Editorials

An urgent alternative watershed management strategy is needed The world has vast natural reservoirs of geological arsenic. The ubiquitous nature of this element means that in some countries arsenic contaminates drinking water, enters the food chain and imposes significant human health risks. Globally, up to 100 million people are at risk of exposure to excessive levels of naturally occurring arsenic in well water or groundwater.1 The countries where arsenic levels in drinking water supplies exceed acceptable levels include Argentina, Bangladesh, Bolivia, Chile, China, Hungary, India, Mexico, Nepal, Peru, Romania, Taiwan, the United States and Vietnam.1,2 A young girl drinking water from a tube-well. (Reproduced with permission: PE-12G-003/Shehzad Noorani/UNICEF Bangladesh.) In Bangladesh, the problem is particularly widespread. Many of the tube-wells in Bangladesh, which supply 95% of the water to 138 million people,3 are contaminated with arsenic at concentrations much higher than the current recommended levels.4,5 If no action is taken now, it is likely that within 20 years a substantial proportion of the Bangladeshi population will develop arsenic-related disease, including cancer. Here, we describe the magnitude and the consequences of the problem, and consider what actions are being pursued and what more needs to be done to prevent this potential public health catastrophe from becoming a reality. Arsenic is a human carcinogen.6 Chronic arsenicosis is characterised by hyperpigmentation and hyperkeratosis of the skin and cancers of the skin, lungs and bladder. Other adverse health effects include hypertension, cardiovascular disease (ischaemic heart disease), cerebrovascular disease, diabetes and reproductive effects including low birthweight, higher occurrence of spontaneous abortions and stillbirths, and congenital malformations in the offspring.7 The World Health Organization’s Guidelines for drinking-water quality8 set a provisional level for arsenic in drinking water of 10 μg/L (or 10 ppb [parts per billion]). In Australia, the guideline value set by the National Health and Medical Research Council and the Agricultural and Resource Management Council of Australia and New Zealand is 7 μg/L.9 However, in many developing countries, including Bangladesh, 50 μ g/L is commonly adopted as the guideline value, often for economic reasons, thus exposing the population to long-term risks.10 In Bangladesh, since the 1970s, in an effort to curb water-borne diseases from pathogen-contaminated surface water sources, over 10 million tube-wells have been installed by aid agencies and non-government organisations as sources of clean drinking water. Unfortunately, arsenic was not measured in tube-well water until the 1990s, and it is now known that 30%–90% of the wells in many of the villages tested contain levels in excess of the national standard of 50 μg/L — placing tens of millions of Bangladeshis at even higher risk.4,11 Arsenic-related skin lesions and the other non-cancerous conditions caused by arsenic contamination have a latency period of about 5–10 years, whereas the latency period for arsenic-related cancers is about 20–30 years. A full survey of contaminated wells in Bangladesh has yet to be completed, but initial estimates predict the cancer burden on the health system will be substantial. Lifetime excess mortality risks (per 100 000 persons) from liver, bladder and lung cancer attributable to arsenic in drinking water have been reported as 0.9, 21.5, and 175.9 in males, and 3.4, 2.1, and 48.3 in females, respectively.12 In countries such as Bangladesh whose gross domestic product or gross national income is dwarfed by those of developed nations (Bangladesh is rated 54th of 60 countries),13 the burden of arsenicosis will have a significant impact on the economy, health system and social structure. Construction of a dug-well in Bangladesh which uses a shallower aquifer to provide “arsenic free” water. An urgent alternative watershed management strategy is needed to prevent further arsenic poisoning, and several options are currently being investigated. Bangladesh’s high annual rainfall means that a key option is large catchments and dams with proper disinfection facilities to treat pathogens from surface water supply. But this is considered a long-term solution, requiring large capital investments beyond the resources of Bangladesh. For an immediate solution, relatively inexpensive interventions are being trialled at the family or village levels. These include the use of alternative water sources with low arsenic concentrations, such as dug-wells, deep tube-wells and rainwater storage. Other strategies have included the use of slow sand-filtration systems with or without chlorination and low-cost domestic filtration and/or precipitation systems using iron compounds, alum, or coal fly ash. Ultimately, it is likely there will be more than one solution. The advantages and disadvantages of these strategies have been discussed.5 Cost and compliance will be the governing factors — but we can be certain that action must be taken now. Since the problem was discovered, international aid agencies have been working with the government of Bangladesh and non-government organisations in an attempt to test every tube-well in Bangladesh to identify which wells have arsenic-free drinking water. They are also implementing many small to medium sized water treatment technologies to reduce arsenic contamination, as discussed above. However, future priorities should focus on large-scale nationally managed watershed programs and better utilisation of the vast surface water source that exists in Bangladesh. In addition, international effort is needed to find effective therapies for the people who have developed arsenicosis. Some view this as a problem that only concerns the developing world. However, continuing pressures on water resources in many developed countries, coupled with the presence of geological arsenic and acid sulfate soils, indicate that the events now occurring in Bangladesh could be repeated elsewhere. For example, in mineral-rich countries, where acid sulfate soil is prevalent in many areas, the acid-generating potential of the soil will mobilise arsenic present in ore bodies resulting in arsenic contamination in the groundwater. Recently, we have focused on the effect of the catastrophic tsunami in Asia, hurricanes in the United States, and the earthquake in Pakistan and Kashmir — natural disasters that have claimed many lives. Generally, acute disasters get a lot more media and political attention and international aid. But we also need to look to the horizon to reduce the arsenic-induced casualty that is happening in Bangladesh where tens of millions of people’s lives are potentially at risk.

Jack C Ng PhD, DABT · Michael R Moore PhD, DSc

The Western Australian Audit of Surgical Mortality is a prototype for a national scheme Most surgical care is conducted to a high standard; when a death occurs under surgical care, the patient is usually elderly, with comorbid disease, and a gathering momentum of events leads towards death. However, this does not abrogate the need for accountability in the safety and quality of surgical care. Across the world, established programs promote a culture of reflective practice in surgery and anaesthesia1,2 which have been used as the basis for developing guidelines for perioperative care.3 For sustained accountability, programs require a high degree of perceived clinical ownership, confidentiality, safeguards for the process and participants (such as legal privilege), transparency, and a health care system oriented towards system improvement. Other requirements are robust quality assurance and safeguards to prevent suppression of process or practice failures, as well as full participation and complete data collection, with protected time for individual clinicians, if improvements in health care are to be facilitated. . . . the WA audit model is a promising advance and is likely to contribute to improving surgical care in Australia and New Zealand In this issue of the Journal, Semmens and colleagues report the successful transfer of an established program of auditing deaths after surgery from a public health care system in Scotland4 to a mix of public and private practice in Western Australia.5 While the long-term impact on surgical practice of the Western Australian Audit of Surgical Mortality remains to be determined, its reported early success merits reflection. Although the WA audit was voluntary, participation was high (96%), as occurred in the Scottish Audit of Surgical Mortality.6 The proportion of patient reviews completed in WA (54%) should improve with time, towards the 91% achieved by the Scottish audit,6 although only 100% completion can give the assurance the public deserves. The finding of the WA audit that 6% of the people who died were patients of surgeons who opted out of the audit reveals another aspect requiring improvement if significant outliers are to be identified. The “headline” finding in WA that 20% of surgery-related deaths were associated with deficiencies of care, with 5% caused by these deficiencies, and 2% considered preventable, exhibits a refreshing honesty on the part of participating surgeons. Technical errors featured prominently, in contrast to the process deficiencies identified in the Scottish audit.6 Of particular concern were the 24% of deaths that occurred after elective admissions (compared with 9% in Scotland), with a nearly twofold greater risk of having a deficiency of care in elective compared with emergency surgical patients. Furthermore, the finding that a consultant was the operating surgeon in 50% of cases, regardless of whether it was the patient’s first, second or third operation during the admission, is worrying, as subsequent operations are likely to be unplanned and to present complex challenges. Surgical audits are not new to Australia — they can be traced back to the 1950s.7 Despite this history and the increasing audit requirements of the Royal Australasian College of Surgeons, a recent national survey of medium-to-large hospitals revealed that over two-thirds of Australian surgical units did not conduct an audit according to College requirements.8 This failure was attributed to resource constraints. A method to measure the audit process itself, focusing on system issues as well as individual accountability, has recently been described.9 Although the surgical audit process has been slow to mature and progress in Australia, the WA audit model is a promising advance and is likely to contribute to improving surgical care in Australia and New Zealand, as it has done in Scotland.6 Involving other health professionals, such as anaesthetists and nurses,6 and using data from incident reporting systems,10 would further enhance the process. Implementing an integrated national audit in individual states is a challenge. Meanwhile, the many doctors who have instigated, piloted and participated in the WA audit should be congratulated. So, too, should the Royal Australasian College of Surgeons for endorsing in principle the introduction of a surgical mortality audit based on the WA model across Australia and New Zealand.

Alastair Thompson MD, FRCs(Ed) · Peter A Stonebridge FRCS(Ed) · Allan D Spigelman FRACS, FRCS, MD

One in 25 Australians carries a cystic fibrosis gene mutation, but most do not know it until they have an affected child The technology for safe, cheap screening for the principal gene mutations responsible for cystic fibrosis has long been available. Nearly 10 years ago, the US National Institutes of Health recommended “testing for gene mutations that cause [cystic fibrosis] be offered as an option to all pregnant couples and those planning a pregnancy”.1 A similar recommendation has been made by a joint committee of the American College of Obstetricians and Gynaecologists and the American College of Medical Genetics.2 In 1998, this Journal published an editorial emphasising the need for Australia to follow suit in promoting carrier screening for cystic fibrosis.3 There has been little response despite the fact that each year 70 babies are born in Australia with cystic fibrosis, almost all to parents with no family history.4 Cystic fibrosis is the most common severe autosomal recessive disease of childhood, with an incidence of 1 in 2500 and carrier frequency of 1 in 25. Clinical manifestations include progressive, irreversible suppurative lung disease and pancreatic exocrine insufficiency. Although most children with cystic fibrosis can expect to survive into adulthood, the daily therapies are rigorous, and there are many years of ill health. The median life expectancy is in the mid-30s, with end-stage lung disease the major cause of death. There is still no cure. Most patients with cystic fibrosis are detected by newborn screening, using a biochemical test (for immunoreactive trypsinogen [IRT]) for all babies, followed by cystic fibrosis gene mutation analysis for those with a raised IRT level. Newborn screening facilitates the early diagnosis of cystic fibrosis and genetic counselling for affected families. Couples identified with an affected infant can choose prenatal testing using gene mutation analysis from a chorionic villus sample for subsequent pregnancies to ascertain the status of the fetus. The genetic test used for diagnosis of cystic fibrosis and prenatal testing can also be used to identify carriers of a cystic fibrosis gene mutation. Testing for cystic fibrosis gene mutations is reliable, and, with a 12-mutation panel, nearly 85% of possible severe mutations can be detected. It can be performed using a painless cheek swab. However, testing for carrier status is generally not offered in Australia to couples without a family history, and most of those who carry a mutation do not know until an affected child is born. While we acknowledge the benefits of newborn screening, we believe it would be better to offer cystic fibrosis gene mutation screening to all couples, before they had their first baby with cystic fibrosis. Prenatal screening for a variety of conditions is routine in Australia. All women have a full blood count early in pregnancy, and those who are iron replete with a low mean cell volume are tested for thalassaemia carrier status. The outcome is that it is now uncommon for babies to be born with thalassaemia. Prenatal screening for Down syndrome (using a combination of ultrasound examination and measurement of serum markers) has been offered since 1996, and more than two-thirds of pregnant women in Victoria participate in this screening. Populations with a high frequency of genetic conditions such as Tay–Sachs disease are also offered prenatal or preconceptual screening. Paradoxically, the carrier frequency of cystic fibrosis in the general Australian population is almost the same as the carrier frequency of Tay–Sachs disease in the Ashkenazi Jewish population.5 Lack of awareness about cystic fibrosis no doubt contributes to the lack of community pressure to screen. A successful prenatal screening program for cystic fibrosis has been pursued in Edinburgh for many years.6 This program uses a model of couple testing for carrier status with the offer of prenatal genetic testing of the fetus when both partners are carriers and has halved the incidence of cystic fibrosis in that community.7 Uptake of the service is 80%,6 similar to the uptake in a smaller Dutch study.8 In Victoria, 67% of couples with an infant with cystic fibrosis have used prenatal testing for subsequent pregnancies.9 Some families have opted for pre-implantation genetic diagnosis (with in-vitro fertilisation technology) to avoid pregnancy termination. We advocate a cystic fibrosis screening program in which both parents are encouraged to be screened at the same time, which will give the most accurate risk assessment of the couple having a baby with cystic fibrosis (Box). Ideally, screening would be performed before conception, to allow the couple time to decide on the best reproductive option. In reality, many women do not present for pre-pregnancy assessment, so a screening model that allows prenatal testing of the couple should remain available. Furthermore, we advocate that both parents receive their individual carrier result to maximise the opportunities for cascade family testing. Any program offering carrier screening needs to include genetic counselling for carrier couples, individual carriers and relatives of carriers who may also wish to be tested. Extensive data clearly demonstrate the cost effectiveness of cystic fibrosis screening. The lifetime cost of care for a patient with the condition outweighs the cost of screening women of child-bearing age.10,11 Cystic fibrosis carrier screening should be a federal initiative. Currently, the care of patients with cystic fibrosis and the newborn screening programs are state funded, and there is little incentive for a national program. A Medicare-rebatable test would allow universal access and encourage uptake. Surely, it is time to fund carrier screening for cystic fibrosis in Australia. Screening for cystic fibrosis gene mutations

R John Massie PhD, FRACP · Martin B Delatycki FRACP, PhD · Agnes Bankier FRACP

Specific priority actions and screening programs should target sexually active young people The incidence of sexually transmitted infections (STIs) is increasing in many parts of the world including Australia,1 and the release of the first Australian National Sexually Transmissible Infections Strategy to deal with STIs is timely.2 Three very appropriate priority areas have been identified: Aboriginal and Torres Strait Islander sexual health, STIs in men who have sex with men, and control and prevention of infection with Chlamydia trachomatis among young people. Given that an implementation plan is under development, it is timely to comment on the Strategy, pointing out its strengths and weaknesses, so as to ensure that an effective, comprehensive approach is implemented. Experience from the United Kingdom, where a national STI strategy was developed in 2001,3 suggests that this is the first stage of a long, difficult and contentious process to improve sexual health within the community. The control of STIs involves a range of activities. As well as research, surveillance, and adequate training and support of professional staff, it is essential that we not only increase access to health care (including screening, treatment and contact tracing), but that we also promote health and educate the young about sex. While the Strategy satisfactorily covers surveillance, service provision and research, sex education and behavioural prevention are not adequately addressed, except with reference to gay and other homosexually active men. There are no specific priority actions focusing on sexually active young people, and a lack of clarity with regard to the targeting of screening programs for young people. The Australian Study of Health and Relationships, a recent survey of the sexual relationships and practices of 19 307 people aged between 16 and 59 years, showed that the median age of first intercourse among Australians aged between 16 and 19 was 16 years, and that the reporting of multiple sex partners was significantly associated with younger age and with identifying as bisexual or homosexual.4,5 As the authors noted: “This early onset of sexual activity indicates that it is important to ensure that all young people have information about contraception and disease prevention before they begin their sexual careers and not simply in their final years of schooling.”5 Health promotion, including mandatory sex education, is essential for all young people, male as well as female, and those under as well as those over 16 years of age. A study comparing sexual health outcomes in young people in the context of sex educational policies in the Netherlands, the United States, France and Australia found that in France and the Netherlands, where there is mandatory secondary school sex education, there are fewer STIs than in Australia and far fewer than in the US, where sex education is patchy.6 Increasing access to health care is not enough. There is also evidence that school-based education is likely to be more effective if it is sex positive, that is, if education does not focus solely on delaying or abstaining from sex.6 In the UK, where STI rates are at an all-time high, a survey of young people’s experience of sex education came to the conclusion that such education was “too little, too late and too biological.”7 We should learn from such experience. The Strategy refers to raising awareness of STIs among sexually active young people and recommends that there be a national health promotion campaign. However, the approach is coy. Although safer sex is mentioned, the only mention of condoms occurs under the action plan for gay men, where the Strategy mentions “reinforcing safer sex and condom use.” The consistent use of condoms is a highly effective method of reducing the risk of acquiring STIs, in particular the bacterial infections (gonorrhoea, chlamydia and syphilis) and HIV.8 Condoms have been and continue to be a major factor in the reduction in the incidence of HIV in homosexually active men in Australia. Widespread condom use is also the single most important factor in the continued low incidence of all STIs in commercial sex workers in Australia.9 Young sexually active people need to be aware of the risk of STIs and use condoms to prevent their transmission. The continued promotion and widespread availability of condoms must be one of the key elements of any successful STI strategy. The incidence of chlamydia infection in Australia is increasing and has more than doubled between 2000 and 2004 with over 35 000 notifications, with the largest increases noted in women aged 15–19 and 20–29 years.1,10 In the Minister for Health’s press release, which accompanied the launch of the Strategy, funding of $12.5 million over 4 years was announced for increased awareness, improved surveillance and a pilot testing program for chlamydia infection,11 and this is very welcome. However, while the Strategy highlights the need to develop “a chlamydia screening pilot targeting sexually active young adults”, the Minister’s press release had a different spin, suggesting that the pilot testing program for chlamydia will target women aged 18–30 years. However, younger women and men, particularly young men, who seldom seek health care, should also be the target for the pilot.12,13 In the US and Sweden, where national chlamydia screening policies based largely on opportunistic screening of women have been in place for several years, rates of chlamydia infection remain high.14 There are many long-term physical consequences of STIs, in particular, pelvic inflammatory diseases and consequent infertility, and cervical and other genital tract tumours. In addition, STIs are often associated with psychological morbidity. The release of the Strategy provides a unique opportunity to reduce the prevalence of STIs and their consequences. We must ensure that we make the most of this opportunity.

Adrian Mindel MD, FRACP, FRCP · Susan Kippax BA(Hons), PhD, FASSA

We urgently need to expand clinical teaching into the private sector In clinical school common rooms around the country, a common refrain of frustrated medical students is “ There aren’t any patients in the wards we can see!” In this issue of the Journal, Olson and colleagues (page 461) report an investigation of hospital inpatients’ accessibility to medical students that strongly suggests that our students’ complaints are real.1 . . . there are not enough suitable public hospital inpatients for the clinical teaching programs of the new medical schools The study simulated the experience of students attempting to see patients without the assistance of junior or senior medical staff. Four University of Newcastle medical students audited the wards of four public hospitals on three separate days, each 2 months apart. Inpatients were classified as present, present but not accessible, unfit to be seen on clinical grounds, or absent. Those who were present and accessible were asked if they would agree to a student taking a history and performing a physical examination. Of 1960 patients, 959 (49%) were present and accessible and, of these, 673 (70%) said they would allow a student to take a history and 645 (67%) would allow a student to perform a physical examination. Half of all patients not available to be seen were classified as unsuitable on clinical grounds, either by nursing staff or by the students. In some wards the students were told by nursing staff that all patients were unsuitable. In short, just over a third of the inpatients in these four hospitals were accessible to medical students.1 Those responsible for clinical teaching programs in public hospitals are only too aware of this problem, which is caused by several factors. Reduced length of stay and “hospital in the home” programs designed to avoid or shorten admissions mean that inpatients are sicker and less inclined to see students. Moreover, as the average age of inpatients rises, an increasing proportion of inpatients are unable to give a history because of confusion or cognitive impairment. Another factor is that most elective surgical patients are now admitted on the day of their operation, leaving little time for students to make contact, and many are discharged the same day. In addition, some routine elective surgical procedures that students need to learn about are now very rarely performed in public hospitals. Finally, privatisation of hospital outpatient clinics has significantly reduced students’ exposure to ambulatory care. Thus, there is increasing competition for scarce “clinical material”. Medical students must also compete with early postgraduate and vocational trainees, especially before postgraduate exams, and with overseas-trained doctors preparing for the Australian Medical Council exam. The recent expansion of medical school places provides a major challenge for clinical educators.2 Australia urgently needs more medical graduates to deal with patently obvious workforce shortages, but there are not enough suitable public hospital inpatients for the clinical teaching programs of the new medical schools, or for their graduates to complete postgraduate training programs. The apparent lack of planning in decisions about the new medical schools will almost certainly exacerbate the problem identified by Olson and colleagues.1 It is difficult to see how the clinical resources in New South Wales will be adequate for the projected increase in student numbers; yet, in Victoria, there has been virtually no increase despite a need for more graduates and capacity to train them. This might have been avoided if the recent spate of medical school expansion had been based on consultation with educators rather than driven by political considerations. Are there any solutions? Olson and colleagues recommend better integration of students into clinical teams. This is sensible, but the magnitude of the problem demands more fundamental changes. The most obvious is to provide exposure to patients in other settings: general practice, specialists’ private rooms, privatised clinics and private hospitals. Many of the patients who used to be available for teaching in ambulatory settings in public hospitals have been diverted to these sites by state government cost-shifting. The Practice Incentives Program (PIP) has been an effective incentive for general practitioners to take on an enhanced role in clinical teaching, but very few students have access to patients seen in specialists’ rooms or privatised outpatient clinics, where there are significant financial disincentives to teaching.3 We urgently need to explore ways of delivering and funding clinical teaching in these locations. Pilot programs that address the financial disincentives would be an excellent place to start, but would require a level of collaboration between federal and state governments, hospitals and universities that has been conspicuously absent in the decisions on new medical school places. Private hospitals are major beneficiaries of the Australian medical education system yet most contribute little to the training of their medical staff. A few have made arrangements to accept students, but there is clearly capacity to provide clinical teaching for many more.4 Australian taxpayers provide large sums of money to support the private health system. We should insist that some of this money is allocated to training its future workforce. Another potential solution is to expand the use of simulation-based clinical teaching.5 Simulation-based teaching is no substitute for direct contact with patients, but it is an effective way to impart some clinical skills and may have some advantages; it can be delivered at the appropriate stage of the curriculum, students have more opportunity to practise in a non-threatening environment, and it is safer, particularly for procedural skills. Australian medical schools make extensive use of clinical skills laboratories in the early years of training, but our hospitals have been slow to acquire these facilities and have often developed them for nursing staff or postgraduate medical trainees rather than for the resource-deprived medical students. The high fidelity simulation centres, which have been developed in capital cities, are not accessible or affordable for day-to-day medical student teaching. Hospital-based clinical skills laboratories are expensive to build and equip and require substantial funding for recurrent costs: teaching staff, surrogate patients, equipment and disposables. International experience suggests that they can help to compensate for declining numbers of accessible inpatients, but this won’t occur without adequate funding or systematic planning by hospitals, universities and both levels of government.5 Australia has begun a long overdue, but poorly planned, expansion of medical schools. Olson and colleagues’ report suggests that we are already struggling to provide clinical teaching for our current students in public hospitals.1 If tomorrow’s doctors are to graduate with adequate clinical skills, we urgently need to expand clinical teaching into other sites — specialists’ private rooms, privatised clinics and private hospitals — and to develop multidisciplinary clinical skills laboratories in all training hospitals.

Brendan J Crotty MB BS, FRACP, MD

A recent report outlines the good and the bad news about asthma Asthma is a common chronic condition among Australians, particularly children. In recent years, federal and state governments have responded to community and health professionals’ concerns by investing in strategies to improve asthma management.1 Coinciding with this, new pharmaceutical formulations have become available for managing asthma. The latest publication from the Australian Centre for Asthma Monitoring and the Australian Institute of Health and Welfare, Asthma in Australia 2005,2 provides a timely review of the good and the bad news about asthma over the past few years (Box). The prevalence of asthma is high in Australia compared with other countries,3 affecting 14%–16% of children and 10%–12% of adults. However, Asthma in Australia 2005 shows that, after a substantial rise in the number of children with asthma during the 1980s and early 1990s, this trend has reached a plateau. Although this pattern is consistent with observations in other countries, including Hong Kong, Switzerland and the United Kingdom,4 the reasons for this rise and subsequent plateau remain unknown. Nevertheless, the observation highlights the value of ongoing surveillance for asthma. Over the past 5–10 years, rates of general practitioner visits and hospitalisations for asthma have declined substantially. Furthermore, deaths due to asthma have fallen by more than 50% since the early 1990s. Despite these overall gains, there are important inequalities in the outcomes of asthma among Australians. Aboriginal and Torres Strait Islander people, particularly adults, have more asthma and higher rates of hospitalisation for asthma than other Australians. Adults living in rural or remote areas and people living in the most socioeconomically disadvantaged localities also have higher rates of hospitalisation for asthma. The reasons for these inequalities need exploring. The burden of GP consultations, emergency department visits and hospitalisations for asthma is highest among children and probably reflects their higher rate of disease exacerbations. At the beginning of school terms, particularly in February, rates of emergency department attendance for asthma are higher than usual and the episodes are more severe than usual among pre- and primary-school-age children. A similar return-to-school increase has been observed in other countries, and has been attributed to increased transmission of respiratory infections.5 This observation highlights the need to develop and test interventions to prevent exacerbations. Regular use of inhaled corticosteroids can reduce asthma symptoms and prevent severe episodes of worsening asthma.6,7 However, Asthma in Australia 2005 highlights evidence that inhaled corticosteroid therapy, the cornerstone of drug therapy for asthma, is not well targeted. Many people who would benefit from using them regularly are not doing so. Furthermore, most formulations are prescribed at the highest doses, in spite of evidence that many people with asthma can be well controlled, with fewer side effects, at lower doses of inhaled corticosteroids.8 This discrepancy with current evidence is further highlighted by the rapid market penetration of inhaled formulations that combine long-acting β-agonists with corticosteroids, a combination which achieves effective asthma control in most people with moderate to severe asthma with lower doses of inhaled corticosteroids.9 These combined formulations accounted for 64% of inhaled corticosteroids distributed in Australia in 2004. Hence, more work is needed to improve appropriate prescribing of inhaled corticosteroid therapy for people with asthma. The Asthma 3+ Visit Plan is an Australian Government initiative introduced to improve the quality of care for people with moderate to severe asthma by promoting structured care of asthma in general practice. However, it is estimated that only 14.1% of eligible people have used this program since its introduction in 2002. Respondents to a survey of GPs in Sydney indicated that the administrative complexity of the program acted as barrier to its uptake.10 Another cause for concern is the limited use of written asthma action plans. Despite evidence that these improve the outcomes of asthma,11 their use has decreased in recent years.12 Asthma in Australia 2005 shows that the outcomes of asthma in Australia are improving, but there is still a long way to go to ensure access to the best quality care for all Australians. We need to understand more about the barriers to effective care and the basis for inequalities in health outcomes for people with asthma.10,13 To investigate these issues, we need more detailed asthma-specific data at a population level, qualitative research in specific populations of health care users and providers, and randomised controlled trials of interventions designed to improve care and outcomes, particularly in disadvantaged groups. Major findings of the Asthma in Australia 2005 report Gains The rising trend in the prevalence of asthma among children during the 1980s and early 1990s has reached a plateau. Currently, 14%–16% of children and 10%–12% of adults have asthma. In 1990, there were 822 deaths attributed to asthma in Australia (5.6 per 100 000), whereas in 2003 there were 314 deaths (1.5 per 100 000). Hospitalisation rates for asthma have declined from 920 patient-days per 100 000 in 1993–94 to 419 patient-days per 100 000 in 2003–04. No gains Hospitalisation rates for asthma in 2002–03 were higher among: Aboriginal and Torres Strait Islander people compared with others in Australia (1003 v 418 patient-days per 100 000); Adults in rural and remote areas compared with adults in major cities and regional areas (728 v 331 patient-days per 100 000); and People with greater levels of socioeconomic disadvantage (528 patient-days per 100 000 in the most disadvantaged quintile v 309 patient-days per 100 000 in the most advantaged quintile). Only 34% of people with asthma aged 15 years and over are using inhaled corticosteroids, but 71% of inhaled corticosteroids are supplied in the highest dose formulations. In South Australia, the proportion of people with asthma who stated that they owned a written asthma action plan declined from 42% in 1995 to 22% in 2001.

Guy B Marks MB BS, PhD, FRACP · Patricia K Correll MPH · Margaret Williamson MPH

There is clear evidence of long-term benefits The Early Breast Cancer Trialists’ Collaborative Group (EBCTCG) 2000 overview of adjuvant systemic treatment trials for early breast cancer has demonstrated clear evidence of substantial and significant reductions in both recurrence and mortality, with follow-up now to 15 years.1 This is the fourth EBCTCG overview of adjuvant systemic therapies, conducted at 5-year intervals since 1985.2-6 The EBCTCG 2000 analysis, based on individual patient data from 145 000 women diagnosed with early breast cancer, involved 194 trials started by 1995 in which chemotherapy and hormonal therapy were evaluated alone and in combination for their effects on recurrence, breast cancer mortality and total mortality. This overview, with data from more trials than the earlier overviews, more patients and more years of follow-up, provided new and long-term information on adjuvant chemotherapy in women aged 50–69 years, tamoxifen duration, combined modality therapy, and cause-specific mortality (Box). What were the benefits?Chemotherapy regimens included single agents or polychemotherapy, either cyclophosphamide, methotrexate and fluorouracil (CMF), or anthracycline-containing regimens, mostly fluorouracil, adriamycin, and cyclophosphamide or substituting epirubicin for adriamycin. Anthracycline-containing regimens of about 6 months’ duration reduced the annual breast cancer death rate by 38% in women younger than 50 years, and by 20% in women aged 50–69 years. Similar reductions in annual recurrence rates were seen. The benefits were largely independent of the use of tamoxifen, oestrogen receptor status, or nodal status. Anthracycline-containing regimens were significantly better than CMF regimens for recurrence (2P = 0.0001 [2P is a two-sided P value]) and mortality (2P = 0.00001). There were insufficient trials involving women older than 69 years (< 5% of women) to reliably determine treatment effects. Hormonal therapies studied were tamoxifen (in most trials), ovarian ablation or ovarian suppression. The 15-year follow-up provided an opportunity to evaluate both early and late effects on recurrence and breast cancer mortality for each modality, given alone or in combination with chemotherapy. With respect to mortality, in women with oestrogen-receptor-positive tumours, 5 years of tamoxifen use reduced the annual breast cancer death rate by 31% and the annual recurrence rate by 40%, independent of patient age, the use of chemotherapy, progesterone receptor status or tumour characteristics. However, there was no advantage for a higher dose of tamoxifen than 20 mg per day. Tamoxifen given for 5 years was significantly superior to 1–2 years of therapy, but the evidence for any effect of continuing tamoxifen for more than 5 years remained inconclusive. With respect to recurrence, a significant trend was seen with increasing reduction of annual recurrence rates with increasing age (40–49 years, 29%; ≥ 70 years, 51%; age trend 2P = 0.05). The overview did not include any trials in which tamoxifen and chemotherapy given concurrently were compared with one modality followed by the other. However, as the benefits of tamoxifen and of chemotherapy were largely independent of whether treatment included the other modality, a mortality reduction of 57% for women younger than 50 years and 45% for women aged 50–69 years could be expected by using both modalities together. Do benefits occur early or late?Most of the benefit of polychemotherapy on recurrence was seen in the first 5 years (absolute reductions of recurrence of 12.5%, 12.4% and 12.4% at 5, 10 and 15 years follow-up, respectively, for women younger than 50 years), whereas the benefit for mortality continued to increase for 15 years (absolute reductions in breast cancer mortality of 4.7%, 7.9% and 10.0% at 5, 10 and 15 years, respectively). The early effect of chemotherapy on recurrence had been well established in the previous overview,6 but the continuing late mortality benefit has only now been established by the longer follow-up. The late mortality benefit was less apparent for chemotherapy in women aged 50–69 years. The pattern of benefit from 5 years of tamoxifen was similar to that seen with chemotherapy for women aged less than 50 years, but was apparent in all age groups. Again, most of the effect on recurrence occurred in the first 5 years (absolute reductions for recurrence: 10.4%, 13.6% and 11.8% at 5, 10 and 15 years), whereas much of the benefit on breast cancer mortality occurred after the first 5 years (absolute reductions of 3.6%, 7.9% and 9.2% at 5, 10 and 15 years). This extended mortality benefit, seen with both chemotherapy and tamoxifen, is striking and suggests that an important number of patients with residual disease after primary therapy are cured of their original tumour by adjuvant tamoxifen or chemotherapy, although they remain at continuing risk of new contralateral breast cancer in the long term. Given the similar pattern for clinical benefits observed for the two treatment modalities, the biological outcomes of their effects at the cellular level may have more in common than has previously been recognised. Ovarian ablation or suppression also had a significant, beneficial effect on recurrence (2P < 0.00001) and mortality (2P < 0.004). The pattern of benefit — an early effect on recurrence and a later effect on mortality — was similar to tamoxifen. However, in contrast to tamoxifen, the effect of suppression or ablation was less in trials where all women also received chemotherapy, perhaps because the chemotherapy also suppressed ovarian function. This question is being addressed in current trials. What were the harms?There were minimal long-term effects of all of these agents on non-breast cancer mortality. Chemotherapy was associated with a small, non-significant increase in mortality from heart disease, leukaemia and lymphoma (0.2%); tamoxifen was associated with a small excess mortality from uterine cancer and pulmonary embolus (0.2%). However, the small increase in non-cancer deaths (a few per 10 000 patients per year) was very much less than the reduction in breast cancer deaths seen for each treatment modality. What are the implications?The data from the earlier EBCTCG overviews have already contributed to widespread changes in practice and a recent fall in breast cancer mortality of around 20% in several developed countries. The findings of the 2000 overview will encourage an even wider use of systemic therapies and should contribute to further reductions in mortality.7 Overall, the most important finding from the 2000 overview is that important practical and biological information is gained from long periods of follow-up. Not only has this overview produced definitive results relevant to breast cancer management but, importantly, it has clearly demonstrated two important biological principles. First, that an early reduction in recurrence rates is invariably followed by a reduction in mortality. Hence, recurrence rate reduction may be an acceptable basis on which to recommend changes in practice before survival data is obtain-able. Second, despite the substantial benefits of 5 years of tamoxifen, 2% of patients continue to have a breast cancer recurrence each year from years 5 to 15 after diagnosis. This is a several-fold greater risk of new breast cancer events than was required for the “high risk” women to be eligible for the tamoxifen prevention trials.8 New strategies for ongoing management of these women should be considered. Further, other questions will need to be addressed by the overview process, including the value of tamoxifen or other endocrine therapies beyond 5 years and addition of a taxane to chemotherapy regimens.9 What are the limitations?The current overview only encompassed therapies used up to 1995, which — although clearly effective — are not optimal for all patients in 2005. The 2000 overview did not involve taxanes (there are now more than 10 000 patients in several trials) or aromatase inhibitors (about 30 000 patients in seven trials).10,11 Nor did it include trials with trastuzumab (Herceptin) for women with tumours expressing HER2.12 However, answers to other specific questions such as the value of long-term aromatase inhibitors and of targeted therapies will likely be based on a smaller number of larger trials rather than an overview of many smaller trials. Many such trials, including the important “SOFT”, “TEXT”, and “PERCHE” trials of different combinations of chemotherapy, aromatase inhibitor and tamoxifen for younger women, as well as trials for older women, and trials of taxanes and of trastuzumab, are being conducted in Australia by the Australian New Zealand Breast Cancer Trials Group through international collaboration. These trials should be the subject of separate meta-analyses, conducted in a timely manner to facilitate rapid dissemination of the results. However, long-term follow-up is a particularly valuable feature of the EBCTCG overviews, and the EBCTCG investigators are pursuing strategies to ensure that data from the 2005 overview will be made available sooner and more widely. Key findings of the Early Breast Cancer Trialists’ Collaborative Group 2000 overview Overview of 194 randomised trials of systemic therapies for early breast cancer started by 1995, including data at 10 and 15 years follow-up. Anthracycline-containing regimens are superior to cyclophosphamide, methotrexate and fluorouracil (CMF). Anthracycline-based polychemotherapy reduced annual death rates by 38% (standard error [SE], 5) for women younger than 50 years, and by 20% (SE, 4) for women aged 50–69 years. Tamoxifen reduced annual mortality rates for oestrogen-receptor-positive tumours in all age groups (31%; SE, 3). Combination therapy with tamoxifen and chemotherapy may produce a larger mortality reduction (45%–57%). Effects on recurrence occur early; effects on mortality occur later. Long-term benefits maintained to 15 years. Long-term non-breast cancer deaths from treatment are a few per 10 000 per year, and are greatly outweighed by the reduction in breast cancer deaths. More rapid data dissemination from overviews is required.

John F Forbes FRACS, FRCS, MS · Jack Cuzick PhD

The NHMRC is at a fork in the road — which route will the government take? When the then Commonwealth Minister for Health, William (Billy) Hughes defined the role of the newly formed National Health and Medical Research Council (NHMRC) in 1936, he noted that:1 . . . the new Council will stimulate a national vision of the infinite possibilities in human health and happiness as the underlying factor in social welfare . . . [and] . . . the new Council must have regard to a balanced policy in which the application of existing knowledge will be steadily maintained, and at the same time all possible efforts towards the acquisition of new knowledge must be made. Research must be actively pursued and developed and as fast as new knowledge is acquired it must be applied. The new Council had 15 members and an initial research budget of £30 000.1 Like its immediate predecessor, the Federal Health Council,1 it was embedded within the structure of the Federal Department of Health. Today, almost 70 years later, an announcement on changes to the governance of the NHMRC is imminent. The pathway that the Australian Government chooses to take to modernise the NHMRC is as critical for the Australian community as the decision that marked its establishment. In 1992, empowered by an Act of parliament, the NHMRC became a statutory body. It has an annual research budget of close to $400 million, and is governed by a council of about 30 members who are elected every 3 years.2 However, its scope and function have remained unchanged, as witnessed by the Council’s current mission statement: “to ensure that excellence in research, research and health ethics, and health advice improves the health of all Australians.”2 Now, 5 years into the 21st century and at the end of another NHMRC triennium, questions are being raised about whether the NHMRC can meet the challenges of delivering its mission in the new century.3 There is a view that the time has come for the NHMRC to modernise and mirror itself on the National Institutes of Health in the United States, the Canadian Institute of Health Research, and other organisations such as the Wellcome Trust in the United Kingdom.3 The attributes these organisations share include a high public and political profile, dynamic leadership, effective and accountable governance, strategies to achieve clearly defined goals, and a cadre of health and research professionals who communicate consistently and widely with other research and health organisations, universities, and the private sector. In contrast, the mould and modus operandi of the NHMRC have remained largely unchanged over the past 30 years.3 The three areas of responsibility of the NHMRC are ethics of research, health more generally, and health and medical research. The ethics component of the NHMRC function is world class, but recently the other areas have drawn increasing, albeit muted, criticism. There are perceptions that the NHMRC is arthritically conservative and has difficulty in establishing a national and international profile; is tangled up in Canberra’s bureaucratic culture of self preservation and political manoeuvring; and is bereft of executive power because of a lack of clarity in the roles of the Chair of Council and the Chief Executive Officer, with the latter having conflicting reporting responsibilities (Box 1).4 There are also perceptions that the purpose and strategy of the NHMRC are driven by crowded committees that have an apparent consensus orientation and undercurrents of the tensions that exist between investigator-driven curiosity research and practice- and policy-driven priority research; and that it has difficulty recruiting and retaining suitable staff.4 Furthermore, there have been assertions that the NHMRC’s health advice is protracted and bogged down by red tape and statutory requirements; that its processes for policy development and priority determinations are slow and at times suboptimal — as instanced by the recent attempts to develop a policy on chronic disease5 and enact one of the Australian Government’s four National Research Priorities proclaimed in 2002: “Promoting and maintaining good health”;6 and, finally, that it has no overt accountability to society for its policy and research directions and its expenditure of what is essentially the public’s money. In some ways it casts an image of an elitist organisation, but overriding all is a sense that its governance and structure is outmoded.3,4 What can be done? A radical option I would suggest is for the NHMRC to shed all its functions except health and medical research and in so doing emulate the National Institutes of Health, the Canadian Institute of Health Research and the UK Medical Research Council. But the Australian research psyche shuns the revolutionary in favour of incremental change. In this context are the excellent governance recommendations advanced in the report Sustaining the virtuous cycle for a healthy, competitive Australia4 delivered to the government nearly a year ago, but which have elicited no response. The review recommended that the NHMRC should be an independent and stand-alone entity, directly responsible to the Federal Minister for Health. It also recommended that it should be governed by a small board of 10–12 members, who could be drawn from society as well as the public health, medical research, and private sectors. The board should be led by a dynamic Executive Chair who might also assume the responsibilities of the Chief Executive Officer (Box 1). Added to this framework, there should be a delineation of the organisation into separate but cohesive units, with overriding responsibilities for research ethics, national health, health research, and medical research. These separate units should be staffed by health and research professionals recruited and retained by challenging work, attractive career pathways, and remunerations not hobbled by public service guidelines. The NHMRC Board and its units should be supported and advised by appropriate committees, including an overarching health and research advisory council of 10–15 members, addressing strategies, policies and priorities for the nation’s health and for curiosity and priority-driven health research. The latter need to focus on the prevailing national health problems in Indigenous health, disease prevention, chronic disease and health care delivery. The NHMRC should also develop innovative approaches to forging research partnerships, such as those pioneered by the Canadian Health Services Research Foundation and the Health Research Council of New Zealand. The overriding aim should be that all policy and practice must be supported by evidence, and, in the absence of evidence, this should be acquired through research. The activation of ad-hoc working committees (Box 1) should be on a needs basis. Ideally, these would be task- and outcome-focused, time limited and made up of experts drawn from an approved “College of experts”. Out of necessity, this College would be continually rejuvenated by “young blood”. This modern NHMRC could also shed some of its current functions. Health advice, particularly regarding acute threats to the nations’ health, could be the business of an Acute Response Taskforce of experts, including representatives from federal, state and territory health departments. Australia’s response to the bovine spongiform encephalitis threat is an exemplar of this approach. The ad-hoc Taskforce would obtain its research capacity from the NHMRC. The NHMRC’s role in clinical guidelines development and dissemination could be devolved to the National Institute of Clinical Studies, as is the case in the UK, where elaboration of guidelines is a function of the National Institute of Clinical Excellence.7 Long overdue questions as to the purpose of guidelines, the processes for their development and dissemination, and the nature of the final product, need to be addressed. The Board could take a radical approach and assess the success of its sponsored research not only by the traditional methods of published articles and granted patents, but also by asking “what exactly is society getting for its money?”8 Three UK bodies — The Medical Research Council, The Academy of Medical Sciences (a non-grant-giving body that promotes medical science) and The Wellcome Trust — are addressing the question of the societal value of health and medical research, to justify escalating government expenditure on this research and convince the public that these vast amounts of money contribute to individual and national health.8 The Board could even be so bold as to invite the public and policy makers to determine research priorities.9 These suggestions for modernising NHMRC governance have one purpose: to ensure that the organisation is clearly accountable to the Minister and is dynamic, flexible, adaptive, effective, and in tune with the 21st century. The recent achievements of the National Institutes of Health10 and Canada’s Institute of Health Research11 indicate that, with the right individuals and culture, all this is achievable. Above all, these changes would fulfil the goal of Billy Hughes that: “Research must be actively pursued and developed and as fast as new knowledge is acquired it must be applied.”1 However, all this discourse on modernisation is academic in the absence of a commitment by the Australian Government to provide appropriate research funding for the NHMRC with built-in annual growth. After all, who would want to lead an enterprise that by world standards is static or falling behind? PostscriptThree days after this editorial was published online on 4 September 2005, the Federal Minister for Health and Ageing announced that from 1 July 2006, the NHMRC will become a fully independent statutory agency within the Health and Ageing portfolio, and that this change “will streamline the council’s governance arrangements and improve its ability to respond to emerging health and research priorities”.12 The newly announced governance structure (Box 2) — a hybrid of the recommendations made by the Grant Report4 and those of the 2004 report of the National Audit Office on NHMRC governance13 — is undoubtedly an improvement compared with the present governance arrangements. There is a clearer delineation of responsibility, and accountability in management, advice and strategic development. However, there are good reasons for the medical and research community to vigorously oppose the suggested governance structure. It will potentially place the NHMRC under the complete control of the Minister and, indirectly, his political or departmental advisors. Under these circumstances, only a very strong CEO, a person with considerable power and influence, would be able to take the NHMRC and its agenda forward, and people of this calibre are hard to find. To improve the proposed new NHMRC governance structure, there should be a Board, a small statutory body operating in classical corporate governance mode, with the CEO responsible to the Chair and the Board, and the CEO corporately responsible to the Minister. In the new governance structure as depicted in Box 2, the Management Advisory Committee would be omitted and the Board would be placed between the CEO and the Minister, with an advisory connection between the Council and the Board. A framework for the modernisation of the NHMRC has been put in place. But, with the potential for political control of the modernised NHMRC, will it become “dynamic, flexible, adaptive, effective, and in tune with the 21st century”? There are 9 months remaining before the new governance structure is activated. During this time, the government might reconsider the governance issue and put in place a structure that will ensure the NHMRC’s independence. For advice on this matter, there is a wealth of interest, expertise and experience available, and the time has surely come for the government to move beyond the GOBSAT (Good Old Boys Sat Around a Table) principle. By embracing a commitment to consultation, communication and change, modernisation of the NHMRC might ultimately be achieved. But it will require leadership and a clear vision, and a commitment to what is good for the community rather than for politicians. 1 Current and proposed National Health and Medical Research Council (NHMRC) structure 2 New governance structure of the NHMRC

Martin B Van Der Weyden MD FRACP FRCPA

The scientific benefit is clear, but translating this into practice requires advocacy Fourteen years ago, randomised controlled studies in the United Kingdom1 confirmed observational studies from Australia,2 the United States,3 and elsewhere, showing that an adequate intake of folic acid by women at around conception prevents most neural tube defects in their babies.4 These three countries now (i) have government-sponsored public health campaigns which encourage women of childbearing age to increase their daily intake of folic acid; (ii) have food standards permitting the food industry to voluntarily add folic acid to cereal and other foods; and (iii) have health benefit claims related to the prevention of birth defects. In 1996, the US (along with Canada) introduced mandatory fortification of virtually all wheat flour products. Despite recommendations by the National Health and Medical Research Council in Australia and other scientific bodies and scientists in the UK, mandatory fortification has yet to be introduced in these countries. Why should this be? After mandatory wheat flour fortification in the US, median serum folate levels in non-pregnant women of reproductive age more than doubled.3 Mandatory fortification has resulted in a 30% reduction of neural tube defects, or 1000 fewer cases every year.2 Each case of spina bifida prevented saves an estimated US$500 000 in lifetime costs.5 Even so, more could be achieved in the US compared with other countries where mandatory fortification requires higher amounts of folic acid to be added to flour than in the US.6 Examples include Canada7 (50% reduction in neural tube defects) and Chile8 (70% reduction). It is well past the time that the Australian and the UK governments should have drafted food standards with sufficient folic acid to provide 400 μg of synthetic folic acid a day to women of child-bearing age. In Australia, while the number of preventable cases (about 500 a year) has been reduced by voluntary fortification,2 this has not occurred across all of society, with resulting inequities.9,10 The reduction of cases of lifelong disability from neural tube defects has largely resulted from antenatal detection, with pregnancies being terminated (now the leading cause for late-stage termination of pregnancy in Australia and the UK). Preventing 500 neural tube defect cases each year in Australia would relieve the huge time commitment, financial cost and emotional burden from not only the affected individual, but his or her network of family, friends, work colleagues and other associates and caregivers. In the 10 years since we have known how to prevent neural tube defects, this would have meant 50 000 highly affected people in Australia alone. Folic acid fortification of flour is cheap — less than 0.1% the cost of flour (ie, less than 20 cents Australian per ton of flour). As thiamine is already a required additive, the costs of preparation and of administering quality control of the process, as well as of changing the labels on some foods, are small. Some millers and grocery companies in Australia do not favour mandatory flour fortification because they fear loss of market share for already fortified foods. However, a number of the largest milling companies, including Allied Mills and the Manildra Group, have publicly stated their support for mandatory flour fortification. The mandatory fortification of flour in the US not only prevents neural tube defects, but has also brought a wider benefit to the population, especially to older people beset with chronic and degenerative diseases. The exact degree of this benefit is still being defined, but current evidence indicates the increase in serum folate concentrations in the population is sufficient to prevent almost all folate deficiency anaemia.7 The association between lower risks for heart attack and stroke with lower homocysteine concentrations has been established.7 Since mandatory flour fortification with folic acid in the US, there have been about 17 000 fewer heart attacks and 31 000 fewer strokes.7 In addition, several recent scientific articles have credited folic acid supplementation with protection against loss of cognitive function in the elderly and Alzheimer’s disease,11 and against several cancers (including neuroblastomas). The benefits described above are clear and significant, but what are the perceived risks? One is the possibility of masking pernicious anaemia (the result of vitamin B12 deficiency) in the elderly and evolution of its neurological manifestations. Mild forms of dietary vitamin B12 deficiency in the elderly do occur, but there is no relationship between folate and vitamin B12 deficiencies. A second perceived risk is an increased risk of certain cancers, such as colon and breast cancer; however, there is mounting evidence that the overall risk of cancer is reduced, as the genome is less stable and at higher risk of mutagenesis when people are deficient in certain micronutrients, including folic acid.12 Since the US first demonstrated the benefits of flour fortification, more than 40 countries around the world have made it mandatory.13 Recently, leaders from over 50 key organisations formed The Flour Fortification Initiative, a United Nations-registered public, private, and civic alliance in support of the UN Millennium goals. With Australians in the forefront of this global movement, it is time that Australians at home also gain the benefit of this substantial public health measure. If there were a toxin (such as lead and mercury) or an infectious agent (such as the mad cow product) in the nation’s food supply, action would be swift and decisive. The ethical issue here is not what harm the mandatory fortification of flour with folic acid would do; rather, it is the harm inflicted each day that fortification is delayed by those who know how to prevent the damage from folic acid deficiency. In 2005, The National Institute of Clinical Studies Evidence-Practice Gaps Report14 identified mandatory folate fortification of flour as a key issue, and the Australian, New Zealand and UK governments will decide for or against this measure during the next 6 months. If the medical community will not rally and become advocates for this public health issue, who will? And at whose expense?

Glen F Maberly BSc(Med), MD, FRACP · Fiona J Stanley AC, FAFPHM, FRACP, FRANZCOG

Major advances continue apace in therapy and in understanding its molecular pathogenesis Myeloma is a malignancy of plasma cells in the bone marrow and presents with bone lesions, renal failure, anaemia and hypercalcaemia. Back pain, often associated with vertebral body collapse, is the most common presenting feature. In Australia, about 1200 new patients are diagnosed with multiple myeloma each year, with a median age at diagnosis in the early 60s. The aetiology of myeloma remains essentially unknown, although recent studies suggest links to agricultural exposures and lifestyle factors, such as low socioeconomic status and obesity.1 The major risk factor is the presence of a monoclonal immunoglobulin (paraprotein) in the blood. The incidence of paraproteins increases with age, and they are found in up to 3%–5% of people aged over 80 years. They are termed “benign paraproteins” or, more commonly, MGUS (monoclonal gammopathy of undetermined significance). By definition, this condition is not associated with other myeloma abnormalities. A patient with this type of gammopathy has an annual risk of about 1%–1.5% of developing active myeloma.2 A variant of myeloma — smouldering or indolent multiple myeloma — is associated with an infiltrate of over 10% monoclonal plasma cells in the bone marrow, but no organ dysfunction. Patients with this variant can be safely monitored for the onset of increasing paraprotein levels or organ dysfunction, suggesting transformation from smouldering myeloma to active disease. Melphalan chemotherapy was introduced in the 1960s, but there was little further change in our ability to affect the natural history of myeloma until the past decade, which has witnessed dramatic therapeutic advances. Currently, all patients aged under 65 years are offered autologous stem cell transplantation, using bone marrow stem cells harvested from the peripheral blood, unless precluded by other comorbidities. Stem cell transplantation is usually preceded by 3–6 months of induction therapy aimed at reducing tumour load and contamination of stem cell harvests by malignant cells.3 The role of a second stem cell transplant 3–6 months after the first is under investigation; it appears to benefit patients who do not have a full response to the initial transplant.4 The effect of a second transplant is also being compared with the new targeted drug therapies (see below). While allogeneic transplantation is usually precluded by age at presentation of myeloma, new techniques that require less intensive chemotherapy and gain their efficacy from the immunological effect of the stem cell graft on the malignant plasma cells (so-called “non-myeloablative” transplants) are now being used for patients who have a suitable matched sibling donor, are young, and have relapsed after autologous stem cell transplantation. The role of ongoing chemotherapy after transplant is unknown at present and the subject of a number of clinical trials. Lytic bone disease, bone pain and hypercalcaemia are major clinical manifestations of myeloma. In the past, no effective therapy was available for bone disease, but now all patients with myeloma receiving chemotherapy are also treated with a bisphosphonate. This reduces the number of skeletal events, such as vertebral collapse and pathological fracture of long bones, and reduces bone pain. Despite the increasing recognition of the uncommon side effect of osteonecrosis of the jaw, bisphosphonate therapy continues to be a standard intervention for all patients with myeloma who are receiving active chemotherapy.5,6 Of great interest are the new targeted therapies. Currently, three drugs — thalidomide, its analogue lenalidomide, and the proteasome-inhibitor bortezomib — are available for use in North America and are undergoing clinical trials in Australia. Extensive clinical experience with these drugs in refractory disease shows that they have a response rate of about 30%, which rises to 60%–70% when combined with dexamethasone.7 Major side effects include neuropathy (thalidomide and bortezomib) and myelotoxicity (lenalidomide). Current investigations are assessing the value of these drugs at initial diagnosis and as maintenance therapy after stem cell transplantation.7-9 Thalidomide and dexamethasone have been shown to be as effective for induction before stem cell transplantation as standard therapies. However, as they may be administered orally they are considered more convenient than therapies requiring venous access. Current studies involve the use of lenalidomide and bortezomib in induction therapy, while a recent French study has shown that thalidomide taken after stem cell transplantation both prolongs event-free survival and prevents relapse compared with no therapy.10 In April this year, the 10th International Myeloma Workshop in Sydney was attended by over 1000 experts in myeloma, indicating the current research interest in this condition. Abstracts and presentations of the meeting are available at the Haematologica website (www.haematologica-thj.org/supplements.html). The work presented at the meeting offered great hope for the future, both in our understanding of the molecular pathogenesis of multiple myeloma and, more importantly, in new therapies for our patients.

Douglas E Joshua DPhil(Oxon), FRACP, FRCPA

When will Australians be able to count on receiving health care that is safe? The Oxford English dictionary defines safety as “freedom from danger and risks”, and there is little doubt that the question of safety is foremost in the minds of many Australians on admission to our hospitals. These concerns were heightened when, 10 years ago, the Quality in Australian Health Care Study (QAHCS) revealed that admission to hospital was associated with a 16% risk of an adverse event, including permanent disability or death.1 In the years that followed, public concerns about hospital safety were reinforced by a series of sensational scandals involving patient care at the King Edward Memorial Hospital in Perth, Western Australia (1999),2 the Canberra Hospital in the Australian Capital Territory (2000),3 and Campbelltown and Camden Hospitals in New South Wales (2002).4 Not surprisingly, all these incidents had common characteristics:3 compromised patient safety not detected by sentinel event reporting; suboptimal clinical governance; health care professionals, who, frustrated by inaction after internal reporting of adverse events, brought the matter to the attention of politicians; and, finally, all incidents provoked one or more independent inquiries.3 There is little doubt that, pari passu with these scandals, the public’s trust in hospitals and doctors has taken a pounding, as has the perception of the profession’s ability to regulate itself. And now, in 2005, we have the Bundaberg Hospital scandal in Queensland. Not surprisingly, this incident shares most of the features of the preceding hospital scandals. But it is also different — it reaches into the hearts of the Medical Board of Queensland, Queensland Health and the Queensland Government. The Bundaberg Hospital incident might revolve around the performance of Dr Jayant Patel, but it is in fact a symptom of an affliction affecting health care Australia-wide. In 2003, Patel was appointed as a surgical medical officer at Bundaberg Hospital and subsequently promoted to Director of Surgery. Over the following 2 years, he operated on about 1000 patients, of whom 88 died and 14 suffered serious complications.5 A clinical review has since found that Patel directly contributed to the deaths of eight patients and “may have exhibited an unacceptable level of care in another eight patients who died”. The report noted that although “in the comfortable majority of cases examined, Dr Patel’s outcomes were acceptable . . . [he] lacked many of the attributes of a competent surgeon”.6 All this may not have happened had the 2003 registration of Patel by the Queensland Medical Board been more rigorous. An in-depth review would have uncovered that Patel was placed on probation for 3 years in 1983 for “gross negligence” in his practice at Rochester Hospital in New York State; that in 2000 the Oregon Board of Medical Examiners in the United States restricted the scope of his surgery; and, in 2001, under threat of having his licence revoked in New York State, he instead obtained permission to surrender his licence to practise.7 The subsequent questioning of Patel’s performance at Bundaberg Hospital did not emerge from a clinical governance system but from concerns of individual doctors and nurses about his surgical performance and prowess. It was a letter from the nursing staff about this matter which, when tabled in Queensland Parliament, resulted in the establishment of a Commission of Inquiry headed by Anthony Morris QC. In the meantime, Patel left the country unimpeded. Inquiries are established to ascertain the facts, to learn from the events, to provide a catharsis for stakeholders, to hold people and organisations accountable, to reassure the public that something is being done, and to serve the interests of governments.8 It was hoped that the Morris Inquiry with these tasks and terms of reference9 would have shed light on: Patel’s appointment to Bundaberg Hospital; the role of the Queensland Medical Board in assessing, registering and monitoring overseas-trained doctors deemed to be necessary for areas of need; the role of federal, state and territory governments and the clinical colleges in these processes; systems to ensure accountability and monitoring of appropriate performance of individuals and clinical services; and systems to receive, process and resolve complaints about clinical performance or services. Now, with the termination of the Inquiry on the grounds of perceived bias, the public and the profession will have to wait.10 But, despite this, answers to these issues will have to be unearthed. They are not only pertinent for Queensland — they have national implications. We have had report after report11-13 on quality and safety, and bodies devoted to safety and quality such as the Australian Council on Healthcare Standards, the Australian Council for Safety and Quality in Health Care, the National Institute of Clinical Studies and, more recently, the NSW Clinical Excellence Commission. And the list goes on. Yet we continue to suffer hospital scandals affecting lives and limbs, which, for all we know, are only the tip of the iceberg. Ten years after the QAHCS and 5 years after the establishment of the Australian Council for Safety and Quality in Health Care, we still have no nationally accepted framework for clinical governance to ensure the safety and quality of Australian health services or the means to comprehensively monitor these indices.14 Based on QAHCS outcomes, 25 patients die each day in our hospitals from preventable adverse events and another 22 suffer preventable permanent disability (Dr R M Wilson, Director, Northern Centre for Healthcare Improvement, Royal North Shore Hospital, St Leonards, NSW, personal communication, 2005). Whether, 10 years after QAHCS, being treated in Australian hospitals still results in the same number of preventable human tragedies, we simply do not know, and this ongoing vacuum is an indictment of our health ministers and organised medicine. The time has long passed for Australia’s political leaders to abandon their leisurely bureaucratic approach to quality and safety15 and to insist on fast-tracking a national program that ensures quality and safety for all Australians accessing health care. It can only be hoped that the Bundabueg Hospital scandal will prompt out political leaders to act more decisively. In tandem with the dismantled Morris Inquiry, there is a wide-ranging Inquiry into the health system in Queensland, instigated by the Queensland Premier in April this year. This Inquiry, driven by two eclectic working groups, both headed by Peter Forster, issued an interim report at the end of July which is not flattering of Queensland Health.16 It is depicted as a gigantic dysfunctional conglomerate with a corporate centre that is more concerned with performance indicators, revenue generation and cost control, than with people. It appears to be preoccupied with tortuous decision processes and ineffective workforce management systems, and with workforce planning that is not linked to service delivery. In short, its command-and-control ethos has resulted in a chasm between administration and front-line health services. In the field, Queensland Health’s focus on cost containment and revenue raising has caused concern, frustration and even anger among clinicians who “feel undervalued and marginalised from a system which does not allow them sufficient time to undertake teaching and research, where they face ever increasing patient loads . . . [and] have limited ability to influence the way the health system is run”.16 There is an even deeper reason for clinicians’ discontent — Queensland is an impoverished health care state! It has the lowest number of doctors per head of population in Australia and is critically dependent on overseas-trained doctors, who now account for nearly one in four doctors in Queensland.16 But there is more. Queensland’s average recurrent expenditure on health is the lowest in the nation, and in 2002–03 its recurrent expenditure on public hospitals was 20% below the national average, and this is despite the greater geographic dispersion of health care facilities in Queensland. And to top off this bleak picture, the remuneration of hospital-salaried medical staff is the second lowest in the country.16 These telling statistics might be trumpeted by politicians and bureaucrats as reflecting good fiscal management, or blamed on the politically convenient federal–state health divide. But others may see it as an inhumane and unnecessary capping of the health budget. Whatever the rhetoric, the impoverishment of the Queensland health system cannot be sheeted home to Queensland Health. It lies squarely with the Queensland Premier and it will be interesting to follow the Queensland Government’s response to the final report of the Forster Inquiry, which is due at the end of this month. But the response will not require rocket science. There is a dire need for Queensland Health to be dragged into the 21st century by a restructuring of its monolithic and disconnected organisation into more diverse and discrete health structures. These should be open, transparent and, most importantly, connected to local communities and to clinicians empowered to make decisions about health care delivery. Queensland could do no worse than to emulate the clinician-led ongoing reform of NSW hospitals.17 Queensland is also in dire need of a boost to its health budget. It also needs to consider attracting clinicians to work in Queensland hospitals — by making its recruitment and retention packages for salaried staff competitive with those of other states, and by providing incentives for clinicians to work in non-metropolitan areas. The reward system does not have to be all monetary. It could include innovations such as a program of continual professional development and refreshment of non-metropolitan doctors through regular periods of secondment to major metropolitan centres. An attitudinal change to the role of visiting medical officers in public hospitals might also help. Despite having more medical schools than any other Australian state or territory, Queensland will be dependent on overseas-trained doctors for some time to come.18 There is a risk of some of these doctors not being suited to the local culture and practice expectations, or not having the necessary skills.6 Their continuing professional and cultural development needs to be met by structured programs involving the clinical colleges, as well as regular monitoring and constructive feedback. It’s time to cease the apparent neglect of overseas-trained doctors, not only in Queensland but nationwide.19 In a recently released book, Patient safety: achieving a new standard of care, there is a simple statement: “Americans should be able to count on receiving health care that is safe.”20 So should all Australians, whether in provincial Queensland or elsewhere.

Martin B Van Der Weyden MD, FRACP, FRCPA

Is it time to walk the line between overtreating indolent disease and undertreating aggressive disease? Few other health care issues in Australia have been as contentious as the diagnosis and treatment of early prostate cancer. Debate centres on two hotly contested but important issues: do prostate cancers diagnosed by an elevated serum prostate-specific antigen (PSA) level pose a significant threat to health, and if they do, can intervention alter the natural history of the disease? In this editorial, we consider the contribution that two recently published studies make to this debate, with a focus on survival and the role of surgical management. Study one: In the first study, Albertsen and colleagues presented an update of a retrospective cohort study first published in 1998.1 They estimated 20-year survival after clinically localised prostate cancer was treated without curative intent in 767 men diagnosed with this condition between 1971 and 1984. After a median of 24 years, the men’s current vital status was obtained and the contribution of prostate cancer to any subsequent mortality was determined by examining death certificates. Survival was assessed on a competing risk analysis, and stratified for age and tumour differentiation. The primary finding was that the risk of death from localised prostate cancer did not increase significantly with time from diagnosis — leading the authors to suggest that aggressive management of localised prostate cancer is perhaps unnecessary. The study also found that prostate cancer graded as Gleason sum 7 and above (moderately to poorly differentiated) is lethal. These results can directly inform our current debate only if the population studied is comparable to contemporary patients, and as these men were diagnosed in the pre-PSA era, there are major differences in this regard. Of the men in the cohort, 71% were diagnosed on the basis of surgical intervention for benign prostatic hyperplasia, either by transurethral resection of the gland or open prostatectomy. Both of these procedures sample the transition zone exclusively, where less than 25% of all prostate cancers originate. A relatively high proportion of these T1 tumours are true “transitional zone tumours”, which are well recognised to be smaller in volume and better differentiated, and to run a more indolent biological course. This is reflected in the finding that 33% of the cohort had cancers with Gleason sums of between 2 and 5 — well differentiated tumours. In contrast, significant or lethal prostate cancer with high Gleason sums is found predominantly in the posterolateral part of the prostate, the peripheral zone. Prostate cancer diagnosed after a finding of an elevated PSA level with sampling of the peripheral zone shows cancer with a Gleason sum of less than 6 in less than 5% of cases, with most cancer detected by PSA testing scoring 6 or 7 (moderately differentiated). Thus, this study cohort contained a high number of clinically insignificant prostate tumours that would be less likely to be diagnosed by needle biopsy. Any comparison with contemporary prostate cancer series detected by PSA testing is also confounded by the late age of diagnosis (median, 69 years) and the high rate of significant comorbidity in this cohort. Further, 42% of patients with clinically localised disease received some form of androgen deprivation therapy within 6 months of diagnosis (which was presumably continued until death), despite there being no evidence of disease progression. It is now becoming increasingly appreciated that hormonal therapy creates a disease in itself, which can contribute significantly to mortality from other causes (particularly cardio-vascular mortality from diethylstilboestrol).2 Despite its differences from more contemporary studies, the study by Albertsen and colleagues does offer striking insights into the biology of conservatively treated prostate cancer. Clearly, cancers graded Gleason 7 and above are lethal when managed conservatively, even in a population of sick elderly men. Conversely, at least up to 15 years of follow-up, cancers graded Gleason 2 to 5 run an indolent course, which suggests that in elderly and medically compromised men, a more conservative course can be followed. However, data from another series which is less contaminated with transition zone tumours suggested that low grade tumours can dedifferentiate and metastasise, which has particular relevance to men diagnosed at a younger age.3 Study two: In the second study under consideration, Bill-Axelson and colleagues directly addressed the second point of contention — can intervention alter the natural history of prostate cancer?4 Again, this was an updated analysis of a previously reported study. It was an elegant study premised on a beguilingly simple hypothesis that: by removing prostate cancer that is confined to the gland via radical prostatectomy, metastases can be prevented; by preventing metastases, death from prostate cancer can be reduced; and by reducing death from prostate cancer, overall survival is improved. Radical prostatectomy is the surgical removal of the prostate and seminal vesicles by dividing the prostate at the bladder neck and urethra, and suturing a vesicourethral anastomosis over the catheter. It has been performed by open abdominal surgery and, more recently, by a minimally invasive laparoscopic or robotic approach. In Bill-Axelson and colleagues’ randomised controlled trial, 695 men with clinically localised prostate cancer were allocated to either radical prostatectomy or “watchful waiting”. In both groups, hormonal therapy (medical or surgical castration) could be introduced at the discretion of the treating physician. Mean age at diagnosis was 64 years, and mean serum PSA level at diagnosis was 13 ng/mL. Median follow-up was 8.2 years. Importantly, this study is more representative of the era in which PSA testing is used to detect prostate cancer. Diagnosis was by contemporary sextant, ultrasound-guided needle biopsy of the peripheral zone, and only 11% of diagnoses were at transurethral resection of prostate, although a higher proportion had palpable disease than a modern series might. In this study, 77% of cancers were T2 (organ-confined) prostate cancers. In contrast to the Albertsen study, 77% of tumours were graded Gleason 5 to 7, and only 13% were graded Gleason 2 to 4. Nearly half (48%) of Bill-Axelson and colleagues’ cohort had a PSA level greater than 10 ng/mL at diagnosis. In all, this cohort of patients represents a somewhat more advanced disease group than would be representative in Australia in 2005 (where PSA testing is now more prevalent, and more cancer is being discovered in the 4–10 ng/mL PSA range). Nonetheless, the results presented by Bill-Axelson and colleagues are instructive, underscoring the biological truth of the study hypothesis. In men treated with surgical intervention, the incidence of metastatic disease and risk of death from prostate cancer was significantly reduced compared with those who were managed by watchful waiting. This led to a significant reduction in all-cause mortality, providing evidence for the first time that radical intervention for localised prostate cancer can deliver a real health benefit. This health benefit was highest in men younger than 65 years of age, with 19% of watchful-waiting patients compared with 8% of patients treated with surgery dying from prostate cancer at 10 years. Although the study authors remained cautious, suggesting further research needs to be done before introducing an immediate change in clinical practice, their results were impressive in terms of metastatic rate (14% in the surgery group versus 23% in the watchful-waiting group) and local progression of prostate cancer (64 in the surgery group versus 149 in the watchful-waiting group, showing a 25% risk reduction in local progression in the surgery group at 10 years). Further, 177 of the patients in the watchful-waiting arm versus 110 in the surgery arm received hormone therapy, with a median time to hormone therapy treatment of 4 years. So, now that Bill-Axelson and colleagues have shown in a randomised controlled trial that surgery for prostate cancer saves lives, do we have all the answers? Would that this were so. These data are extremely important in guiding men about the relevance of PSA testing, the risk of death and risk of metastatic and local progression from untreated histologically significant prostate cancer. However, the injudicious application of prostate testing has opened a Pandora’s box. We have seen an explosion in diagnosis of potentially insignificant non-life-threatening prostate cancer. There is now a strong push in the United States to have the PSA cutpoint for prostate cancer biopsy lowered from 4 ng/mL to 2.5 ng/mL or even lower.5 Some suggest all men have a prostate biopsy at the age of 50 years. The PSA test is good, but not great. It doesn’t help us differentiate between the indolent and dangerous prostate cancer. Gleason histology grading does help as a differentiator. But what is the cost–benefit balance of making a diagnosis of indolent microfocal Gleason 6 prostate cancer in a 78-year-old man with a PSA level of 6 ng/mL? We can take comfort in the proven knowledge that surgery is indicated for younger men with at least 15 years of life expectancy. However, a more judicious approach in managing older men with comorbidities will be needed. Countering this, newer technical developments in prostate cancer surgery, including laparoscopic and robotic radical prostatectomy, will further improve outcomes for men by reducing the morbidity of the operation and improving cancer control.6-8 Perhaps the next big question (and answer) in prostate cancer surgery has been articulated by Klotz.9 They are conducting a program of active surveillance with regular PSA testing and repeat biopsy, with surgical intervention with curative intent if there is cancer progression, in men with defined low-risk prostate cancer. This approach may help us to reduce unnecessary treatment in men at low-risk of disease progression. Eventually, an improved molecular understanding of the biology of these cancers will help us to predict precisely long-term outcomes in patients with prostate cancer and, thus, to decide on the most appropriate management for each individual patient.

Anthony J Costello FRACS, MD · Niall M Corcoran MB, AFRCSI · Scott Van Appledorn MD

Results of a recent Australian trial suggest it is time to stop equivocating about screening and treatment The 1998 consensus guidelines on the management of gestational diabetes mellitus from the Australasian Diabetes in Pregnancy Society emphasised that, “due to a lack of good quality randomised controlled clinical trials in the area of [gestational diabetes mellitus], these guidelines are based on what is a reasonable consensus of informed opinion in Australasia”.1 The clear benefits of treating women with gestational diabetes according to these guidelines have now been demonstrated by the Australian Carbohydrate Intolerance Study in Pregnant Women (ACHOIS).2 This study randomised 1000 women with gestational diabetes to either routine antenatal care or to an intervention that comprised home glucose monitoring, review by a diabetes educator, dietitian and physician, and insulin therapy if glycaemic targets were not met. Serious adverse perinatal outcomes occurred in 1% of the intervention group versus 4% of the routine-care group (adjusted relative risk, 0.33 [95% CI, 0.14–0.75]). The percentage of infants who were large for gestational age was lower in the intervention group (13% v 22%), with no increase in those who were small for gestational age. Although induction of labour was more common in the intervention group (39% v 29%), rates of caesarean delivery were similar (around 31%). Measures of maternal quality of life were more favourable in the intervention group. To prevent one serious perinatal outcome, 34 women needed to be treated. The 1998 guidelines were equivocal in regard to screening for gestational diabetes, allowing either for universal screening or for selective screening based on clinical risk factors in relatively low-risk populations. In the light of the findings of ACHOIS, we believe that universal screening should now be accepted and implemented. There are multiple arguments in favour of this approach: Most women with gestational diabetes have no symptoms, and many have none of the classic risk factors associated with gestational diabetes.3 Screening based on risk factors adds an extra complexity to busy routine clinical practice and may lead to some women failing to undergo appropriate testing. Furthermore, ACHOIS patients were relatively “low risk”, being predominantly of European background, with a mean age of around 30 years, and a mean body mass index of around 26 kg/m2. Many would not have been tested based on risk factors. Nonetheless, the benefits of treatment were impressive. The precise level of hyperglycaemia that carries increased pregnancy risk remains to be defined. ACHOIS used as its inclusion criterion a 2-hour venous plasma glucose level on oral glucose tolerance testing ≥ 7.8 mmol/L but < 11.0 mmol/L. The women included in the study had a median fasting glucose level of 4.8 mmol/L and a median 2-hour glucose level of 8.6 mmol/L. The current Australian criteria suggest fasting and 2-hour cut-offs of ≥ 5.5 mmol/L and/or ≥ 8.0 mmol/L, respectively, for the diagnosis of gestational diabetes.4 To avoid the confusion which could occur if multiple sets of criteria were promulgated, we suggest that the diagnostic thresholds for gestational diabetes should not be revised until the blinded prospective international epidemiological study HAPO (Hyperglycemia and Adverse Pregnancy Outcome) reports its results, which are expected by mid-2007.5 Screening for gestational diabetes also offers benefits from a public health viewpoint, at a time of increasing prevalence of obesity and type 2 diabetes.6 Screening allows identification of women with undiagnosed type 2 diabetes and those at increased risk of developing this condition in the future. Detection of gestational diabetes has the potential to benefit not only the women involved, but also their children, through intervention.7 Preventing progression from gestational diabetes to type 2 diabetes is already considered cost-effective.8 Introduction of routine screening for gestational diabetes clearly carries cost and resource implications. The number of women diagnosed with gestational diabetes will increase, and appropriate provision must be made for their care. In ACHOIS, the intervention group received care from a multidisciplinary team, which generally comprised a dietitian, diabetes educator and physician, in addition to the obstetrician and midwives. This level of care is congruent with the 1998 Australasian guidelines, but may be difficult to implement on a large scale across Australia. Other models of care may be required, with increasing involvement of midwives, general practitioners and other health care providers. There is some evidence to support the efficacy of such treatment protocols.9 However, the ACHOIS data2 suggest that something more than “routine antenatal care” is required for optimal outcomes in this patient group. Therefore, less intensive models of care should be rigorously evaluated rather than promoted ad hoc on the basis of potential cost savings. The extra costs involved in providing optimal care for women with gestational diabetes are likely to be far outweighed by savings due to reduction in adverse perinatal outcomes. Evidence and recommendations on gestational diabetes Treatment for gestational diabetes substantially reduces adverse perinatal outcomes and improves maternal quality of life. Optimal proven treatment for gestational diabetes includes review by a diabetes educator, dietitian and physician, with insulin used if glycaemic targets are not achieved. Screening for gestational diabetes should be offered to all pregnant women. Maternity service providers should ensure that adequate resources are devoted to the detection and treatment of gestational diabetes.

H David McIntyre FRACP · N Wah Cheung PhD, FRACP · Jeremy J N Oats DM, FRCOG, FRANZCOG · David Simmons MD, FRACP

It is time to focus on issues of roll-out and quality control “Hospital in the home” can mean different things in different countries and contexts. A Cochrane review defined it as “a service that provides active treatment . . . in the patient’s home of a condition that otherwise would require acute hospital in-patient care”.1 This definition includes services that substitute acute care by home-based management (admission avoidance) and those that support discharge with community-based post-acute care and rehabilitation (discharge support). The review found “insufficient evidence to support expansion or contraction” of home-based alternatives to inpatient hospital care.1 Two articles in this issue of the Journal contribute to the clinical evidence base for home care as an admission-avoidance service. There is a growing list of well-defined conditions that have been shown. . . to be manageable in home care. . . There is less consensus about whether treatment at home saves money. . . In a randomised controlled trial of an admission-avoidance hospital-in-the-home scheme in patients with mild to moderate community-acquired pneumonia, Richards et al (page 235) in New Zealand found no clinically important differences in time to discharge, duration of intravenous and oral antibiotic use or general functioning, but higher levels of satisfaction and lower costs for patients treated at home.2 In a retrospective case series of patients with pulmonary embolism in an admission-avoidance hospital-in-the-home scheme conducted in New South Wales, Ong et al (page 239) found outcomes similar to those in hospital cohorts, but acknowledged these results need to be confirmed in a trial.3 There is a growing list of well-defined conditions that have been shown in adequately powered trials or meta-analyses to be manageable in home care, provided either as a complete alternative to hospital admission or to support early discharge from inpatient care. These include cellulitis,4 chronic obstructive pulmonary disease5 and deep vein thrombosis.6 These findings should reassure clinicians who had concerns that similar overall outcomes in trials with a varied casemix may have masked important differences in outcomes for specific conditions. There is also consistent evidence from these studies that patients and carers prefer treatment at home. There is less consensus about whether treatment at home saves money, partly because of the difficulty of measuring costs realistically within a trial rather than a “real world” context,7 but also because costs are highly influenced by the health care system in which hospital in the home operates. A recent study from Victoria of 924 patients treated at home and matched hospital controls showed that home care was cheaper — especially if inpatient admission was completely avoided, in which case costs were 38% less.8 Costs also need to be considered as part of a whole system of health and social care provision. For example, it has been estimated that the Victorian hospital-in-the-home scheme provides the equivalent of more than 400 beds, and so has effectively provided care that would otherwise require the building and maintenance of a large metropolitan hospital.9 In contrast, in the United Kingdom, schemes are generally too small to have a detectable effect on hospital provision. If the evidence does support expansion of the scheme, clinicians and policymakers will need to know which key elements need to be replicated. Nearly all the evidence cited above relates to models with specific admission criteria, which include medical assessment by a specialist, generalist or both, either at home, in an accident and emergency department, or before transfer from inpatient care. Care is also supported by ongoing medical review, provided either in primary care or as hospital outreach. These schemes explicitly provide substitute, not additional, care and require detailed cooperation between the acute and community care providers. Interestingly, the development of hospital at home and other forms of intermediate care in the UK is going largely in the opposite direction. Since publication of the National service framework for older people in 2001,10 the emphasis has been on providing a wide range of schemes in response to local need, in part to prevent “avoidable admissions” (ie, those whose needs are primarily non-medical).11 Many schemes adopt low technology, and are nurse- or therapist-led, with admission rights extended to community nursing and social work teams.12 These developments have contributed to resistance, especially from physicians involved in the care of older people, who are concerned that inadequate assessment of geriatric clinical syndromes will disadvantage frail older people and reverse advances in clinical care made in the second half of the 20th century.13 These concerns are accompanied by fears held by general practitioners that they are neither equipped nor available to provide medical support to intermediate care. Although Richards et al point to the opportunities for involvement in home care schemes to increase the skills and experience of GPs,2 it seems only a minority of GPs in the UK will use the service if they have to assume medical responsibility. This proportion is likely to decline as most urban practices opt out of providing out-of-hours care.14 A national evaluation of intermediate care has recently been completed, but results have yet to be published. It seems likely that recent trial evidence will influence an updated Cochrane review, but problems appraising the evidence remain. Firstly, it may not be useful to combine data from intensive outreach interventions designed to substitute for inpatient hospital care (as seen in Australia and New Zealand) with more rehabilitative approaches designed to avoid unnecessary admissions and support discharge from inpatient hospital care. Furthermore, many of the advantages of hospital in the home, such as reducing risk of hospital-acquired infection and delirium and the social and psychological consequences of a hospital stay, occur only if admission is avoided, again suggesting that pooling data including supported discharge is not helpful. Finally, the Cochrane review will not include important evidence from large observational studies, which are more able than trials to detect uncommon complications and provide realistic estimates of cost. The articles by Richards et al and Ong et al add to the evidence for the effectiveness of a model of hospital in the home in which Australia and New Zealand are leading the world by providing services of sufficient scale to offer a real alternative to inpatient care. The evidence needed now goes beyond the remit of a Cochrane review, and should focus on issues of roll-out and quality control.

Andrew D Wilson MD, FRCGP · Stuart G Parker MD, FRCP

We need to acknowledge the inevitability of death to have some choice in the manner of our dying The tragic story of Maria Korp, the Victorian woman with severe irreversible hypoxic brain damage after an alleged murder attempt, has been prominent in the Australian media over the past few weeks. The clear, considered, and humane intervention by the state’s Public Advocate to authorise the cessation of artificial feeding has drawn both widespread praise, and some condemnation, especially from right-to-life activists.1 Once again, care and decision-making at the end of life is in the public arena. Earlier this year, world media attention focused on a young American woman, Theresa Marie Schiavo, who had been in a permanent vegetative state for more than 15 years. A prolonged legal and political battle in state and federal jurisdictions of the United States eventually led to the cessation of tube feeding, and her death. Interestingly, there was broad agreement between the courts and medical opinion that feeding should stop.2 In the preceding November, a much less publicised case was played out in Australia. The Supreme Court of New South Wales ruled that treatment could be withdrawn from Isaac Messiha, a man whose life was supported by ventilation and tube feeding, after he had experienced severe cortical brain damage resulting from a cardiac arrest. Faunce and Stewart review the Messiha and Schiavo cases concerning treatment abatement (a term adopted by Weir3 to encompass both stopping and not starting treatment) for incompetent persons (page 261) and weigh up two options for dispute resolution: an institutional clinical ethics committee ruling, and a judicial declaration on futility.4 Although both may occasionally have their place, basic process questions need to be posed by clinicians5 (Box 1) before recourse to external arbitration. It is noteworthy that in neither case was an advance directive in place. An important difference between the two cases lies in the time that elapsed after catastrophic hypoxic brain injury before treatment abatement was considered — years for Theresa Schiavo, and initially only 4 days for Isaac Messiha. It is clearly essential that abatement decisions should not be made prematurely. They should only be made after the patient’s failure to improve has been demonstrated over a period of observation and care that is widely agreed (by appropriate specialist neurological opinion, and supported by any relevant clinical evidence) to be reasonable for the diagnostic category concerned (stroke, post-coma unresponsive state, or brain death). Patients in a post-coma unresponsive state (previously known as permanent or persistent vegetative state) constitute a small subset of those who are incompetent to make medical decisions for themselves, and can be further subdivided into those whose condition is the end-stage of a terminal (albeit slowly progressive) illness (for example, the Victorian BWV case6), and those who are the victim of anoxic insult or trauma and are being maintained by nutritional support indefinitely, as in the Messiha and Schiavo cases, and the United Kingdom case of Anthony Bland.7 Leaving questions of advance directives to one side (their uptake rate has been poor nearly everywhere), Australian health legislation is not obviously helpful with the Bland-type cases, whereas some headway has been made with the first subset, as seen in the BWV case, and the drafting of the Consent to Medical Treatment and Palliative Care Act 1995 (SA). Whether the underlying condition is progressive or static, nobody should be locked indefinitely into an existence on life support, often without consent, and usually with no prospect of recovery. Treatment abatement decisions for those who are unable to speak for themselves should usually be resolved where they traditionally have been, between clinicians and families or duly appointed agents. Recourse to public tribunals and courts should be minimised, reserved for situations of intractable disagreement, if only because such processes address, but can also encourage, adversarial style mediation. Reducing the amount of futile medical treatment and introducing the timely deployment of appropriate palliative care to all who need it should be our preferred process. In bioethics, the concept of “futile” treatment has had a rough ride, mainly because of the inevitable uncertainties of medical prognostication. However, the “prognostic paralysis” described by Murray and colleagues is a real challenge,8 and we cannot ignore the fact that medicine has its limits. Despite polls reporting a widespread public pragmatism about death and dying (“I would never want to be a vegetable”, “When my time comes I do not want to be kept alive artificially”), when clinicians do try to discuss treatment abatement with patients and families, they often meet disbelief, even hostility. Clearly, polls reflect public attitudes as distinct from personal situations. In personal health care encounters, the idea that cure is improbable or impossible, or that continued life support is inappropriate or unkind, is unacceptable to many families. The wider problem here is that acknowledgement of the inevitability of death, and preparation for it, have largely lost their place in our culture. For many, an almost child-like faith in medicine and science has taken its place. We need to take up the challenges, and solutions, offered by health-promoting palliative care (Box 2).9,10 We need to shift from seeing the treatment of dying people, and the maintenance of those who are permanently unconscious but biologically alive, as “curative”. Instead, treatment of dying people with curative intent should be seen as an inappropriate and unkind obstruction of the natural dying process (given that our natural biological inheritance is to die) and a misuse of medicine.11 Thus, we should first try to save the lives of those who are sick and injured, but when this is no longer a reasonable prospect, the goals of care need to reflect that reality (Box 3).12 Mere emphasis on individual choice, important as it is, is not enough. A wider social understanding about the anticipated results of treatment of the dying and comatose person is essential, not medical heroics or legal and moral gymnastics. Health care workers and society need to move beyond curative domination and a view of death as medical defeat or failure. We need to question the place of death in the culture and processes of hospitals and aged care facilities, where most of these treatment abatement decisions occur. Appropriate care and decision-making at the end of life can only occur when death and the dying process are acknowledged, worked with, and regarded as an integral part of modern health care. Research into policy-based approaches, such as advance directives13 and care pathways for the dying in hospitals,14 is important. Results of their evaluation in Australia are eagerly awaited. In the meantime, many hospitals in Australia still do not have adequate consultative palliative care resources. When in place, and adequately funded, they can assist with imparting bad news, adapting to impending death, providing holistic care for patient and family, and with the transition, where appropriate, to community-based palliative care, or a palliative care bed. Evidence concerning good practice in communication about these issues is now well established.15,16 Death and dying is everyone’s business. Good clinical practice, integrating all we have learnt about communication and support for patients and families facing death, will go a long way to easing these tough journeys. But clinical approaches are not enough. We need to work with the policy-makers to place death and loss back on the public health and community agenda. We cannot control the fact of death, but we can have some influence on the manner of our dying. Medicine can make a wonderful contribution to quality of life until death; and it can make it miserable. This choice is ours. 1 Key questions to be addressed by a health care team if treatment abatement is considered Are the clinical facts of the case well established? Is the diagnosis correct? Has sufficient time elapsed to be reasonably confident that there is no reasonable prospect of substantial improvement or recovery? Is there consensus among the clinicians about the diagnosis, prognosis and most appropriate course of medical action? Is a case conference necessary? Identify the key decision maker(s) in the family, or friends. Have the patient’s family, carer(s) or legally appointed agent been advised of the above? Have they had a chance to express their opinions, and been involved in the decision-making process? Has the patient’s general practitioner been involved? Has the abatement decision been documented? The plan for implementing it may involve a “time trial” of continued life-sustaining treatment. How will subsequent objections to the decision be dealt with? Has a consultative palliative care team referral been considered? 2 Goals of health-promoting palliative care Provide education and information for health, dying and death Provide both personal and social supports Encourage interpersonal reorientation towards a “natural” death Encourage reorientation of palliative care services towards public health ideas of prevention, harm-reduction and community participation Combat death-denying health policies and attitudes 3 Goals of care Curative (“beating it”) Cure or durable remission Prognosis: years Palliative (“living with disease, anticipating death”) Disease incurable and progressive Prognosis: weeks, months (but can be years) Terminal (“dying very soon”) Death imminent Prognosis: hours or days Modified from Ashby and Stoffell.12

Michael A Ashby MD, FRACP · Allan Kellehear BA, PhD · Brian F Stoffell PhD

Millennium Development Goals for the world’s poorest nations need to be matched by Health Priority Goals for prosperous nations, to relieve the burden of wealth-related disease We have a set of clear and challenging goals — the Millennium Development Goals, adopted by the United Nations in 2000 — to improve the health of the poorest 760 million people on earth,1 but none for health development for the rest of us, and it is time that we did. Twelve per cent of the world’s population, inhabiting 50 countries, live on US$3 a day or less.2 Four and a half billion people live in less impoverished circumstances in Asia (excluding Japan), Latin South America, the Caribbean and some of Africa.1 Their countries have built the economic, legal and political infrastructure to attract investment, and they have achieved prosperity through the commercial, industrial and financial processes of global market participation. Birth rates and infant mortality have fallen, life expectancy has risen, and infectious diseases have been brought more or less under control. A further 1.2 billion people live long and prosperous lives in economically sound nations. Let us call these three groups Worlds A, B and C. The health needs of World A are those of people caught in desperate poverty, where infant and maternal mortality is high, infectious disease is out of control, and essential medical care for readily cured life-threatening illness is hard or impossible to obtain. HIV, malaria, respiratory and gastrointestinal infections and tuberculosis are the warlords that molest and kill. In 2000, the UN adopted the Millennium Development Goals to help World A gain its feet. The Millennium Development Goals called for global assistance through debt relief, direct aid, and scaling up of critical infrastructure, to cut in half the prevalence of abject poverty by 2015.3 The Millennium Development Goals correctly and appropriately concentrate on infant and maternal deaths, HIV and other diseases, but there are things that should be done now to prevent future chronic disease epidemics, for example, in tobacco control. For US$70 billion a year, less than the cost to the United States of the Iraq war, it would be possible to put in place a graded program of infrastructure development and community strengthening as a springboard for health gain and development. Part of poverty entrapment is health entrapment, and it may be easier to tackle this than try regime change as a means of social uplift. Although World A struggles desperately, it is now on the global radar. International aid agencies commit most of their resources to its relief. The Group of Eight (G8) summit recently agreed to a doubling of aid for Africa by US$25 billion a year by 2010, as part of an overall increase of US$50 billion for all developing countries. The G8 partners also cancelled 100% of the multilateral debts of the Highly Indebted Poor Countries.4 No one who understands the Millennium Development Goals claims that money is the whole answer, but while not sufficient, it is necessary. World B, meanwhile, is coming to terms with the impact of diseases that stem from the urbanisation, changing diet, tobacco, and transport changes that characterise their growing prosperity. Birth rates and infant mortality have fallen, and life expectancy is converging on that of World C, so that the global average life expectancy today is 65 years.1 Cardiovascular disease is now the truly global disease, evenly spread through Worlds A, B and C. World C has succeeded in pushing cardiovascular disease (both its death toll and much of its morbidity) into people’s late 70s and beyond. Not so in World B, where a third of deaths and suffering from cardiovascular disease occur among men and women, of working age.5 While the needs of World A are now on aid agendas, those of World B receive scant attention. Heart disease and stroke top the list of causes of disease burden worldwide. While the World Health Organization, the World Bank and the International Monetary Fund (to a lesser extent) have been steadily producing regional and national reports on the continuing and serious illnesses afflicting World B, no global commitment equivalent to the Millennium Development Goals has yet been proposed. As a result, efforts to control these problems are poorly directed and effective interventions all too rarely applied. A different set of goals — Health Prosperity Goals — is needed for World B. These goals should specify cuts in the toll of chronic disease, which is rising in developing countries. Specifically, smoking should be reduced by 20% in 10 years, and death from cardiovascular disease among people aged under 65 should be reduced by 15%. These goals could be discussed with town planners, food producers and retailers, insurers, employers (whose workforces cardiovascular disease adversely affects), unions (whose members suffer from cardiovascular disease), doctors and nurses, ministries of finance, educators, and the other people who must help us define the problem and solve it. Four benefits would follow from articulating a set of Health Prosperity Goals that would clearly define our intentions and bring to global attention the need to act on these conditions. First, Health Prosperity Goals would redirect us from repeatedly describing the size of our current health problems to concentrating thought on how to relieve them. To take cardiovascular disease again, we do not need to prove repeatedly that it is a serious problem. More to the point, we know we can achieve much through programs that manage people at elevated risk medically, combined with efforts to modulate the social and economic forces that promote those risks. Let us therefore aim for a 15% reduction in death from heart disease in people aged less than 65 by 2015 throughout Worlds B and C. Second, Health Prosperity Goals would establish accountability. Those who manage health programs then have an aim for which the community can hold them accountable. Third, we might frame the Health Prosperity Goals so that they specify broad strategies, based on evidence of effectiveness, but leave the details to individual nations to determine. Fourth, by concentrating on intervention, we will see how crucial it is that those involved in producing prosperity and its untoward side-effects contribute ideas and support to preventing and relieving those side effects. Discussion with city planners, developers, insurers, employers, union representatives, and non-government organisations may lead to a redefinition of health problems such as cardiovascular disease and proposals for their solution that introverted public health professionals, meeting in closed seminar rooms, might not think of in a decade.

Stephen R Leeder PhD, FRACP, FFAPHM

Fighting the current epidemic requires intensive education of clinicians and men who have sex with men, as well as targeted screening A research article (page 179)1 and a letter to the editor (page 218)2 in this issue of the Journal should leave you in no doubt that syphilis is back. After falling precipitously with the onset of the HIV epidemic in the early 1980s, syphilis infection rates are rising dramatically in Australia and the developed world among men who have sex with men.3 Why has this occurred, and what can be done about it? Australia’s response will determine if the current syphilis epidemic is remembered as an isolated epidemic or the return of endemic infection. The prevalence of a sexually transmitted infection (STI) is determined by three factors: the probability of transmission per partnership, the rate of partner change, and the duration of infectiousness. The particular importance of the duration of infectiousness is illustrated by the dramatic 100-fold fall in the prevalence of syphilis following the introduction of antibiotics.4 Another example is in situations where access to health care is poor and duration of infectiousness is therefore prolonged, as in isolated Indigenous communities in Australia. In such communities, both syphilis and gonorrhoea are common, despite rates of partner change being similar to those in the rest of Australia.5 In contrast, gonorrhoea or syphilis struggle to exist in communities with adequate access to health care, unless the rate of partner change is high. What then has changed among men who have sex with men to cause this sudden rise in syphilis infections in New South Wales and Victoria? Sexual behaviour has changed, with rates of any unprotected anal intercourse among men who have sex with men having increased by 50% in Australia over the last 10 years — this was also a strong risk factor for incident syphilis in the Health in Men (HIM) study6 mentioned in the research article by Jin et al.1 Oral sex is also transmitting syphilis, despite being considered relatively safe in terms of HIV transmission. Over half of the men in Jin et al’s cases series believed they had contracted syphilis through oral sex,1 and oral sex has been reported as the sole risk factor in up to 50% of cases reported overseas.3 HIV-positive men who have sex with men appear to be at increased risk of syphilis in Australia, representing between 40% and 54% of the cases reported by Jin et al1 and Guy et al.2 In addition, unprotected anal intercourse with an HIV-positive man was a strong risk factor for incident syphilis among HIV-negative men in the HIM Study.1 These findings are consistent with overseas reports that syphilis is more commonly diagnosed in HIV-positive men.3 The critical issue is what can be done now to control this epidemic. Clearly, increasing the use of condoms is important, particularly for anal sex. It is unlikely, however, that condoms will be widely used for oral sex, even though this practice is transmitting syphilis. In addition, reducing the rate of partner change is important, but it has been difficult to demonstrate large effect sizes in controlled studies.7 Substantially reducing the duration of infectiousness may be possible through educational campaigns, increased screening and enhanced contact tracing. Intensive educational campaigns for clinicians and men who have sex with men are fundamental for promoting early diagnosis and treatment, and screening high-risk individuals. Remember, most doctors under the age of 45 have not seen a case of syphilis, and young men are also less likely to be aware of the symptoms and clinical presentation of the infection. Educational campaigns that use the Internet can be relatively cheap and effective. For example, one banner advertisement on gay websites resulted in 32 270 click-throughs to public health websites with syphilis information.8 The cost per “click” varied from $0.05 to $10.8 Increased screening is the only way to detect asymptomatic infection; up to 33% of infections reported by Jin et al in the syphilis case series and the HIM study were asymptomatic.1 Guidelines suggest yearly testing for syphilis for any man who has had sex with another man in the past 12 months.9 This is easily justifiable given the syphilis incidence rate of 0.78 per 100 person years among men in the HIM study, but not necessarily easy to implement because it involves reaching all men who have sex with men, not just those attached to the gay community.1 Screening at every clinic visit for syphilis among HIV-positive homosexually active men may be necessary in view of the higher incidence of syphilis in this group. STI control is most cost effective if programs are focused on core group members who have large numbers of sexual partners. In the syphilis case series, up to two-thirds of the men had attended sex-on-premises venues or saunas where rates of STI infections have been previously reported to be extremely high.1,10 Contact tracing is an essential part of effective STI control but is difficult among men who have sex with men, whose partners are often anonymous. Nevertheless, innovative programs can prove effective. One study found that contact tracing was relatively effective even though the only identifying information available to public health officials were the “screen names” used in internet chat rooms. In this study, 41 of the 97 contacts of men infected with syphilis were traced through their “screen names”.8 Lastly, information about the epidemic, including the typical clinical features, who is affected, and risk factors for infection, is critical to inform intervention, as indeed both Jin et al1 and Guy et al2 have shown. For example, Jin et al provided much needed information about the usual clinical presentation of syphilis, finding that rash was the most common symptom (42%), but an ulcer or sore was also common (40%).1 As the rash of secondary syphilis is extremely infectious, identifying such cases early will significantly improve control. Australia’s response will determine if the current syphilis epidemic is remembered as an isolated epidemic or the return of endemic infection. Endemic syphilis will be expensive; both in human and financial costs, not least because it promotes HIV transmission. We need to learn from Australia’s effective and early response to the HIV epidemic that was characterised by community partnership, bipartisan government support, a commitment to harm minimisation and dynamic, original strategies.

Christopher K Fairley MB BS, PhD, FRACP · Jane S Hocking MPH, MHlthSc, PhD · Nicholas Medland MB BS

It may be difficult for patients to distinguish current concepts of immune function from other, non-conventional explanations of illness Each year, as many as 50%–70% of adults and children with allergic disease consult alternative practitioners.1-3 Some will undergo unproven diagnostic “allergy testing” as used by some alternative (and some conventionally trained) medical practitioners. The potential for adverse outcomes from using unproven diagnostic techniques is not only insidious but also potentially more serious than the more commonly debated issues surrounding costs,1 or the risks and benefits of alternative therapies such as naturopathy, chiropractic, acupuncture, homoeopathy or so-called “allergy elimination therapy”.4,5 Particular concerns arise when “positive test results” are followed by advice to restrict diet, a practice that our combined clinical experience tells us occurs not infrequently, regardless of the presenting problem — even in cases of asthma, allergic rhinitis or recurrent infection in which food allergy is not considered to play a pathogenic role. Such advice may unnecessarily delay more appropriate therapy and sometimes impair nutrition and growth.6 It is not difficult to understand why patients with allergic disease seek help where they can find it. Most people affected by allergic disease are young adults, or parents of young children with eczema, food allergy or allergic respiratory disease — groups that may find concepts of chronicity, and palliation rather than cure, unattractive. Parents of young children may be attracted to non-invasive (“no needles”) allergy testing. Furthermore, the field of allergy and immunology is a non-organ-based specialty, making it difficult for some patients to distinguish current concepts of immune function (or dysfunction) from other, non-conventional explanations of illness. Blurring the meaning of “allergy” to refer to any perceived response to an environmental agent, and use of the term “impaired immunity” interchangeably with “fatigue” (in the media as well as among some alternative practitioners), is conducive to blending concepts of immunology, neurology and spirituality to explain the pathogenesis of disease by some non-conventional philosophies.7 Factors that may contribute to the uptake of unproven diagnostic and therapeutic techniques include congruence with patients’ own philosophies about the pathogenesis of some disorders, a desire for autonomy, long waiting lists for specialty allergy services (and the lack of any publicly-funded clinics in some states, such as Tasmania and Queensland), advice from friends and family, internet-derived information (and misinformation) and uncritical media attention.1-3 Some of the non-conventional “allergy” tests in current use arose in the early 20th century, when allergy practice was essentially empirical.8 At that time, without mechanistic explanations or reliable tests to confirm an immune origin, disorders with a similar phenotype (eg, allergic and non-allergic urticaria) and some non-specific symptoms (eg, migraines, fatigue) were attributed to allergy, if skin tests were positive, or to “allergic toxaemia”, if results were negative.9 Cytotoxic food testing (“Bryans’ test”, and the ALCAT variant — whereby a patient’s leucocyte morphology is assessed after incubation with food extracts) was one, now considered unconventional, technique to arise from a search for more “reliable” tests to explain these phenomena.9 This test continues to be used today, despite evidence that results are not reproducible, are different when duplicate samples are analysed blindly, do not correlate with those from conventional testing, and “diagnose” food hypersensitivity in people with conditions in which food allergy is not considered to play a pathogenic role.10 In the meantime, modern allergy practice relies on understanding the biological mechanisms underlying allergic disorders and the correlation of symptoms with standardised tests to detect allergen-specific IgE.11 Reliable allergy testing increases diagnostic accuracy and facilitates the identification of avoidable inhaled or ingested triggers.12 Advances in scientific understanding have also facilitated the development of medications to block specific inflammatory pathways and novel approaches to immunotherapy.11 By contrast, many non-conventional diagnostic techniques are used without published evidence of clinical utility, and those subjected to formal evaluation have produced uniformly negative results. For example, in a blinded study, iridology practitioners were unable to distinguish healthy from diseased individuals and gave different diagnoses using iris photographs from the same patients taken minutes apart.13 Furthermore, the theoretical basis for iridology — that disease is reflected in iris patterns — is undermined by the use of iris patterns as biometric identification markers because they are considered to be unchanging and unique to individuals, differing even between genetically identical twins. Kinesiology (muscle testing) has been shown, in controlled studies, to be no more accurate than guessing.14 Vega (electrodiagnostic) testing, whereby skin electrical resistance is measured with food extracts present in the same circuit, was unable to distinguish between healthy and allergic individuals, or between control and allergen extracts, and yielded results that did not correlate with conventional test results.15 Rigorous study of other non-conventional methods such as IgG food antibody testing, food immune complexes and sublingual provocation/neutralisation have provided similarly negative results. (These and other techniques are reviewed in more detail at <http://www.allergy.org.au/pospapers/unorthodox.htm>.) In light of the evidence, how can we, as doctors, best serve our patients? First, we need to understand our patients’ belief systems and understand conventional and non-conventional approaches to diagnosis and treatment of allergies. Second, when assessing polysymptomatic patients with normal clinical and laboratory findings, we need to resist the temptation to label medically unexplained illness as “allergic disease”, and should question an allergy diagnosis made by the patient or based on unproven diagnostic techniques. By doing so, we may be able to help our patients to direct their efforts into more productive areas, and minimise unnecessary expenditure resulting from the use of unproven diagnostic techniques. We may also then be able to reconcile concepts of patient autonomy with the medical principle of primum non nocere (first, do no harm) and reduce the possibility that patients may inadvertently harm themselves or their children by pursuing unproven diagnostic techniques.

Raymond J Mullins PhD, FRACP FRCPA · Robert J Heddle PhD, FRACP, FRCPA · Pete Smith PhD, FRACP, FRCPA

This new definition should assist both researchers and clinicians The metabolic syndrome — the clustering of abdominal obesity, dyslipidaemia, hyperglycaemia and hypertension — is a major public health challenge worldwide.1,2 The metabolic syndrome is not benign; it is associated with a substantially elevated risk of type 2 diabetes (5-fold) and of cardiovascular disease (CVD) (2–3-fold),1 and its increasing prevalence could possibly reverse the gains made through recent declining CVD mortality. The metabolic syndrome is not a new condition. It was first described in the 1920s by Kylin, a Swedish physician, as the association of hypertension, hyperglycaemia and gout.3 In the 1940s, attention was drawn to upper body adiposity (android or male-type obesity) as the obesity phenotype commonly associated with type 2 diabetes and CVD.4 This constellation of CVD risk factors has been given a number of names, including “deadly quartet”, “syndrome X”, and “insulin resistance syndrome”,1 but “metabolic syndrome” is likely to hold sway for the foreseeable future. Just as the metabolic syndrome has borne a variety of different names, numerous definitions have also surfaced. The World Health Organization definition,5 and two others, developed by the European Group for the Study of Insulin Resistance6 and the National Cholesterol Education Program — Third Adult Treatment Panel (ATP III),7 have been the main ones in use. Each of these agreed on the core components of obesity, hyperglycaemia, dyslipidaemia and hypertension. However, the definitions differ in the cut-points used for each component, and the way in which the components are combined, leading to considerable confusion.1 The confusion has been particularly apparent in attempts to compare the burden in different populations, where the use of different definitions has seriously hampered the ability to make comparisons between and within communities.1,2 The parameters for assessing obesity have been most problematic, with the current definitions failing to account for ethnic differences for cut-points in waist circumference and body mass index. It was also uncertain which of the definitions best predicted those at risk of CVD and diabetes, although from a clinical perspective, the ATP III definition was probably the most practical for alerting health care professionals to subjects at risk.1,7 Because of the confusion, the International Diabetes Federation (IDF) embarked on the process of developing consensus on a new global definition (Box). The definition recognises the mounting evidence that visceral adiposity is common to each of the components of the metabolic syndrome. Thus, an excessive waist circumference (a good proxy measurement for visceral adiposity) is now a necessary requirement for the metabolic syndrome. Furthermore, as it is clear that the level of obesity at which the risk of other morbidities begins to rise varies between population groups,1,10 ethnic-specific waist circumference cut-points have been incorporated into the definition, so that for South and South-East Asians, 90 cm and 80 cm are the cut-points for men and women, respectively. The cut-points for lipids and blood pressure are unchanged from those used by ATP III, and the glucose cut-point is the value most recently recommended as the upper limit of normal by the American Diabetes Association. As with many previous attempts to define diagnostic criteria for obesity, diabetes, hypertension, and dyslipidaemia, there is always the possibility that new research will force changes, including the possible incorporation of new components such as C-reactive protein and adiponectin. The IDF consensus also includes recommendations for future research into components not currently included in the core definition of the metabolic syndrome. It further highlights strategies for treatment of the metabolic syndrome and its components.8 It addresses both clinical and research needs and: provides a simple entry point for primary care physicians to diagnose the metabolic syndrome; provides an accessible diagnostic tool suitable for worldwide use, taking into account ethnic differences in waist circumference and associated type 2 diabetes and CVD risk; and establishes a comprehensive “platinum standard” list of additional criteria that should be included in epidemiological studies and other research into the metabolic syndrome. Using this new definition, analysis of AusDiab indicates that 29.1% of Australian adults (aged 25 and over) have the metabolic syndrome, compared with 19.3% according to ATP III (P Z Z, J E S, unpublished data). Much recent discussion about the metabolic syndrome has appropriately raised questions about its definition, its clinical role, and even its existence.1,11 At its heart, the syndrome represents the association between a range of factors that appear to be united both in terms of aetiology and consequences. The new IDF definition should provide researchers with a common platform for investigating the metabolic syndrome and its consequences. It should provide a useful practical tool that reminds health care professionals of the metabolic consequences of obesity, and identifies individuals at risk of CVD and type 2 diabetes who are likely to benefit from (lifestyle) interventions. The 2005 International Diabetes Federation definition of the metabolic syndrome8,9 According to the International Diabetes Federation definition, for a person to be defined as having the metabolic syndrome, they must have: Central obesity (defined as waist circumference ≥ 94 cm for Europid men and ≥ 80 cm for Europid women, with ethnicity specific values for other groups*) plus any two of the following four factors: raised serum triglyceride level (≥ 1.7 mmol/L) reduced serum HDL-cholesterol level (< 1.03 mmol/L in males and < 1.29 mmol/L in females), (or specific treatment for these lipid abnormalities) raised blood pressure (systolic blood pressure ≥ 130 mmHg or diastolic blood pressure ≥ 85 mmHg), or treatment of previously diagnosed hypertension impaired fasting glycaemia (fasting plasma glucose [FPG] ≥ 5.6 mmol/L), or previously diagnosed type 2 diabetes * South Asian and South-East Asian men ≥ 90 cm, women ≥ 80 cm; Japanese men ≥ 85 cm, women ≥ 90 cm.

Paul Z Zimmet MD, PhD, FRACP · Jonathan E Shaw MD, MRCP(UK), FRACP · K George M M Alberti FRCP, PhD

We know what to do, but doing it is the challenge In 1992, the late Fred Hollows warned of the catastrophic effects that HIV would have in remote Indigenous communities. His trademark candour caused considerable stir, and a number of important initiatives were implemented, such as the Tri-state HIV/STI Project in Central Australia and the National Indigenous Australians’ Sexual Health Strategy. However, it would be hard to argue that HIV is widely believed to be a priority in Indigenous health 13 years later. Health-seeking behaviour based on the presence of genital symptoms or awareness of risk is limited in many Indigenous communities . . . Until now, the prevalence of HIV in the Indigenous community has been considered similar to that in the non-Indigenous community.1 In this issue of the Journal (page 124), Wright et al present evidence of a higher rate of HIV among Indigenous people in Western Australia than in the non-Indigenous population.2 They report that, while the rate of HIV notifications in the non-Indigenous population declined between 1985 and 2002, it increased in the Indigenous population. The difference in risk for Indigenous women was striking — 39% of all female HIV notifications in WA since 1994 have been for Indigenous women, giving an Indigenous : non-Indigenous age-standardised rate ratio of 18. In contrast, the rate ratio for Indigenous males was 2. Wright et al also confirmed the marked differentials in risk of other sexually transmitted infections (STIs) in the Indigenous population — with Indigenous : non-Indigenous age-standardised rate ratios of 242 for syphilis, 77 for gonorrhoea and 16 for chlamydia. The data in this study are likely to predominantly reflect the situation in rural and remote regions of WA, and the authors acknowledge the difficulties of interpreting surveillance data. Nevertheless, the findings demand attention. Health-seeking behaviour based on the presence of genital symptoms or awareness of risk is limited in many Indigenous communities: the concept of “sexual health” is a construct usually confined to well-resourced urban populations. Few Indigenous children in remote areas complete high school and, as a result, there are few reliable means of informing young people about health risks. Although many Aboriginal Health Services have instituted local programs of distribution, condom use appears to be uncommon,3 and there is anecdotal evidence of an increase in injection drug use in remote areas. In settings of social disruption and dislocation, such as among individuals who congregate on the fringes of major urban areas, sex is often exchanged for favours, alcohol and other substances. Not surprisingly, reinforcement and maintenance of health messages and wide implementation of interventions are difficult to achieve in these settings. It is not entirely clear why the prevalence of HIV has remained low in remote Aboriginal Australia; however, this might be explained by the structure of local sexual networks. In simple terms, the sexual network identifies who is having sex with whom, how often and where. Individuals in a sexual network operate in a social space, not necessarily a geographic space. Because of the sensitivity surrounding this issue, there has been very little published on the complex sociocultural factors that determine the structure of Indigenous sexual networks in remote Australia. It is known that Indigenous people living in remote areas may travel extensively across the country, but are likely to choose partners they already know and who share the same background. This has been termed “assortative” partnering, and has been observed in other populations.4 The absence of HIV from a network protects all its members — it is only when an HIV-infected individual enters the network that transmission occurs. Such individuals may have travelled to large urban areas and contracted HIV through injection drug use or homosexual contact. As a result, a substantial proportion of the members of the sexual network will become infected, although in small communities the absolute numbers will remain low. This implies that control of HIV in the Indigenous population will require multiple small interventions that target individual sexual networks, as well as reflecting the local sociocultural conditions. In the 1990s, the rates of curable STIs (chlamydia, gonorrhoea and trichomoniasis) were found to be many times higher in the Indigenous population in the Northern Territory, compared with the non-Indigenous population. However, the rate of a non-curable, viral STI (human papillomavirus) was higher in the non-Indigenous than in the Indigenous population. This suggested that a major reason for the disparity in rates is the limited access to and use of clinical services in remote areas, rather than differences in average rates of partner change.5 Health professionals who have worked in remote health settings know how hard it is to do more than simply react to the patients who walk through the clinic doors with an acute problem. Maintaining population health programs, such as immunisation, health promotion and risk factor modification, is always difficult in these settings, and these programs are first to suffer when a medical crisis occurs. The opportunity costs of a local HIV epidemic are considerable: HIV does not just affect the individual who is infected — sexual partners are also at risk, and transmission can occur antenatally and during breastfeeding. Ongoing risk behaviour after a diagnosis of HIV is documented, driven by psychiatric and substance abuse-related factors. The medical system is compelled to react to the presence of HIV infection in a particular community. In one remote community, this required an increase in the staff of the local public health unit from three to eight, and other programs fell by the wayside (unpublished data). This migration of resources may be one of the major costs of an HIV epidemic in remote Indigenous Australia. Evidence from Africa suggests that STI control early in an HIV epidemic may be effective in limiting the spread of HIV,6 but this strategy is less useful once the HIV epidemic is established. Good STI control requires a coordinated program that addresses health promotion, diagnostic and screening services, rapid access to appropriate treatment and locally appropriate contact tracing. This is not easy, nor cheap, but it is possible — as seen with a successful program in Central Australia.7 Others have also implemented relatively effective programs.8 Primary care providers can use a new Medicare rebate item (item 710) to screen for STIs in Indigenous people as part of a broader preventive health assessment. The new National Aboriginal and Torres Strait Islander Sexual Health and Blood Borne Virus Strategy, to be announced later in the year, will provide a useful review of existing programs, and recommendations for specific action. HIV testing is central to HIV control: it determines the extent of the epidemic and helps plan local interventions. Antenatal screening and antiviral treatment of an HIV-infected mother can almost eliminate the risk of transmission of HIV to the neonate; appropriately timed therapy has obvious benefits for the individual in terms of morbidity and mortality, and successful treatment reduces the viral load and decreases the risk of transmitting HIV through sexual contact. There is no need to reinvent guidelines for testing in Indigenous settings — they already exist. Sustainable implementation is the challenge that faces primary care providers. The data from Wright et al provide a compelling reason for meeting this challenge now.

Francis J Bowden FRACP, MD

Estimating glomerular filtration rate using a simplified formula will lead to a vast increase in detection of chronic kidney disease in Australia In patients with chronic kidney disease (CKD), the degree of reduction in the glomerular filtration rate (GFR) is closely linked to the development of complications of CKD, and GFR is the best index for classifying the severity of the disease. In 2002, a US working party produced a five-stage classification of CKD, with guidelines for management according to stage, based largely upon GFR (Box).1 The classification is logical and simple and has enjoyed worldwide endorsement. However, one problem has impeded widespread usage of the classification — most clinicians do not measure or calculate GFR. Why estimate GFR?The gold standard for measurement of GFR is kidney clearance of inulin, but this method is a research tool and not practical for clinical practice. GFR may be accurately measured by determining the clearance rate of exogenous radioisotopes, such as radiolabelled Cr51-EDTA. Alternatively, the measurement of 24-hour creatinine clearance provides a reasonable, though less accurate, approximation. Both methods are inconvenient, time-consuming and costly. Serum creatinine concentration is widely used as a surrogate marker of GFR, but is crude and insensitive. For example, among the nationally representative AusDiab cohort of 11 247 Australian adults, 1.1% had elevated serum creatinine levels whereas 11.2% had a calculated GFR < 60mL/min.2 Because of these anomalies, much effort has been directed at deriving formulas that use serum creatinine level together with other clinical variables, such as age, sex and weight, to yield an accurate estimated GFR (eGFR). The abbreviated MDRD (Modification of Diet in Renal Disease) formula for deriving eGFR has been extensively validated in US populations and is endorsed for the classification of CKD.1 The inputs required for the (predominantly white) Australian population are serum creatinine level, age and sex (the performance of the formula is less satisfactory among people of Chinese origin,3 and thus possibly others of Asian ethnicity, and is untested among Indigenous Australians). Thus, all data required for calculating eGFR using the abbreviated MDRD formula are currently provided on the typical pathology request form, making automated reporting of eGFR potentially feasible. The growing burden of CKDThe burden of CKD has long been underappreciated. Stage 5 CKD (end-stage kidney disease [ESKD]), which requires dialysis or transplantation to prevent death from kidney failure, provides the most obvious burden of CKD, as dialysis and transplantation are highly visible and enormously costly health problems. Earlier stages of CKD are more prevalent and may be even more costly than ESKD. Projections based on data from the AusDiab survey suggest that 1.4 million Australian adults (11.4% of the non-institutionalised population) had CKD stages 3–5 in 2000.2 Of these, 11 660 (< 1%) were living on dialysis or a functioning kidney transplant.4 For the 99% with CKD who were not receiving dialysis or had not had a transplant, two major consequences have become apparent: increased risk of developing ESKD and increased cardiovascular risk compared with the normal population. Both of these risks are associated with a progressive increase in mortality rate through successive stages of CKD, as was demonstrated in a longitudinal study of subjects in a large health maintenance organisation in the United States (figures represent 5-year mortality rates): no CKD, 10.2% ± 0.5%; stage 2, 19.5% ± 1.9%; stage 3, 24.3% ± 0.8%; stage 4, 45.7% ± 3.5%.5 Indeed, overwhelming evidence now shows that CKD is an independent risk factor for cardiovascular disease and should be added to the list of “traditional” risk factors.6 The need to identify CKDIdentifying cases of CKD may help to prevent ESKD and the attending increase in cardiovascular morbidity and mortality. There is clear evidence that intervention may slow the rate of decline in GFR for people with CKD, particularly if identified at an early stage. Blood pressure control, use of angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists for patients with proteinuric nephropathies, blood sugar control and regular clinical follow-up are all proven to be of benefit.7 Reduction in the cardiovascular burden associated with CKD through aggressive management of traditional and non-traditional (eg, elevated calcium phosphate product) cardiovascular risk factors appears likely to be effective, although definitive studies are awaited. CKD is generally asymptomatic. Subject awareness at all stages other than stage 5 is almost non-existent, and clinician awareness is similarly low.8 Thus, detecting CKD requires GFR measurement or estimation. In this issue of the Journal (page 138), a working group representing the peak bodies of Australian nephrology, pathology and biochemistry plus Kidney Health Australia has proposed that eGFR be automatically calculated whenever a serum creatinine measurement is requested through any pathology service in Australia. The eGFR will be reported whenever the value is < 60 mL/min, enabling classification of the patient within CKD stages 3–5. Values above 60 mL/min will not be reported, because of inaccuracies in eGFR in that range and because the complications of CKD are mainly seen at GFR < 60 mL/min. The program will include a comprehensive, ongoing strategy for quality control of laboratory serum creatinine measurements, as this is critical to the accuracy of eGFR, and a major education campaign designed to provide clinicians with guidance on interpreting eGFR and managing CKD. This initiative may prove to be incredibly important if Australia is to limit the current escalation in the burden of CKD. One crucial aspect will be to determine whether automated reporting of eGFR and early detection of CKD result in better health outcomes for the general population, by formally assessing the impact on the health system and individuals before and after the recommended change in eGFR reporting. As with any bold undertaking, there are certain risks and limitations. Firstly, an enormous number of patients will be identified, particularly among elderly Australians. The AusDiab study suggests the majority of patients with stage 3 CKD will be elderly women.2 The natural history of CKD in older people is poorly understood, as is the difference between the impact of normal ageing versus disease on GFR. The potential for increased costs to the health care system through an increase in tests, prescriptions and referrals to nephrologists may be significant, and the potential benefits are uncertain. The increase in workload for nephrologists, in particular, may be unsustainable. Education of clinicians will be crucial here, as will further research into the natural history of CKD in older people. Secondly, although eGFR is well validated for adult whites, caution will be required in applying eGFR to other patient groups such as Indigenous Australians and people of Asian origin.3 Finally, clinicians must not fall into the trap of interpreting an eGFR of > 60mL/min as indicative of healthy kidney function. While GFR is the best overall measure of kidney function and therefore the dominant determinant of the stage of CKD, for people at risk of kidney disease, testing for other markers of kidney damage — such as hypertension, haematuria, abnormal structure and, most importantly, albuminuria/proteinuria — must not be forgotten. K/DOQI classification of chronic kidney disease1 CKD stage Definition Prevalence in Australian adults2 1 Kidney damage (albuminuria, haematuria or abnormal kidney imaging), eGFR > 90 mL/min 0.9% (n = 112 000) 2 Kidney damage, eGFR 60–90 mL/min 2.0% (n = 250 000) 3 Moderate kidney failure, GFR 30–59 mL/min 10.9% (n = 1 400 000) 4 Severe kidney failure, GFR 15–29 mL/min 0.3% (n = 40 000) 5 End stage kidney disease requiring dialysis or transplant, GFR < 15mL/min 0.1% (n = 13 000) CKD = chronic kidney disease. eGFR = estimated glomerular filtration rate. K/DOQI = Kidney Disease Outcomes Quality Initiative.

Steven J Chadban PhD, FRACP · Francesco L Ierino PhD, FRACP

In the competition for official development assistance, health is losing out to governance and security Governance, law and justice were “big ticket” items in the 2005–06 Australian federal budget, reflecting the increasing focus on national security in Australia and elsewhere. Our current aid budget reflects this trend. Australian official development assistance (ODA) seeks “to advance Australia’s national interest by assisting developing countries to reduce poverty and achieve sustainable development”.1 According to AusAID, the agency responsible for the ODA program, poverty reduction remains central, reflecting Australia’s humanitarian values and its economic and security interests. The Australian Government has committed to a number of interrelated policy, program and partnership initiatives. In 2005–06, these initiatives seek to promote a closer partnership with Indonesia and engagement with fragile states, to stimulate broad-based economic growth, to strengthen efforts to promote better governance, to tackle transnational threats (notably HIV/AIDS), and to contribute to greater stability and security. A fair contribution?Australian contributions to ODA, now $2.49 billion a year, have been increasing over the past 5 years — a step in the right direction. Budget allocation has risen from 0.25% of gross national income (GNI) in 2001–02 to 0.28% in 2005–06. However, this gradual rise must be seen against the much larger decline over the past 30 years: in 1975–76, 0.45% of GNI was allocated to ODA, falling to 0.43% in 1985–86, 0.32% in 1995–96; and 0.28% in 2005–06.2 Current levels are well below the 0.42% committed, on average, in 2004 by nations belonging to the OECD (Organisation for Economic Co-operation and Development).3 This prompts questions about how Australia will achieve the ODA targets required to meet the United Nations’ Millenium Development Goals, to which we committed in 2000. If it is to do so, a timetable for achievement should be reiterated, with Australian ODA reaching 0.5% of GNI by 2009, nearly double the current level, and 0.7% by 2015.4,5 Without allocating considerably more resources, Australia will be substantially under target. Who benefits?Australia’s ODA is increasingly directed to near neighbours; around 42% is allocated to just three countries — Indonesia, Papua New Guinea and the Solomon Islands. The allocation to the whole continent of Africa, where poverty and conflict cut deepest,6 and where the impediments to achieving the Millenium Development Goals are greatest, stands at only 3% of Australia’s ODA. Support for other resource-constrained countries in South and East Asia is not much greater. Assistance to those in greatest need remains crucial if the benefits of greater equity, stability7 and control of infectious diseases,8 for example, are to be achieved. Attainment of the Millenium Development Goals needs better governance, but also increased and more effective aid for basic services in the poorest countries. One of the agreed indicators of effective aid targeting is the proportion going to countries classified as “Least Developed” by the UN’s Economic and Social Council. As little as 0.05% of Australia’s GNI goes to Least Developed Countries, one of the lowest rates of all OECD donors.9 A notable trend in Australia’s latest aid budget is the increased focus on governance, which now attracts 36% of ODA, squeezing out other commitments (Box). Almost half of this governance expenditure goes towards law and justice, with large tranches allocated to the Department of Defence and the Australian Federal Police for their activities overseas. This commitment to a “whole of government” approach has seen greater involvement of Australian experts with limited experience of developing countries, and inadvertently undermines the concentration of development expertise within AusAID itself. A healthy contribution?In 2005–06, Australia is devoting only 12% of ODA to health, substantially less than countries such as the United Kingdom (22%),10 and much the same proportion as in the past few years. Within this health allocation, an increasing share is devoted to multisectoral HIV/AIDS programs; their funding has increased from around $25 million in 2001–02 to around $70 million in 2005–06. While increased HIV/AIDS funding is necessary and welcome, commitment to non-HIV health-related expenditure has declined, in some cases markedly. Countries such as Laos, Cambodia and Vietnam no longer receive AusAID funds for health and, in the case of Laos, had primary health care funds cut precipitously. Health is significantly linked to poverty, but there are no short-cuts or easy solutions to re-establishing, reforming, and reshaping functional, efficient, and more equitable health systems. Basic health care requires sustained investment in human resources, infrastructure, community-level health promotion, and essential services for primary care, as well as attention to the social determinants of ill health. While supporting basic services is not the most glamorous issue, with neither the profile of HIV/AIDS nor the visibility of uniformed police and defence force personnel, these services remain the cornerstone to promoting health and to ensuring that communities can participate in, shape and control their own development. The Australian Council for International Development (ACFID), an independent association of Australian non-government overseas aid and development agencies, estimates that a fair Australian contribution to the global aid requirements for health would be around A$580 million, substantially above our current commitment of A$299 million.2 Keeping track of where ODA goesKeeping track of ODA is important. Otherwise, we cannot assess the range of activities underway and their outcomes. In recent years, the monitoring of ODA has been made more difficult because of the greater proportion devoted to governance and security, the control of funds by government departments other than AusAID, the failure to separate HIV/AIDS from general health sector reporting, and a reduction in detailed statistical presentation (eg, AusAID has not published a detailed listing of all funded projects since 2001). The level of funding allocated to Australian government departments exposes us to the criticism of “boomerang aid”. The ability to track and account for where funds have actually gone, the proportion tied to purchase of Australian products,11 and the share that goes into basic infrastructure and service delivery in the social sectors, or other forms of direct poverty reduction, should be enhanced. Aid effectiveness remains a key challenge.12-14 While there are no simple answers, numerous international organisations have made a commitment to promoting evidence-informed policy and allocating resources to learning lessons and reflecting on current practice, in partnership with academic and country-based experts.15 Australian commitment to this trend is to be encouraged. Will government follow the lead of a generous public?The response of the Australian community to the 2004 earthquake and tsunami in the Indian Ocean demonstrated popular concern for the needs of others. In fact, even before the tsunami, private contributions by Australians to aid and development were increasing by around 10% per year in real terms (from around $380 million in 2000 to $443 million in 2004, both figures in 2004–05 dollars [G Luke, Policy Adviser to Australian Council for International Development, personal communication, June 2005]), indicating strong interest and support for development cooperation. We need to tap into this public solidarity and ensure that ODA, despite its limitations, obtains more resources and attention. Increasing commitment to health and education will reinforce governance and security, but this is not why they should be supported. Health and education should attract funds because we care about other people,16 because we have a commitment to promoting human security in the region, and because we find it unacceptable that women die in childbirth because of lack of health services, that preventable diseases kill so many children before the age of 5, and that infectious and non-communicable diseases are decimating economies. Basic services require support, which cannot be provided within the existing aid envelope. The Australian Government White Paper on aid, currently being drafted and due in early 2006, is an opportunity to reinforce commitments to dramatically increase ODA and should place health firmly back on the agenda. The Australian public has demonstrated a willingness to contribute directly. Can we mobilise a matching political commitment? Australian official development assistance by sector* * From analyses of AusAID budgetary data (G Luke, Australian Council for International Development, personal communication). Funds not earmarked for a particular sector (either because they go to multisectoral initiatives, such as gender and environment, or to development banks and United Nations agencies) are excluded. †Expressed in 2004–05 Australian dollars.

Anthony B Zwi PhD, FAFPHM · Natalie J Grove BOccThy, MPH · Maria-Theresa Ho MHP, MD

Treatment has advanced, but a stigma still surrounds this disorder Epilepsy affects some 120 000 to 200 000 Australians. It is defined as a disorder with recurrent unprovoked seizures, but 4%–5% of the population may experience at least one seizure at some point in their lives.1 About half the people who develop epilepsy present in the first two decades of life. A second peak occurs in people older than 60 years. Pathophysiology and clinical geneticsFor 25 years, the classification of epilepsy syndromes has been embedded in the seizure type (partial or generalised onset) and the presence or absence of an underlying brain disorder (symptomatic or idiopathic),2 along with acceptance that there is a genetic basis with complex patterns of inheritance for idiopathic epilepsy. Indeed, in the past decade or so, examination of large pedigrees with multiple affected members has led to the discovery of several epilepsy genes. These gene defects most commonly disrupt the function of voltage-gated or neurotransmitter-gated ion channels, producing alterations in neuronal excitation within brain networks.3 These discoveries have enhanced our understanding of seizure pathophysiology, but they have also begun to cast doubt on the current classification of the epilepsies. The distinctions between partial and generalised and between idiopathic and symptomatic are difficult to support when individuals sharing gene defects present with very different epilepsies.4 Despite this, the known epilepsy genes do not yet explain the most common epilepsies, where gene combinations interacting with environmental or epigenetic factors are expected to provide the answers. NeuroimagingThere have been tremendous advances in neuroimaging technology. Magnetic resonance imaging (MRI) can demonstrate a variety of cerebral pathologies not reliably found with computed tomography (CT). These include hippocampal atrophy in mesial temporal lobe epilepsy, focal and diffuse malformations of cortical development, and vascular malformations and focal encephalomalacia. A CT brain scan is no longer an adequate investigation for epilepsy. The ability to measure volumes of specific brain structures and quantify signal change has opened new areas of neuroscience research in humans with epilepsy. Cross-sectional and, more recently, longitudinal studies of regional brain volumes have provided evidence of progressive brain damage with intractable focal seizures.5 Functional neuroimaging with positron emission tomography (PET) and single photon emission computed tomography (SPECT) are valuable in assessment for epilepsy surgery, but have contributed little to our understanding of the aetiology of epilepsy. The development of new PET and SPECT ligands and MRI spectroscopy holds the promise of advances using in vivo neurochemistry. Treatment and prognosisWith therapy, 60%–70% of people with epilepsy will have a good prognosis with complete control of seizures on the first medication tried. In the past 10–15 years we have seen the introduction of lamotrigine, vigabatrin, gabapentin, tiagabine, topiramate oxcarbamazepine and levetiracetam to the therapeutic armoury. These new antiepileptic drugs (AEDs) provide a greater range of options and differing side-effect profiles than existed with the older array of AEDs (barbiturates, phenytoin, carbamazepine and valproate).6 However, 20%–30% of patients will not respond completely to medication and there has been no major change in the proportion of children and adults whose seizures remain refractory to medication — even with the release of these new AEDs. There has been a growing awareness of the futility of years of different AED trials in individuals and AED polytherapy.7 The failure of two well-supervised medication trials in partial epilepsy should alert the physician of the need to consider options such as epilepsy surgery. A randomised, controlled trial of surgery for temporal-lobe epilepsy has shown 58% of the surgical candidates were seizure-free at one year, compared with 8% of medically treated patients.8 Surgery should not be seen as the last resort, but as a complement to medical treatment in refractory cases. Comorbidity of epilepsyDoctors have become very adept at counting seizures to determine the success of interventions. In the past decade, attempts have been made to assess the impact of epilepsy and its treatment upon a person’s quality of life. We are becoming more aware of the effects of the older AEDs on endocrine function and their teratogenic potential.9 Long-term AED use is associated with osteopenia, and vitamin D and calcium supplements are appropriate. More than 30% of patients with epilepsy may suffer depression. The depression is not simply the result of a chronic medical illness; it seems that the two disorders may share a common pathological substrate. Recognition and treatment of depression is important to the success of the treatment of the epilepsy itself.10 The futureIn the next decade or so, we can expect that genetic testing for particular epilepsies will complement and perhaps lessen our current dependence on clinical profiles and electroencephalography. It is conceivable such testing may aid us in selecting the most appropriate AED and predicting hypersensitivity side effects of AEDs. Currently, AEDs are administered to control seizures or the clinical expression of epilepsy, but we have no means to intervene to prevent epileptogenesis. Advances in our knowledge will certainly occur in the next decade. But without a greater understanding of epilepsy and seizures in the community, we will not lessen the stigma that still surrounds the disorder in schools and the work place. Epilepsy is a common disorder and deserves attention in public education programs.

Andrew F Bleasel MB BS, PhD, FRACP

How to submit a manuscript using Editorial Manager Prepare your submission To submit your manuscript online, you will need: 1. An electronic manuscript file that contains no identifying information (no author names or addresses, no acknowledgements). 2. An abstract of your manuscript. All articles except Letters to the Editor, Obituaries and Book Reviews require an abstract of some kind (see <www.mja.com.au/public/information/instruc.html>). Even an editorial requires a one- or two- sentence descriptive abstract. 3. Details of your co-authors: name, qualifications, position, institution, email address. 4. A disclosure statement completed for all authors. Our disclosure form is available at <www.mja.com.au/ public/information/disclosure.doc>. 5. High-resolution copies of any figures or photographs in separate files (if your manuscript is illustrated). 6. A covering letter in support of your submission (not required for Letters to the Editor, Book Reviews or Obituaries) saved in a separate electronic file. Register with Editorial Manager Everybody needs a username and password to log in to the MJA’s Editorial Manager site. If you haven’t used Editorial Manager with the MJA before, you will need to register first. Go to <www.editorialmanager.com/mja/>, click on “Register”, and follow the steps. We have registered all MJA reviewers already. If you are a reviewer, you should have received your username and password in an email. Submit your article Go to <www.editorialmanager.com/mja/> and click on “Submit a manuscript”. There are several steps to making a submission. Each time you complete a step, the system saves your work. If your session is interrupted for any reason, you can come back and complete your submission at a later time. Problems? Call Kerrie Harding or Christine Hooper in the editorial office: +61 2 9562 6666. No internet access? Send your submission by post. We would appreciate receiving the manuscript on a disk as well as on paper, if that is possible. On 1 July 2005, the MJA began using an online manuscript submission and peer review system called Editorial Manager. Provided by Aries Systems in the US, Editorial Manager is used by many journals throughout the world (including Australian Health Review, American Heart Journal, Annals of Emergency Medicine, and Cell). Indeed, many MJA authors and reviewers have already used Editorial Manager or a similar system. Editorial Manager records manuscript submission and peer review in a database accessible via the world wide web. This administrative technique is very efficient. Authors enter their submissions directly into the database, receiving instant confirmation that their work has been received. Using Editorial Manager, authors are less likely to omit required information from their submission, and this reduces delays. Editorial Manager streamlines the communication between editors and potential reviewers, and makes it easy and quick for reviewers to receive a copy of the manuscript. The same streamlined method of communication is used to submit reviews, request manuscript revisions, and receive a final article. Journals using Editorial Manager commonly report that the administrative work and time taken to reach a decision on manuscripts are greatly reduced, and the number of manuscripts submitted rises. Editors, authors and reviewers can log in at any time to check the status of their manuscripts. Because Editorial Manager is a web-based system, it is available wherever and whenever there is an internet connection, not just in the office. This accessibility also makes it easier for authors and reviewers overseas to contribute to the MJA. So, we are expecting Editorial Manager to bring many benefits — benefits that should ultimately be expressed in better articles published more quickly in the MJA. We are also nervously prepared for the potential downside. New computer systems never appeal to everybody. The website provides plenty of written instructions, but we are also ready to spend time on the phone with new users answering their questions. We encourage all users of the system to give us feedback to guide future development of the system. And, although we are encouraging all authors to use Editorial Manager, no author will be discriminated against for not using the system. You can still post us a handwritten essay, if that is your modus operandi, and the editors (some with a thrill of nostalgic pleasure) will respond in like style. We do feel, however, that most authors will be much better served by the new system, and strongly urge them to take it up.

Craig M Bingham BA · Christine Hooper · Kerrie Harding

Our unsustainable health care system needs reforms that capitalise on GPs’ passion for patient care “. . . it takes all the running you can do, to keep in the same place. If you want to get somewhere else, you must run at least twice as fast as that!” Lewis Carroll July 1999 saw the first MJA general practice issue emerge, by dint of some careful gathering of relevant articles for Family Doctor Week. Over time, this special issue has become an annual fixture, and this year we had the luxury of being able to choose from a bumper crop of articles submitted especially for the issue. Our dilemma now is not, “How do we fill the issue?” but “How do we pick from the crop?”. We particularly wanted to reflect the priorities of general practitioners and did what any self-respecting journal does — waved a magic wand towards the GPs in our current reviewer database, and asked what they most wished for to help them in their clinical practice. Their greatest desire turned out to be more time to spend with their patients. And they are not alone. In 2000, generalist and specialist physicians in five countries — Australia, Canada, New Zealand, the United Kingdom and the United States — wanted health care reforms that gave them more time with patients.1 What GPs want is indisputably linked with more satisfied patients and better outcomes.2 Yet, it seems that Australian GPs are, to some extent, already having their wish fulfilled and are spending more time with their patients, as are their UK and US counterparts.3 In the 10 years to June 2004, claims to the Health Insurance Commission for “brief office consultations” dropped by 42% to 5774 services per 100 000 population, and for “standard consultations” (up to 20 minutes) by 12% to 348 946 per 100 000.4 Meanwhile, claims for “long consultations” (over 20 minutes) rose by 52% to 49 399, as did “prolonged consultations” (over 40 minutes) by 59% to 4824. So, why do we still feel pressed for time? Our patients’ needs are greater — we battle with chronic disease, complex comorbidities and the frailties of age. Expectations are higher on all fronts — from society, government and the profession itself. Greater patient participation in consultations, an agenda extended to include health promotion, access difficulties and lack of continuity of care also add to time pressures.2,3 To fathom how consultation length is affected by a GP’s age, sex, training and other characteristics, as well as the type of patients and problems managed, turn to the analysis by Britt et al of over 70 000 general practice consultations on page 68. Of course it’s not just GPs who want more time — everyone else in our society does too. But few other professionals attempt to undertake complex tasks in 20- or even 40-minute spurts. Our health care juggernaut creaks with infrastructure and payment systems inherited from an age when acute care was paramount. Remedial patches, such as financial incentives and Medicare items to promote quality care, are applied with reels of red tape.5 On page 64, Zwar and colleagues show that it is mainly paperwork that stops GPs using the government’s Asthma 3+ Visit Plan for organised asthma care. The phrase “hamster health care” has been coined for a system that depends on everyone running faster on a treadmill.6 It is not sustainable and “the answer must be to redesign health care”. But many GPs prefer instead to spend less time as hamsters. According to Schofield and Beard (page 80), employment and retirement patterns of Australian doctors and nurses show that “generation X” GPs are working shorter hours than “baby boomers” did at the same age. But some hamsters just can’t break the habit; our workforce is ageing, with older GPs working beyond the traditional retirement age of 65 years. Others, however, are branching out into special interest areas, and Wilkinson et al (page 84) canvass the pros and cons of this solution. The path to reform“There’s no use trying,” [Alice] said: “one can’t believe impossible things.” “I daresay you haven’t had much practice,” said the Queen. “. . . Why, sometimes I’ve believed as many as six impossible things before breakfast.” Lewis Carroll In this issue, we only ask you to believe two things: 1) that health care reform is possible and will save time — eventually; and 2) that GPs are still passionate about what they do. We asked a small sample of GPs how they would grant the wish for more time for clinical practice. They conjured up remuneration that rewards time spent with patients, less paperwork, better IT support and more efficient collaboration with allied health professionals. Pegram (page 94), Aloizos (page 96) and Wenck and Lutton (page 95) give concrete suggestions for these, drawing on some real-life local examples. Similar models being tested elsewhere include cohesive primary care teams in the UK and the US, comprising health professionals from different disciplines, which have been shown to benefit patients and doctors.7 There has been slow headway in the paperwork battle. In June, in response to the 2003 Red Tape Taskforce review,8 new Medicare Enhanced Primary Care items were announced. It is hoped that these will reduce the administrative complexity of care planning and improve allied health access for GPs managing patients with chronic disease.9 While most general practices are computerised, our ability to save time by harnessing the digital revolution for communication and information management is still in its formative stages.10 Beilby et al (page 99) confront what is required to achieve systems that allow effortless communication across health sectors, and seamless movement between patient records, decision support tools, and practice audits. A groundbreaking analysis of pharmaceutical advertisements in prescribing software (Harvey et al, page 75) illustrates some of the pitfalls of new technologies; and a linked editorial by a former pharmaceutical industry insider Ruff, and colleague Haikal-Mukhtar (page 73), sheds light on how relationships between stakeholders in modern health care might evolve. Difficulty getting timely appointments introduces another time pressure. An innovative appointment scheduling system applied in the UK and the US provides patients with same-day appointments with their doctor of choice. This model is set to roll into 300 Australian general practices at a cost of $15 million, and the initial experience of two Australian practices (Knight et al, page 101) shows it is feasible and can boost staff morale and working conditions. Clearly, sensible health policy reform should come from quality primary care research (Glasgow et al, page 97), but McAvoy (page 110) draws attention to the huge discrepancy between funding for primary care research and that for hospital- and laboratory-based research not only in Australia, but also in New Zealand, the Netherlands and the UK. Despite this, Kamien (page 91), Weller (page 92) and Jackson (page 93) attest to the achievements and map the future tasks of academic general practice. They want fairer funding, and a redoubling of efforts, firstly, to engage non-academic GPs (and general practice registrars) in a research culture and, secondly, to make general practice integral to shaping our health care future. We have included in this issue several reports of useful research embedded in the general practice setting, including a randomised trial of different injection techniques for vaccinating babies and toddlers (Cook and Murtagh, page 60), and evaluations of two different psychiatric services (Simpson et al, page 87; Bradstock et al, page 90). The passion of GPsMartin and Sturmberg (page 106) argue that reforms focused solely on structure and behaviour change will fail without an understanding of the GP’s role in complex, living, relationship-based systems. And our general practice issue would be incomplete without stories of such relationships: a tale of patient persistence and GP passion (see Box) and Cowap’s Personal Perspective on page 72. These are the real reasons we want reform. However, we should take care that the individual discourse of general practice is not overshadowed by reform incentives leading to a purely biomedical or population health model (Russell, page 104). Don Berwick, a leading proponent of health care reform in the US, is wary of financial incentives to individuals: “I think people respond to joy and work and love and achievement and learning and appreciation and gratitude — and a sense of a job well done.”11 Incentives without passion are meaningless. As this issue goes to print, it is disappointing to hear that discussions have stalled between the Council of Australian Governments (COAG) and an unprecedented coalition of over 40 health professional and consumer groups (the Australian Health Care Reform Alliance, AHCRA) (Professor John Dwyer, Chairman, AHCRA, personal communication). It appears that, rather than capitalise on the passion at the frontline with a broader collaborative approach, the task of developing strategies for reform is now in the hands of government officials, who will report in December 2005.12 We hope that they will engage frontline clinicians and consumers. Without this engagement, any plans for reform are doomed to failure and the time-poor will remain with us. Just another day at the practice . . . A young woman D confronts her new GP, Dr T, with gangrenous, bone-exposed toes, a complication of previous meningococcaemia. Her other leg looked similar, she says, until the below-knee amputation. The specialists advise amputating this one too, an option she refuses to consider. Dr T seeks opinions from other specialists, who advise the same. But both GP and patient refuse to give up hope. Dr T contacts a surgeon with extensive overseas experience in reconstructive surgery for patients with leprosy. This surgeon intervenes and the leg is saved (minus a few toes). The story doesn’t end there. D wants to lead as normal a life as possible, and next Dr T and the prosthesis team scout for a waterproof prosthesis so that she can waterski. Now, she not only waterskis, but mountain climbs, visits building sites as part of her job, and has had a child after a complicated pregnancy, all with the support of her GP and other health professionals.

Mabel Chew FRACGP, FAChPM