Editorials

Editorial Mortality from cardiovascular disease is too high outside capital cities Do we accept this situation or look for ways of changing it? MJA 2000; 172: 360-361 The report by Sexton and Sexton1 in this issue of the Journal updates our knowledge about geographic differences in death rates from cardiovascular disease (CVD) in Australia. Their major finding is that deaths from coronary heart disease (CHD) in 1996 were 30% higher for men and 21% higher for women who live outside our capital cities than for those who live in capital cities. The gap widened over the period of study -- in 1986 the CHD mortality difference (in both men and women) was 13%. The gratifying decline in deaths from CVD over the last number of years has been greater for those who live in capital cities, and this has led to a widening of the geographic gradient in CVD deaths. Of particular concern in the report is that the excess mortality outside capital cities is greater among younger age groups. The demonstration of social and geographic gradients in death rates is not new.2,3 The findings of Sexton and Sexton are disturbing -- what could be the explanation? What can we do about them? There are two reasons for excess CHD deaths -- risk factors among the population and inadequacies in the level of medical care provided. A combination of changes in these factors has been found to be the explanation for the recent decline in CHD deaths seen in Australia.4Sexton and Sexton allude to differences in socioeconomic status between urban and rural areas, which together with higher levels of unemployment outside capital cities may be part of the "explanation" of the higher CHD mortality. Their report does not examine separately death rates in Aboriginal people, and, while these are likely to contribute to the overall picture, Indigenous people constitute too small a proportion of the total population for this to be the whole explanation. Data on risk factor levels are scarce outside capital cities, but some limited data discussed in the report suggest that differences in risk factor levels mirror the excess rural mortality. The strength of the article by Sexton and Sexton is the demonstration of a widening of the mortality gap over time. There have been major changes in the provision of medical care for patients with heart disease between 1986 and 1996, and it seems most appropriate to focus here on the level of healthcare provided in and outside capital cities. The data from Sexton and Sexton do not allow us to distinguish between disease incidence and case fatality, but other data indicate that there are differences in case fatality and in medical care for acute myocardial infarction (AMI) between metropolitan and non-metropolitan hospitals.5,6 There are differences in the types of hospital in and outside capital cities and in the distribution of specialist cardiologists. There is ample evidence that hospital type and size and the speciality of the treating physician are related to the outcome and the practice of evidence-based care for patients with CHD.7-10 A recent report in this Journal found that the evidence-based use of drugs after AMI was lower among doctors in smaller non-metropolitan hospitals in New South Wales.7 It is not beyond credibility to suggest that at least part of the reason for the widening geographic gradient in CHD deaths in Australia is differential levels of care for those with the disease. Rural areas have smaller hospitals and fewer cardiologists (who prefer to have access to investigative facilities, which have become such an important part of their speciality). We must find solutions to the need to practise evidence-based care and prevention throughout the Australian healthcare system, irrespective of access to specialist services and tertiary care facilities. Guidelines and clinical pathways have been promulgated as a response to the demonstration of variations in medical care, and may have an impact on changing patterns of care.11,12 However, the solution to the structural inequalities in the provision of care is likely to be much more complex than the use of these clinical decision aids, especially given the relatively small impact they might be expected to have.12 Do we just accept that people who live outside capital cities in a large country where the population is thinly spread will inevitably have less access to high quality medical care (as they have less access to many other resources such as the arts and retail outlets)? These are fundamental questions about societal expectations. Where is the consumer pressure for change? What is the responsibility of the health professions for the health of the whole of the population, and how is this expressed? A number of these questions were discussed at the recent Federal Government Regional Australia Summit, at which, despite the comment that "There are no easy solutions facing regional Australia", a number of key priorities and proposed strategies were identified.13 For example, two of the key priorities under the health theme are: "Regional, rural and remote communities require improved and expanded access to healthcare services . . ." and "Resource allocation for regional, rural and remote communities must be equitable in terms of health need relative to the urban population." One of the proposed strategies to achieve this latter priority is "A health services plan will be established to set optimal levels of services for communities of different sizes. The Commonwealth Health Department will act as broker for funding to any community which wishes to invoke those benchmarks." Maybe the demonstration of a reduced geographic gradient for CVD deaths could be a future marker of the success of this and other interventions. Richard F Heller Professor of Community Medicine and Clinical Epidemiology Centre for Clinical Epidemiology and Biostatistics Faculty of Medicine and Health Sciences The University of Newcastle, Newcastle, NSW Sexton PT, Sexton T-L H. Excess coronary mortality among Australian men and women living outside the capital city statistical divisions. Med J Aust 2000; 172: 370-374. Taylor R, Chey T, Bauman A, Webster I. Socio-economic, migrant and geographic differentials in coronary heart disease occurrence in New South Wales, Australia. Aust N Z J Public Health 1999; 23: 20-26. Marmot M, Ryff CD, Bumpass LL, et al. Social inequalities in health: next questions and converging evidence. Soc Sci Med 1997; 44: 901-910. Dobson AJ, McElduff P, Heller R, et al. Changing patterns of coronary heart disease in the Hunter Region of New South Wales, Australia. J Clin Epidemiol 1999; 52: 761-771. Huy Dinh Vu, Heller RF, Lim LLY, et al. Hospital mortality after acute myocardial infarction is lower in metropolitan than non-metropolitan regions. J Epidemiol Commun Health. In press. Lim L, O'Connell R, Heller R. Differences in management of heart attack patients between metropolitan and regional hospitals in the Hunter Region of Australia. Aust N Z J Public Health 1999; 23: 61-66. Lim LLY, Heller RF, O'Connell R, D'Este C. Stated and actual management of acute myocardial infarction among different specialties. Med J Aust 2000; 172: 208-212. Chen J, Radford MJ, Wang Y, et al. Do "America's best hospitals" perform better for acute myocardial infarction? N Engl J Med 1999; 340: 286-292. Jollis JG, Delong ER, Peterson ED, et al. Outcome of acute myocardial infarction according to the speciality of the admitting physician. N Engl J Med 1996; 335: 1880-1887. Weitzman S, Cooper L, Chambless L, et al. Gender, racial, and geographic differences in the performance of cardiac diagnostic and therapeutic procedures for hospitalised acute myocardial infarction in four states. Am J Cardiol 1997; 79: 722-726. Kitchiner DJ, Bundred PE. Clinical pathways [editorial]. Med J Aust 1999; 170: 54-55. Gupta L, Ward JE, Hayward RS. Clinical practice guidelines in general practice: a national survey of recall, attitudes and impact. Med J Aust 1997; 166: 69-72. Regional Australia Summit communiquŽ. Presentation of the summit recommendations. <http://www.dotrs.gov.au/regional/summit/communique.htm> (Accessed 23 March 2000). Make a comment

Richard F Heller

Editorial The Bone and Joint Decade: 2000-2010 The United Nations has endorsed a Decade to focus attention on worldwide epidemic of musculoskeletal diseases MJA 2000; 172: 307-308 In January this year, the Bone and Joint Decade was launched in Geneva by the World Health Organization. The Decade was initiated because of the epidemic of musculoskeletal disease that is occurring worldwide as the population ages.1 In late November 1999, the Secretary-General of the United Nations, Kofi Annan, signed the UN Declaration of Support for the Decade. The launch came after almost two years of negotiation by health professionals, led principally by orthopaedic surgeons and rheumatologists. These health professionals garnered support from other musculoskeletal medicine specialists and patient groups. It is hoped that orthodox and complementary practitioners and patient groups involved in musculoskeletal disease and trauma will become involved as the Decade develops. Following the official launch, some 80 delegates from around the world spent three days at the World Health Organization, evaluating the significant burden of musculoskeletal disease on both developed and developing societies. In the WHO/World Bank Global Burden of Disease Project, musculoskeletal conditions represent more than half of all chronic conditions2 and are the most common cause of severe long-term pain and physical disability.3 There is now...evidence that, for chronic rheumatic diseases, something can be done. In Australia, musculoskeletal diseases are the second most common cause of presentations to a general practitioner4 and the third leading cause of health system expenditure, with an estimated total cost of over $3 billion in 1993-19945 (Box). This compares with an estimated total cost of $3.5 billion for circulatory diseases, $2.5 billion for respiratory diseases and $1 billion for endocrine disorders.6Furthermore, in 1993-1994,1 musculoskeletal diseases accounted for nearly 300 000 hospital admissions, nearly 15 million medical services and over 13 million prescriptions.5 Significant disability due to musculoskeletal disease has been noted in more than half of people aged over 65 years,7 and is also commonly self-reported in population samples.8 Indeed, osteoarthritis (the most common form of arthritis) accounts for over 5% of years lost due to disability in Australia.9 What is the Bone and Joint Decade and what is its intended impact? One objective is to create national networks of professional and patient organisations which will establish their own national goals and agendas. The desire is to develop a patient "focus", with individuals living with rheumatic disease being significantly involved in the process. Some 80 countries have established national coordinators, and over 20, including Australia, have endorsed the Decade. The Decade has four major aims: To raise awareness of the growing burden of musculoskeletal disorders on society; To promote prevention of musculoskeletal disorders and empower patients through education campaigns; To advance research on prevention, diagnosis and treatment of musculoskeletal disorders; and To improve diagnosis and treatment of musculoskeletal disorders. Groups such as the Arthritis Foundation of Australia, the Australian Rheumatology Association and the Australian Orthopaedic Association are already actively pursuing some of these aims and will play major roles in developing activities for the Decade in Australia. Although one focus of the Decade may well be on the aged and diseases causing disability (eg, osteoporosis, osteoarthritis and back pain), the Decade will also address the increasing problem of musculoskeletal trauma. This is of particular relevance to young populations in both developed and developing countries. Much more information is needed on the epidemiology of trauma, risk factors, ways of minimising damage to tissues after trauma, and strategies to enhance rehabilitation. The recently advertised National Health and Medical Research Council Trauma Research Partnerships will be helpful in this regard. The past decade has seen enormously exciting advances in the management of osteoporosis and in our understanding of the basic mechanisms of inflammation, which produces so much pain and disability in diseases such as rheumatoid arthritis. These advances include an understanding of the role of genetic markers in osteoporosis, elucidation of risk factors for falls and subsequent fractures, and development of the bisphosphonates. More recently, exciting advances have occurred in the therapeutics of musculoskeletal diseases, previously little changed for decades. These include the development of monoclonal antibodies to substances such as tumour necrosis factor, new specific antirheumatic drugs, and the cyclooxygenase-2 (COX-2) specific inhibitors, which have the potential to reduce pain and inflammation without major gastrointestinal adverse reactions. Musculoskeletal surgery, particularly joint replacement, has revolutionised the lives of many elderly (and some younger) Australians. Hip and knee replacements are among the most cost-effective interventions in medicine, comparing favourably to coronary bypass surgery and renal dialysis,10 and very significantly improve the quality of life in patients with a variety of rheumatic diseases.11 In addition, data suggesting that osteoarthritis of the knee is related to obesity and can be alleviated to some extent by weight reduction present a cogent argument for primary prevention.12 Many musculoskeletal conditions produce chronic pain, which itself strongly contributes to disability and decreased quality of life. Strategies to address chronic musculoskeletal pain will also be a priority of the Decade. The hope is that the Bone and Joint Decade will focus attention on these important diseases, demonstrating to healthcare providers that a relatively modest investment can produce significant benefits. The Bone and Joint Decade will try to bring together these important strands of research, education and service to improve the lot of the millions of Australians who suffer each week from a rheumatic condition. A meeting of professional groups, patients and patient organisations and healthcare providers will shortly be convened to begin planning for the Decade in Australia. The 1990s were designated the Decade of the Brain, and spawned enormous interest around the world in the neurosciences, which is now starting to have significant spin-offs in treatment. It should be remembered that that Decade began with a significant financial investment from the United States Congress, while the Bone and Joint Decade has had no such funding as yet. This week is National Arthritis Week and professional and patient groups around Australia will focus attention on these important chronic and disabling diseases and their impact on society. They should proceed in the knowledge that there is now a considerable groundswell of energy worldwide and evidence that, for chronic rheumatic diseases, something can be done. Peter M Brooks Executive Dean, Health Sciences University of Queensland, Brisbane, QLD John A L Hart Clinical Associate Professor of Surgery Monash University, Melbourne, VIC and Australian Coordinator of the Bone and Joint Decade Hazes JM, Woolf AD. The bone and joint decade 2000-2010. J Rheumatol 2000; 27: 1-3. Dieppe P. Osteoarthritis. Acta Orthop Scand Suppl 1998; 281: 2-5. Murray JL, Lopez AD, editors. The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Cambridge, Mass: Harvard University Press, 1996. Britt H, Sayer GP, Miller GC, et al. General practice activity in Australia 1998-1999. Canberra, ACT: Australian Institute of Health and Welfare, 1999. AIHW Cat No. GEP 2. Mathers C, Penn R. Health system costs of injury, poisoning and musculo-skeletal disorders in Australia 1993-94. Canberra: Australian Institute of Health and Welfare, 1999. AIHW Cat No. HWE 12 (Health and Welfare Expenditure Series No. 6). Mathers C. Burden of disease and health system costs of heart disease, depression and back problems in Australia. Presented at the National Health and Medical Research Council National Forum. Canberra; 24 Mar 1998. March LM, Brnabic AJM, Skinner JC, et al. Musculoskeletal disability among elderly people in the community. Med J Aust 1998; 168: 439-442. Hill CL, Parsons J, Taylor A, Leach G. Health related quality of life in a population sample with arthritis. J Rheumatol 1999; 26: 2029-2035. Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. Canberra: Australian Institute of Health and Welfare, 1999. AIHW cat. no. PHE 17. Liang MH, Cullen KE, Larson MG, et al. Cost effectiveness of total joint arthroplasty in osteoarthritis. Arthritis Rheum 1986; 29: 937-943. March LM, Cross MJ, Lapsley H, et al. Outcomes after hip or knee replacement surgery for osteoarthritis. A prospective cohort study comparing patients' quality of life before and after surgery with age-related population norms. Med J Aust 1999; 171: 235-238. Hart DJ, Spector TD. The relationship of obesity, fat distribution and osteoarthritis in women in the general population. The Chingford Study. J Rheumatol 1993; 20: 331-335. Make a comment Back to text

Peter M Brooks

Editorial Routine antenatal screening: a need to evaluate Australian practice Are current screening practices evidence-based and cost effective? MJA 2000; 172: 311-312 Screening is defined as a procedure to identify, in an organised way, a specified disease or condition among asymptomatic individuals.1 Before introducing a screening test into pregnancy care, it is imperative that the following criteria be met: there is detailed knowledge of the effect of the condition on both the pregnant mother and her fetus; a highly accurate and specific diagnostic test is readily available to make the definitive diagnosis; the condition is a significant health problem; the test and any actions based on its results are ethically acceptable to the community; and increasingly important in the current climate of restricted healthcare funding, the economic implications of either performing or not performing the test have been evaluated. As in many areas of medical practice, various screening tests have been introduced into obstetric practice without being evaluated according to these criteria, while others which might satisfy the criteria are not widely used. Antenatal screening tests currently recommended by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) are shown in the Box. In 1997, I surveyed use of a selection of these tests at the 11 hospitals then belonging to Women's Hospitals Australia (an Australian and New Zealand organisation which represents major women's hospitals; almost a quarter of Australian babies are cared for in member hospitals). This survey revealed that, although all 11 hospitals routinely undertook a blood group and antibody screen, full blood count, tests for rubella antibody status and syphilis serology, and a second-trimester ultrasound examination, use of other tests was more variable. Tests for hepatitis B serology were routine at nine hospitals, urine microscopy and culture at four, measurement of serum α-fetoprotein level at two, and the triple test for Down's syndrome at one. The survey also revealed considerable variation in screening for gestational diabetes: six of the 11 hospitals screened all women, while the others selectively screened women with perceived risk factors (eg, maternal age over 30 years, family history of diabetes, poor obstetric history, maternal obesity, and ethnic group with high prevalence of diabetes). The RANZCOG does not recommend routine screening of all pregnant women for gestational diabetes, contrary to the guidelines of the Australasian Diabetes in Pregnancy Society.3 The place of screening for gestational diabetes and the criteria for its diagnosis are the subject of an international, multicentre project funded by the National Institutes of Health (US) -- HAPO (Hyperglycemia and Adverse Pregnancy Outcome). This should be completed in four years. The low rate of screening for asymptomatic bacteriuria (also not recommended as a routine test by the RANZCOG2) is at variance with the recommendations of Rouse based on his analysis of published studies.4 He reported that, of the 2%-10% of pregnant women who have asymptomatic bacteriuria, 30% will develop acute and potentially serious infections. He concluded that screening and treatment prevents symptomatic infection and is cost effective. Screening later in pregnancy for maternal carriage of group B streptococci (GBS) is also controversial. In this issue of the Journal, Connellan and Wallace describe the variation in GBS screening practices in Victoria.5 They recommend development of consensus practice guidelines to help prevent early-onset GBS disease in neonates (EOGBSD). Such guidelines have been developed in Queensland after a systematic review of the literature and a large Brisbane case-controlled study.6 The recommended strategy is not to perform routine antenatal screening but to consider administering intrapartum antibiotics for defined risk factors (preterm birth before 35 weeks' gestation; membranes ruptured for > 18 hours before delivery; maternal temperature ≥ 38ºC; GBS colonisation or GBS bacteriuria ever detected; or previous infant with EOGBSD) (Professor James King, Mater Perinatal Epidemiology Unit, Mater Misericordiae Mothers' Hospital, Brisbane, Qld, personal communication). The implementation of these evidence-based clinical guidelines is now being evaluated. This process could serve as a template for the evaluation and development of guidelines for all antenatal screening tests. Routine screening for HIV is now recommended by the RANZCOG,2 but most units do not comply with this directive -- in 1995, only 20% of pregnant women were so screened.7 The need to revise current policies, especially as antiretroviral drug therapy can reduce the risk of HIV transmission from mother to child from 30% to below 2%,8 was recently reviewed by Ziegler.9 In addition, calls for routine screening of thyroid function have followed publication of a study that found long-term developmental abnormalities in the offspring of women with even mild degrees of untreated hypothyroidism.10 The prevalence of undiagnosed hypothyroidism was 1.9 per 1000, and the offspring had a mean score on the Wechsler Intelligence Scale for Children four points lower than matched control children. To identify each at-risk fetus, 500 pregnant women would need to be tested. Again, this emphasises the pressing need for full analysis of the clinical and economic implications of such tests before they enter clinical practice. Australia is not alone in the variation in screening practice. In a recent survey of obstetric centres in the United Kingdom, only 24% of births occurred in units with a universal testing policy for hepatitis B.11 Conversely, universal screening for syphilis was the norm, although a number of centres were considering dropping this policy.11 There is a paucity of accurate data on the cost of current antenatal screening practices to the Australian community. However, the economic impact is sure to be substantial. In 1997, 252 370 women gave birth in Australia.12 If the RANZCOG screening recommendations were followed for all, then, based on the Medicare schedule fee structure, the annual cost would be around $48 million for routine haematological, serological, biochemical and cytological screening, and an additional $17 million for the triple test and hepatitis C serology. Furthermore, in 1996-1997, Medicare benefits in excess of $33 million were paid for ultrasound examinations in pregnancy.13 Yates et al estimated in 1991 and 1992 that 97% of pregnant women had at least one ultrasound scan, and that 46% had two or more.14 It is not possible to calculate the cost of "routine screening" scans from these data. However, if all pregnant women have a second-trimester scan, the cost to Medicare is $25.5 million annually, with the cost to the community likely to be higher, as many scans are billed at rates above the Medicare schedule fee. The introduction of first-trimester ultrasound scans of nuchal translucency, which identify up to 85% of fetuses with Down's syndrome15 and, potentially, fetuses with an increased risk of other structural abnormalities, including cardiac defects, will inevitably increase the number of routine ultrasound examinations. However, as these scans also identify fetuses with a low probability of Down's syndrome, they have the potential to reduce the numbers of chorionic villus samplings and amniocenteses performed in women with a high theoretical risk of trisomy 21. In addition, improvements in ultrasound resolution and our understanding of the markers of fetal anomalies may allow this late first-trimester scan to replace the second-trimester scan. Although antenatal screening appears well accepted as a significant healthcare issue in Australia, it has not been subject to systematic assessment. The need for funding to critically evaluate all currently used tests seems self-evident. However, currently such funding has not been granted by the Commonwealth or State governments or Medicare, who carry the major financial burden for antenatal testing. The potential to redirect some of the healthcare dollar to other, needier areas is a further reason for appropriate funding to establish practitioner-credible, evidence-based practice. Jeremy J N Oats Director of Obstetrics and Gynaecology, Mater Misericordiae Mothers' Hospital, Clinical Professor of Obstetrics and Gynaecology University of Queensland, Brisbane, QLD joatsATmater.org.au Reprints: Professor J N Oats, Department of Obstetrics and Gynaecology, Mater Misericordiae Mothers' Hospital, Raymond Terrace, South Brisbane, QLD 4101. Peters TJ, Wildschut HIJ, Weiner CP. Epidemiologic considerations in screening. In: Wildschut HIJ, Weiner CP, Peters TJ, editors. When to screen in obstetrics and gynecology. London: WB Saunders, 1996: 1. Royal Australian and New Zealand College of Obstetricians and Gynaecologists Statements. 2.2. Screening in pregnancy. <http://www.ranzcog.edu.au/open/ statements/2_2.htm> Hoffman L, Nolan C, Wilson JD, et al. Gestational diabetes mellitus -- management guidelines. The Australian Diabetes in Pregnancy Society. Med J Aust 1998; 169: 93-97. Rouse DJ. Asymptomatic bacteriuria in pregnancy. In: Wildschut HIJ, Weiner CP, Peters TJ, editors. When to screen in obstetrics and gynecology. London: WB Saunders, 1996: 163-169. Connellan M, Wallace EM. Prevention of perinatal group B streptococcal disease: screening practice in public hospitals in Victoria. Med J Aust 2000; 172: 317-320. Flenady V, King J, Woodgate P, et al. Early onset neonatal GBS sepsis: a case controlled study. Proceedings of the 2nd Annual Congress of the Perinatal Society of Australia and New Zealand. Alice Springs, NT. 29 Mar-1 Apr 1998. Sydney: PSANZ, 1998. Elford J, MacDonald MA, Gabb RG, et al. Antenatal HIV antibody screening in Australia. Med J Aust 1995; 163: 183-185. Riley LE, Greene MF. Elective cesarean delivery to reduce the transmission of HIV. N Engl J Med 1999; 340: 1032-1033. Ziegler JB. Antenatal screening for HIV in Australia: time to revise policies? Med J Aust 1999; 171: 201-203. Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999; 341: 549-555. Newell M-L, Thorne C, Pembrey L, et al. Antenatal screening for hepatitis B infection and syphilis in the UK. Br J Obstet Gynaecol 1999; 106: 66-71. Day P, Sullivan EA, Ford J, et al. Australia's mothers and babies 1997. Perinatal Statistics Series No 9. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit 1999; 7. (AIHW Cat No PER 12.) Simes J. Diagnostic ultrasound: discussion paper. Presented at the Forum on Ultrasound. Sydney; 13-14 June 1998. Canberra: Australian Health Technology Advisory Committee, 1998: 41. Yates JM, Lumley J, Bell RJ. The prevalence and timing of obstetric ultrasound in Victoria 1991-1992: a population-based study. Aust N Z J Obstet Gynaecol 1995; 35: 375-379. Hyett JA, Perdu M, Sharland GK, et al. Increased nuchal translucency at 10-14 weeks of gestation as a marker for major cardiac defects. Ultrasound Obstet Gynecol 1997; 10: 242-246. Make a comment Current recommendations on antenatal screening by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists2 At the first antenatal visit, tests should be offered for: blood group and antibody screen; full blood count; rubella antibody status; syphilis serology; hepatitis B serology hepatitis C serology (if significant risk); HIV serology; and cervical cytology. In addition, the doctor should discuss: the availability of maternal serum screening for Down's syndrome ultrasound examination at 18-20 weeks' gestation Back to text

A recent draft proposal for revising the Declaration has provoked heated controversy The World Medical Association (WMA) Declaration of Helsinki1 is regarded internationally as the pillar of ethical standards for biomedical research involving humans. In 1997, the American Medical Association presented a draft proposal to the WMA to update the Declaration to bring it more into line with contemporary ethical thinking,2-4 whereupon the WMA began the current process of revising the Declaration. Since 1964, the Declaration has evolved from a relatively broad set of ethical principles to a more defined, prescriptive set of guidelines, but it is extremely difficult to obtain global consensus on the Declaration because perceptions and ethical standards are not universal. ... we must determine just how the Declaration can remain relevant in the current biomedical research environment... Ethical standards are a product of cultural, linguistic, moral, religious, and social considerations; hence, many nations develop their own ethical guidelines for biomedical research -- for example, the National statement on ethical conduct in research involving humans,5 released recently by Australia's National Health and Medical Research Council. In June 1999, the WMA circulated a draft Proposed Revision of the Declaration of Helsinki6 to all National Medical Associations (NMAs). An international outcry ensued over the proposed amendments to issues such as informed consent, access to healthcare, placebo use, and publications (see Box).8-10 Some argued that the Proposed Revision established a model for human biomedical research ethics that encouraged utility and efficiency at the expense of patient autonomy and wellbeing.9 Those who defended the amendments said they were more in line with contemporary ethical thinking and did not impose unnecessarily stringent standards of practice.11 In this issue of the Journal, Loff and Black discuss some of the complexities associated with this debate and raise further questions.13 As a result of the lack of consensus between NMAs on the Proposed Revision, the WMA decided, at its General Assembly in October 1999, to develop a new draft revised Declaration in consultation with the public and WMA members.14 The difficulties imposed by the Declaration's prescriptive model are exemplified in the proposed amendments to placebo use (see Box). Robert Levine, Professor of Internal Medicine at Yale University School of Medicine, argues that the current Declaration's restrictions on placebo use, if taken literally, not only rule out the development of all new treatments other than for those diseases without a proven therapeutic treatment, but also forbid the use of a placebo when a standard therapy exists.11 Levine asserts that the current Declaration incorporates overly stringent ethical standards that needlessly impede biomedical research. However, a literal interpretation of the Proposed Revision's approach to placebo use gives cause for alarm. It proposed to change the standard from not allowing placebo use where a proven therapy exists to freely allowing placebo use as long as participants do not die or become disabled as a result.8 In so doing, it failed to recognise other adverse health effects that could arise from placebo use, such as pain, discomfort, or psychological stress, which might constitute unacceptable risks of the treatment. Indeed, even the perception of an "acceptable risk" in biomedical research finds little uniformity.8,15 The WMA should take heart from the fact that the Declaration of Helsinki can still provoke such strong passion and emotion almost 40 years after its adoption. The recent controversy is a true testament to just how important the Declaration is to those with a vested interest in biomedical research. As we head into the new century, we must determine just how the Declaration can remain relevant in the current biomedical research environment while not diminishing the fundamental ethical principles surrounding patient autonomy and wellbeing. Alternatives do exist to following the prescriptive model. A recent workshop on revising the Declaration of Helsinki, held by the Royal Society of Medicine, London,16,17 presented a reasonable alternative to pursuing the prescriptive approach: The Declaration should not be rewritten; The Declaration should remain a slim set of principles, not regulations, that could remain unchanged for a long time; and Guidance on such issues as informed consent could be addressed in accompanying commentaries which could easily be revised while leaving the Declaration intact.17 By using this or a similar alternative, the Declaration of Helsinki will not be further denigrated in the way it has been over the past year, and will continue to prevail as the definitive statement of ethical principles in human biomedical research. Kate Stockhausen Senior Research Officer, Health Services Australian Medical Association Federal Secretariat Canberra, ACT World Medical Association Declaration of Helsinki as adopted by the 18th World Medical Assembly, Helsinki, Finland, June 1964. American Medical Association. Proposed Revision of the World Medical Association Declaration of Helsinki. Ferney-Voltaire, France: World Medical Association, 1997. (WMA document 17. CRev/97/A). American Medical Association. Background comments and text comparison aid for the proposed draft of the World Medical Association Declaration of Helsinki - recommendations guiding physicians and other investigators in biomedical research involving human subjects. Ferney-Voltaire, France: World Medical Association, 1997. (WMA document 17. CRev/97/B). Crawley F, Hoet J. Ethics and law: the Declaration of Helsinki under discussion. Bull Med Ethics Aug 1999: 9-12. National Health and Medical Research Council. National statement on ethical conduct in research involving humans. Canberra: Commonwealth of Australia, 1999. (Available from AusInfo government bookshops.) Medical Ethics Committee of the World Medical Association. Proposed Revision of the World Medical Association Declaration of Helsinki. Ferney-Voltaire, France: World Medical Association, 1999. (WMA document 17. C/Rev1/99). World Medical Association Declaration of Helsinki as amended by the 48th General Assembly, Somerset West, Republic of South Africa, October 1996. Australian Medical Association. AMA submission on the Proposed Revision of the World Medical Association Declaration of Helsinki (WMA document 17. C/Rev1/99). Canberra: Australian Medical Association, 1999. (Available from AMA, PO Box E115, Kingston, ACT 2604.) Brennan TA. Proposed revisions to the Declaration of Helsinki - will they weaken the ethical principles underlying human research? N Engl J Med 1999; 341: 527-531. Lurie P, Wolfe SM. Letter to Dr Delon Human, World Medical Association, on Helsinki Principles. Distributed by Public Citizen, Washington DC, March 1999. Levine RJ. The need to revise the Declaration of Helsinki. N Engl J Med 1999; 341: 531-534. Stockhausen K. Ethical hazards in new Declaration of Helsinki. Aust Med Aug 1999; 11: 10-11. Loff B, Black J. The Declaration of Helsinki and research in vulnerable populations. Med J Aust 2000; 172: 292-295. Summary minutes of the 51st WMA General Assembly, Tel Aviv, Israel, October 1999. Woodward B. Challenges to human subject protections in US medical research. JAMA 1999; 282: 1947-1952. Bulletin of Medical Ethics, European Forum for Good Clinical Practice. The 150th issue devoted to a workshop on revising the Declaration of Helsinki: a fresh start. Bull Med Ethics Aug 1999; 150. Report of a Workshop held at the Royal Society of Medicine, London. Revising the Declaration of Helsinki: a fresh start. Bull Med Ethics Oct 1999; 151: 13-17. Some controversial issues raised by the draft Proposed Revision of the Declaration of Helsinki (17. C/Rev1/99)6 Documentation of informed consent Article I.9 of the current Declaration states that a physician should "obtain a patient's freely-given informed consent, preferably in writing".7 Article 24 of the Proposed Revision introduces a waiver of written consent "when the research involves only slight risk or when the procedures to be used are customarily used in the practice of medicine without documentation of consent".6 Benefit of the amendment The amendment could reduce the time and effort needed to obtain written documentation of consent from every research participant. Objection to the amendment It allows a great deal of leeway to waive written consent based on subjective standards such as risk.8-10 It also fails to recognise that research is inherently different from clinical practice and research participants require specific protection that may not be required in clinical practice.10 Access to health care Article II.3 of the current Declaration states that "every patient - including those of a control group, if any - should be assured of the best proven diagnostic and therapeutic method".7 Article 18 of the Proposed Revision states that "every patient should be assured of the best proven diagnostic, prophylactic or therapeutic method that would otherwise be available to him or her" (emphasis added).6 Benefit of the amendment It may be economically and logistically unfeasible for a researcher to provide the same standard of health care found in an industrialised nation to participants in a developing nation (as required by the current Declaration). The amendment would allow research sponsors in industrialised countries to help developing countries establish affordable treatments and preventive interventions for debilitating diseases, eg HIV/AIDS. 11 Objection to the amendment It diminishes the researcher's moral and ethical commitment to protecting the patient's well-being.8-10 For economically disadvantaged individuals, the local standard of health care may be nothing; thus, providing an economic incentive to conduct biomedical research in economically disadvantaged areas and exploiting particular groups of research participants for commercial benefit.8-10,12 Placebo use and risk Article II.3 of the current Declaration states that "in any medical study, every patient - including those of a control group, if any - should be assured of the best proven diagnostic and therapeutic method. This does not exclude the use of inert placebo in studies where no proven diagnostic or therapeutic method exists."7 Article 19 of the Proposed Revision states that "when the outcome measures are neither death nor disability, placebo or other no-treatment controls may be justified on the basis of their efficiency".6 Benefit of the amendment In certain circumstances, it permits placebo use even when a standard therapy already exists. This allows researchers to trial new and improved treatments in a more efficient, cost-effective manner.11 Objection to the amendment In freely allowing placebo use as long as participants do not die or become disabled, it fails to recognise other adverse health effects that could arise from placebo use, such as pain, discomfort or psychological stress.8

Kate Stockhausen

Long-acting testosterone/progestin combinations show great promise as contraceptives Any suggestion that men cannot be trusted with contraceptive responsibility ignores the widespread use of existing methods which involve their cooperation -- condoms, periodic abstinence and interrupted intercourse are used by millions of couples worldwide.1 For those wanting an alternative to these methods, only female contraceptive methods, permanent sterilisation or "natural" methods have been available. A wider choice of effective methods would be highly desirable, and male hormonal contraception (MHC) is likely to offer a reliable alternative in the near future. Male hormonal contraception The physiological principles of MHC have long been recognised, but the past 20 years have seen important research in this area, notably that sponsored by the World Health Organization (WHO). Real evidence for MHC effectiveness has been provided from trials involving 600 couples in 10 countries, including Australia.2,3All MHC strategies involve the administration of testosterone, which profoundly reduces serum gonadotropin (follicle-stimulating hormone [FSH] and luteinising hormone [LH]) levels.4 A reduced serum LH level markedly reduces intratesticular testosterone levels, which, in combination with a reduced serum FSH level, reversibly interrupts sperm production. (Following cessation of testosterone treatment, sperm counts return to pretreatment levels in 4-6 months.) In the WHO trials, two-thirds of men were rendered azoospermic (ie, having sperm counts of zero), while 91% of the men achieved sperm counts below 1 x 106/mL (normal value, > 20 x 106/mL).3 The pharmaceutical industry has not been active in the MHC area in the past, perhaps because of a belief that the potential market was small, or because of concerns about product litigation. Very recently, the industry has cautiously entered the area. Fortuitously for MHC development, current pharmaceutical interest in new types of androgen replacement therapies will assist this process. Marketing male hormonal contraceptives Key factors to consider in planning a marketing strategy for male hormonal contraceptives are contraceptive effectiveness, acceptability and safety. Contraceptive effectiveness. No contraceptive is 100% effective. For the female contraceptive pill the failure rate is approximately 3 conceptions per 100 person-years in the first year of use, a figure which represents a reasonable target comparator for MHC. The WHO study showed that azoospermia confers high contraceptive cover (0.8 conceptions/100 person-years; 95% CI, 0.02-4.5).2 While azoospermia continues to be the goal, the WHO data suggest that the suppression of sperm counts to very low levels (eg, less than 1 x 106/mL) may provide contraceptive cover comparable to that of the female contraceptive pill, and would almost certainly be superior to other widely used methods such as condoms.3 No pretreatment marker predicts whether an individual will attain azoospermia using MHC. Apart from interracial variation (eg, 98% of Chinese men become azoospermic2,3), there appear to be no differences in serum gonadotropin or testosterone levels, or in testosterone pharmacokinetics, between those who become azoospermic and those who do not.5 Some data suggest that men in whom sperm production is not fully suppressed have a higher level of 5a-reductase enzyme activity, which converts testosterone to the potent androgen metabolite dihydrotestosterone and thus maintains spermatogenesis.6 Understanding the variability of response to MHC is important in formulating regimens which produce the highest rates of azoospermia. Acceptability. Men's willingness to use MHC will depend upon its effectiveness, convenience of use and side effect profile. Methods which are painful, costly, or inconvenient, or which require extensive monitoring or interfere with sexual function or general health, will be declined or soon discarded. Current MHC treatments encounter problems in this area, particularly the need for frequent testosterone injections (every 1-2 weeks) or testosterone implants (every 4-6 months). Supraphysiological doses of testosterone given by intramuscular injection in the WHO studies led to androgenic side effects (acne, mood change) in 21% of men,2,3 but more physiological testosterone levels achieved with implants can reduce these problems.7 Safety. The effects of male hormonal contraceptives on prostate and cardiovascular health are of prime concern in assessing the safety of MHC. So far, prostate problems have not been encountered in MHC trials of up to 18 months' duration. Furthermore, there is no evidence for the induction or acceleration of benign or malignant prostate disease with androgen replacement therapy in hypogonadal men. A fall of around 15% in HDL-cholesterol levels was observed in MHC trials using injectable testosterone;8,9 however, these changes were not seen with the more physiological profile of testosterone delivery via implants.7 Such physiological androgen delivery should reduce androgenic side effects (eg, polycythaemia) associated with intramuscular testosterone replacement, while maintaining libido and sexual function. MHC using combined preparations Testosterone treatment alone will not reliably suppress sperm production to the point of azoospermia. The addition of a gonadotropin-releasing hormone antagonist to testosterone treatment effectively suppresses sperm production,4 but practical difficulties and expense make this a non-viable option. The combination of testosterone and a progestin promotes rapid and profound suppression of serum gonadotropins and sperm counts, and the search for the ideal testosterone-plus-progestin regimen is now the main focus of MHC research. Recent studies have used levonorgestrel,8 desogestrel and medroxyprogesterone acetate.7 One study using cyproterone acetate, an antiandrogenic progestin, produced azoospermia very rapidly and consistently.10 It was proposed that the efficacy of cyproterone acetate was due to its inhibition of testosterone action within the testis (which has a unique need for high testosterone levels) while not interfering with androgen action elsewhere in the body. The question of whether the progestin component of combined male hormonal contraceptives may have specific effects (eg, mood change) in some men requires further study. Delivery methods Delivery methods providing stable physiological levels of testosterone are critical to male hormonal contraceptive development. Delivery could be either oral or by infrequent injection or implants (the latter perhaps being preferable, to assist with compliance). In this area, there is renewed interest from the pharmaceutical industry to work collaboratively with clinical scientists. Testosterone undecanoate or buciclate are esters which are slowly absorbed from intramuscular injection sites and provide testosterone delivery for 2-3 months. Methylnortestosterone is a more potent androgen than testosterone (reducing the mass of steroid to be delivered),11 and, furthermore, its 5a-reduced metabolite is inactive and thus avoids stimulation of the prostate. Finally, our improved knowledge of steroid ligand/receptor interaction may permit the synthesis of a single agent which activates both androgen and progestin receptors in the male, thereby providing gonadotropin suppression within the testis while maintaining androgen activity elsewhere in the body. Conclusions The combination of testosterone and progestin, delivered in the form of a single long-acting injection, shows great promise for providing equally effective (or better) contraception than current widely used male contraception methods. Large and long-term MHC trials are needed to establish the optimal formulations, to provide essential safety and efficacy data, and to spur the interest of industry, which is essential in bringing these products to the market. Robert I McLachlan Associate Professor and Principal Research Fellow Prince Henry's Institute of Medical Research Monash Medical Centre, Clayton, VIC Handelsman DJ. Contraception in the male. In: DeGroot LJ, editor. Endocrinology. 3rd edition. Philadelphia: WB Saunders, 1995: 2449-2458. World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia in normal men. Lancet 1990; 336: 955-959. World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia and oligozoospermia in normal men. Fertil Steril 1996; 65: 821-829. Amory JK, Bremner WJ. The use of testosterone as a male contraceptive. Baillieres Clin Endocrinol Metab 1998; 12: 471-484. Handelsman DJ, Farley TMM, Peregoudov A, et al. World Health Organization Task Force on Methods for the Regulation of Male Fertility. Factors in non-uniform induction of azoospermia by testosterone enanthate in normal men. Fertil Steril 1995; 63: 125-133. Anderson RA, Wallace AM, Wu FCW. Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. III. Higher 5a-reductase activity in oligozoospermic men administered supraphysiological doses of testosterone. J Clin Endocrinol Metab 1996; 81: 902-908. Handelsman DJ, Conway AJ, Howe CJ, et al. Establishing the minimum effective dose and additive effects of depot progestin in suppression of human spermatogenesis by a testosterone depot. J Clin Endocrinol Metab 1996; 81: 4113-4121. Wu FCW, Farley TMM, Peregoudov A, et al. Effects of testosterone enanthate in normal men: experience from a multicentre contraceptive efficacy study. Fertil Steril 1996; 65: 626-636. Bebb RA, Anawalt BD, Christensen RB, et al. A promising male contraceptive approach: combined administration of testosterone and levonorgestrel. J Clin Endocrinol Metab 1996; 81: 757-762. Meriggiola MC, Bremner WJ, Paulsen CA, et al. Cyproterone acetate and testosterone enanthate as a potentially highly effective male contraceptive. J Clin Endocrinol Metab 1996, 81: 3018-3023. Noe G, Suvisaari J, Martin C, et al. Gonadotropin and testosterone suppression by 7α-methyl-19-nortestosterone acetate administered by subdermal implant to healthy men. Hum Reprod 1999, 14: 2200-2206.

Robert I McLachlan

Editorial Breast cancer guidelines in action The challenge is to develop and sustain audit programs on an ongoing basis MJA 2000; 172: 196-197 In 1995, when the National Health and Medical Research Council (NHMRC) released Clinical practice guidelines for the management of early breast cancer,1 the first of their evidence-based recommendations, the initial response by clinicians was very positive: 97% regarded them as a good summary of recent evidence and 85% believed they would be useful in improving management.2This was encouraging, but the more important question was whether the guidelines would result in evidence-based care for women with breast cancer. Until recently, there has been little national information about breast cancer management in Australia, a lack noted by the House of Representatives in 1995, whose response was to recommend a comprehensive national monitoring system.3 However, it was not until 1999 that an accurate national picture of breast cancer management emerged. A report by the NHMRC National Breast Cancer Centre,4 analysing the surgical management of 4237 women with breast cancer in 1995 (ie, 88% of all women in Australia diagnosed with breast cancer in the six months before release of the guidelines), showed that, at that time, most women were receiving care in accord with most of the recommendations. However, some aspects of care were not in line with the guidelines: for example, the report highlighted the need to encourage the use of tamoxifen in women with oestrogen receptor positive tumours (particularly in women less than 50 years); to decrease rates of testing for distant metastases at the time of diagnosis of early breast cancer; and to increase participation in clinical trials. Progress will occur only if other local groups also see value in promoting evidence as their mast-head and recognising the fundamental role of audit in evidence-based treatment Information about current practice plays a key role in supporting evidence-based care. It enables the best use of scarce resources, as costly implementation strategies can be targeted at aspects of care not in accord with the recommendations. The process of audit itself is also effective in changing practice, particularly if individual clinicians can compare their own practice with evidence-based recommendations or with the practice of their peers.5,6 In this context, the article in this issue of the Journal by Craft et al 7 is of considerable significance, as it demonstrates the feasibility of a community-based audit of breast cancer management by a multidisciplinary team (the Australian Capital Territory and South Eastern New South Wales [ACT and SE NSW] Breast Cancer Treatment Group). The Group is to be commended both for its meticulous approach to encouraging evidence-based care through local audit and for the high standards of care provided. The results presented by Craft et al7 suggest that more women than in the national survey were managed in accordance with the NHMRC guidelines. For example, in the national data, 85% of women with breast-conserving therapy received radiotherapy, compared with 98% of the sample studied by Craft et al, and all women in the sample aged under 50 with axillary node involvement received adjuvant chemotherapy. We do not know, of course, to what extent these results can be generalised to the 21% of cases occurring in the region and not included in the audit. Although these differences may show an embracing of the guidelines since their release, it is unclear whether these changes would be apparent across Australia or whether they are due to intensive efforts within the ACT and SE NSW region. However, an audit conducted in a surgical practice in Echuca, a rural town in Victoria, also demonstrated patterns of care generally in accordance with the guidelines.8 The report by Craft et al also shows the role of local ownership of guidelines and a multidisciplinary team approach to management. The ACT and SE NSW Breast Cancer Treatment Group was formed to consider priorities within the region and to select indicators of local significance for inclusion in their audit. Consumer input was included. Further, the audit was not limited to one institution, but attempted to include all clinicians, including potentially more isolated clinicians in the region, making it more likely to have an impact on outcomes. The strategies used by the Group appear to have been successful, with 23 of 24 clinicians participating and the identification of an estimated 79% of all cases of breast cancer occurring in the region. There is some evidence that a multidisciplinary team approach is more likely to result in evidence-based care and better patient outcomes than clinicians working in isolation.9,10 Recent initiatives within Australia are designed to foster multidisciplinary care, including Victoria's Breast Care Enhancement Program and the federally funded National Multidisciplinary Care Demonstration Project coordinated by the National Breast Cancer Centre. After Craft et al's conclusive demonstration of the value of local audit, the challenge now is to develop and sustain other audit programs on a continuing basis. There is a real danger that the evidence-based approach will founder from a lack of resources for guideline implementation at the local level and for support of audit programs. A commitment from State and local health services to resourcing these programs is vital. The recent initiative by the Royal Australasian College of Surgeons in developing an audit system for breast cancer should prove particularly valuable in future assessment of guideline adherence. The audit is national and provides contributing surgeons with feedback about their practice compared with that of their peers. There are also benefits to daily clinical practice: the audit provides a standardised record, which can be used in patient notes or to inform general practitioners or patients. Apart from surgery, other disciplines are also considering developing similar approaches to audit in breast cancer, notably the Royal Australian and New Zealand College of Radiologists (Faculty of Radiation Oncology) and the Medical Oncology Group, all in association with the National Breast Cancer Centre. Progress will occur only if other local groups also see value in promoting evidence as their masthead and recognising the fundamental role of audit in evidence-based treatment. In demonstrating the feasibility of this approach, the achievement of the ACT and SE NSW Breast Cancer Treatment Group could serve as a model for other regions. Sally Redman Director, NHMRC National Breast Cancer Centre, Sydney, NSW Tom S Reeve Executive Officer, Australian Cancer Network, Sydney, NSW National Health and Medical Research Council. The management of early breast cancer. Clinical Practice Guidelines. Canberra: NHMRC/AGPS, 1995. Carrick S, Bonevski B, Redman S, et al. Surgeons' opinion about the NHMRC clinical practice guidelines for the management of early breast cancer. Med J Aust 1998; 169: 300-305. House of Representatives Standing Committee on Community Affairs. Report on the management and treatment of breast cancer in Australia. Canberra: AGPS, 1995. Hill D, Jamrozik K, White V, et al. Surgical management of breast cancer in Australia in 1995. Sydney: NHMRC National Breast Cancer Centre; 1999. Thomson MA, Oxman AD, Davis DA, et al. Audit and feedback to improve health professional practice and health care outcomes (Parts I and II) (Cochrane Review). Oxford: The Cochrane Library 1999: Issue 1. NHS Centre for Reviews and Dissemination, University of York. Getting evidence into practice. Effective Health Care 1999; 5(1). Craft PS, Zhang Y, Brogan J, et al, and the Australian Capital Territory and South Eastern New South Wales Breast Cancer Treatment Group. Implementing clinical practice guidelines: a community-based audit of breast cancer treatment. Med J Aust 1999; 172: 213-216. Tulloh BR, Goldworthy ME. Breast cancer management: a rural perspective. Med J Aust 1997; 166: 26-29. Sainsbury R, Haward B, Rider L, et al. Influence of clinician workload and patterns of treatment on survival from breast cancer. Lancet 1995; 345: 1251-1252. Gillis CR, Hole DJ. Survival outcome of care by specialist surgeons in breast cancer: a study of 3786 patients in the west of Scotland. BMJ 1996; 312: 145-148. Make a comment

Editorial Genetically modified food: consternation, confusion, and crack-up The controversy over genetically modified food exposes larger issues about public trust in science and the role of science in policymaking MJA 2000; 172: 148-149 "The great pioneers of our subject were tormented by crises of belief and uncertainty, which we need to understand in facing our own problems today. It is only today, after 70 years, that such understanding is coming within our reach -- and may soon slip out of our reach."1 Did this desperate plea come recently from a scientist in defensive retreat? A scientist, perhaps, embroiled in the debate about genetically modified food, who flinched on reading that Stanley Ewen and Arpad Pusztai had found an "unexpected proliferative effect" of genetically modified potatoes on rat gut?2Not, thankfully, on this occasion. These were the opening remarks of a respected senior botanist, C D Darlington, in an issue of the Philosophical Transactions of the Royal Society of London devoted entirely to the manipulation of genetic systems in plant breeding. He was writing over 20 years ago. Interference with our systems of food production has always aroused public alarm, occasionally with justification. From soaking crops with pesticides to taking short cuts in the feeding of cattle (bovine revenge being wreaked on Britain with variant Creutzfeldt-Jakob disease), food is a lightning-rod for public fears about scientists' allegedly reckless indifference to safety. But, even by these high standards of public sensitivity, the debate surrounding genetically modified organisms became the scientific controversy of 1999,3 a debate that is summarised in this issue of the Journal, with restrained good temper, by Huppatz and Fitzgerald on one side 4 and Leeder on the other.5 Four larger issues have been exposed by these kinds of exchange in the last months of the 20th century, and the arguments they incite threaten the fragile remnant of trust that remains between the public and scientists. First, how can two (reasonably) well-regarded organisations peer review the same work -- Ewen and Pusztai's research on the effects of feeding genetically modified potatoes to rats -- and yet come to such radically opposite conclusions about its validity, as did the Royal Society and The Lancet? All six Royal Society reviewers pronounced the research "flawed", while five out of six of The Lancet's reviewers judged that Ewen and Pusztai's work should be published.6 Peer review as a reliable technique for assessing the validity of scientific data is surely discredited. The mistake, of course, is to have thought that peer review was any more than a crude means of discovering the acceptability -- not the validity -- of a new finding. Editors and scientists alike insist on the pivotal importance of peer review. We portray peer review to the public as a quasi-sacred process that helps to make science our most objective truth teller. But we know that the system of peer review is biased, unjust, unaccountable, incomplete, easily fixed, often insulting, usually ignorant, occasionally foolish, and frequently wrong. A recent editorial in Nature was right to conclude that an over-reliance on peer-reviewed publication "has disadvantages that should be countered by adequate provision of time and resources for independent assessment and, in the midst of controversies, publicly funded agencies providing comprehensive, reliable and prompt complementary information".7 Second, given each outrageously overblown claim and counterclaim about the safety of genetically modified foods, how can the public ever begin to reach a balanced opinion about this important new technology? British -- but hopefully not Australian -- doctors, scientists, politicians, and even journalists, treat the public with little more than patronising contempt when a compelling scientific issue surfaces. According to research published by the United Kingdom's Economic and Science Research Council,8 "the public are not stupid and ignorant about their approach to [genetically modified food] risks but have a sophisticated grasp of the main issues". In the United States, the culture is, as so often, entirely different. Faced with growing public anxiety about genetically modified foods, the Food and Drug Administration (FDA) called three open meetings to discuss the widespread concerns. The FDA plans to channel this public point of view into its own food-labelling and safety policies. Here is a model that other countries might adopt to their advantage. Third, after the latest storm has calmed, how much more do we really know about the safety of genetically modified foods? Regrettably, very little. Considered opinions have been traded,9,10 but few new insights have been gained. The insipid but correct conclusion is that more research -- notably to confirm or refute Ewen and Pusztai's preliminary findings -- is needed. But perhaps the terms of the debate could be refined. Mark Tester, for example, has argued against discussing genetically modified plants as a homogeneous group. Instead, he proposes a classification of such foods based on the type of gene transfer used -- between kingdoms, between plant species, or between genes in a single type of plant genome.11 Each category of transfer carries a diminishing theoretical risk. Careful thinking, and not brutish restatements of old positions, is now required. Finally, this and other recent public health scares have focused attention on the validity of the precautionary principle. This principle states that, where there are significant risks of damage to the public health, we should be prepared to take action to limit those risks, even when scientific knowledge is not conclusive, if the balance of likely costs and benefits justifies it. I have argued that the precautionary principle "offers one useful means to inform decision making".12 By contrast, Aaron Klug, President of the Royal Society, noted in his 1999 anniversary address that the precautionary principle "is no way to deal with uncertainty -- it is a recipe for [scientific] stagnation".13 Therefore, the question remains unresolved: how do policymakers make policy on controversial matters of public health when the scientific evidence is inconclusive? In some ways, this bitter debate is spurious. Huppatz and Fitzgerald repeat a familiar argument -- namely, that "gene technology offers enormous potential for world agriculture". The Royal Society went further, claiming that "we cannot assume that current practices will feed the population of 8 billion expected by 2020";7 hence, genetically modified food offers one solution to a projected global famine. Is this the problem we are trying to solve with genetic modification? If not, then what is? And if so, we may be missing a simpler, but far more profound, answer. The little research that has been conducted about the origins of famine reveals that the solution of "more food" may be no solution at all. There is no direct relation, Amartya Sen concludes in his study of poverty and famine,14 between food availability and starvation. Access to food depends far more on a complex mix of economic, social and political factors -- eg, without an income and a stable environment to exchange money for food, a person may starve in the face of plenty. If Sen's argument is correct, and the evidence he cites is persuasive, seeking a technological food fix for world hunger may be not only the biggest scientific controversy of 1999, but also the most commercially malevolent wild goose chase of the new century. Richard Horton Editor, The Lancet London, UK Reprints: Dr R Horton, The Lancet, 84 Theobald's Road, London, WCIX 8RR, UK. Darlington CD. Genetics and plant breeding, 1910-80. Philos Trans R Soc Lond 1981; B 292: 401-405. Ewen SWB, Pusztai A. Effects of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small intestine. Lancet 1999; 354: 1353-1354. Controversy of the year: GM foods under attack. Science 1999; 280: 2243. Huppatz JL, Fitzgerald PA. Genetically modified foods -- safety and regulatory issues. Med J Aust 2000; 172: 170-173. Leeder SR. Genetically modified food -- food for thought. Med J Aust 2000; 172: 173-174. Horton R. Genetically modified foods: "absurd" concern or welcome dialogue? Lancet 1999; 354: 1314-1315. Dangers of over-dependence on peer-reviewed publication [editorial]. Nature 1999; 401: 727. The politics of GM food: risk, science, and public trust. London: Economic and Science Research Council, 1999. The Royal Society Statement, 1998. Genetically modified plants for food use. London: The Royal Society, 1998. Millstone E, Brunner E, Mayer S. Beyond "substantial equivalence". Nature 1999; 401: 525-526. Tester M. Seeking clarity in the debate over the safety of GM foods. Nature 1999; 402: 575. Horton R. The new new public health of risk and radical engagement. Lancet 1998; 352: 251-252. Klug A. Anniversary address 1999. London: The Royal Society, 1999. Sen A. Poverty and famines. Oxford: Oxford University Press, 1981. Make a comment

Richard Horton

Editorial The health of young Australians Mental disorders account for the major burden of disease in young people MJA 2000; 172: 150-151 Community views on youth health tend to be polarised and contradictory. On the one hand, adolescents are seen as having few overt health needs: mortality is low by comparison to that in older groups, and most young people, and their parents, rate their health as good. On the other hand, the emergence in recent decades of youth suicide, drug abuse and new infectious diseases (eg, HIV) has elicited strong and sometimes conflicting opinions about moral and social threats to young people's health. Individualism, a growth in permissiveness, and a decline in religious affiliations have all attracted debate. The recent report Australia's young people: their health and well-being 1999,1 from the Australian Institute of Health and Welfare (AIHW), provides some clarity. It follows an earlier report on child health2 and gives the first comprehensive national picture of the health of young Australians (see Box for key points). In general, Australian youth remain healthy, and retain a positive view of their health. Some health trends are positive: overall mortality in young people in the 1990s was at historically low levels (mostly due to the substantial reductions in motor vehicle deaths in the previous two decades); and rates of teenage pregnancy were low compared with those of other First World countries. However, new threats to youth health have emerged: Mental and behavioural disorders are increasingly recognised as affecting youth disproportionately and account for over half their disease burden. With the changing profile of infectious disease, newer bloodborne and sexually transmitted diseases have become prominent, with threefold higher notifications of both chlamydia and hepatitis C. The prevalence of syphilis has declined further, but gonorrhoea notifications have doubled. Shifts in young people's lifestyle carry implications for health later in life. Tobacco use remains obstinately high, with 40% of young adults continuing to smoke. Physical activity declines across the teens, so that fewer than a third of women aged 20-24 years take part in regular, moderate to vigorous physical exercise. Moreover, 22% of 15-24 year olds already have a body mass index in the overweight or obese range for adults. Some groups have disproportionately high levels of health problems. Low socioeconomic status is linked to higher death and hospitalisation rates, as well as to lower self-rating of health. Recent death rates for young Aboriginal and Torres Strait Islanders are close to three times higher in males and twice as high in females compared with rates for non-Indigenous youth. High levels of mental disorders and substance abuse are major contributors at one level, but the fundamental causes are more likely to be found in social and economic conditions, the loss of cultural identity and the disaffection of youth in many of these communities. The report's findings will inevitably prompt questions about current health provision for young Australians. At present, young people's primary care attendances, for example, are mostly for relatively minor respiratory conditions, musculoskeletal problems or acne. The conditions contributing to the disease burden in young people are less common reasons for general practice presentations, suggesting scope for the development of "youth-friendly" primary-care services capable of responding to youth health problems. With training in adolescent health care, general practitioners can both learn and retain the skills for responding to youth health needs,3 and such training could be linked to health education for young people about access, availability and use of health services. Health promotion has an even greater role. Health problems cluster not only in particular groups but also in individuals. For example, the young regular tobacco user is more likely to engage in heavy alcohol consumption and illicit drug use, have poorer mental health and an overall less healthy lifestyle.4 The clustering can mostly be traced back to common determinants of health in family, community, school and developmental backgrounds. Recent North American research has emphasised the protective influence of family and school attachment on problems ranging from deliberate self-harm and emotional distress to tobacco and illicit substance use, violence and early sexual activity.5 Such findings have been mirrored in recent Australian research.6,7 More importantly, preventive intervention targeting these social risk and protective factors is feasible and can be effective.8,9 Family and school-based interventions, both in adolescence and during childhood, have been shown to reduce adolescent problems as diverse as antisocial behaviour, substance abuse and sexually risky behaviour.9 Similarly, strategies based on community mobilisation, peer support, mentoring and legislative enforcement show promise in specific areas. Many gaps in our knowledge remain. Mental health problems loom large, but available data provide an incomplete picture of current need, changes over time and effectiveness of current health provision. Health profiles of groups with the greatest needs -- the young, the homeless and the disabled -- are incomplete, as are those of Aboriginal and Torres Strait Islanders. Much remains to be learned about health interventions and their effectiveness. Most importantly, data on the psychosocial processes that underpin youth health are not available. Health promotion should be guided not only by knowledge of the health problems of young people, but also by an understanding of relevant risk and protective factors. For mental health problems, these are likely to include parental care, the experience of psychosocial adversity, trauma and violence, victimisation, school failure and underemployment. This understanding is of value, not only in selecting the focus of health promotion, but in helping to ensure its continued relevance and sustainability. A recent report from the World Health Organization noted that most investment has gone into innovation rather than continuing programs, with only one in five youth health programs extending beyond five years.10 Sustainable preventive health programs for youth necessarily depend on effective cooperation with government sectors such as education, justice and employment, as well as non-governmental organisations involved with youth, younger children and their families. As the most comprehensive available account of the health of young Australians, the AIHW report will do much to inform the intersectoral dialogue that must underpin the setting of priorities and, in turn, the development of a rational advocacy. However, implementing effective responses to these priorities will require further work to build a more complete picture of the psychosocial determinants of the major health problems of young people. George C Patton Professor of Adolescent Health, Department of Paediatrics University of Melbourne Centre for Adolescent Health, Melbourne, VIC pattonATcryptic.rch.unimelb.edu.au Lynelle J Moon Senior Analyst, Population Health Unit Australian Institute of Health and Welfare, Canberra, ACT Reprints: Professor G C Patton, Department of Paediatrics, University of Melbourne, Centre for Adolescent Health, 2 Gatehouse Street, Parkville, VIC 3052. Moon L, Meyer P, Grau J. Australia's young people: their health and well-being. PHE19. Canberra: Australian Institute of Health and Welfare, 1999. Moon L, Rahman N, Bhatia K. Australia's children: their health and well-being. PHE7. Canberra: Australian Institute of Health and Welfare, 1998. Sanci LA, Coffey C, Veit FCM, et al. Evaluation of an educational intervention for general practitioners in adolescent health care: randomised controlled study. BMJ 2000; 320: 224-230. Hibbert M, Caust J, Patton G, et al. The health of young people in Victoria. Melbourne: Centre for Adolescent Health, 1996. Resnick MD, Bearman PS, Blum RW, et al. Protecting adolescents from harm: findings from the National Longitudinal Study on Adolescent Health. JAMA 1997; 278: 823-832. Glover S, Burns JBH, Patton GC. The Gatehouse Project: the scope of school based intervention for the prevention of adolescent depression. Family Matters 1998; 49: 11-16. Silburn SR, Zubrick SR, Garton AF, et al. Western Australian Child Health Survey: Family and Community Health. Perth: Australian Bureau of Statistics, 1996. (Catalogue No. 4304.5) National Crime Strategy (Homel R, editor). Pathways to prevention. Canberra: Attorney General's Department, 1999. Toumbourou JW, Patton GC, Sawyer S, et al. Guidelines to inform planning and purchasing of evidence-based practice: interventions for promoting health in the adolescent population. Melbourne: Department of Human Services, 1999. WHO/UNFPA/UNICEF Study Group. Programming for adolescent health and development. Geneva: World Health Organization, 1999. Make a comment Key points from the report Australia's young people: their health and well-being 19991 Young Australians remain in good health... Two-thirds of young people rated their own health as "excellent" or "very good" and getting better. Overall death rates for 12-24 year olds declined by 29% over the period 1979-1992 to 60/100000 (partly due to a 60% decline in motor vehicle accident deaths, 1979-1997), and have remained stable since then. but there are areas of concern... The major burden of disease (combined effect of mortality and disability) for this age group is from mental disorders. Injury is the leading cause of death for 12-24 year olds (40/100000 per year in 1997), with two-thirds of all deaths attributed to some form of injury, including accidents and suicide. Suicide (15.1/100000 per year) and drug-related deaths (4.2/100000 per year) have not followed the declines in most other causes of death, particularly for young men. In 1998, 25% of young people aged 14-19 years and 40% of those aged 20-24 years were regular or occasional smokers. While 54% of 15-24 year olds in 1995 were of acceptable weight, 22% were overweight or obese. The proportions of young people reporting exercising at a "vigorous" or "moderate" level for sport or recreation declined with age. and some groups are worse off. Recent death rates (1995-1997) for Aboriginal and Torres Strait Islander youth were 2.8 times higher for males (278/100000 per year) and 2.0 times higher for females (70/100000 per year) than those of their non-Indigenous counterparts (males, 101/100000 per year; females, 35/100000 per year). The 20% of males in the lowest socioeconomic group were 1.7 times more likely to die and 1.4 times more likely to be hospitalised than males in the highest group; for females, these ratios were 1.4 and 1.2, respectively. Twenty per cent of unemployed youth in 1995 assessed their health status as being fair or poor, compared with 9% of employed youth and 8% of students. Back to text

George C Patton · Lynelle J Moon

Editorial Mood disturbances and coronary heart disease: progress in the past decade Psychological factors are increasingly being identified as important contributors to the onset and course of coronary heart disease MJA 2000; 172: 151-152 Psychological conditions, such as life event stress, mood disturbance and personality disorders, are believed to be important risk factors for coronary heart disease (CHD).1-3 Building on the work of the past decade, growing evidence is emerging that mood disturbances can contribute substantially to CHD. This work has studied the effect of a range of emotional conditions, including hostility and anger, but we will focus here on anxiety and depressed mood. Anxiety Studies of patients with pre-existing CHD show that anxiety, independently of conventional risk factors, can be predictive of recurrent acute CHD events.4 Moreover, prospective studies of anxiety in normal populations show that there is an association between anxiety assessed at enlistment and subsequent CHD mortality over many years, even when conventional risk factors are controlled for -- the relative risks are significant, being of the order of 5-6 for sudden death and 2-3 for fatal acute myocardial infarction (AMI).5 Impressive data also come from prospective studies of panic disorder, which show that CHD mortality risk may be doubled in people with the disorder.6,7 There has been strong supportive psychophysiological evidence -- for example, in patients with pre-existing CHD undergoing ventriculography and exposed to trivial experimental stressful tasks, a significant but transient reduction (of up to 50%) in coronary muscle perfusion can occur.2,8 At the other end of the evidence hierarchy are the clinical case reports of patients with panic disorder, found to be free of CHD at angiography, who have had an acute AMI or ongoing angina following panic attacks.9 It has furthermore been shown that patients with panic disorder, while lacking any demonstrable peripheral elevation in serum catecholamine levels, nonetheless have significant release of adrenaline from the coronary sinus during panic attacks.10 This may in turn adversely affect coronary perfusion, cardiac rhythm, shear forces on atheromatous plaques, and platelet function.11 States of severe emotional arousal can also affect underlying pathophysiological risk factors for CHD, including platelet function and haemostasis.12,13 Longer-term effects of anxiety on cardiovascular pathophysiology are also possible; it has been shown that subjects with an exaggerated blood pressure response to mental stress may experience more rapid progression of carotid atherosclerosis.14 Depressed mood Depressed mood is emerging as an important risk factor for CHD. Depressed mood in CHD patients is associated with increased mortality.15 The increased risk is not trivial (relative risk > 3), being of the same order as other risk factors such as prior AMI and impaired left ventricular function after infarction. Even in long-term studies of normal CHD-free populations, depression at enlistment doubles the risk of subsequent acute coronary events16 and increases mortality risk.17 States resembling depression, such as "vital exhaustion" (characterised by fatigue, irritability and demoralisation),18 have been shown to be associated with acute myocardial events in normal populations even when conventional risk factors are controlled. Unlike the more acute effects of anxiety, the effects of depression are not immediate. Indeed, in one prospective study, mortality rates in women with depression did not begin to increase until after 16 months of follow-up.19 Thus, depression may well have a prolonged mode of action on CHD risk. One study found that one component of depression (ie, hopelessness) was associated with more rapid progression of atherosclerosis.20 The CHD risk of a person with chronic depression or dysphoric mood, either as an induced state or an enduring trait of "depressive" personality, needs further study. Personality Recently the "type D ('distressed') personality" has been described by Denollet et al as a result of finding significant differences in CHD outcome in those with certain personality traits. The type D personality is identified by two components: the continual experience of negative emotions, including depression, and the inhibition of social expression of these emotions. In a sample of patients undergoing cardiac rehabilitation, deaths from cardiac causes were increased fourfold in those with type D personality even after controlling for conventional risk factors.21 This suggests that type D personality (whether as a biological construct of temperament or a constellation of habitual behaviours) is a risk factor at least equivalent in importance to the other, "conventional" coronary heart disease prognostic factors. Implications It is possible that the association between mood and CHD risk is not causal, but that the two are linked by some common underlying genetic factor, perhaps associated with vascular disease in general. Weighted against this interpretation are the experimental findings showing the effect of emotions on cardiovascular pathophysiology. To explore the possibility of covariance, prospective aetiological and interventional studies are necessary to examine both mood state (which is episodic) and the personality-based predisposition (trait) to depression. Intervention studies are now in progress to assess whether antidepressants may reduce CHD events in those with depression following AMI.22 In the meantime, in patients with pre-existing CHD or those at increased risk of CHD, the identification and treatment of mood disorders, including anxiety and depression, is important for improving quality of life and for reducing the risk of CHD events and mortality. Christopher C Tennant Professor, Department of Academic Psychiatry Loyola McLean Lilly Psychiatry Research Training Fellow Department of Academic Psychiatry Royal North Shore Hospital, St Leonards, NSW tennantATmed.usyd.edu.au Hemingway H, Marmot M. Evidence-based cardiology: psychosocial factors in the aetiology and prognosis of coronary heart disease. Systematic review of prospective cohort studies. BMJ 1999; 318: 1460-1467. Rozanski A, Blumenthal JA, Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation 1999; 99: 2192-2217. Tennant CC, Palmer KJ, Langeluddecke PM, et al. Life event stress and myocardial reinfarction: a prospective study. Eur Heart J 1994; 15: 472-478. Moser DK, Dracup K. Is anxiety early after myocardial infarction associated with subsequent ischemic and arrhythmic events? Psychosom Med 1996; 58: 395-401. Kawachi I, Gollditz G, Ascherio A, et al. Prospective study of phobic anxiety and risk of coronary heart disease in men. Circulation 1994; 89: 1992-1997. Coryell W, Noyes R, House JD. Mortality among outpatients with anxiety disorder. Am J Psychiatry 1986; 143: 508-510. Weissman MM, Markowitz JS, Ouellette R, et al. Panic disorder and cardiovascular/cerebrovascular problems: results from a community survey. Am J Psychiatry 1990; 147: 1504-1508. Tennant C. Experimental stress and cardiac function. J Psychosom Res 1996; 40(6): 569-583. Mansour VM, Wilkinson DJ, Jennings GL, et al. Panic disorder: coronary spasm as a basis for cardiac risk? Med J Aust 1998; 168: 390-392. Wilkinson DJ, Thompson JM, Lambert GW, et al. Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks. Arch Gen Psychiatry 1998; 55: 511-520. Deedwania PC. Hemodynamic changes as triggers of cardiovascular events. Cardiol Clin 1996; 14: 229-238. Grignani G, Pacchiarini L, Zucchella M, et al. Effect of mental stress on platelet function in normal subjects and in patients with coronary artery disease. Haemostasis 1992; 22: 138-146. Malkoff SB, Muldoon MF, Zeigler ZR, Manuck SB. Blood platelet responsivity to acute mental stress. Psychosom Med 1993; 55: 477-482. Kamarck TW, Everson SA, Kaplan GA, et al. Exaggerated blood pressure responses during mental stress are associated with enhanced carotid atherosclerosis in middle-aged Finnish men: findings from the Kuopio Ischaemic Heart Disease Study. Circulation 1997; 96: 3842-3848. Frasure-Smith N, Lesperance F, Talajic M. Depression and 18-month prognosis after myocardial infarction. Circulation 1995; 91: 999-1005. Ford DE, Mead LA, Chang PP, et al. Depression is a risk factor for coronary artery diease in men: the precursors study. Arch Intern Med 1998; 158: 1422-1426. Simonsick EM, Wallace RB, Blazer DG, Berkman LF. Depressive symptomatology and hypertension-associated morbidity and mortality in older adults. Psychosom Med 1995; 57: 427-435. Appels A, Otten F. Exhaustion as precursor of cardiac death. Br J Clin Psychol 1992; 31: 351-356. Whooley MA, Browner WS. Association between depressive symptoms and mortality in older women. Arch Intern Med 1998; 158: 2129-2135. Everson SA, Kaplan GA, Goldberg DE, et al. Hopelessness and 4-year progression of carotid atherosclerosis. The Kuopio Ischaemic Heart Disease Risk Factor Study. Arterioscler Thromb Vasc Biol 1997; 17: 1490-1495. Denollet J, Stanislas US, Stroobant N, et al. Personality as independent predictor of long-term mortality in patients with coronary heart disease. Lancet 1996; 347: 417-421. Shapiro PA, Lesperance F, Frasure-Smith N, et al. An open-label preliminary trial of sertraline for treatment of major depression after acute myocardial infarction (the SADHAT Trial). Sertraline Anti-Depressant Heart Attack Trial. Am Heart J 1999; 137: 1100-1106. Make a comment

Christopher C Tennant · Loyola McLean

Editorials Complementary and alternative medicine: an educational, attitudinal and research challenge We need to understand more about these treatments, why they are being used, and what makes them effective MJA 2000; 172: 102-103 Complementary and alternative medicine (CAM) has become increasingly popular over the past decade. Out-of-pocket expenditure in the United States has doubled between 1990 and 1997, from $US14 billion to $US28 billion,1 a situation that is likely to be mirrored in Australia, both in the general population and among cancer patients.2,3CAM is difficult to define. The British Medical Association (BMA) has suggested that it encompasses treatments not taught as part of the medical undergraduate curriculum.4 The major CAM treatments are usually considered to be acupuncture, homoeopathy, herbal medicine, manipulative medicine (osteopathy and chiropractic) and nutritional medicine, although this is based on patient and practitioner use rather than on definitive evidence.5 Further, the use of CAM treatments varies regionally. For example, while homoeopathy is particularly popular among general practitioners in the United Kingdom and Holland,6,7 acupuncture seems to be the CAM treatment of choice in Australia.8 This is not necessarily related to evidence of efficacy, but correlates with a number of historical and cultural factors, including, in Australia, the enthusiasm of a small number of medically qualified acupuncturists in the late 1970s and early 1980s, which led to the reimbursement of acupuncture through Medicare. Patients may...not be seeking proof of efficacy of particular treatments, but meaning and context for their illness... In this issue of the Journal, articles by Pirotta and colleagues,9 and by Newell and Sanson-Fisher10 address doctors' knowledge and use of CAM in general practice and in cancer care. Both articles highlight extensive use of CAM among both doctors and patients. Pirotta et al found high levels of acceptance of acupuncture, hypnosis and meditation among GPs, and that considerable proportions of GPs had trained in, or expressed interest in training in, these and other CAM treatments, but that they still underestimate its use in the Australian population.9Newell and Sanson-Fisher show that Australian oncologists have very variable knowledge of the therapies that are being used by 22% of their patients,3,10 and that, while they appear to accept and understand meditation, acupuncture and chiropractic, they have very little knowledge of the widely available homoeopathic approaches used for cancer in Germany, such as Iscador. Newell and Sanson-Fisher suggest that Australian oncologists viewed this therapy as potentially dangerous,10 while preliminary evidence suggests that it may be both useful and safe.11 In the UK, doctors who practise CAM are predominantly GPs, and a similar situation seems likely in Australia. As GPs act as mediators between the public demand for treatment and the evidence-based provision of medical services,12 it is inevitable that economic and social pressures in a free market system such as Australia's will encourage the development of CAM in the general practice environment. Further, it is GPs who manage patients with chronic illnesses for which conventional medicine all too often offers inadequate solutions. Disenchantment with conventional medicine is not necessarily the reason why patients turn to CAM.13 One suggestion is that patients are increasingly knowledgeable about CAM and seek a more egalitarian process within the consultation.14 It has been confirmed that patients seek CAM because of an intuitive feeling that it could offer them a more appropriate medical model for their illness.15,16 Patients may therefore not be seeking proof of efficacy of particular treatments, but meaning and context for their illness, thus allowing them the freedom to benefit from therapeutic consultations within their chosen milieu.17 Why should we impose our medical model on patients? Their use of CAM may be their process of empowerment, which in turn allows them to contain and manage their chronic illness. It is perhaps difficult for those of us educated within the conventional medical system to allow our patients the freedom to make such journeys in a truly egalitarian manner. As physicians, we do, of course, have statutory and moral responsibilities. We are obliged to attempt to design and conduct studies for evaluating CAM treatments so that they can be safely integrated into medicine, and so that patients can make informed choices about the risks and benefits of particular treatments. Clinical trial work within CAM presents enormous challenges. How do we evaluate physical therapies such as acupuncture and individualised approaches such as homoeopathy?18 CAM research, like the development of general practice research in the 1970s, needs specific skills and teamwork. It requires proactive policies and, as Bensoussan suggests, a collegiate approach,13 whereby those involved in CAM and in conventional medicine genuinely communicate with each other to develop a research agenda. Such a process has recently been completed in the United Kingdom with the support of the Foundation for Integrated Medicine. A research agenda looking specifically at the problems of priority setting, research methods, research capacity and support, potential funding streams and the dissemination of CAM research has been established.5 Core funding for centres of excellence was considered an essential part of developing a specific academic discipline for CAM. It was envisaged that, once established with relatively small amounts of funding, such centres could compete equally for specific project grants. Bensoussan's vision of cooperative ventures13 could then inform all practice, both through original research and through access to appropriate databases and systematic reviews. The BMA has responded very clearly to the expansion of CAM by expressing a desire to expand both undergraduate and postgraduate CAM education.4 Over half the medical schools in the UK and nearly all those in the US now include some CAM familiarisation courses in their undergraduate curricula. The BMA, as well as Pirotta and Newell, indicate that such educational initiatives would also be of great value at the postgraduate level. CAM is clearly popular among patients in Australia and throughout the Western world, but it may be a mistake to read too much into the use of any particular therapeutic intervention. Patients may be using CAM largely to empower themselves in the management of their chronic illnesses. We certainly need to understand more about CAM, why patients choose it, why doctors provide it, and what is it within CAM that seems to be effective. On the other hand, while it may be easier to answer these questions than to conduct large, randomised controlled trials into complex therapeutic interventions, such research may usefully challenge many of our preconceptions about conventional medicine. Without adequate research funding and the establishment of a high quality research network, as well as a critical and evaluative approach to education and practice, it will be impossible for us to answer these vital questions about the increased use of CAM and its individual or combined therapeutic efficacy. CAM may have much to teach us about the practice of medicine and the increasing desire for patients to play an active part in the management of their own illness. George T Lewith Honorary Senior Research Fellow and Honorary Consultant Physician School of Medicine, University of Southampton, United Kingdom Eisenberg DM, Davis RB, Ettner SL, et al. Trends in alternative medicine use in the United States, 1990-1997. JAMA 1998; 280: 1569-1575. MacLennan A, Wilson D, Taylor A. Prevalence and cost of alternative medicine in Australia. Lancet 1996; 347: 569-573. Begbie SD, Kerestes ZL, Bell DR. Patterns of alternative medicine use by cancer patients. Med J Aust 1996; 165: 545-547. Integrated healthcare. A way forward for the next five years? Discussion document. The Foundation for Integrated Medicine on behalf of the Steering Committee for the Prince of Wales Initiative on Integrated Medicine, London: Foundation for Integrated Medicine, October 1997. British Medical Association. Complementary medicine: new approaches to good practice. Oxford: Oxford University Press, 1993. Lewith G, Reilly D. An examination of the effectiveness of complementary and alternative medicine in the UK NHS, with focus on homoeopathy. Health Matters in Prisons 1999; 6: 13-17. Visser G, Peters L. Alternative medicine and general practitioners in The Netherlands: towards acceptance and integration. Family Practice 1990; 7: 227-232. Easthope G, Gill GF, Beilby JJ, Tranter BK. Acupuncture in Australian general practice: patient characteristics. Med J Aust 1999; 170: 259-262. Pirotta MV, Cohen MM, Kotsirilos V, Farish SJ. Complementary therapies: have they become accepted in general practice? Med J Aust 2000; 172: 105-109. Newell S, Sanson-Fisher RW. Australian oncologists' self-reported knowledge and attitudes regarding non-traditional therapies used by cancer patients. Med J Aust 2000; 172: 110-113. Kiene H. Klinische Studien zur Misteltherapie karzinomatoser Erkrankungen. Eine Ubersicht. Therapeuticon 1989; 3: 347-353. Wharton R, Lewith G. Complementary medicine and the general practitioner. BMJ 1986; 292: 1498-1500. Bensoussan A. Complementary medicine -- where lies its appeal? Med J Aust 1999; 170: 247-248. Vincent C, Furnham A. Complementary medicine. A research perspective. Chichester, UK: John Wiley & Sons Ltd, 1997. Moore J, Phipps K, Marcer D, Lewith G. Why do people seek treatment by alternative medicine? BMJ 1985; 290: 28-29. Astin JA. Why patients use alternative medicine. JAMA 1998; 279: 1548-1553. Mitchell A, Cormack M. The therapeutic relationship in complementary health care. Edinburgh: Churchill Livingstone, 1998: 149-159. Lewith G, Vincent C. The evaluation of the clinical effects of acupuncture. A problem reassessed and a framework for future research. Pain Forum 1995; 4: 29-39. Make a comment

George T Lewith

Editorials Measles in an era of measles control As measles becomes rare in Australia, clinical diagnosis becomes increasingly inaccurate MJA 2000; 172: 103-104 It has been a long road to the control of measles in Australia. Live attenuated measles vaccine was licensed in 1968, and included in childhood vaccination schedules in 1971. Even after the first national measles campaign, in 1988, coverage remained too low (85%)1 to achieve herd immunity, as evidenced by major measles outbreaks in many areas in 1993-1994. In 1994, a second dose of measles-mumps-rubella (MMR) vaccine was introduced for all children aged 10-16 years. Although the incidence of measles declined, seroprevalence studies2 indicated that further measles outbreaks were likely. In response to these findings, the Australian Measles Control Campaign (MCC) was launched in July 1998. The centrepiece of this campaign was administration of a dose of MMR vaccine to all primary school children in the second half of 1998. This "catch-up" dose was needed before lowering the recommended age for the second dose of MMR vaccine to four years in 1999. After the MCC, an estimated 96% of children aged five to 12 years had received two doses of MMR vaccine.3 As a result of this campaign and the continuing efforts to eradicate measles, it is hoped that Australia will soon be shown to have joined other countries, such as the United States,4 the United Kingdom5 and Finland,6 where indigenous measles transmission has been interrupted. The better the control of measles, the lower the probability that someone presenting with fever and rash will have measles, and the poorer the positive predictive value (PPV) of a clinical diagnosis. Even in 1990-1993, before any major measles control measures, a study of 58 people notified with measles in eastern Sydney found that only 49% of cases were serologically confirmed.7 A case definition of morbilliform rash, cough and fever at rash onset had a PPV of 69%.7 In this issue of the Journal, there is a report of a larger study of enhanced measles surveillance in Victoria from July 1997 to December 1998 (ie, primarily conducted before the MCC) which showed a much lower level of confirmation.8 Only 8% of the 248 notified cases that could be classified on the basis of serological results were confirmed as measles. The PPV of the National Health and Medical Research Council (NHMRC) clinical case definition for considering public health action9 was as low as 5% when secondary cases from clusters were excluded.8 Since the MCC, the proportion of serologically confirmed cases is likely to have fallen even further. In the UK, after a similar school-based MMR program in 1994,5 and in Finland 12 years after high coverage with a two-dose MMR schedule,6 only about 1% of suspected cases were shown to be measles. These developments necessitate major changes in the approach of medical practitioners to suspected measles, especially in general practice where most cases will be seen. The latest draft of the revised NHMRC guidelines for measles control emphasise that confirmation by detection of measles IgM in a serum specimen is essential when measles is clinically suspected.10 This policy is also recommended by the authors of the Victorian study and by the National Measles Surveillance Strategy.11 Confirmation is particularly important in sporadic cases, where the prior probability of measles is especially low, and should also be obtained from at least two cases during an outbreak. The high level of laboratory testing achieved in Victoria is encouraging. However, overall, only 44% of the 428 cases accepted as measles notifications in Australia between January 1998 and June 1999 were laboratory confirmed (personal communications from State and Territory health departments). It may be possible to improve this percentage -- although teams of venepuncturists are impractical for many areas of Australia, arrangements to bleed patients can usually be made in consultation with local public health authorities. Considerable interest has also focused on non-invasive diagnostic methods, such as salivary testing. This method has been used in the UK but has technical difficulties,11 making timely testing more difficult than for serological testing. Even when serological testing is done, as measles becomes rare the likelihood of a falsely positive measles IgM will rise, as found in Victoria and elsewhere.4 A positive measles IgM test should therefore be confirmed by a reference laboratory, especially in sporadic cases. Clinicians should be aware that many viral infections in children may resemble measles clinically, and that measles is more likely in older children and young adults than in infants. After control of measles in Finland,6 37% of 993 children with suspected measles had serological evidence of infection caused by parvovirus, enteroviruses, adenovirus or human herpesvirus type 6 (HHV-6).12 The most common serological diagnoses were parvovirus infection, in children aged four to 15 years, and enterovirus and HHV-6 infection, in children aged under four years. In Sydney, in 1990-1993, the mean age of patients with confirmed measles was 11.3 years,7 and, in Victoria in 1997-1998, more than half (53%) the patients with confirmed measles were aged at least 10 years.8 An outbreak of measles in Victoria in 1999, after the MCC, indicates the likely future pattern of measles in Australia -- 84% of patients were aged 18-30 years and all patients aged one to eight years were unvaccinated.13 Sustained measles control will require further efforts in young adults as well as continued high coverage with two doses of measles vaccine in children. Young adults, especially those attending tertiary institutions or planning travel to areas where measles remains endemic, should be encouraged to have a second dose of MMR or serological confirmation of measles immunity. Peter B McIntyre Deputy Director Heather F Gidding Epidemiologist National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases, Royal Alexandra Hospital for Children and University of Sydney, Sydney, NSW Gwendolyn L Gilbert Director, Centre for Infectious Diseases and Microbiology and University of Sydney, Sydney, NSW Australian Bureau of Statistics. National health survey. Children's immunisation, Australia, 1989-90. Canberra: ABS, 1992. (Catalogue no. 4379.0.) Gilbert GL, Chan S-W, Escott R, et al. Seroepidemiology of measles in New South Wales, 1997. Report to the National Centre for Disease Control, Commonwealth Department of Health and Aged Care, 1998 (available from the Department). National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases. Australian measles control campaign 1998. Evaluation report. Sydney: University of Sydney, Royal Alexandra Hospital for Children, 1999. Watson JC, Redd SC, Rhodes PH, Hadler SC. The interruption of transmission of indigenous measles in the United States during 1993. Pediatr Infect Dis J 1998; 17: 363-366. Gay N, Ramsay M, Cohen B, et al. The epidemiology of measles in England and Wales since the 1994 vaccination campaign. Commun Dis Rep CDR Rev 1997; 7: R17-R21. Peltola H, Hienonen OP, Valle M, et al. The elimination of indigenous measles, mumps, and rubella from Finland by a 12-year, two-dose vaccination program. N Engl J Med 1994; 331: 1397-1402. Ferson MJ, Young LC, Robertson PW, Whybin LR. Difficulties in clinical diagnosis of measles: proposal for modified clinical case definition. Med J Aust 1995; 163: 364-366. Lambert SB, Kelly HA, Andrews RM, et al. Enhanced measles surveillance during an interepidemic period in Victoria. Med J Aust 2000; 172: 114-118. National Health and Medical Research Council. Measles: guidelines for the control of outbreaks in Australia. Canberra: NHMRC, 1996. National Health and Medical Research Council. Measles: guidelines for the control of outbreaks in Australia [draft]. Canberra: NHMRC, 2000. Heath T, Burgess M, McIntyre P, Catton M. The national measles surveillance strategy. Commun Dis Intell 1999; 23: 41-49. Davidkin I, Valle M, Peltola H, et al. Etiology of measles and rubella-like illness in measles, mumps, and rubella-vaccinated children. J Infect Dis 1998; 178: 1567-1570. Lambert S, Lynch P, Morgan M, Gercovich D. Measles outbreak -- young adults at high risk. Victorian Infect Dis Bull 1999; 2: 21-22. Make a comment

Peter B McIntyre · Heather F Gidding · Gwendolyn L Gilbert

Editorial Defibrillation for out-of-hospital cardiac arrest Strengthening that most important link in the "chain of survival" MJA 2000; 172: 53-54 Cardiac arrest outside hospital is a common mode of unexpected death in our society. The arrest is usually caused by coronary artery disease, and indeed may be its first manifestation, occurring in apparently fit and well individuals. The causative arrhythmia is usually ventricular fibrillation, but by the time help arrives and the rhythm is recorded it has often degenerated into asystole. In this issue of the Journal, Meyer et al1 present a detailed medical perspective of this problem, and outline the steps we need to take to improve the survival rate for victims of out-of-hospital cardiac arrest, particularly the "chain of survival" -- the critical links in the resuscitation process. When a cardiac arrest is witnessed, the first priority is defibrillation, but in most situations cardiopulmonary resuscitation (CPR) needs be undertaken before defibrillation. The spectacular success of implantable defibrillators in terminating lethal arrhythmias2 in patients known to be at extreme risk of ventricular fibrillation raised the possibility that the same sensing technology and defibrillator waveforms might be incorporated into an external defibrillator, without the need for rhythm interpretation by a medical or paramedical attendant. Such devices were introduced over 10 years ago, and have been widely implemented, with results for successful defibrillation by junior ambulance officers that were as good as those of paramedics.3 By 1990, the New South Wales Ambulance Service had introduced semiautomatic defibrillators into all its frontline ambulances (ie, those not used for routine transport) to complement the care given by paramedics with manual defibrillators. Similar systems have since been initiated in other Australian States. By 1991, the concept of public access defibrillation (PAD) was re-emerging. This idea was first conceived by the pioneer of prehospital coronary care, Frank Pantridge of Belfast,4 who developed a small but primitive defibrillator in the late 1960s which could be installed next to every fire extinguisher and used in the same way, simply and easily, and by whoever was closest. Pantridge asked the question "Is property more important than life?". With the re-emergence of this concept within the American Heart Association, the aim was to have semiautomatic defibrillators so widely available, and sufficient members of the public trained, that a person who suffered a cardiac arrest in a public place might have the benefit of a defibrillator before the arrival of an ambulance and when the chance of a successful outcome may be well over, rather than well under, 50%.5 Semiautomatic defibrillators are now deployed in what may seem to be the most unlikely places,5 and Australia has played a leading role. They were first installed in the QANTAS International fleet and in Australian airports during 1991.6 The long-term survival rate for people treated on the ground or in the air by QANTAS International staff is 32%,7 now exceeded by the seven of 14 (50%) for people treated by American Airlines staff over the past 18 months.8 Defibrillators are deployed widely in Chicago's O'Hare Airport and are available for public access. Deployment of public access defibrillators in airports is becoming commonplace, and Sydney's international and domestic terminals will be equipped with a system similar to Chicago's within months. Installation in airliners is becoming the industry standard throughout the world,8 with programs completed or under way for most major international and domestic airlines (including QANTAS and Ansett Domestic). Use in airports and airliners has followed awareness of the fact that deaths from cardiac arrest in the air are far more common than deaths from aircraft crashes,7,8 while deaths in terminals of people undergoing unaccustomed exercise are more common than at other locations9 (except at sporting venues, where deaths in older spectators are common). Survival rates of 70% have been reported from the Melbourne Cricket Ground10 and in Las Vegas casinos:11 in both situations remote monitoring of crowd activity enables quick recognition, which, together with appropriate placement of personnel and devices, ensures a prompt response. Deployment of defibrillators in police cars, complementing the ambulance service in the environs of the Mayo Clinic, has increased community survival after cardiac arrest in Rochester, Minnesota, to near 50%.12 St John Ambulance, as the leading teacher of community resuscitation and first aid in Australia, has endorsed training in defibrillation with CPR, and is embarking on an ambitious program, through its training and operational arms, to make public access defibrillation widely available throughout the nation. Such a program must mesh with the existing professional ambulance service, and complement this by strengthening that most important earliest link in the "chain of survival" -- the prompt reversal of ventricular fibrillation by whoever can do so first, and fastest. In strife-torn Belfast, Pantridge's idea lapsed because no system was available at the time for automatic recognition of ventricular defibrillation, so the device had to be used in the manual mode, and could have been used as a weapon. The introduction of safe semiautomatic defibrillators which will only operate in the presence of ventricular fibrillation has changed this situation. A satisfactory answer can now be given to Pantridge's question. As peace emerges in Ulster, the concept proposed by Pantridge and Geddes4 has taken firm root throughout the whole world. Michael F O'Rourke Professor of Medicine University of New South Wales and St Vincent's Hospital and Clinic, Sydney, NSW Meyer ADMcR, Cameron PA, Smith KL, McNeil JJ. Out-of-hospital cardiac arrest. Med J Aust 2000; 172: 73-76. Moss AJ, Hall WJ, Cannon DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med 1996; 335: 1933-1940. O'Rourke MF, Hall J. Pre-hospital cardiac arrest in New South Wales (1992). Aust N Z J Med 1994; 24: 619. Geddes JS, editor. The management of the acute coronary attack: the J Frank Pantridge Festschrift. London: Academic Press, 1986. Nichol G, Hallstrom AP, Kerber R, et al. American Heart Association Report on the Second Public Access Defibrillation Conference, April 17-19, 1997. Circulation 1998; 97: 1309-1314. Donaldson E, O'Rourke MF. Defibrillators on QANTAS aircraft. Med J Aust 1992; 156: 293. O'Rourke MF, Donaldson E, Geddes JS. An airline cardiac arrest program. Circulation 1997; 96: 2849-2853. Crewdson J. Code blue: survival in the sky. Chicago Tribune Aug 1, 1999: C1-C3. Becker L, Eisenberg M, Fahrenbruch C, Cobb L. Public locations of cardiac arrest: implication for public access defibrillation. Circulation 1998; 97: 2106-2109. Wassertheil J, Keane G, Fisher N, Leditschke JF. Cardiac arrest outcomes at the Melbourne Cricket Ground and Shrine of Remembrance using a tiered response strategy -- a forerunner to Public Access Defibrillation. Resuscitation 2000. In press. Valenzuela TD, Bjerke HS, Clark LL, et al. Rapid defibrillation by non-traditional responders. The Casino project. Acad Emerg Med 1998; 5: 414-415. White RD, Hankins DG, Bugliosi TF. Seven years' experience with early defibrillation by police and paramedics in an emergency medical services system. Resuscitation 1998; 30: 145-151. Make a comment

Michael F O'Rourke

Editorial Preventing hepatitis C virus transmission in Australians who inject drugs Prevention, through harm minimisation, remains preferable to cure MJA 2000; 172: 55-56 Hepatitis C virus (HCV) infection is an uncontrolled epidemic in both the developed and the developing world. However, it is only in the developed world where average life expectancy is long enough to be influenced by the sequelae of HCV infection. The disease is very slowly progressive, and causes cirrhosis in approximately 15% of infected people over two or more decades; in approximately half of these, it then causes hepatic decompensation or hepatocellular carcinoma over another one or two decades.1Most people currently dying of HCV infection in Australia are middle-aged or elderly immigrants from Southern Europe, the Middle East and Asia. To date, 31.3% of liver transplants performed for hepatitis C infection in Australia2 and 52.4% of hepatocellular carcinomas diagnosed in people with HCV infection in Victoria3 have been in this group. These people have acquired the infection in their country of birth from cultural practices involving skin penetration, or medical interventions, including injections. Maintenance and expansion of the needle and syringe exchange programs will remain the single most important component of Australia's harm minimisation efforts However, current transmission of HCV infection in Australia is occurring largely within the culture of injecting drug use. Although the risk of transmission by an individual needlestick is not high (up to 6.1%4), the high prevalence of HCV infection among users, the frequency of injecting and the practices used have established a self-perpetuating system of transmission.5,6 Thus, it is likely that the future disease burden of hepatitis C-related illness in Australia will be carried largely by current or past injecting drug users. In this issue of the Journal, MacDonald et al examine the influence of harm reduction programs by measuring seroprevalence of HCV in people who attended a cross-section of needle and syringe exchange programs throughout Australia in 1995, 1996 and 1997.7 Their findings, which show that seroprevalence fell from 63% in 1995 to 50% in 1997, are encouraging. There may have been selection bias, but, if one assumes that this bias applies equally to all three years studied, there has been a 21% reduction in seroprevalence during that time. The results were even more striking in recent users, in whom there has been a 41% reduction. For some reason there was no additional reduction between 1996 and 1997. Does this mean the effect of harm reduction programs has plateaued? That there is a limit to their efficacy? That only a certain proportion of users can be influenced by education programs? While further studies are needed over the next two or three years to clarify this, these data strongly support the need for ongoing efforts at harm reduction and maintenance of needle and syringe exchange programs. Can we do more to reduce seroprevalence of HCV in people who inject drugs? There has been a great deal of debate in the public domain about the various prevention and treatment strategies for drug dependency. There is little to add, except to emphasise the need for continuing support services and harm-minimisation programs for those people who decide to embark on or continue with an injecting drug habit. Such support includes widespread availability of needle and syringe exchange programs and ready access to counselling and education facilities. Education includes strategies for primary and secondary prevention of injecting drug use, including diverting users to non-injecting routes of drug administration. Does antiviral treatment have anything to offer as a strategy to prevent transmission? The combination of interferon alfa and ribavirin has now become the benchmark for treatment of HCV infection, with a long term response rate of over 40% -- double that of interferon alfa monotherapy. As the marker of response (the polymerase chain reaction test for viral RNA) measures viraemia, it can be assumed that those who "respond" are not infectious. It is expected that the combination therapy will be licensed for treatment-na•ve patients in Australia in 2000. Currently, combination treatment is licensed under section 100 (s100) of the National Health Act 1953 (Cwlth) for people who have relapsed after interferon alfa monotherapy. With a response rate of over 40%, should we not be using this treatment in injecting drug users? The current s100 criteria for interferon alfa do not preclude treatment of current injecting drug users. However, there are three major potential problems which lead to caution in liver clinics. Firstly, there is the risk of reinfection: an injecting drug user needs to use scrupulous technique 100% of the time in order to avoid reinfection. Secondly, there is the risk of serious psychiatric effects with interferon alfa (psychotic reactions, cognitive impairment, severe depression including suicide attempts, and homicidal ideation),8 with suicides having occurred in Australia and overseas.9 Psychiatric reactions are more common in people with pre-existing psychological problems, chaotic lifestyles and those who lack social networks and supports. Interferon alfa can cause recidivism to injecting drugs, particularly in recent users, and this recidivism has been associated with major psychiatric problems.8 Unfortunately, funding for interferon in Australia has not been tied to any funding for counselling or psychiatric services. Thirdly, the other drug, ribavirin, is clearly teratogenic at low dose in all animal species studied, and can potentially cause embryotoxicity from either male or female parents.10 Additionally, ribavirin may be present in semen and cause teratogenicity in a woman already pregnant. It has a large volume of distribution and a long half-life (298 hours; see product information, available from Schering-Plough Pty Ltd, PO Box 231, Baulkham Hills, NSW 2153). Thus, people contemplating a course of ribavirin must be counselled about contraception -- both men and women must make sure no pregnancies occur during treatment and for six months afterwards, and additionally there should be no unprotected intercourse with a woman already pregnant. The product information for ribavirin advises two separate methods of contraception, one for the male and one for the female of a partnership. Clearly, at this stage, antiviral treatment cannot be safely advocated as a widespread public health method of reducing transmission of HCV in people who inject drugs. As a general rule it is safer to defer treatment until individuals have stopped injecting drugs for a long time, particularly as the rate of progression of HCV-related liver disease is so slow. While antiviral treatment may then be effective in clearing virus in those who have stopped injecting, it will have no effect on transmission, as these individuals are no longer part of the injecting population. The emphasis must therefore remain on concerted efforts to reduce the numbers of Australians who inject drugs, to provide support during this period in their lives, to reduce the number of times they actually inject, and to promote a safe, "self defence" injecting technique with every injection. Maintenance and expansion of needle and syringe exchange programs will remain the single most important component of Australia's harm-minimisation efforts. Adherence to the principles of harm minimisation is the only way to control this epidemic until a vaccine becomes available -- and this is unlikely to occur within a decade. Katrina J R Watson Deputy Director Department of Gastroenterology St Vincent's Hospital, Melbourne, VIC Seeff AB. Natural history of hepatitis C. Hepatology 1997; 26 (3 Suppl): 215-285. Zekry A, Whiting P, Crawford D, et al. Long term outcome of hepatitis C virus infection post liver transplantation. The Australian and New Zealand experience [abstract]. J Gastroenterol Hepatol 1999; 14: A171. Roberts SK, Sulaiman N, Giles G, et al. Rising incidence and risk factors for hepatocellular carcinoma in Victoria [abstract]. J Gastroenterol Hepatol 1999; 14: A194. Dore G, Kaldor J, McCaughan G. Systematic review of the role of polymerase chain reaction in defining infectiousness among people with hepatitis C virus. BMJ 1997; 315: 333-337. Crofts N, Thompson S, Kaldor J. Epidemiology of the hepatitis C virus. Communicable Diseases Intelligence Technical Report Series No. 3. Canberra: National Centre for Disease Control, Commonwealth Department of Health and Aged Care, and Communicable Disease Network Australia and New Zealand, May 1999. Australian National Council on AIDS and Related Diseases Hepatitis C Sub-Committee. Hepatitis C Virus Projections Working Group: estimates and projections of the hepatitis C virus epidemic in Australia. Sydney: National Centre in HIV Epidemiology and Clinical Research, University of NSW, August 1998. MacDonald MA, Wodak AD, Dolan KA, et al. Hepatitis C virus antibody prevalence among injecting drug users at selected needle and syringe programs in Australia, 1995-1997. Med J Aust 2000; 172: 57-61. Dusheiko G. Side effects of alpha interferon in chronic hepatitis C. Hepatology 1997; 26 (Suppl 1): 1125-1215. Hepatitis C National Data Base Project. Final report 1999. Newcastle: Hepatitis C National Data Base, 1999. Kochbar DM. Effects of exposure to high concentrations of ribavirin in devloping embryos. Pediatr Infect Dis J 1990; 9 (9 Suppl): S88-S90. Make a comment

Editorial Allies or enemies? Evidence-based medicine and consumer choice MJA 2000; 172: 5-6 In this era of promoting evidence-based medicine, the study by Fitzgerald and Phillipov in this issue of the Journal on consumers' attitudes to three "best practice" recommendations raises key questions:1 How do consumers respond to the medical profession's determination of "best practice"? Are there tensions between the movements for evidence-based medicine and for greater consumer choice? Although not immediately addressed by this study, other important questions include: Should "best practice" be determined only by professionals' judgements? Could the use of evidence in fact enhance consumers' ability to make healthcare choices that suit them best? Fitzgerald and Phillipov suggest that patients may be more averse to risks of interventions, particularly preventive ones, than are doctors. Consequently, the course of action recommended by the profession may not be seen as the best option by patients, and, Fitzgerald and Phillipov argue, disclosing risks may run counter to the goal of implementing best-practice recommendations.1 This should come as no surprise. The values and concerns of patients and doctors are often quite different. Studies comparing the concerns of patients with what their practitioners believe are most important to patients show at least discrepancies, and often great gulfs, between doctors and patients.2-6 This must at times translate into different value judgements about healthcare treatments, and a different attitude to individual risks, benefits, and the trade-offs between them. Part of the problem in translating evidence-based recommendations into action is that the evidence often does not reflect the major concerns of the person who has to make a choice. Trials on the effects of healthcare often measure mortality and other easily measured outcomes, and often overlook key issues of concern to patients, such as quality of life and long term effects. Researchers exploring people's experiences of healthcare, or charting long term progress, are more likely to be using methods other than trials. These will be given less weight by the individuals determining "best practice" according to the hierarchies of evidence that count the randomised controlled trial as the "gold standard".7 Some guideline developers, such as the National Health and Medical Research Council in Australia7 or the Agency for Health Care Policy and Research in the United States,8 consider evidence from literature on consumers' experiences, and include consumer representatives in guideline development groups. However, that is not the way that researchers, medical colleges, and other organisations involved in guideline development traditionally function. To assess consumer attitudes to three such professionally derived "best practice" recommendations, Fitzgerald and Phillipov presented risk-benefit scenarios to various groups of people.1 Each group was presented with scenarios related to hormone replacement therapy (HRT), thrombolysis after myocardial infarction, and coronary artery bypass surgery. The drugs and procedure were not named. However, bypass surgery would have been recognisable to many, and thus they would be able to call on frames of reference other than simply the information presented by the researchers. This is important, as only some of the risks and benefits of these interventions were discussed. For example, HRT was presented solely as a therapy to prevent heart disease, with no mention of its principal effects and purpose. The three scenarios were presented together, perhaps leading survey participants to compare them directly as options for preventing heart attacks. One scenario was a long term daily drug where there was no real disease, one a single injection for dissolving clots after a heart attack, and the third scenario was presented as one-off surgery to correct a diagnosed problem. The study was hypothetical: imagine you are someone of a specific age, sex, and medical history that may be unfamiliar territory, and an intervention you do not really have to face. The individuals surveyed were by no means a representative sample of the population, nor were they necessarily candidates for these interventions (for example, a third of those being asked if they would take HRT were men). This seriously undermines the ability to extrapolate the results to people's real lives. People's willingness to accept the risk of an intervention can be very different if they are living with the risks and effects of the disease itself.6 The authors considered the effect of risk-framing techniques on people's potential reactions, and so presented absolute risk information rather than the more dramatic relative risk equivalent. This is critical, as, for example, it has been shown that these different ways of framing risks even affect doctors' willingness to prescribe HRT.9 However, there are many other ways to bias framing, and some are exemplified in Fitzgerald and Phillipov's study. Consider this somewhat emotive statement about coronary artery bypass surgery: "Unfortunately as well as having to endure major surgery, there is a 1 in 20 chance that the surgery will cause death or a stroke."1 This highlights another of the main issues at the heart of this debate. If evidence is to be an ally rather than an enemy to consumers, then it needs to be used to help inform people's decisions, rather than dictate what should be done or manipulate people down certain tracks. If this is to be achieved, healthcare practitioners need to become far more skilled at communicating meaningfully and objectively about the relative benefits and risks of treatments. Although many aspects of their study undermine the weight that can be given to its results, Fitzgerald and Phillipov raise some critical issues. At its best, evidence-based medicine will expose many of the value differences between doctors and the individuals and communities they serve. This is to be welcomed. So too is the challenge to improve health professionals' communication skills. The answer to these challenges is not, as the authors appear to suggest, to question whether information should be provided. It is to question who gets to decide "best practice" for the whole community, how evidence is best used, and whose values are driving the evidence-based medicine agenda. Hilda Bastian Chairperson, Consumers' Health Forum of Australia Convenor, Consumer Network of the Cochrane Collaboration Blackwood, SA hilda.bastianATflinders.edu.au Fitzgerald SP, Phillipov G. Patients' attitudes to commonly promoted medical interventions. Med J Aust 1999; 172: 9-12. Catalan J, Brener N, Andrews H, et al. Whose health is it? Views about decision-making and information-seeking from people with HIV infection and their professional carers. AIDS Care 1994; 6: 349-356. Freda MC, Anderson HF, Damus K, Merkatz IR. What pregnant women want to know: a comparison of client and provider perceptions. J Obstet Gynecol Neonatal Nurs 1993; 22: 237-244. Jachuk S, Brierley H, Willcox P. The effect of hypotensive drugs on quality of life. J R Coll Gen Pract 1982; 32: 103-105. Orth-Gomer K, Britton M, Rehnqvist N. Quality of care in an outpatient department: the patients' view. Soc Sci Med 1979; 13A: 347-351. Slevin ML, Stubbs L, Plant HJ, et al. Attitudes to chemotherapy: comparing views of patients with cancer with those of doctors, nurses, and general public. BMJ 1990; 300: 1458-1460. National Health and Medical Research Council. A guide to the development, implementation and evaluation of clinical practice guidelines. Canberra: Commonwealth of Australia, 1999. Agency for Health Care Policy and Research. Using clinical practice guidelines to evaluate quality of care, vol 1: Issues. US Department of Health and Human Services and Public Health Service, 1995. Nikolajevic-Sarunac J, Henry DA, O'Connell DL, Robertson J. Effects of information framing on the intentions of family physicians to prescribe long term hormone therapy: results of a randomised controlled trial. J Gen Intern Med. In press. Make a comment

Hilda Bastian

Editorial Hepatitis A, liver transplants and Indigenous communities Vaccination plus improved living conditions and healthcare are needed to combat hepatitis A in remote Indigenous communities MJA 2000; 172: 6-7 In this issue of the Journal, Hanna et al highlight the serious problem of acute hepatitis A in Indigenous children in far north Queensland communities.1 This should come as no surprise, as these communities are plagued by poverty, educational disadvantage and poor living conditions -- the very circumstances in which this infection occurs. Indeed, Indigenous children in rural and remote Australia generally have an extraordinarily high burden of infectious disease, with attack rates for conditions such as invasive pneumococcal disease as high as any in the world.2 The incidence of hepatitis A virus (HAV) infection in north Queensland in 1996-1997 was up to six times higher among Aboriginal and Torres Strait Islander people than among non-Indigenous people.3 Indigenous people accounted for 29% of all HAV infections but only 8.1% of the population, and contracted HAV infection at a mean age of 12 years compared with 30 years for the general population. The most common risk factor for HAV infection was living in or visiting a rural Aboriginal or Torres Islander community. An effective hepatitis A control program requires effective vaccines as well as generic programs for improving Indigenous health. An effective vaccine for HAV infection exists,4 but it has been suggested that HAV vaccination is not necessary in Aboriginal and Torres Strait Islander communities, as HAV infection is endemic (eg, a 1994 study found that 98.5% of people over the age of 10 years had had HAV infection5). However, young children (aged three to five years) are both very vulnerable to severe infection and significant transmitters of infection, and could be targeted by community-wide HAV vaccination programs.3 The patients reported by Hanna et al highlight a severe complication of HAV infection -- fulminant hepatic failure. As the case fatality rate for HAV infection in Australia is thought to be 0.2%,6 cases of fulminant hepatic failure are not unexpected in communities with a high prevalence of HAV infection. Generally, outcomes of fulminant hepatic failure are better if it is secondary to HAV infection than to other causes, such as drugs, hepatitis B or hepatitis "X" (caused by unidentified viruses).7 However, children aged under 10 years and adults aged over 40 years do worse, irrespective of cause.7 The children reported by Hanna et al were all under 10 years, had severe hepatitis and were transferred to tertiary care centres relatively late in the course of their illness. All three died of cerebral oedema, raising the important issue of fluid management in patients with fulminant hepatic failure: aggressive fluid replacement is not part of the management of acute liver failure and may even be detrimental by precipitating cerebral oedema. In the children reported by Hanna et al, delayed diagnosis and late referral were probably contributing factors to cerebral oedema. Early indicators of fulminant hepatitis include a serum bilirubin level of > 300 µmol/L, prolongation of clotting time and hypoglycaemia.7 These cases also raise the issue of organ transplantation in Aboriginal and Torres Strait Islander populations. Aboriginal people from remote regions have worse outcomes than non-Aboriginal people after renal transplantation, probably because of their higher rates of comorbidity, especially "syndrome X" disorders (insulin resistance, associated obesity and hyperlipidaemia).8 Obviously, this would be much less of a problem for liver transplantation in Aboriginal children with fulminant hepatic failure.8 There is no reason that Aboriginal and Torres Strait Islander people would have inherently poorer outcomes after liver transplantation than other people, although issues related to primary health care and long term follow-up must be addressed. Indeed, the high prevalence of hepatitis B in the adult Aboriginal community makes the issue of liver transplantation even more relevant. Liver transplantation should clearly be considered a therapeutic option for severe liver disease in the Aboriginal population. The Australian National Liver Transplant Unit has performed liver transplants on two Aboriginal adults with good medium-term outcomes. However, none of the above issues can be addressed in isolation from general issues of Aboriginal health. Prevention and detection of disease and treatment of severe infection are possible only if the basic requirements for improving Aboriginal health are in place. These include improved environmental and living conditions and comprehensive and competent primary healthcare delivery systems. There is now considerable evidence that poor living conditions in Aboriginal communities can be improved by focusing on delivery and maintenance of "health hardware" (such as waste removal and supply of cold and hot water and the means to clean living areas).9 Furthermore, effective vaccination programs and appropriate primary care management of sick children can occur only in the setting of sustainable, primary healthcare systems. This requires a range of initiatives, in particular supply of a competent rural health workforce. Appropriate protocols for referring sick children are also needed, as well as access to rapid and appropriate evacuation to large regional hospitals. We believe that the recommendations of Hanna et al on when to refer are far too conservative. Surely, any young child with clinical or biochemical hepatitis needs to be referred at least to a large base hospital, where immediate investigation and assessment is possible. The patients reported by Hanna et al raise many issues about healthcare in Aboriginal and Torres Strait Islander communities, including the need to: provide and maintain functioning "health hardware"; establish sustainable primary healthcare systems; deliver effective vaccines for common infectious diseases; develop protocols for patient referral; provide rapid access and evacuation to large regional hospitals; and demystify organ transplantation as an effective therapeutic procedure for fulminant hepatic failure. These are all achievable! Geoffrey W McCaughan A W Morrow Professor of Gastroenterology and Hepatology A W Morrow Gastroenterology and Liver Centre Australian National Liver Transplant Unit Royal Prince Alfred Hospital and University of Sydney, Sydney, NSW Paul J Torzillo Medical Director, Nganampa Health Council, Umuwa, SA Clinical Associate Professor of Medicine Department of Respiratory Medicine Royal Prince Alfred Hospital and University of Sydney, Sydney, NSW Hanna JN, Warnock TH, Shepherd RW, Selvey LA. Fulminant hepatitis A in Indigenous children in north Queensland. Med J Aust 2000; 172: 19-21. Torzillo PJ, Hanna JN, Morey F, et al. Invasive pneumococcal disease in central Australia. Med J Aust 1995; 162: 182-186. Merritt A, Symons A, Griffiths M. The epidemiology of acute hepatitis A in North Queensland 1996-1997. Commun Dis Intell 1999; 23: 120-124. Bader TF. Hepatitis A vaccine. Am J Gastroenterol 1996; 91: 217-222. Bowden SJ, Currie BJ, Miller NC, et al. Should Aboriginals in the "Top End" of the Northern Territory be vaccinated against hepatitis A. Med J Aust 1994; 161: 372-373. Amin J, Heath T, Morrell S. Hepatitis A in Australia in the 1990s: future directions in surveillance and control. Commun Dis Intell 1999; 23: 113-120. O'Grady JG, Alexander GHM, Haylor KM, Williams R. Early indications of prognosis in fulminant hepatic failure. Gastroenterology 1989; 97: 439-445. Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure amongst Aboriginal Australians. Med J Aust 1998; 168: 537-541. Pholeros P, Rainow S, Torzillo PJ. Housing for health -- towards a healthier living environment for Aborigines. Sydney: Healthabitat, 1994. Make a comment

Geoffrey W McCaughan · Paul J Torzillo

Editorial Doctors and the "environment" A "call to arms" for medical practitioners in Australia MJA 1999; 171: 576-577

Editorial William Osler: a model for the 21st century? Osler's teachings are as relevant now as they were 100 years ago Whatever way my days decline, I felt and feel, tho' left alone, His being working in mine own, The footsteps of his life in mine. MJA 1999; 171: 577-579

Michael F O'Rourke

Editorial Humour in medical teaching The place of humour in medical teaching seems paradoxical MJA 1999; 171: 579-580

John B Ziegler

Editorial The burden of disease and injury in Australia: time for action Another report or the beginning of a new era? MJA 1999; 171: 581-582

Editorial The impact of culture on technology How do we create a clinical culture of innovation? MJA 1999; 171: 508-509 Human knowledge, we are told, is growing exponentially, and so too, by implication, is the development of technology. The theme of this special issue of the Medical Journal of Australia is the Impact of New Technologies in Medicine, and the Journal joins 43 other medical journals internationally in exploring this theme. Together, they create a global snapshot of the rise of technological medicine at the close of the 20th century. However, it is not just our ability to innovate that is growing. The complexities of predicting the impact of new technologies on our bodies, our society and our world are increasing too. For example, while our ability to map the human genome and manipulate its structure is only in its infancy, the speed of this technological development has already outstripped our collective capacity to develop appropriate moral approaches and social and environmental policies about its application. The same group of technologies that might deliver a cure for cystic fibrosis could also tamper with our food crops, with possible widespread and unexpected implications for public health. So, is it time for the Luddite clan to regather, or is it time to take another leap of faith into the future? This is the dilemma we have already faced many times this century. The nuclear industry developed both weapons of mass destruction and engines of energy, and the debate raged about whether one was possible without the other. With hindsight we now know that the two could not be separated.1 An almost unspoken assumption about technology is that its development is inevitable, and that, for good or bad, we must come to terms with the changes that follow. However, technology does not develop in a vacuum; the direction of its evolution is not a fundamental law of nature. The potential for innovation is probably infinite, and we make active choices in developing one set of technologies over others. Since human resource is finite, we have to ration our efforts. We see this in the often-implicit priority-setting of governments, research-funding agencies and industry. As a community, we also make decisions to resist particular innovations. Rogers' classic work The Diffusion of innovations is filled with examples of the barriers that any innovation must cross before it comes into common use.2 Among the greatest of these barriers is the culture of organisations and societies, because it is within cultures that we decide what is valuable and what is not. Thus, in medicine, if a new technology is seen to threaten our role as doctors or to diminish our importance, then it is likely to be resisted. If our peers scorn the use of a particular technology, or favour another, then we are more likely to follow suit. So, our culture shapes the technologies we build and the technologies that we adopt. One of the problems facing practising clinicians is that much of the technological innovation is coming from outside our own professional culture. It is hard not to feel deluged by the offerings of the pharmaceutical, biotechnology and information industries. Why is the situation not reversed? What is it about the clinical culture that makes us predominantly adopters of, rather than innovators of, technology? If we scan the pages of our medical journals, we see that much of clincal science revolves around assessing the "evidence". Somehow, whether consciously or unconsciously, clinicians have assumed the role of gatekeeper, vetting the creations of others. But before a drug or technology comes to randomised clinical trial, there has been a long and expensive path of invention and experimentation. Indeed, this hidden process of innovation applies to most technologies, where probably only one in ten ideas makes it off the drawing board and into an applicability trial. When others are better equipped than clinicians to do the inventing, the system works well. When clinicians are faced with challenges that require us to be the inventors, we run into trouble. We are very good at being critical and analytical, but are not used to being lateral, fuzzy and playful in our thinking. New ideas require nurturing, cajoling and bending and can easily get crushed if we prematurely apply our skills of critical evaluation. Yet it is this creative and necessarily fluid process of innovation that is desperately needed today. Struggling with an ever more burdened healthcare system, we know we must re-invent the way we work, and redefine our roles and the way that we structure the delivery of care. To do this, we will need to be as innovative as we are critical. Unfortunately, the healthcare culture shares many of the attributes of large organisations that struggle with, or fail to adapt to, change. In common with many other established organisations, the success of the existing way of doing business makes the cultural norm one of steady, incremental change rather than radical change. Further, the older the organisation, the richer are the interdependencies between groups in that organisation.3 If one or more small groups are threatened by an innovation, its passage through the larger organisation is likely to be stifled. Indeed, those who study the interactions between professional subcultures within healthcare consider the conflicting beliefs of these different groups to be a major barrier to health reform.4 If we look to the strategies of enduring organisations that successfully adopt innovations, we see a willingness to recognise that change is essential, and an ability to relinquish old hard-won skills and ideas in favour of the new. Such organisations have the skills to create a vision of what they wish to become, and to set about making that vision come true. The process of continuous renewal is one of seeking advantage in change, and of finding new evolutionary niches in the changing competitive landscape. So, if healthcare is to evolve in pace with the rest of society, it needs to focus on creating a sustainable and flexible culture that does not fear innovation. Whether we are enraptured by the promise of technology, or are in fear of it, simply being reactive to its development is not appropriate. Our culture's beliefs and values shape what we create and what we dream. An anti-technology stand leaves us room only to react to what is done by others, and, with the potential to innovate accelerating as it is, now is the time to be pro-active. Many of us believe that medicine will be profoundly transformed in this coming generation, and that our power to build new technologies will be pivotal in engineering that transformation. But it is not the technology that will transform medicine -- it is our vision of medicine that will define the change. Our skills of invention will then shape the technology we need to make the vision reality. Enrico Coiera MJA Guest Editor Professor, Faculty of Medicine University of NSW Sydney, NSW ewcATpobox.com Malchijiani A, Hu H, Yih K. Nuclear wastelands: a global guide to nuclear weapons production and its health and environmental effects. Boston: MIT Press, 1995. Rogers EM. Diffusion of innovations. New York: Free Press, 1995. Utterback JM. Mastering the dynamics of innovation. Boston: Harvard Business School Press, 1994. Degeling P, Kennedy J, Hill M, Carnegie M, Holt J. Professional sub-cultures and hospital reform. Sydney: UNSW Centre for Hospital Management and Information Systems Research, 1998. Make a comment

Enrico Coiera

Editorial Sentinel node biopsy: evaluating a new technique Can we safely avoid axillary clearance in selected women with breast cancer? MJA 1999; 171: 452-453 Breast cancer is one of the most-researched areas of medicine, and best practice has evolved from well conceived and conducted randomised trials. For instance, we know that outcomes after breast-conserving surgery and mastectomy are equivalent, that adjuvant therapies improve survival, and that breast screening reduces mortality. Yet, many questions remain unanswered. In breast cancer, the status of the axillary nodes is one of the strongest prognostic indicators, and a major factor in determining adjuvant systemic therapy. Although the landmark National Surgical Adjuvant Breast Project (NSABP 04) study concluded that treatment of the axilla per se did not affect long-term survival,1 the issue of whether or not good local control (ie, radiotherapy or axillary clearance) affects survival is still debated,2,3 and the evidence to date suggests that at least Level 2 dissection -- 10 or more nodes -- is required for reliable assessment of axillary involvement.4 A proportion of women will experience complications after axillary dissection, including shoulder dysfunction, paraesthesiae and chronic lymphoedema.5 The question then arises: can we avoid axillary clearance in selected patients -- for example, by the technique of axillary node biopsy? This technique is based on the assumption that the status of the first node in the draining basin of the primary tumour is an accurate indicator of the overall status of that field of drainage; with a tumour-free sentinel node, axillary dissection may be unnecessary. Now that screening and evidence-based improvements to treatment are starting to have an impact on survival, we need to be wary of replacing well established methods with new techniques that have not been rigorously evaluated. Can sentinel node biopsy be implemented safely, with real long term benefits for our patients? In this issue of the Journal , Kollias and colleagues report their results with the sentinel node biopsy technique,6 which compare favourably with other international series. Sentinel nodes were identified successfully in 95 of the 117 women by a combination of three techniques -- lymphoscintigraphy, blue dye and a hand-held gamma probe (the latter two for intraoperative identification). Lymphoscintigraphy is an important prelude to sentinel node biopsy, but in the series of Kollias et al it successfully mapped the sentinel node in only 63.2% of cases. However, the authors point out that they were able to improve the accuracy by increasing the injection volume. The skill and persistence of the nuclear physician are key factors in obtaining optimal lymphoscintigraphy. In Australia, we are fortunate to have a radiopharmaceutical (99mTc-labelled antimony sulfide colloid) that is superior to those available in other countries. This means that we may produce more accurate maps of lymphatic drainage, and thereby identify sentinel nodes more often. Research reported from the Royal Prince Alfred Hospital in Sydney has shown that drainage patterns from individual tumours can be quite unexpected.7 This new area of study means that we will have to re-evaluate the whole notion that "skip metastases" occur, and their significance in determining overall prognosis.8 If a decision on whether to dissect the axilla had been based on a confirmed tumour-negative sentinel node, then 66 of the 117 women in the study of Kollias and colleagues would have been spared axillary dissection, although in two women this would have been a false negative diagnosis (two of the 31 women with nodal involvement had sentinel nodes negative for tumour). This rate (6.5%) is comparable with those in other series.9,10 Although we should be concerned about the false negative rate of sentinel node biopsy, we should also recognise that some occult metastases are not detected in standard haematoxylin-eosin histopathological sections. With standard staining methods, the false negative rate in a series of patients reported from St Vincent's Hospital in Melbourne was 12%; in that series, antimucin monoclonal antibodies showed micrometastatic deposits in 41 of 343 patients previously classified as having node-negative breast cancer by haematoxylin-eosin staining.11 False negative assessments are inevitable when lymph nodes are sampled, but the more detailed examination of one or two "sentinel" nodes may prove more beneficial than the standard examination of many nodes. The detection of micrometastatic deposits introduces a new area of uncertainty requiring further study -- we have yet to determine their significance. How do they affect prognosis and how should we treat them? Ongoing evaluation of locoregional recurrence and distant disease is essential. At first glance, sentinel node biopsy appears invitingly easy, but success in completing the sometimes technically difficult procedures involved will define the oncological relevance of the technique. Simply removing a "hot" or "blue" node is not enough -- we have to reappraise our indications for treating the internal mammary nodes and the supraclavicular nodes, as well as those in the axilla, as nodes from more than one site may be involved. It is equally important that women with breast cancer be managed in consultation with oncologists: women treated in a multidisciplinary setting tend to have better outcomes.12 While Kollias et al conclude that sentinel node biopsy is an accurate method of assessing axillary lymph node status, the accuracy has varied in other series. Reported detection rates range from 66% to 100% and false negative rates from zero to 17%.13 Why is there such a discrepancy? A possible explanation is the different techniques used in individual series. Some surgeons used only one method of localisation; others used different combinations of the three techniques -- different dyes, different radiopharmaceuticals, different times between injection and surgery, different methods of injection, and even different criteria by which sentinel nodes are searched for and removed. In Australia, we have a window of opportunity to work towards a standardised approach to sentinel node biopsy, using agreed protocols and prospective and uniform data collection. Kollias and colleagues, and other representatives from the major breast units and the Section of Breast Surgery of the Royal Australasian College of Surgeons, are working together and have proposed an Australasian prospective randomised trial with the capacity to involve all surgeons who are interested in breast cancer management. New techniques require proper evaluation. As a group, surgeons have been quick to adopt new procedures before scientific validation.14 In addition, consumer pressures, and sometimes market pressures, are at work. For comparison, consider laparoscopic cholecystectomy, which has now gained widespread approval. The learning curve was steep -- the early reports of this technique were full of enthusiasm and the procedure was adopted rapidly. There is no doubt that, in those early days, considerable morbidity for many patients could have been avoided with more caution and less haste.15 The technical aspects of these two quite different operations are not comparable; the parallel to be drawn relates to the way new procedures may be incorporated into, and perhaps finally adopted as, standard procedures. It therefore behoves us to ensure that, with any new procedure, consumers are not placed at increased risk, particularly if it is performed with limited expertise. Owen A Ung Clinical Services Director New South Wales Breast Cancer Institute, and Breast and Endocrine Surgeon Westmead Hospital, Sydney, NSW owenuATbci.org.au Neil R Wetzig Chairman, Section of Breast Surgery Royal Australasian College of Surgeons and Senior Surgeon Princess Alexandra Hospital, Brisbane, QLD Fisher B, Redmond C, Fisher ER, et al. Ten-year results of a randomized clinical trial comparing radical mastectomy and total mastectomy with or without radiation. N Engl J Med 1985; 312: 674-681. Harris JR, Osteen RT. Patients with early breast cancer benefit from effective axillary treatment. Breast Cancer Res Treat 1985; 5: 17-21. Overgaard M, Hansen PS, Overgaard J, et al. Postoperative radiotherapy in high-risk premenopausal women with breast cancer who receive adjuvant chemotherapy. Danish Breast Cancer Cooperative Group 82b Trial. N Engl J Med 1997; 337: 949-955. Axelsson CK, Mouridsen HT, Zedeler K, on behalf of The Danish Breast Cancer Cooperative Group (DBCG). Axillary dissection of level I and II lymph nodes is important in breast cancer classification. Eur J Cancer 1992; 28A: 1415-1418. NHMRC National Breast Cancer Centre. Lymphoedema: prevalence, risk factors and management: a review of research. Sydney: NBCC, 1997. Kollias J, Gill PG, Chatterton BE, et al. Reliability of sentinel node status in predicting axillary lymph node involvement in breast cancer. Med J Aust 1999; 171: 461-465. Uren RF, Howman-Giles RB, Thompson JF, et al. Mammary lymphoscintigraphy in breast cancer. J Nucl Med 1995; 36: 1775-1780. Danforth DN, Findlay PA, McDonald HD, et al. Complete axillary lymph node dissection for stage I-II carcinoma of the breast. J Clin Oncol 1986; 4: 655-662. Giuliano AE, Kirgan DM, Guenther JM, Morton DL. Lymphatic mapping and sentinel lymphadenectomy for breast cancer. Ann Surg 1994; 220: 391-398. Krag DN, Ashikaga T, Harlow SH, Weaver DL. Development of sentinal node targeting technique in breast cancer patients. Breast J 1998; 4: 67-74. Hainsworth PJ, Tjandra JJ, Stillwell RG, et al. Detection and significance of occult metastases in node-negative breast cancer. Br J Surg 1993; 80: 459-463. Sainsbury R, Haward B, Rider L, et al. Influence of clinical workload and patterns of treatment on survival from breast cancer. Lancet 1995; 345: 1265-1270. McIntosh SA, Purushotham AD. Lymphatic mapping and sentinel node biopsy in breast cancer. Br J Surg 1998; 85: 1347-1356. Solomon MJ, McLeod RS. Surgery and the randomised controlled trial: past, present and future. Med J Aust 1998; 169: 380-383. The Southern Surgeons Club. A prospective analysis of 1518 laparoscopic cholecystectomies. N Engl J Med 1991; 324: 1073-1078.

Editorial Where has all our iodine gone? The possible re-emergence of iodine deficiency in Australia needs to be investigated in national surveys MJA 1999; 171: 455-456 Most countries in the world, including Australia, are signatories to the United Nations-sponsored "Declaration for the Survival, Protection and Development of Children", which states that "every child has the right to an adequate supply of iodine to ensure its normal development".1 One teaspoon of iodine is all a person requires in a lifetime, yet iodine deficiency at critical stages of development in fetal life and early childhood remains the world's single most important and preventable cause of mental retardation.2For the past three to four decades iodine deficiency has not been of significant concern in Australia (except in Tasmania); it was considered largely a problem of developing countries. That is what we thought until Gunton and colleagues give us a wake-up call with their article in this issue of the Journal 3. They found evidence of mild to moderate iodine deficiency in pregnant women, patients with diabetes and a small group of volunteers attending a Sydney teaching hospital. In their study, median urinary iodine concentrations ranged from 64 µg/L in the volunteers to 104 µg/L in pregnant women. The World Health Organization's standard for iodine-deficiency disorders in population surveys recommends that a median urinary iodine concentration above 100 µg/L is evidence against significant iodine deficiency in that population.4 Other population indicators of iodine deficiency, including total goitre rates in school-age children and serum thyrotropin (TSH) levels in the newborn, were not assessed in the Sydney study. The data of Gunton and colleagues indicate that the pregnant women they tested are ingesting less than half the recommended iodine intake in pregnancy of 200 µg/day. Although this study was not a national survey, and the sample size was small, the findings are alarming and raise concern that a major public health problem may be developing in the Australian community which could put future generations at risk of iodine-deficiency disorders. The key factor in the genesis of iodine-deficiency disorders is decreased production of thyroxine from the thyroid gland. While endemic goitre is the most easily recognised and best-known consequence of iodine deficiency, it is probably the least important. At critical periods in fetal development and in early childhood, biochemical hypothyroidism, due to iodine deficiency, results in a wide range of devastating and irreversible effects now known as iodine-deficiency disorders.5 More recently, we have come to appreciate that there is a general diminution in intelligence in iodine-deficient communities such that iodine deficiency is considered to be the commonest cause of preventable intellectual disability worldwide.2 Further, there is now very good evidence that a small decrease in serum free thyroxine level during pregnancy, either because of iodine deficiency or thyroid disease, is an important risk factor for impaired psychomotor development in infants.6,7 The recent demonstration of intellectual impairment in the children of American women who had mild hypothyroidism in pregnancy highlights the need for better detection and treatment of hypothyroidism in early pregnancy, irrespective of its cause.8 Tasmania is the only Australian State where regular surveillance of iodine nutrition is undertaken and records are maintained. Other data are available from the Australian Centre for Control of Iodine Deficiency Disorders (ACCIDD), located at Westmead Hospital, which has performed sporadic surveys of urinary iodine excretion levels in small samples of Australians for the past two decades. In 1992 we reported that the mean urinary iodine excretion level in Sydney residents was 180 µg/L, and over 200 µg/L in Tasmanian children.9 Since then, our sporadic surveys have shown a gradual but sustained decline in urinary iodine excretion levels in Sydney residents. We recently found similar results to those of Gunton et al 3 in a survey of primary schoolchildren from western Sydney who had a median urinary iodine concentration of 84 µg/L, and in 16% of whom the iodine concentration was less than 100 µg/L. Further, unpublished results we obtained in healthy pregnant women were also very similar to those of Gunton et al, indicating that widespread mild iodine deficiency threatens to affect the most vulnerable in our community. Why is our iodine intake decreasing in Australia? Gunton and colleagues implicate a combination of factors. Firstly, for over three decades, we have been dependent on iodine in milk contaminated by cleaning solutions used in the dairy industry; these solutions are gradually being replaced by others which leave less iodine in milk. Secondly, we seem to be using less iodised salt, through a combination of purchasing uniodised salt for domestic consumption, probably decreasing our salt consumption, and consuming most of our salt in processed foods, which, as far as we can ascertain, is uniodised. The problem is not unique to Australia, as similar downward trends in iodine intake have recently been noted in other developed countries such as the United States10 and New Zealand.11 What actions should be taken in response to these findings? Firstly, we need more information through a national survey of urinary iodine excretion and goitre rates to determine the status of iodine nutrition throughout Australia. Secondly, we need to educate the population and healthcare providers about the insidious and harmful effects of iodine deficiency, especially during pregnancy and early childhood. Finally, we must institute effective and sustainable means of iodine supplementation to our whole community through legislating for universal salt iodisation, so that all salt used for human and animal consumption in Australia is iodised. Iodising all edible salt will cost less than 10 cents per person annually. In the past this intervention has been viewed as politically unacceptable, but the debate was conducted with a view to eliminating endemic goitre without any real understanding of the often subtle, but devastating, consequences of impaired brain development. In the interim, every effort should be made to ensure every pregnant woman ingests an adequate amount of iodine to ensure her unborn child experiences normal mental development. Until we have educated the population as a whole about the risks of iodine deficiency and instituted mandatory iodisation of all salt for human and animal consumption, it may be prudent to recommend supplementary iodine for all pregnant women from the time of conception until weaning of the infant. Creswell J Eastman, AM Director, Institute of Clinical Pathology and Medical Research Westmead Hospital, Westmead, and Clinical Professor of Medicine University of Sydney, Sydney, NSW World Declaration on the survival, protection and development of children and a plan of action for implementing the world declaration on the survival, protection and development of children in the 1990s. New York: United Nations, 1990. World Health Organization. Progress towards the elimination of Iodine Deficiency Disorders (IDD). WHO/NHD/99.4. Geneva: WHO, 1999. Gunton JE, Hams G, Fiegert M, McElduff A. Iodine deficiency in ambulatory patients attending a Sydney teaching hospital: Is Australia truly iodine replete? Med J Aust 1999; 171: 467-470. World Health Organization. WHO, UNICEF, ICCIDD. Indicators for assessing iodine deficiency disorders and their control through salt iodisation. WHO/NUT/94.6. Geneva: WHO, 1994. Boyages SC. Clinical Review 49, Iodine deficiency disorders. J Clin Endocrinol Metab 1993; 77: 587-591. Pop VJ, Kuijpens JL, van Baar AL, et al. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy. Clin Endocrinol 1999; 50: 149-155. Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neurological development of the child. N Engl J Med 1999; 341: 549-555. Utiger RD. Maternal hypothyroidism and fetal development. N Engl J Med 1999; 341: 601-602. Eastman CJ. The status of iodine nutrition in Australia. In: Delange F, Dunn JT, Glinoer D, editors. Iodine deficiency in Europe -- a continuing concern. New York: Plenum Press, 1993: 133-139. Dunn JT. What's happening to our iodine? [editorial]. J Clin Endocrinol Metab 1998; 83: 3398-3400. Thomson CD, Colls AJ, Conaglen JV, et al. Iodine status of New Zealand residents as assessed by urinary iodide excretion and thyroid hormones. Br J Nutrition 1997; 78: 901-912.

Creswell J Eastman

Editorial Monitoring drinking water: the receding zero Testing is only one part of an overall preventive strategy to ensure high quality affordable drinking water MJA 1999; 171: 397-398 For related article see Byleveld et al Improvements in analytical methods now allow us to measure minute quantities of chemicals and microorganisms in water which a decade ago would have been undetectable. However, our understanding of the impact on public health of low-level exposures to these contaminants lags far behind the technological expertise which enables us to detect them. The rationale for testing drinking water needs to be placed in perspective with the more important aspects of overall system management and risk minimisation. Testing of drinking water shares some similarities with laboratory testing in medicine. Before embarking on a testing regimen, the reliability of the testing method needs to be established, the purpose of the test should be clear, and there must be an adequate response plan to deal with the result. The mere fact that a particular test exists does not justify its use -- these three requirements must also be fulfilled. Some critical factors in drinking water require continuous monitoring, as even temporary disruption can have major health consequences. An obvious example is monitoring of chlorine concentrations to ensure effective destruction of waterborne pathogens. Failure of chlorination systems is one of the more common causes of waterborne disease outbreaks.1 Also frequently monitored are levels of faecal coliform bacteria, which, although not pathogenic, are an early indication of faecal contamination. Increased levels provide a warning of failure in water treatment or a break in the integrity of the distribution system, or possible contamination with pathogens. Tests for faecal coliform bacteria are cheap, reliable, and rapid. High levels of faecal coliforms may indicate an elevated risk of waterborne gastroenteritis.2 Chemical contaminants in drinking water (eg, arsenic or pesticides) require considerably less frequent measurement, because exposure to the guideline level does not pose a significant health risk over a lifetime's consumption. These health guideline levels are very conservative and have built-in safety factors to compensate for limitations in scientific knowledge and variation in sensitivity among the exposed population.3 For all potential waterborne contaminants, including individual pathogens such as Cryptosporidium and Giardia, there is a great temptation to attempt to apply numerical limits. This is understandable: a numerical value is easily understood and compliance can be clearly judged by regulators and water authorities alike. However, as illustrated by the at times frenzied debate accompanying the water contamination episode in Sydney in 1998, some contaminants can not be equated with a meaningful health-based guideline value.4 Despite this, the United Kingdom government is pressing ahead with enforcing a numerical limit for Cryptosporidium in drinking water and daily monitoring of a large number of water supplies. The legislation will impose a legally enforceable maximum concentration of 10 oocysts/100 L for water supplies considered to be at risk of contamination.5 The presence of Cryptosporidium oocysts above this level will constitute a criminal offence, and could result in an unlimited fine. The impetus for this legislation is complex and relates to an inability under UK law to prosecute water authorities for outbreaks of waterborne cryptosporidiosis on the basis of epidemiological evidence. It is estimated that the cost of testing treated drinking water for Cryptosporidium in the UK will be at least £8 million per year. It has been assumed that this improved management of drinking water treatment plants may prevent about 150 reported cases of waterborne cryptosporidiosis annually. Thus, the cost of preventing each reported case would be about £53 000.5 Reported cases probably represent about one-tenth of community cases,6 making the cost per community case prevented closer to £5300. These data illustrate the potentially enormous costs of water testing for individual pathogens, and the disproportionate cost-benefit relationships generated when arbitrary limits are imposed without regard for public health evidence. Overemphasis on numerical guidelines also leads to compliance with "the numbers" becoming the primary focus of drinking water quality management. This simplistic interpretation disregards the proper and intended role of numerical guidelines as a basis for verifying the integrity of operational barriers and water treatment processes. Deviation from normal values may not necessarily constitute an immediate public health risk, but it signals a need to identify the cause and, if neccessary, intervene to restore operational control. The Australian Drinking Water Guidelines drawn up by the National Health and Medical Research Council (NHMRC) in 19963 recognise the primary importance of the multibarrier approach for minimising health risks in water supply systems, but there has been a recent tendency for this message to be overlooked by both regulators and water utilities. The Sydney contamination episode has had widespread repercussions in the Australian water industry, but one very positive outcome has been the recognition that a preventive risk management approach offers a better means of protecting public health than a reactive response centred around intensified testing of drinking water. The current review of the 1996 NHMRC Australian Drinking Water Guidelines7 will consider expanding the existing elements of system management and integrating them into a comprehensive risk-based framework for water quality management, emphasing prevention rather than reaction. For example, improved management of agriculture and recreation in catchment areas will reduce the potential for contamination. This approach includes (i) systematic assessment of each water system from catchment to tap to identify hazards and prioritise risks specific to the system; (ii) establishment and documentation of effective operating procedures to define the processes and procedures for critical activities serving as barriers to contamination; and (iii) operational control measures and verification protocols to ensure that the barriers are functioning effectively. This approach offers Australia a rational and cost-effective alternative to the excessively complex and costly regulatory systems in the United States and Europe. Routine water testing for a variety of chemical, physical and microbial parameters will remain important for operational monitoring and verification of system performance, but our drinking water supply will not be improved by measuring for measuring's sake. There needs to be a very clear rationale for testing drinking water and an understanding of what the result of each measurement means. Testing is only one part of an overall preventive strategy to ensure high quality drinking water at an affordable cost. Christopher K Fairley Head, Infectious Disease Epidemiology Unit Martha I Sinclair Senior Research Fellow Samantha Rizak Research Fellow Cooperative Research Centre for Water Quality and Treatment Department of Epidemiology and Preventive Medicine Monash University, Monash Medical School, Alfred Hospital, Melbourne, VIC christopher.fairleyATmed.monash.edu.au Surveillance for waterborne disease outbreaks -- United States, 1995-1996. MMWR Morb Mortal Wkly Rep 1998; 47(SS-5): 1-34. Indicator organisms and the coliform concept. In: Gleeson C, Gray N, editors. The coliform index and waterborne disease. London: E&FN Spon (Chapman & Hall), 1997: 38-59. National Water Quality Management Strategy: Australian Drinking Water Guidelines. National Health and Medical Research Council (NHMRC), Agriculture and Resource Management Council of Australia and New Zealand (ARMCANZ). Canberra: NHMRC/ARMCANZ, 1996. Sinclair MI, Fairley CK, Hellard M. Protozoa in drinking water: is legislation the best answer? Med J Aust 1998; 169: 296-297. Public health and drinking water: preventing Cryptosporidium getting into public drinking water supplies. Consultation paper. London: Department of the Environment, Transport and the Regions; May 1998. Wheeler JG, Sethi D, Cowden JM, et al. Study of infectious intestinal disease in England: rates in the community, presenting to general practice, and reported to national surveillance. BMJ 1999; 318: 1046-1050. National Health and Medical Research Council (NHMRC) and Agriculture and Resource Management Council of Australia and New Zealand (ARMCANZ). National Water Quality Management Strategy. Revised Australian Drinking Water Guidelines. Draft -- July 1999. Available from: <http://www.nhmrc.health.gov.au/ advice/water.htm> (accessed 16 September 1999). No longer available, but see revised and updated version at http://www.health.gov.au/hfs/nhmrc/publicat/synopses/eh19syn.htm Accessed 10 May

Christopher K Fairley · Martha I Sinclair · Samantha Rizak

Editorial Erectile dysfunction in the Australian community This problem is both increasingly recognised and increasing in prevalence with the ageing of our population MJA 1999; 171: 342-343 Erectile dysfunction (ED) is the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual activity.1 Worldwide, 100 million men are estimated to have some degree of ED, with around 30 million men in the United States1 and around one million men in Australia affected. With our ageing, but relatively fit, population the incidence of ED is certain to escalate. The first major community-based study on ED was the Massachusetts Male Aging Study (MMAS),2 an observational study (conducted from 1987 to 1989) of a random sample of men aged between 40-70 years living in and around Boston, Massachusetts. This study yielded, for the first time, an understandable concept of ED; comparable studies in Australia have been singularly lacking. The first report on the prevalence of ED in our community was a study by Chew et al from the Keogh Institute for Medical Research in Perth3 (formerly the Reproductive Medicine Research Institute). The generalisability of this 1996 study was limited as it only included men who presented to general practices in Perth. The South Australian community study by Pinnock and colleagues in this issue of the Journal,4 which recruited men from the general community through a 1997 household survey, provides data that are, firstly, drawn from a more general community sample than the one in the Perth study, and secondly, more suited to our own demographic situation than data from overseas surveys. The South Australian study confirms that age is the strongest contributing demographic factor to ED, with 60 years of age being the turning point where desire exceeds potency and sexual frequency diminishes.4 The MMAS found that 52% of men aged between 40 and 70 years had some form of ED, with almost 60% of 60-year-old men having this complaint.2 Both studies found that sexual function was also affected by risk factors such as smoking, hypertension, obesity and a high total cholesterol level with a low concentration of high density lipoprotein. Vigorous exercise was found to be protective. The Perth study also found diabetes mellitus (types 1 and 2) to be significant contributors to ED. It should be noted that Pinnock et al used a questionnaire based on the UCLA Prostate Cancer Index that covered sexual function parameters including desire and orgasm, frequency of intercourse, prostate surgery and erectile function. As this index has not been validated in patients who do not have prostate cancer, its use in a randomly based population study represents a methodological flaw. A more appropriate questionnaire for this study would have been the better-known International Index of Erectile Function (IIEF),5 a 15-question survey that includes similar parameters, assesses intercourse and overall satisfaction, but excludes questions related to prostate cancer. The higher incidence of ED reported in the South Australian study4 compared with the MMAS2 probably reflects improvements in public awareness and keenness to discuss and report ED over the past 10 years. The study by Pinnock et al4 clearly shows that cardiovascular disease and ED have similar risk factors and present in a similar age group. Thus, it seems possible that, by improving their risk factor profile, men may benefit both their cardiovascular health and their sexual function. Pinnock et al also suggest non-cancer prostate surgery appears a more important contributor to ED than previously recognised. Erectile dysfunction is clearly an established and recognised male health problem -- one that is decreasingly being regarded as an inevitable consequence of ageing. The estimated 10% of men currently seeking help will increase, as more men will seek help in the future. Doctors will need to improve their skills in obtaining patients' sexual histories as more men request help. A full assessment of men, with emphasis on cardiovascular risk factors, will help direct the consultation to discussion of sexual matters -- it makes good sense to combine cardiac and sexual issues. Sildenafil is the first effective oral medication for ED, and its arrival on the market was well timed with the increasing interest in ED and the increasing numbers of men wanting a simpler treatment. Initial media interest over coital deaths associated with sildenafil has abated, and the drug is now accepted as a safe treatment when prescribed within the recommended guidelines. These guidelines advise caution when prescribing sildenafil to male cardiac patients who may not be fit enough to engage in sexual activity. Sildenafil is also absolutely contraindicated in men receiving nitrate therapy and those who use amyl nitrite "poppers". When sildenafil is contraindicated or fails to achieve the desired result, the use of injectable vasoactive agents is appropriate. Penile injection therapy is still considered the "gold standard", having been used for over 10 years. Alprostadil is the only approved injectable prostaglandin medication available on the Pharmaceutical Benefits Scheme. Alprostadil is also available as an intra-urethral pellet. Vacuum erection devices have been available for over 20 years and are still an acceptable choice for some men. Penile prostheses may be used in more difficult cases. The Australian community-based studies on male sexual function show a pattern similar to that in overseas studies, and highlights two important points in this era of increasing demand for treatment for ED: Doctors need to understand "normal" sexual function for men at different age groups, as knowing the effects of ageing on sexuality is important when counselling patients and advising on treatment; and Knowing that an apparently healthy patient presenting with ED may have underlying cardiovascular disease can advantage the patient's health outcome, and conversely, reducing a patient's cardiovascular risk factors may benefit both cardiovascular health and sexual function; the implications for sexual function may add weight to the arguments against obesity, smoking and excessive alcohol intake. Michael P Lowy Sexual Health Physician Australian Centre for Sexual Health St Luke's Hospital Complex, Sydney, NSW NIH Consensus Conference. Impotence. NIH Consensus Development Panel on Impotence. JAMA 1993; 270: 83-88. Feldman HA, Goldstein I, Hatzichristou DG, et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol 1994; 151: 54-61. Chew KK, Earle CM, Stuckey BGA, et al. Erectile dysfunction in general medical practice. A study in Perth, Australia. Int J Impotence Res 1997; 9 (Suppl 1): A17. Pinnock CB, Stapleton AMF, Marshall VR. Erectile dysfunction in the community: a prevalence study. Med J Aust 1999; 171: 353-357. Rosen RC, Riley A, Wagner G, et al. The international index of erectile function (IIEF): a multidimensional scale for assessment of erectile dysfunction. J Urol 1997; 49: 822-830.

Michael P Lowy

Editorial Screening, case finding and evidence-based guidelines There are functional questions about the nature of screening and the exact clinical scenarios to which screening guidelines apply MJA 1999; 171: 344-345 Screening has been defined as "the examination of asymptomatic people in order to classify them as likely or unlikely to have a disease".1 When public health authorities recommend screening for otherwise healthy people they assume a substantial degree of responsibility. Clear evidence should exist that the disease in question can be identified at an earlier and more treatable stage in its natural history. Moreover, the resulting fall in morbidity or mortality should be achieved without too great a burden of adverse effects. In particular, the side effects of the procedures necessary to establish a diagnosis and those associated with the treatments employed should not be excessive. Screening for prostate cancer has spurred considerable controversy, particularly since the introduction of prostate-specific antigen (PSA) testing.2,3 Most authorities within Australia and other countries recommend against such testing.4 The reasons include a lack of confidence that present interventions improve the prognosis of lesions discovered at screening. Furthermore, the interventions available (surgery and radiotherapy) are associated with a fairly high frequency of impotence and incontinence.5 These may be a high price to pay in the absence of proven benefit. Negative sentiments about routine prostate cancer screening have been incorporated into guidelines by four Australian bodies.6-9 In this issue of the Journal, Girgis et al examine the impact of such guidelines on the behaviour of general practitioners faced with a 58-year-old man requesting screening at the behest of his wife.10 They found that 90% of respondents would accede to the patient's request. After being acquainted with the Australian guidelines, three-quarters of the respondents would still choose to test the patient. Only 15% of respondents were confident that the guidelines would assist their case if a patient whom they had refused to test subsequently developed prostate cancer and sued. Few believed that they were at risk of being sued if patients suffered complications of investigation or treatment of which they had not been warned before screening. The authors conclude that evidence-based guidelines have little influence on GPs' approach to prostate cancer screening and raise the issue of "more deliberate implementation". They also regard the lack of confidence in a legal defence derived from national evidence-based guidelines as troubling and recommend that steps be taken to clarify their legal standing. As readers of the discussion in the Journal's Internet peer review trial would be aware,11 these conclusions have been challenged and have raised fundamental questions about the nature of screening and the exact clinical scenarios to which screening guidelines apply. In practice, screening can be carried out in a variety of settings. These range from organised mass population screening to advice provided to a single patient presenting to a doctor on account of some other problems (the latter is referred to as case finding). The common feature is that the medical profession has taken the initiative to promote the testing, and most screening guidelines have been developed with this implicit assumption. If this view is accepted, then a request by a patient to have a PSA test would not qualify as screening. When the request has been made by an asymptomatic patient without any particular concerns, the risk-benefit ratio is likely to be similar to that of a typical screening scenario, and it would be appropriate to be guided by the same advice. In other words, in a setting strictly as described by Girgis et al, where the patient requested testing at the suggestion of his wife, it might well be appropriate to be guided by the same published guidelines for prostate cancer screening. If special concerns about the presence of prostate cancer have led to the request, a GP might reasonably conclude that the extra component of reassurance is sufficient to justify the test. However, men with uncomplicated lower urinary tract symptoms should be advised that there are no data to suggest that they are at increased risk of prostate cancer.9 In real life clinical practice other complexities may also arise and must be taken into account. When patients seek PSA testing, simple refusal is rarely an option for GPs wishing to successfully balance their varied roles of therapist, educator, friend, small businessman and guardian of the public purse. Most GPs would agree that their principal task is to provide a balanced account of the pros and cons of testing. This would include the fact that a positive test could initiate a potentially costly chain of events that might leave the person incontinent and/or impotent without improving his life expectancy. If these facts have been conveyed accurately and the patient still requests testing then continued refusal may be seen as unreasonable and paternalistic. For a simple screening investigation such as PSA, where controversy is known to exist, it is difficult to be critical of practitioners who would provide testing. The other key issue raised by Girgis et al is the extent to which defensive medicine influences the use of clinical investigations in Australia. The fact that 46% of GPs perceived a medicolegal risk if they failed to accede to the patient's request, despite being presented with evidence that the testing was inappropriate, illustrates the extent of this problem. It has been anticipated that the provision of clinical practice guidelines might assist practitioners dealing with controversial clinical problems by providing a legally defensible approach with which to manage patients. However, this study suggests that, at least in the case of prostate cancer screening, guidelines do not provide this reassurance. The authors point out that, unless the legal standing of guidelines can be clarified, they are unlikely to provide a useful response to the problem of defensive medicine. Like many vigorous controversies, the arguments about prostate cancer screening result from a lack of evidence of value rather than evidence of no value. The definitive information to guide practitioners will be derived from clinical trials large enough to establish the balance of benefits and costs in a population. Trials of this type are presently under way in both the United States and Europe.12,13 Findings are expected in 2002 or sometime thereafter. If these provide an unequivocal result, then the response of practitioners to various testing scenarios will be guided by much firmer evidence. John J McNeil Professor, and Head, Department of Epidemiology and Preventive Medicine Monash University, Melbourne,VIC Paul E O'Brien Professor, Department of Surgery Monash University, Melbourne, VIC Mornson AS. Screening. In: Rothman KJ, Greenland S, editors. Modern epidemiology. Philadelphia: Lippincott-Raven, 1998; 499. Mulley AG, Barry MJ. Controversy in managing patients with prostate cancer. Banish dogma, get more data [editorial]. BMJ 1998; 316: 1919-1920. Woolf SH. Screening for prostate cancer with prostate-specific antigen -- an examination of the evidence. N Engl J Med 1995; 333: 1401-1405. Feeney T. To screen or not to screen. In: Fundamentals of prostate cancer detection and treatment [web site]. <http://rattler.cameron.edu/ww/index.html>. Revised 27 January 1999. Accessed 1 September 1999. Coley CM, Barry MJ, Fleming C, et al. Early detection of prostate cancer. Part II: Estimating the risks, benefits, and costs. Ann Intern Med 1997; 126: 468-479. Australian Cancer Society. Prostate cancer screening: guidelines for health professionals. Cancer Forum 1995; 19: 47-50. Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice. 4th ed. Sydney: RACGP, 1996; 26. National Health and Medical Research Council. Clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: Commonwealth of Australia, 1997. Girgis S, Ward JE, Thomson CJH. General practitioners' perceptions of medicolegal risk. Using case scenarios to assess the potential impact of prostate cancer screening guidelines. Med J Aust 1999; 171: 362-366. Girgis S, Ward JE, Thomson CJH. Potential impact using case scenarios of guidelines discouraging prostate cancer screening on general practitioners' perceptions of medicolegal risk [second revised version with peer review discussion]. <http://www.mja.com.au/public/issues/iprs2/girgis/girgisframe.html>. Accessed 1 September 1999. Kramer BS, Brown ML, Prorok PC, et al. Prostate cancer screening: what we know and what we need to know. Ann Intern Med 1993; 119: 914-923. Auvinen A, Tammela T, Stenman U-H, et al. Screening for prostate cancer using serum prostate-specific antigen: a randomised population-based pilot study in Finland. 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