Volume 183 Issue 4

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

Dr Lee, Medical Director, Wyeth Australia (left), presenting the 2004 MJA/Wyeth prize to Associate Professor Damien Jolley. Mr Jim Robertson announcing the inauguration of the Wyeth Prize in 1994 On 12 July 1994, at a ceremony celebrating the 80th year of continuous publication of The Medical Journal of Australia, Mr Jim Robertson, the then General Manager of Wyeth Australia, announced the inauguration of the annual MJA/Wyeth Prize, to be awarded for the best clinical research published in the Journal, as judged by independent experts. The first prize was presented at the 1996 AMA National Conference in Canberra by Dr Greg Rough, then Marketing and Sales Director of Wyeth Australia. Since then, the MJA/Wyeth Prize has been strongly supported by Wyeth Australia and the organisation’s managing directors, Greg Rough, Geno Germano and, more recently, Erica Mann, and has been awarded for an eclectic array of first class clinical research, encompassing acute medicine, environmental and public health, and the health of Australian Indigenous people (listed in the Box). The 10th MJA/Wyeth Prize was awarded at the 2005 National AMA Conference in Darwin by Dr Michael Lee, Medical Director, Wyeth Australia, to Associate Professor Damien Jolley and his co-investigators Robyn Wright, Sunita McGowan, Mark Hickey, Don Campbell, Rodney Sinclair and Kenneth Montgomery. Their research addressed the prevention of a common but unglamorous condition: the pressure ulcer. In a head-to-head randomised trial that compared the efficacy of Australian sheepskin versus usual treatment to prevent pressure ulcers, patients resting on medical sheepskin developed new pressure ulcers at less than half the rate of those undergoing standard treatment. In presenting the award, Dr Lee noted that Wyeth “was particularly delighted to be able to continue its association with and support for the Medical Journal of Australia/Wyeth Research Award”. “As a medical community, we are all keen to see continuing evolution in medical knowledge. It allows us to do more, and hopefully better, for our patients and our community. After all, this is what motivates us. And as participants in the health care system and the health care industry, we can all claim, with the winner of this award today, a small role in making a difference.” Recipients of the MJA/Wyeth Award 1995–2004 1995 Gastric emptying in acute overdose: a prospective randomised controlled trial Susan M Pond, David J Lewis-Driver, Gail M Williams, Adèle C Green, Noel W Stevenson. Med J Aust 163: 345-349. 1996 An outbreak of Japanese encephalitis in the Torres Strait, Australia, 1995 Jeffrey Hanna, Scott A Ritchie, Debra A Phillips, Jack Shield, M Clare Bailey, John S Mackenzie, Michael Poidinger, Bradley J McCall, Phillip J Mills. Med J Aust 165: 256-260. <eMJA full text> 1997 A high incidence of melanoma found in patients with multiple dysplastic naevi by photographic surveillance John W Kelly, Josephine M Yeatman, Cheryl Regalia, Grahame Mason, Amanda P Henham. Med J Aust 167: 191-194. <eMJA full text> 1998 Outdoor air pollution and children's respiratory symptoms in steel cities of New South Wales Peter R Lewis, Michael J Hensley, John Wlodarczyk, Ruth C Toneguzzi, Victoria Westley-Wise, Trevor Dunn, Dennis Calvert. Med J Aust 169: 459-463. <eMJA full text> 1999 Impact of improved diagnosis and treatment on prevalence of gonorrhoea and chlamydial infection in remote Aboriginal communities on Anangu Pitjantjatjara Lands Penny J Miller, Paul J Torzillo, Wayne Hateley. Med J Aust 170: 429-432. 2000 Reducing premature death and renal failure in Australian Aboriginals: a community-based cardiovascular and renal protective program Wendy E Hoy, Philip R Baker, Angela M Kelly, Zhiqiang Wang. Med J Aust 172: 473-478. <eMJA full text> 2001 The effects of quality improvement interventions on inhospital mortality after acute myocardial infarction Ian A Scott, Michael D Coory, Catherine M Harper. Med J Aust 175: 465-470. 2002 Sharing the true stories: improving communication between Aboriginal patients and healthcare workers Alan Cass, Anne Lowell, Michael Christie, Paul L Snelling, Melinda Flack, Betty Marrnganyin, Isaac Brown. Med J Aust 176: 466-470. <eMJA full text> 2003 Effectiveness of ototopical antibiotics for chronic suppurative otitis media in Aboriginal children: a community-based, multicentre, double-blind randomised controlled trial Sophie Couzos, Traven Lea, Reinhold Mueller, Richard Murray, Margaret Culbong. Med J Aust 179: 185-190. <eMJA full text> 2004 Preventing pressure ulcers with the Australian Medical Sheepskin: an open-label randomised controlled trial Damien J Jolley, Robyn Wright, Sunita McGowan, Mark B Hickey, Don A Campbell, Rodney D Sinclair, Kenneth C Montgomery. Med J Aust 180: 324-327. <eMJA full text> Managing Directors of Wyeth Australia and New Zealand (left to right): Greg Rough (1998–2000), Geno Germano (2000–2002), Erica Mann (2003–).

Objectives: To describe trends in the notification of infectious syphilis in New South Wales, the characteristics of homosexually active men recently notified with early syphilis, and the seroprevalence and incidence of syphilis, as well as associated risk factors, in a Sydney cohort of HIV-negative homosexually active men.Design, setting and participants: Secondary analysis of New South Wales infectious syphilis surveillance data from 1998 to 2003; a case series of 57 homosexually active men diagnosed with early syphilis in inner Sydney from December 2002 to January 2004; and a prospective cohort study of syphilis among 1333 HIV-negative homosexually active men in Sydney recruited from June 2001 to December 2003.Main outcome measures: Rates of notification of infectious syphilis in New South Wales and in areas of inner Sydney; behavioural and clinical features of men with syphilis in the case series; and incidence of syphilis and hazard ratios (HRs) associated with sexual behaviours in the cohort study.Results: Infectious syphilis notifications in inner Sydney rose more than 10-fold (from 6 in 1999 to 162 in 2003), and the increase was confined to men. Of 57 men with early syphilis in the case series, 54% were HIV-positive and 32% reported no symptoms of syphilis. These 57 men were highly sexually active and likely to report recreational drug use. In the cohort study, 1292 men (97% of participants) consented to syphilis testing; the incidence of syphilis was 0.78 per 100 person-years, and risk factors included reporting unprotected anal intercourse with HIV-positive partners (HR, 5.31; 95% CI, 2.00–184.93) and insertive oral sex (HR, 4.55; 95% CI, 1.14–18.18).Conclusion: Syphilis has been re-established among homosexually active men in Sydney, and HIV-positive men are over-represented. Frequent screening is needed in this population to curb the transmission of both syphilis and HIV.

Fengyi Jin MPH · Garrett P Prestage PhD · John M Kaldor PhD · Andrew E Grulich PhD, FAFPHM · Susan C Kippax PhD · Catherine M Pell MB BS · Basil J Donovan MD, FAChSHM

Objective: To examine the effects of asbestos exposure and tobacco smoking on the level and rate of change of the diffusing capacity of the lung for carbon monoxide (Dlco).Design and participants: A cohort study of 934 people (including both mine workers and town residents) exposed to crocidolite (blue asbestos) at the asbestos mines and in the town of Wittenoom, Western Australia, between 1943 and 1966. Dlco measurements were taken during a follow-up period from 1992 to 2002.Main outcome measures: Baseline levels of Dlco and change in levels over time.Results: 2980 Dlco measurements were done on 934 people (of whom 818 were men and 724 were workers) who underwent a median of 2 (range, 1–17) measurements during the follow-up period. Radiographic asbestosis at baseline and asbestos exposure at a younger age were associated with lower Dlco values. The average rate of decline in Dlco was 0.33 (95% CI, 0.31–0.35) units per year, plus an additional decrement of 0.22 (95% CI, 0.12–0.32) units per year if the participant had radiographic asbestosis at the beginning of the follow-up period. Compared with never-smokers, current smokers and ex-smokers had lower Dlco at baseline, but smoking status did not affect the change in Dlco during the follow-up period.Conclusions: Our results confirm a continuous deleterious effect of crocidolite on Dlco, especially on people with asbestosis. Smoking was associated with lower Dlco levels, but was not a significant predictor of rate of change in Dlco. Smoking status did not affect the relationships between crocidolite exposure and the level or rate of change of Dlco in this population.

Helman S Alfonso PhD · Lin Fritschi PhD · Nicholas H de Klerk PhD · Nola Olsen MSc · Jan Sleith MSc · Arthur (Bill) W Musk PhD, FRACP

Reporting medical news entails a special responsibility The fundamental question in medical journalism is how best to identify, process and report legitimate medical information to the general public . . . The process . . . is far more haphazard and idiosyncratic than outsiders might ever imagine.1 — Timothy Johnson: Chief Medical Correspondent, American Broadcasting Corporation Media coverage provides an essential link between the providers and users of health care. For health care industries, favourable reports on new drugs, procedures and treatments may translate into improved revenue streams from increased sales and rising share values. For medical researchers, media reporting of research findings enhances citation rates and boosts the public profile of their research institutions.2 For an increasingly educated and attuned public, access to developments in medicine affects individual health decisions. Integral to this whole process are journalists, as they largely determine what information is reported. Equally crucial is the responsibility that their reportage be accurate, adequately researched and conveyed in a clear and unambiguous manner. Indeed, the 2001 Australian Press Council guidelines on reporting medical matters stress the need for a conservative and careful approach to this task.3 The Association of Health Care Journalists (AHCJ) in the United States is even more explicit. Its principles for health reporting note that “ journalists have a special responsibility in covering health and medical news”.4 This includes the “professional standards of truth, accuracy and context in every report”, free from any personal, financial or other conflicts of interest. The AHCJ principles provide pragmatic advice on such matters as being vigilant in selecting sources; understanding the medical research process; avoiding vague and sensational language; explaining research outcomes clearly; and outlining the risks and benefits of any treatment.4 With such an abundance of good advice, a high quality of media reporting of health and medical matters would be expected, but this confidence may well be misplaced. In this issue of the Journal (page 190), Smith and colleagues report on the quality of medical news stories published in three high profile Australian newspapers — The Age (Melbourne), The Australian and The Sydney Morning Herald — and two online outlets — “ABC news online” and “ninemsn”.5 Assessments of individual news stories are posted on the media doctor website (http://www.mediadoctor.org.au) and scored using a three-star rating system based on satisfying 10 criteria, such as evidence of disease-mongering, too much reliance on press releases, appropriate reporting of benefits, harms and costs, and the independence of information sources. Twenty of the 104 articles surveyed scored no stars (overall score < 25% of criteria satisfactory), and 11 scored three stars (score > 75% of criteria satisfactory). Overall, both online and print media outlets scored poorly, with an average score of 56.1% for the print media, and 40.1 % for the online media. Criteria that scored poorly across both print and electronic media news reports included quantification of benefits, and harms and costs of treatment.5 Similar findings have been reported for media outlets in North America.6,7 Given that most people know little about the workings of the media, we invited media insiders — three high level journalists — to give their comments on the findings of Smith et al. Herman and Morgan of the Australian Press Council (page 195) welcomed the findings, but cautioned against expectations that initiatives such as media doctor will lead to any spectacular improvement in the quality of health or medical reporting. They suggest that the somewhat better performance of print compared with electronic media may reflect the promulgation in the print media of the Press Council’s 2001 reporting guidelines. Indeed, such guidelines are conspicuously absent in the current Commercial Television Industry Code of Practice.8 Swan (page 194) and Sweet (page 194), both veteran health commentators, stress the need for better cooperation between researchers and journalists, and Sweet is sceptical that exercises such as media doctor will enhance the quality of medical or health reporting. There is an impression that, in the time-poor and chaotic world of journalism, quality is sometimes overwhelmed by the urgent need for copy, and that outside scrutiny of quality is not particularly welcomed or productive.9 There is, however, a more pertinent issue. At the core of the media, as in medicine, is the principle of self-regulation. In such circumstances, it is the attitudes of journalists, their editors and program executives that drive standards, and in this quest for medical reportage, Schwartz and Woloshin have recently advanced a number of simple principles:10 Don’t report preliminary findings: This recommendation applies particularly to Phase 1 trials, studies using animals, and preliminary reports presented at scientific meetings. More than a quarter of meeting presentations are never published.11 Communicate the absolute magnitude of differences: Convey not only the relative risks, but, more importantly, what these mean in absolute terms. Include study limitations: These should be highlighted along with potential conflicts of interest and funding sources. To make health and medical reports as accurate and accessible as possible, there should be greater cooperation between researchers and reporters. To achieve this objective, the “single overriding communication objectives” (SOCOs) of the press release should be pursued. This strategy, developed by the US Centers for Disease Control and Prevention,12 ensures visibility of the main points that the researcher or health expert believes are important. Press releases should also include relevant caveats on the limitations of the research, industry funding and other financial matters. Essentially, the public places a great deal of trust in the health care system and in medical news, particularly if it is based on peer-reviewed data published by medical experts. It would be a pity to destroy such trust through substandard reporting.

Martin B Van Der Weyden MD FRACP FRCPA · Ruth M Armstrong BMed

Objective: To analyse the reviews of medical news articles posted on media doctor, a medical news-story monitoring website.Design and setting: A descriptive summary of operating the media doctor website between 1 February and 1 September 2004.Main outcome measures: Consensus scores for 10 assessment criteria for the medical intervention described in the article (novelty, availability in Australia, alternative treatment options given, evidence of “disease mongering”, objective supportive evidence given, quantification of benefits, coverage of harms, coverage of costs, independent sources of information, and excessive reliance on a press release); cumulative article rating scores for major media outlets.Results: 104 news articles were featured on media doctor in the study period. Both online and print media scored poorly, although the print media were superior: mean total scores 56.1% satisfactory for print and 40.1% for online; percentage points difference 15.9 (95% CI, 8.3–23.6). The greatest differences were seen for the use of independent information sources, quantification of benefits and coverage of potential harms.Conclusions: Australian lay news reporting of medical advances, particularly by the online news services, is poor. This might improve if journals and researchers became more active in communicating with the press and the public.

on behalf of the media doctor study group*

Taking on two global Goliaths Cheers and groans. Those were my conflicting reactions during a recent perusal of the media doctor website. I cheered in admiration at a good idea and at the temerity of the project’s instigators in taking on two global Goliaths — the media and the medical industries. It is an ambitious task for a project run largely by volunteers on a limited budget. I cheered to see media coverage recognised as a public health issue meriting attention and intervention. It was also pleasing to see a systematic attempt to counter the effective public relations campaigns of commercial, professional and other vested interests in the health sector. Clearly the media and its audiences could do with some help in developing better critical appraisal skills when it comes to health and medical claims. And it is a point well made that responsibility for media coverage must also be borne by medical journals, health professionals, researchers and others who provide information to journalists. But I also groaned as I looked at the website, wondering how it would appear to a busy journalist or media manager with no particular background in epidemiology, who did not know, and cared even less, about such things as randomised controlled trials. Would a quick, casual glance at this website convince them to change their ways? I doubt it, especially considering that many health stories are not covered by specialist health journalists. If the project is to succeed in its goal of changing media reporting, it must first do a better job of explaining why this is necessary. And it must do this in a way which is relevant to journalists and the media. Any attempt to influence behaviour — whether of a patient, a doctor or a journalist — needs to be based in an understanding of what is important to the target and what will motivate them to change. This is yet another initiative targeting individual journalists, who are only one component of the media industry. Other powerful forces, notably the commercial prerogative, also shape how health is covered. An analogy can be drawn with efforts to improve the safety and quality of health care, another chaotic industry. Measures aimed at individual clinicians may be helpful, but it is also important to look at the broader culture, system and industry in which they work. The pharmaceutical industry has been so successful at winning positive media coverage because its goals align neatly with the media’s — stories boldly promising medical breakthroughs sell product for both industries. Those who would like better reporting of the uncertainties and complexities surrounding medical developments will have to work much harder to influence media coverage than those promising miracle cures. Another question arising from this project is whether its good intentions may unintentionally reinforce one of the great deficiencies in media coverage of health. It is far easier to report on the latest research finding or new drug than to investigate other issues which may be of far more significance for the community’s health. Whenever a new drug attracts headlines, scarce newsroom resources are diverted from stories investigating social, structural and policy issues affecting health and health service delivery. Encouraging the media to focus even more on its coverage of medicines may have an opportunity cost. So, how to weigh up the cheers and groans? This website is a great idea. But it needs more work and broader thought. There is a report of its early experience in this issue of the Journal (page 190),1 and I hope there will be a follow-up study, detailing the feedback of journalists, news producers, media managers, and editors. And it raises another question: if the website does lead to more balanced, detailed reporting, what impact might this have on the media’s audiences? They may still hope for miracle cures.

Melissa A Sweet

Media outlets have as much responsibility as ever to maintain standards One of the roughest stories about medical coverage I’ve heard was from a bacteriologist who told me about the effort he’d made with a local journalist over a particular research story. But to his horror, when the article was published in the newspaper, every time the word “bacterium” should have been used, “virus” appeared instead. Outraged, he rang the journalist who gave him the standard response — that it was the subeditor’s fault. Not giving up, our intrepid researcher rang the subbie who told him “It wasn’t me, it was the editor”. So he called the editor whose response was, “I used journalistic licence. I reckoned our readers knew the word virus better. It doesn’t matter does it?” This, of course, is every researcher’s worst nightmare. But it is only a relative risk. It’s true that you don’t advance your academic career by the number of citations on the evening television news. On the other hand, a report of your findings in one TV news slot will reach an audience equivalent to a lifetime’s presentations at learned gatherings, or even, dare I say it, readers of the MJA? So, if the work was worth doing and has been accepted by your peers, it is surely worth telling the community. However, that doesn’t absolve us in the media from getting it right and resisting the influence commercial interests have in pushing products, attitudes and diseases, real or invented.1 The article by Smith et al describing the experience of media doctor in this issue of the Journal (page 190)2 shows the extent to which some of our major media outlets, including the ABC, in their reporting of medical news, fall below the sorts of standards that might allow the community to make rational decisions about their health and medical care. The situation may actually be worse, as media doctor does not monitor talkback radio where public relations companies pushing their clients’ wares can access large numbers of listeners. In addition, there are important problems, such as the way the media can increase stigmatisation of people with major mental illnesses,3,4 that are not necessarily monitored by media doctor’s approach. Before we become too overwrought though, we are not as badly off in Australia as in other countries, particularly the United States and the United Kingdom, where newspaper tabloids can be breathtakingly odious, flaunting science, objectivity, social responsibility and a host of other values in the fight for sales. The solution is not necessarily to have more doctor–journalists. There are several excellent health reporters with no technical background. Their success comes from staying on the job and being determined to learn the analytical skills required rather than moving on to other more prestigious rounds like economics or politics. A growing number of journalism schools teach some of the essentials of science reporting, but cadets and trainees don’t always come with communication degrees. That means media outlets themselves have as much responsibility as ever to maintain standards. However, there is only so much that public embarrassment from media doctor or from the ABC’s weekly TV program Media Watch5 can do. Researchers should complain when they see things done badly, which can make a difference because the line of least resistance should be to do things well. For example, Professor David Pennington, who chaired the “AIDS Task Force” in the early days of the AIDS epidemic, made a significant impact on coverage by intervening actively in the interests of accuracy and defusing prejudice. My gripe with media doctor is that they don’t monitor The Health Report (http://www.abc.net.au/rn/talks/8.30/helthrpt/default.htm). As we in the Fourth Estate like to say, any coverage is good coverage.

Norman Swan FRCP, DCH

Each side needs to appreciate the other’s agenda Media doctor, an attempt by a group of medically well informed people to monitor and rate medical news reports, is a welcome initiative. It aims to improve the standard of health and medical reporting in Australia’s press and the media in general. Whether it can do that, even if expanded to Australia-wide coverage, is a moot point, but well worth considering. No matter how good the website’s intentions, for the project to meet its goals, it is essential to gain the confidence and cooperation of newspaper editors and journalists, as well as their counterparts in radio, TV and the expanding online medium. The media doctor group has made a good start, and a report of their early experience is published in this issue of the Journal (page 190).1 The report is reasonable, reasoned and, clearly, deliberately non-adversarial. Less welcome is the marking and star rating system used for evaluating medical news articles, although the recent move to a five-star, rather than three-star, rating may improve this element, making the rating more sensitive to differences in article quality. We believe, however, that the 10-criteria marking system is subjective and that the criteria themselves may need examining. For example, not all the criteria are of equal weight and some elements, while relevant to refereed papers within the medical profession, may not be as important when assessing lay press reports of medical breakthroughs. The better handling of medical news reporting was one of the motivations that led the Australian Press Council to issue Reporting guidelines in April 2001.2 It is perhaps relevant, and noted in the report by Smith et al,1 that the print media (guided we hope by the Council’s advice) scored significantly higher in terms of the group’s criteria than the electronic/online media, for which a similar guideline has not been issued. A canvassing of opinions on the publishing side is vital to establish the goodwill and cooperation needed to achieve the improved standards media doctor seeks. The Press Council and the bodies dealing with electronic media could undoubtedly help by ensuring that ethical reporting guidelines similar to those of the Press Council are widely disseminated to all segments of the media. The media doctor group is right in not expecting any spectacular improvement in the standards of medical reporting, but is justified in hoping that a judicious and informed examination of medical news reports will improve reporting standards. Again, it needs to be stressed that reports in the general media are not meant to meet the same rigorous standards as those in the medical literature. Moreover, general media reports can be supplemented by well written and accessible commentary from the medical profession to ensure that accurate information is promulgated. Editors cannot guarantee that journalists assigned to cover a medical breakthrough will have the requisite technical knowledge (The New York Times once sent its golfing correspondent to interview Einstein), and this places more responsibility on researchers to ensure that they are clear in what they say to journalists — perhaps, compromising a little to achieve some lay understanding — and are not themselves the cause of the misunderstanding. One weakness in the article by Smith et al is that the authors could not trace many of the press releases from which the stories were derived to see if the “errors” arose from the source rather than the reporter.2 Co-author John Morgan provides one illustrative anecdote: Once I was sent to interview Macfarlane Burnet on immunology. At one stage he talked for about 20 minutes on one aspect. When he finished, I wrote 150 or so words and read them back to him. I asked if what I’d written was right? He told me off for smoking, thought for a while and said: “It’s not entirely right, but it would take 1000 words to make it any better.” Now that’s the sort of help a struggling reporter needs. Good journalists don’t mind being asked to read back what they are writing, but the interviewee must be prepared to take a reasonable approach, to explain any objection and not to renege on some earlier quote. The need for each side to appreciate the other’s agenda should be widely discussed. Doctors should understand that reporters and editors are often better judges of what constitutes news for their readers and that they are subject to (self-) regulation when they commit egregious errors. Most publications are happy to clarify or correct material when errors are made known to them. Journalists are aware of the problems faced by professionals in explaining highly technical matters. Journalists should be aware of their ethical responsibilities, and doctors should be aware of the need to reveal their links to commercial operations or their funding sources. Perhaps the media doctor initiative will help to foster an atmosphere of trust on both sides.

Jack R Herman · John A T Morgan

Objective: To investigate attitudes of Australian health professionals working in oncology to health-related information in the media and on the Internet and to patients who search for this information.Design: Questionnaire-based survey.Setting and participants: Questionnaires were mailed in January 2003 to all 333 health professionals belonging to the Victorian Cooperative Oncology Group.Main outcome measures: 27 items about attitudes to information in the media and the Internet, patient information-seeking and its effects on the doctor–patient relationship.Results: 226 surveys (68%) were returned and assessable. Most respondents took notice of medical information reported on television/radio, in newspapers (80% each) and on the Internet (56%), mainly to be informed when patients ask questions (82%) and to check its accuracy (60%). Most were concerned about this accuracy (64% believed it accurate only sometimes, and 23% rarely), and 91% believed information from the Internet had the potential to cause harm to patients. Nevertheless, they generally supported patients’ information-searching, believing it allowed them to be better informed (58%), and did not affect their ability to cope with their illness (49%), or their trust in, and relationship with, their doctor (69% and 67%, respectively).Conclusions: Oncology health professionals are aware of patients’ use of the Internet and other media to obtain medical information. To ensure oncology patients find reliable and relevant information and to minimise the risk of harm, the health professionals treating them should provide guidance in finding information sources, and assistance in interpreting the information obtained.

Genni M Newnham MB BS(Hons) · W Ivon Burns FRACP · Raymond D Snyder FRACP · Anthony J Dowling FRACP · Nadia F Ranieri · Emma L Gray · Sue-Anne McLachlan MSc, FRACP

The discovery of novel mutations in genes encoding succinate dehydrogenase subunits has revealed that familial phaeochromocytomas are much more common than previously thought. Genetic screening should be offered to patients with apparently sporadic phaeochromocytomas and their first-degree relatives. An increasing proportion of phaeochromocytomas present preclinically on genetic testing or as “incidentalomas” on abdominal imaging, rather than with classic symptoms and signs. Clinical suspicion should prompt measurement of plasma levels of free metanephrine or 24-hour urinary catecholamine and metanephrine levels, followed, if positive, by tumour localisation studies. With appropriate perioperative care, surgical management of phaeochromocytomas is safe and effective. Most tumours can be removed laparoscopically.

Yaser Alderazi MB BS · Michael W Yeh MD · Bruce G Robinson MD, FRACP · Diana E Benn PhD · Mark S Sywak FRACS · Diana L Learoyd PhD, FRACP · Leigh W Delbridge MD, FRACS · Stan B Sidhu PhD, FRACS

The cytokine, tumour necrosis factor-alpha (TNF-α) plays a key role in the pathogenesis of many chronic inflammatory and rheumatic diseases, in particular, Crohn’s disease, rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. Controlled trials have shown that the TNF inhibitors (etanercept, infliximab and adalimumab) significantly reduce symptoms and signs, improve function and quality of life, and reduce radiologically evident damage in patients with rheumatoid diseases. For reasons that are not entirely clear, etanercept does not work in Crohn’s disease. Injection site and intravenous reactions and increased risk of infection (in particular, reactivation of tuberculosis) are associated with the use of these agents. Increased risk of lymphoproliferative disease, the development of lupus-like syndromes and demyelination, including optic neuritis and reactivation of multiple sclerosis, are under evaluation in long-term follow-up studies. The TNF inhibitors are expensive (about $18 000 per year), and in some patients need to be given continuously to maintain benefit, even in the presence of other immunosuppressive therapy.

Peter T Nash MB BS, FRACP · Timothy H J Florin MB BS, FRACP

There is growing recognition in Australia of the importance of early childhood to later health and wellbeing, with developments such as the National Agenda for Early Childhood and the National Public Health Action Plan for Children. To sustain a policy agenda for children and improve long-term outcomes, we need timely, comprehensive and accurate indicators and data on child health, development and wellbeing. Building this evidence requires a national monitoring and surveillance system that involves more than aggregating or linking existing data. Steps to building a national system are: to agree on key indicators of child health, development and wellbeing for regular reporting, to research a comprehensive set of indicators for each domain and ascertain data gaps, and to ensure development and coordination of data relevant to policy-making.

Sharon R Goldfeld FRACP, PhD · Frank Oberklaid FRACP, MD

A 44-year-old woman presented with a 3-day history of worsening right upper quadrant pain associated with nausea, anorexia and fever. She had localised tenderness and guarding in the epigastrium. Initial ultrasound imaging showed a distended gallbladder containing calculi, without wall thickening. A computed tomography scan (performed because of increasing pain) showed a whorled structure in the anterior abdomen (Box 1). At laparotomy this was seen to be torsion of a segment of the greater omentum. Histology of the resected specimen showed congestion of the vessels, haemorrhagic infarction and focal fat necrosis (Box 2). She made an uncomplicated and rapid recovery. Primary omental torsion is a rare cause of acute abdomen. It may affect children and adults, and is commonly misdiagnosed preoperatively as appendicitis. Some cases have presented as acute cholecystitis.1,2 Kimber et al identified 13 cases of omental torsion or infarction in about 8000 cases of suspected appendicitis over a 20-year period.3 Large meals, sudden postural change, and abdominal trauma may be precipitating factors in primary torsion,4 while adhesions, hernia, tumour or focus of inflammation3 occur with secondary torsion. Resection is the preferred treatment,3,4 although some clinicians suggest conservative management2 when the diagnosis is apparent on computed tomography. Laparoscopic resection has also been advocated.5 1 Computed tomography scan of abdomen A whorled structure (arrow) is seen in the anterior abdomen adjacent to the transverse colon. 2 Histological section of omentum There is marked congestion and haemorrhagic infarction, with areas of fat necrosis and an acute inflammatory reaction. (Inset: higher mag-nification shows fat necrosis and a polymorph neutrophil response.)

Wen-Chan Yeow MB BS · Mohan V Jayasundera FRACS, MB ChB · Graham Hool FRACS · Rajalingam Sinniah DSc, FRCPath, FRCPA

Clinical record A 55-year-old woman with chronic epilepsy and psychiatric problems was admitted to hospital in 2004 with a fractured neck of femur after a trivial fall. She had been diagnosed with epilepsy in childhood and treated with phenytoin and phenobarbitone. Management was complicated by multiple, prolonged psychiatric admissions. Anticonvulsant compliance had been verified with measurement of serum phenytoin levels on a number of occasions. As a result of psychiatric problems, the patient became less able to care for herself and, at the age of 46 years, was admitted to long-term psychiatric hostel accommodation. Four years later, she had a non-displaced fracture of the olecranon after a fall; serum 25-hydroxyvitamin D level and bone mineral density were not assessed at that time. During the current admission, the fractured neck of femur was treated surgically. Biochemical testing indicated vitamin D deficiency (Box), which was treated with daily calcium carbonate (1200 mg) and ergocalciferol (vitamin D2) (2000 IU), and substitution of phenytoin with sodium valproate. This patient had recurrent fractures at a young age caused by a preventable complication from long-term use of anti-epileptic medication. Osteoporotic fractures, particularly hip fractures, result in significant individual morbidity and mortality and major financial cost to the community. It is well documented that enzyme-inducing anticonvulsants increase fracture risk by an average of two- to threefold, and that phenytoin causes osteomalacia. A 7-year longitudinal study of 87 people with epilepsy treated with phenytoin showed that they had a fracture rate six times higher than that of the healthy population.1 Fractures were not related to seizures. This high rate of fracture has been confirmed in many subsequent studies.2,3 Phenytoin induces hepatic microsomal enzymes and increases the catabolic clearance of a number of vitamin D metabolites. Hypermetabolism results in vitamin D deficiency, which induces a compensatory increase in serum parathyroid hormone (PTH) and bone turnover. Patients may develop a severe mineralisation defect and consequent osteomalacia. Other enzyme-inducing anti-epileptic drugs, such as primidone and perhaps carbamazepine, have similar effects on vitamin D metabolism. Anti-epileptic drugs have also been shown to cause bone loss in the absence of vitamin D deficiency.4 This effect was greater in patients taking multiple drugs, those with longer duration of epilepsy, and those taking enzyme-inducing drugs.5 This suggests that anti-epileptic drugs have a direct effect on bone turnover and could cause bone loss without inducing vitamin D deficiency. Vitamin D replacement has been studied in patients taking phenytoin. In at least one study, cholecalciferol and ergocalciferol were not bioequivalent.6 Another found that patients taking phenytoin required larger doses of calciferol to reach positive calcium balance than a control group.7 Other factors predisposing to vitamin D deficiency should also be considered. Institutionalisation leads to low sunlight exposure and reduced skin synthesis of vitamin D. This can produce vitamin D deficiency, even in Australia and without the addition of anti-epileptic drugs.8 People living in institutions may require higher replacement doses of vitamin D than those in the community. For example, a dose of 2400 IU calciferol (well above the accepted dose required for nutritional health) was required to reach adequate serum 25-hydroxyvitamin D levels in three-quarters of institutionalised patients treated with anti-epileptic drugs.9 Many medical practitioners fail to consider the diagnosis of osteoporosis or to provide adequate prevention and treatment. In a recent American study of neurologists, only one in four screened for bone disease, and fewer than one in 10 routinely prescribed prophylactic calcium and calciferol for patients taking anticonvulsants.10 There are no published consensus guidelines, but a recent editorial recommended osteoporosis screening in all adults taking anti-epileptic drugs long term.11 We believe appropriate investigations should include annual screening of serum 25-hydroxyvitamin D level. This is particularly important for those who are institutionalised. Patients taking anti-epileptic drugs long term should be advised about optimal dietary calcium intake, smoking cessation and avoidance of excess alcohol consumption, adequate sun exposure and weight-bearing exercise to prevent osteoporosis. Calcium and calciferol could be offered to those who achieve less than three to four serves of calcium daily or those who have a serum 25-hydroxyvitamin D level < 50 nmol/L. A recent position statement in the Journal provided useful advice about vitamin D replacement in people with vitamin D deficiency.12 Vitamin D replacement is particularly important for those taking phenytoin or phenobarbitone. If an osteoporotic fracture has occurred, bone mineral density should be assessed (this is currently not reimbursed by Medicare unless a fracture has occurred), and specific treatment with bisphosphonate drugs could be considered. However, bisphosphonates should be prescribed only after calcium and vitamin D deficiency has been corrected. These measures may help avoid the occurrence of hip fractures in relatively young patients taking anti-epileptic medication long term. Lessons from practice Patients taking anticonvulsant medication have a two- to threefold increased risk of fracture. Lifestyle measures, with exercise, adequate sunlight exposure, smoking cessation and sufficient calcium intake, should be encouraged for all patients with epilepsy taking anticonvulsant medication. Serum 25-hydroxyvitamin D levels should be assessed annually in all those taking anticonvulsant medication long-term. Calcium and calciferol could be offered to those who achieve less than three to four serves of calcium daily and to those with a serum 25-hydroxyvitamin D level < 50 nmol/L. Larger calciferol doses than typically required may be needed to treat vitamin D deficiency induced by anticonvulsant medication. Bone mineral density should be measured in all patients taking anticonvulsant medication long-term who sustain a fracture. Blood test results for a 55-year-old woman with an osteoporotic fracture* On admission Follow-up RR 3 months 9 months Ionised Ca (mmol/L) 1.1 – 1.22 1.14–1.29 Phosphate (mmol/L) 0.7 1.6 1.3 0.8–1.5 Parathyroid hormone (pmol/L) 58.2 14.5 10.9 1.5–8 25-hydroxyvitamin D (nmol/L) 9 34 70 > 50 Creatinine (μmol/L) 51 – – 30–95 Alkaline phosphatase (U/L) 229 112 103 35–105 Haemoglobin (g/L) 143 – – 115–155 Mean cell volume (fL) 97 – – 81–98 RR = reference range. * Results outside the RR are highlighted in bold.

Hannah M Seymour MRCP · Paul Glendenning PhD, FRCPA, FRACP

Bevan Coombes, a distinguished pathologist both in New South Wales and Queensland, died in the company of his family at Southport, Qld, on 18 December 2004, from complications associated with limbic encephalitis. Bevan was born in Sydney on 26 March 1930. He attended Sydney Boys High School and studied medicine at the University of Sydney, graduating in 1955. He did his residency at Sydney Hospital, and in 1962 completed a Diploma in Clinical Pathology. He remained at Sydney Hospital until 1964, by which time he was a Staff Specialist in pathology. In 1964, Bevan embarked on 18 months of investigative study and practice as a Fellow in Pathology at the Memorial Hospital in New York. He was very proud of being the first Australian doctor to have worked there. He became a Fellow of the College of American Pathologists in 1965 and returned to Australia in the same year, where he resumed his pathology career — juggling work, family life and further studies and trying to find time for his favourite pastimes, golf and tennis. From 1966 to 1980, Bevan was a Visiting Medical Officer at Hornsby District Hospital and worked in a partnership with four other doctors. During this time, he was made Senior Pathology Examiner for the Royal Australasian College of Radiologists. In 1980, Bevan moved to Southport, on the Queensland Gold Coast, to take up a position in a small partnership known as Queensland Medical Laboratories (QML). Over the next 22 years, he was influential in the growth and expansion of QML, not only in Queensland but also in New South Wales. He was the main instigator in the formation and operation of the QML practice in country NSW in Tamworth and Armidale. It gave him great pleasure to see the small partnership he had helped grow for over 20 years turn into the largest private medical practice in Australia. In 2002, Bevan decided that after 50 years in medical practice it was time to retire and enjoy the final years of his life travelling and doing the things that such a frantic, demanding and constant career hadn’t allowed him to do. He had always loved sport, and it was only after having a pacemaker fitted (due to heart problems in the early 1990s) and experiencing increasing problems with his knees that he was forced to give up his beloved tennis and, at a later stage, golf. Bevan will be deeply missed by his family and all those who knew him. He was a true gentleman, with an infectious energy for life and learning, who, without question, would go out of his way to help anyone who asked him. In the words of one of his closest friends, Dr Ross Hayes, “he was one of the truly intellectually honest people I have ever met”.

Howard J Coombes · Andrew H Coombes

Rebecca J Guy,* David E Leslie,† Kleete Simpson,‡ Beth Hatch§ Jennie Leydon,¶ Margaret E Hellard,** Heath A Kelly†† * Epidemiologist, ** Head, Centre for Epidemiology and Population Health Research, Macfarlane Burnet Institute for Medical Research and Public Health, GPO Box 2284, Melbourne, VIC 3001; † Microbiologist, ¶ Senior Serologist, †† Head, Victorian Infectious Diseases Reference Laboratory, Melbourne, VIC; ‡ Surveillance Manager, § Partner Notification Officer, Blood Borne Viruses and Sexually Transmissible Infections Program, Department of Human Services, Melbourne, VIC. Rebecca. GuyATburnet.edu.au To the Editor: In Victoria, notifications of infectious syphilis infection (primary, secondary and early latent [< 2 years’ duration]), reported by the Department of Human Services, have increased more than fivefold in the past decade, from 16 in 1995 to 85 in 2004 (Box). An increase in notifications has also been observed in Sydney.1 Whereas previously in Victoria, very few infectious syphilis notifications were reported among men who have sex with men (1 of 16 cases in 1995), in 2004, 63 of a total of 85 cases (74%) were in this group (68% of these were acquired in Victoria). The Victorian Infectious Diseases Reference Laboratory (VIDRL) conducts testing for sexually transmitted infections (STI) and HIV for three Melbourne sexual health clinics with a high proportion of patients who are men who have sex with men. In 2004, 62 male patients tested positive for infectious syphilis, and 40% of these were HIV-positive. This is similar to the situation in Sydney, where in 2003, 54% of infectious syphilis cases were reported among HIV-positive men who have sex with men.1 Syphilis outbreaks among men who have sex with men have been reported elsewhere in recent years. There was an outbreak of syphilis in this group in Greater Manchester; between 1999 and 2002, and 37% of cases were in HIV-positive men.2 In this population, syphilis infection was associated with unprotected oral sex with high numbers of partners, seeking sexual partners at venues (darkrooms, cruising areas and saunas) and use of drugs (GHB [gamma hydroxybutyrate] and poppers [amyl nitrate]).3 A San Fransisco study in 2000, performed in response to a syphilis outbreak among men who have sex with men, reported that meeting sexual partners through use of the Internet was a factor significantly associated with syphilis infection.4 It is likely that some or all of the factors reported in these outbreaks overseas are contributing to the sustained increased in infectious syphilis notifications in Victoria, but it is important to have local data to ensure interventions are targeted appropriately and cost effectively. In Victoria, responses to the increase in syphilis notifications have already included an alert to general practitioners to encourage men who have sex with men to have syphilis testing and individual counselling, and syphilis testing of men who have sex with men at a popular sex-on-premises venue over a 4-week period. Depending on further studies in this population in Victoria, other responses could include enhancing outreach at Internet chat rooms, intensive counselling of HIV-positive men who have sex with men, and education interventions such as peer-led community-based strategies for countering unsafe sex and substance-use behaviours. Finally, it is vital that interventions are multidisciplinary, collaborative and evidence-based. Infectious syphilis notifications by year, Victoria Data from the Notifiable Infectious Diseases Surveillance System Database, Communicable Diseases Section, Victorian Department of Human Services.

Rebecca J Guy · David E Leslie · Kleete Simpson · Beth Hatch · Jennie Leydon · Margaret E Hellard · Heath A Kelly

To the Editor: Lymphogranuloma venereum (LGV) is an uncommon sexually transmitted infection caused by Chlamydia trachomatis serovars L1–3. LGV is not endemic in Australia, and rare Australian cases of LGV have been seen in patients who have either acquired the infection while travelling overseas in an endemic area, or have had local contact with an imported case. Currently, there is an outbreak of LGV in western Europe (in particular, The Netherlands) and the United States.1-4 A case of LGV in an Australian man with no history of overseas travel was managed recently. A 42-year-old bisexual man with previously treated early syphilis and hepatitis C infection presented to a Melbourne hospital in August 2004 complaining of 3 months of tender right inguinal lymphadenopathy. An excisional biopsy showed the formation of necrotising granuloma indicative of LGV. He had no history of penile ulceration, urethritis or proctitis. The surgical wound healed normally. The patient gave a history of attending sex-on-venue premises (“gay saunas”) and “beats”. He reported having oral sex with men, and recently having non-insertive sex involving masturbation with an unknown casual male contact who was apparently an overseas visitor. The patient had a female sexual partner with whom he had irregular, unprotected vaginal intercourse. The diagnosis of LGV was confirmed by polymerase chain reaction (PCR), which detected C. trachomatis, identified as serovar L2 by nucleotide sequencing, from the excised lymph gland. IgG and IgA antibodies to C. trachomatis were demonstrated by enzyme-immunoassay. Tests for other active sexually transmitted infections were negative. The patient was treated with doxycycline (100 mg twice daily for 3 weeks). His asymptomatic female partner was also treated. LGV is endemic in developing countries in our region, but occurs only sporadically in industrialised countries. The first stage of disease consists of a papule or ulcer that may occur on the penis, urethra or cervix. Proctocolitis may also be present, mimicking inflammatory bowel disease. Regional lymphadenopathy develops in the secondary stage of disease when there may be systemic symptoms. Fistula formation at these sites can be prevented by early recognition and treatment. Late, severe genital ulceration is rarely seen. Confirmation of a diagnosis of LGV requires showing C. trachomatis serovars L1–3 by serological tests or PCR on genitourinary specimens. Lymph node resection is not favoured because of the possibility of sinus formation. Prolonged treatment with doxycycline or roxithromycin for 3 weeks is required for affected patients. Asymptomatic contacts are treated with doxycycline for 1 week or a single dose of azithromycin. This case of locally acquired LGV highlights the features of this progressive disease that may now be recognised more frequently in Australian men who have sex with European or North American men. Histological section of the lymph node showing the thickened node capsule and necrotising granuloma Image courtesy of Dr Malcolm Buchanan, Department of Anatomical Pathology, Royal Melbourne Hospital.

Damon P Eisen

To the Editor: A 47-year-old woman presented with a 1-week history of spontaneous prominent and painful bruising and haematomata, 5–6 weeks after commencing meloxicam 15 mg daily for osteoarthritis and plantar fasciitis. The bruises varied in size from 2 cm × 2 cm to 3 cm × 4 cm. She had a past history of acne rosacea, for which she was taking clonidine 100 μg daily, and reflux oesophagitis, for which she was taking pantoprazole 40 mg daily. Meloxicam, being the only new drug taken by the patient, was suspected as the causative agent and was therefore discontinued. Activated partial thromboplastin time (APTT) at presentation was 58 s (reference range, 22 s –38 s). A week after stopping meloxicam, it had fallen to 37 s. All other haematological parameters, including platelet count and international normalised ratio, were normal, as were renal and liver function. New bruises and haematomata stopped appearing 2 days after the patient stopped taking meloxicam. She continued taking clonidine and pantoprazole. Meloxicam is a selective nonsteroidal anti-inflammatory drug (NSAID) (a cyclo-oxygenase 2 [COX-2] inhibitor). It was chosen for this patient in view of her reflux oesophagitis and because she had already been unresponsive clinically to one of the other COX-2 inhibitors. Unlike non-selective NSAIDs, meloxicam has been shown to have negligible effect on platelet function as measured by bleeding time.1-3 Rinder et al4 reported no prolongation of APTT or prothrombin time after 8 days of regular administration of meloxicam at 7.5 mg, 15 mg or 30 mg. In spite of these contrary findings, I believe the prolongation of APTT and spontaneous bruising and haematomata in this patient were directly attributable to meloxicam, as the bruises disappeared 2–3 days after stopping the drug (with no other changes in the patient’s existing medication) and a repeat APTT a week after cessation of the drug was normal.

Anil M Kurien

Diane A Longstreet,* Deanne L Heath,† Robert Vink‡ * Dietitian, † Research Scientist, Townsville Aboriginal and Islander Health Services, 57–59 Gorden Street, Garbutt, QLD 4814; ‡ Head, Department of Pathology, University of Adelaide, SA. dlongstreetATtaihs.net.au To the Editor: Diabetes in Indigenous Australians occurs at a younger age and at almost four times the rate in non-Indigenous Australians. The age-adjusted prevalence of diabetes among Indigenous people is 16% in remote areas and 9% in non-remote areas, with the actual prevalence estimated to be between 20% and 25%, and possibly higher than 30% in some remote areas.1 The cause for this disparity in diabetes incidence is multifactorial, and recent evidence suggests that nutrition — particularly magnesium intake — may play a role. Although central obesity remains a major risk factor, magnesium deficit has been posited to be an underlying common mechanism for the insulin resistance found in type 2 diabetes, as well as in metabolic syndrome, hypertension, and impaired glucose tolerance.2 The clinical correlations between low magnesium and diabetes have been well documented,3 with serum magnesium deficits being reported in 25%–39% of diabetic outpatients in the United States and Switzerland, and up to 73% of diabetic outpatients in Mexico. With magnesium deficits being observed in diabetes, studies examining the effects of magnesium-rich foods on diabetes risk become relevant. The Nurses’ Health Study and the Health Professionals’ Follow-up Study, which included 85 060 women (18 years follow-up) and 42 872 men (12 years follow-up), demonstrated that, after adjusting for confounding variables, a magnesium-rich diet reduced the relative risk of developing diabetes by 34% in women and 33% in men.4 A similar inverse correlation between magnesium intake and diabetes risk was shown in the Iowa Women’s Health Study with a cohort of 35 988 older women,5 and in the Honolulu Heart Program and the Women’s Health Study with cohorts of 8006 men and 39 345 women, respectively.6,7 Despite this growing body of evidence supporting the involvement of magnesium in diabetes, consideration of magnesium status has not been integrated into Australian medical care for diabetes, and more specifically, for Indigenous Australians. It is known that the traditional diet of hunter-gathers such as Indigenous Australians was much more nutrient- and magnesium-rich than the current estimated Australian intake.8 Nonetheless, there remains a lack of information about current magnesium status, including dietary intake, in Indigenous Australians. It is possible that dietary magnesium intake may be too low to maintain normal serum magnesium homoeostasis, and that this might contribute to the development of type 2 diabetes. Further research into this issue may provide this information.

Diane A Longstreet · Deanne L Heath · Robert Vink

To the Editor: The clinical update on venous thromboembolism by Lee and colleagues advises that “Ventilation perfusion (V/Q) isotope scanning reliably establishes the diagnosis of PE [pulmonary embolism] if the V/Q features suggest a high probability of PE . . .”.1 Although this is probably true for patients with intermediate or high pretest probability, a discordant result (low pretest probability and high probability V/Q) should be regarded with suspicion. From the original PIOPED data, high probability V/Q was predictive of angiographically confirmed PE in 80% of patients,2 which drops to 56% by Bayesian analysis if the pretest probability is low. False positive results may be due to previous PE or unrelated parenchymal lung disease. There is significant potential morbidity associated with a false positive result for PE, both from the acute anticoagulation and for future presentations with PE-type symptoms, where PE will be accorded a higher probability because of the previous documented diagnosis. As Lee and colleagues also state, D-dimer testing must be combined with an estimate of pretest probability to be useful. They advocate excluding PE on the basis of low pretest probability and negative D-dimer result. However, a negative D-dimer result (rapid enzyme-linked immunosorbent assay [ELISA] type) may be used to exclude PE in intermediate as well as low probability patients.3 This is dependent on the type of assay available as well as the local PE prevalence, and local guidelines should therefore be developed.

Matthew J Bragg

To the Editor: I read with interest the article by Lee et al regarding the investigation and treatment of pulmonary embolism (PE).1 The investigation of patients presenting with PE as a diagnostic possibility is of great interest to emergency physicians, and such presentations are a daily occurrence in emergency departments around the country. Unfortunately, only a small amount of text is devoted to describing the relative merits of ventilation perfusion (V/Q) scanning and computed tomography pulmonary angiography (CTPA), and no guidance is provided as to which is the test of choice when both are available. The British Thoracic Society has recommended CTPA as the lung imaging modality of first choice for patients presenting with non-massive PE.2 There is a large and increasing body of evidence that CTPA provides superior specificity to V/Q scanning in the detection of PE. CTPA also provides the opportunity of establishing diagnoses other than PE and, in addition, a negative multi-slice CTPA is of sufficient sensitivity to enable the withholding of anticoagulation.3 It is also my experience that CTPA is easier to obtain out of hours, compared with V/Q scanning. The authors state that V/Q scanning “reliably establishes the diagnosis of PE if the V/Q scan features suggest a high probability of PE . . .”.1 Unfortunately, this statement is incorrect. It is essential that V/Q scan results be interpreted in the light of the patient’s clinical probability for PE. In the PIOPED study, only 56% of patients with high probability V/Q scan reports had pulmonary embolism if the pretest probability was low.4 No mention is made of the special situation of pregnant women presenting with pleuritic pain, or which lung imaging test is considered “safest” for both mother and baby. Although the risks of PE are generally agreed to be increased in pregnancy, it is my experience that pregnant women are extremely reluctant to undergo any form of diagnostic investigation that exposes the fetus to radiation. The Wells criteria have been validated for the assessment of PE in emergency department patients only, and provide a means for clinicians with little experience to make an accurate assessment of an individual patient’s clinical probability of PE.5 Once initiated, clinical assessment of the patient with possible PE is straightforward. The key question facing emergency physicians is this: is there a group of patients that have such low probability for PE that no investigation at all is required?

Paul M Bailey

John W Eikelboom,* Graeme J Hankey,† Wai Khoon Ho,‡ Cindy H Lee§ * Haematologist, Thrombosis Service, McMaster University, HHS General Divison, 237 Barton Street East, Hamilton, ON L8L2X2, Canada; † Neurologist, ‡ Fellow in Haematology, § Senior Registrar in Haematology, Royal Perth Hospital, Perth, WA. eikelbj@mcmaster.ca In reply: Pulmonary embolism (PE) remains a complex diagnosis despite the availability of validated prediction models and D-dimer testing to direct the need for diagnostic imaging. We agree with Bailey that the ability to exclude the diagnosis of PE on clinical grounds in patients with a low pretest probability is highly desirable. Unfortunately, clinical features lack sensitivity and specificity for the diagnosis of PE, and clinical prediction models, laboratory investigations, and diagnostic imaging are likely to remain an integral part of the clinical work-up. As suggested by Bragg, it may be possible to simplify the diagnostic approach by using a highly sensitive D-dimer assay, and simplified pretest probability models have been proposed. However, this may come at a cost of reduced specificity,1 which leads to unnecessary diagnostic imaging studies and thus limits the clinical utility of these approaches. Further improvements in the diagnostic approach to PE are clearly needed. There are emerging data demonstrating the accuracy of computed tomography pulmonary angiography (CTPA) for the diagnosis of PE. However, CTPA has limitations (a large contrast load, high radiation dose, and lack of sensitivity of first generation scanners for small thrombi2), some of which are evident in the recently published validation study referred to by Bailey:3 25% of screened patients with suspected PE were not eligible for this study because of renal impairment, a contraindication to CT, or other reasons. The diagnostic algorithm that we provided in our review suggests that either ventilation perfusion (V/Q) scanning or CTPA can be used for patients with suspected PE who require diagnostic imaging,2 with the choice determined by patient factors and availability. The diagnosis of PE during pregnancy is challenging because of concerns about radiation exposure and uncertainty about whether CTPA or V/Q delivers more radiation to the fetus.4 Furthermore, clinical decision rules have not been validated in pregnancy. However, recommendations from experts and professional bodies suggest that V/Q scanning can be used in combination with compression ultrasound to establish or exclude the diagnosis of PE during pregnancy in most cases with minimal fetal radiation exposure.5,6 The comments by Bailey and Bragg concerning the interpretation of high probability V/Q scan results highlight the pitfalls of performing diagnostic imaging without considering the patient’s pretest probability of PE. Although a high probability V/Q scan is diagnostic in patients with a moderate or high pretest probability of PE (prevalence of disease ≥ 90%), the prevalence of disease is only about 50% in those with a low pretest probability.7,8 Therefore, V/Q scanning should not be performed in patients with a low pretest probability unless the D-dimer test is positive. In this situation the algorithm for moderate or high pretest probability should be followed,2 and a high probability scan reliably establishes the diagnosis.

John W Eikelboom · Graeme J Hankey · Wai Khoon Ho · Cindy H Lee

Richard F O’Reilly,* Ian A Burgess,† Bernard Zicat‡ * Physician, † Radiologist, ‡ Orthopaedic Surgeon, Mater Misericordiae Hospital, Rocklands Road, North Sydney, NSW 2060. roreillyATbigpond.net.au To the Editor: In a recent editorial, Gallus estimates the cost of doing ultrasonography in all patients after unilateral hip or knee replacement, with further testing in the 9% or 26% of patients, respectively, found to have deep vein thrombosis (DVT), to be about $200 000 per 1000 patients.1 We agree. He then states, “Many would argue that extended prophylaxis is likely to be the simplest, cheapest and perhaps safest solution”. However, prophylaxis is also expensive. Subcutaneous enoxaparin 40 mg administered daily for 30 days costs $170, or $170 000 per 1000 patients.2 In our study, we found DVTs in 1086 of 5999 patients (18.1%) before discharge,3 so that extended prophylaxis would involve 81.9% of patients receiving prophylactic doses of anticoagulants, with the risk of unwanted bleeding, despite the absence of DVT on ultrasound at Day 7 postoperatively. In addition, if an ultrasound scan was not done before discharge, the 18.1% of patients with a DVT would receive only prophylactic (not therapeutic) doses of anticoagulant for their DVT. We plan a further study to check the prevalence of post-discharge DVT by repeating ultrasonography at 90 days postoperatively in patients without DVT on ultrasound at Day 7. We suspect the prevalence is lower than suggested in the literature, as the data on late presentation of DVTs have been obtained by retrospective study of the number of patients re-admitted to hospital with DVT. Finally, on the question of whether performing ultrasonography on all patients has clinical benefit, we concur with Gallus when he writes that “Logic suggests it should . . .”.

Richard F O’Reilly · Ian A Burgess · Bernard Zicat

In reply: O’Reilly and colleagues belatedly address the need to consider bleeding risk and costs when choosing between management routines designed to prevent venous thrombosis and pulmonary embolism. Their otherwise valuable article1 failed to record bleeding rates when patients (almost 17%) with subclinical calf-vein thrombosis were exposed to therapeutic (not prophylactic) anticoagulant dosages. Nor did they evaluate the dollar and manpower costs of their complex management routines. Present evidence-based international guidelines from the Seventh ACCP (American College of Chest Physicians) Conference on Antithrombotic and Thrombolytic Therapy recommend effective prophylaxis for at least 10 days in all patients having hip or knee replacement, extending to 28–35 days after hip replacement.2 The ACCP guidelines also recommend against routine use of ultrasound screening because it is “neither clinically effective nor cost effective”.2 This is a Grade 1A recommendation from the ACCP (“Grade 1” implies certainty “that the benefits do, or do not, outweigh the risks, burdens, and costs”; “Grade A” refers to recommendations based on “randomized clinical trials with consistent results [that] provide evidence with a low likelihood of bias”).3 To reverse this recommendation would require randomised comparisons between routine prophylaxis alone or routine prophylaxis supplemented by screening ultrasonography — powered to permit meaningful measures, in both groups, of thromboembolism rates, bleeding rates and costs. Routinely screening for subclinical thrombosis after major joint surgery should not be done outside suitably designed clinical trials until such evidence is available. The role of logic in medicine is to generate hypotheses, which must then be tested by clinical trial. Unfortunately, evidence derived from uncontrolled cohort studies remains limited to Grade C (based on “observational studies or [on] generalization from one group of patients included in randomized trials to a different, but somewhat similar, group of patients”).3

Alexander S Gallus

Ian Hamilton-Craig Chairman, MEDPED-FH Australia, North Adelaide Heart Centre, 80 Brougham Place, North Adelaide SA 5006. IhcATsahc.com.au To the Editor: In their editorial, Burnett and colleagues correctly emphasise the importance and cost-effectiveness of cascade family screening in the early diagnosis of familial hypercholesterolaemia (FH) among relatives of known cases. They point out that Australia does not have “a national program for detecting the vast majority of patients with FH in our community . . .”.1 Such an approach has been advocated since the 1980s by the international MEDPED-FH project, initiated in Utah to raise public and professional awareness of the need to detect and treat FH at an early age (MEDPED-FH stands for Make Early Diagnosis to Prevent Early Deaths in Familial Hypercholesterolaemia).2 Since then, the project has spread to over 30 countries, including Australia, and has over 25 000 patients with FH registered worldwide.3 In Australia, the MEDPED-FH program has registered about 700 patients with FH, about 2% of the estimated 33 000 patients overall.4 This proportion is similar to registrations in many other countries (including the US). Only the Netherlands, Denmark and Finland, where government-financed screening programs are in place, have higher proportions of registrations, with 10%–50% of patients with FH registered with MEDPED-FH. Also, in these countries, DNA detection of low-density lipoprotein cholesterol receptor gene mutations is used routinely for the diagnosis of FH. At present in Australia, nurse practitioners are performing FH cascade screening in collaboration with MEDPED-FH physicians in each capital city, supported by Pfizer Australia. Further work on FH is being carried out by Associate Professor David Sullivan and colleagues in Sydney, supported by the Western and Central Sydney Area Health Services. In addition, the Cardiac Society of Australia and New Zealand has established a working party to investigate cardiac genetic disorders, including FH, and is involved in further education among cardiologists regarding screening, diagnosis and treatment of FH. But these efforts are not enough. I support Burnett and colleagues in recommending the establishment of a nationwide screening program for FH, and also recommend that DNA diagnosis be incorporated as an essential component. There is a definite cost benefit of early detection and treatment with statins of patients with FH.

Ian Hamilton-Craig

John R Burnett,* David Ravine,† Frank M van Bockxmeer,‡ Gerald F Watts§ * Medical Biochemist, Department of Core Clinical Pathology and Biochemistry [corresponding author]; † Medical Geneticist, Medical Genetics Unit; ‡ Director, Cardiovascular Genetics Laboratory; § Physician, Department of Internal Medicine, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847. john.burnettAThealth.wa.gov.au In reply: The international MEDPED-FH project has made a major contribution towards introducing family-based cascade screening into the Australian health care system. Although these achievements are important, we agree with Hamilton-Craig’s view that they are dwarfed by the magnitude of what now has to be done to deliver to all at-risk relatives the health gains that can be achieved by a proactive program of population screening. The risk of familial hypercholesterolaemia (FH) for a first-degree relative of an affected index case is 250 times greater than the risk for a member of the general population. The relative cost-efficiency of family-based cascade genetic screening is high, compared with population-wide screening for a dominantly inherited disorder.1,2 We disagree with Hamilton-Craig that DNA diagnosis is an essential component of an effective screening program. Among FH-affected families, biochemical testing has a sensitivity of 95%, and a specificity of 96%.3 The additional diagnostic gain from DNA testing in the context of screening relatives at 50% prior risk is marginal, although of use in determining with certainty whether or not a relative has inherited the family-specific trait. FH offers a paradigm of best clinical practice for improving health care outcomes for a widening range of “monogenic” disorders with complications that can be avoided or reduced by focused health care provision. The time has come when physicians, cardiologists, paediatricians, biochemists, geneticists, public health physicians, general practitioners and those administering the funding of health care delivery in Australia come together and formulate the changes necessary to allow cascade genetic screening for FH to become part of routine health care.

John R Burnett · David Ravine · Frank M van Bockxmeer · Gerald F Watts

Caroline F Finch Director, New South Wales Injury Risk Management Research Centre, University of New South Wales, Level 8, Applied Science Building, Sydney, NSW 2052. c.finchATunsw.edu.au To the Editor: I am prompted to write to you in response to a recent MJA editorial.1 It amazes me that the health sector in Australia, as I think the editorial did, continues to largely ignore the magnitude of the problem of injury in our children. This is despite clear evidence of the excess ill-health burden that injury places on our children, according to the Australian Institute of Health and Welfare (AIHW) report (the subject of the editorial)2 and other reports.3-5 Having said this, the editorial did highlight a very pleasing trend — there has been a steady decline in injury deaths in later childhood. Unfortunately, however, this was the only mention of injury in the editorial, and readers could be forgiven for thinking that this is the end of the story: the injury death rate is declining; therefore, we are doing all we can, and injuries are not a major issue. Nothing could be further from the truth. Our children continue to die from road and drowning accidents and will do so until injury prevention is recognised as paramount. The AIHW report clearly states that the single highest cause of death in children remains injury and poisoning.2 Accordingly, trauma is the single highest contributor to premature mortality and years of potential life lost of any health condition in Australia. If we don’t develop new approaches to reducing the incidence of drownings and road deaths, in particular, we will not see further declines in injury-related death rates, and injury will continue to rate highly as a killer of young people. Importantly, injuries do not only kill young people — they also hospitalise and maim them. The second most common reason for hospitalisation in Australian children is injury.2 Unlike injury deaths, there has been no trend in the rate of hospitalisation for injury. Across age groups, there appears to be a shift from fatalities to an increasing number of people with a high lifetime burden of significant disability, including brain and spinal cord damage. Imagine what this does to the quality of life and life expectancy of a child. How many of these children will be able to lead physically active lives? It is time for the health sector, particularly public health agencies, to properly recognise injury as a critical issue for the ongoing health of Australian children and to formally commit to appropriate preventive actions, commensurate with the priority ranking of childhood injuries.

Caroline F Finch

George C Patton,* Sharon R Goldfeld,† Indrani Pieris-Caldwell,‡ Meredith Bryant,§ Graham V Vimpani¶ * VicHealth Professor of Adolescent Health Research, Centre for Adolescent Health, Murdoch Childrens Research Institute, Flemington Road, Parkville, Melbourne, VIC 3052; † Paediatrician and Research Fellow, Royal Children’s Hospital, Melbourne; ‡ Senior Analyst, § Project Officer, Australian Institute of Health and Welfare, Canberra; ¶ Clinical Chair in Paediatrics, University of Newcastle, NSW. george.pattonATrch.org.au In reply: There is little to disagree with in this excellent summary of injury morbidity and mortality in Australian children. However, the principal point of our editorial1 was to highlight important problems where adequate data are currently unavailable. The Australian Institute of Health and Welfare report was able to give extensive coverage to injuries and accidents in children.2 Indeed, seven indicators specifically addressed aspects of childhood injury, with a range of others (eg, child abuse and neglect, neighbourhood safety) addressing relevant aspects of the family and social context. This emphasis reflected not only the importance of childhood injury, but the extent to which reasonably good data are available. We agree that, despite some favourable mortality trends, the burden of childhood injury remains high, as are associated health care costs. However, childhood injury is an area where advocacy has translated into action.3 One of the reasons for the success of that advocacy has been the availability of sound data, both to make the case and to ensure an appropriate focus in policy responses.4 While there is undeniably much more to do, we can learn much from injury prevention about how to tackle the newly emerging problems of childhood.

George C Patton · Sharon R Goldfeld · Indrani Pieris-Caldwell · Meredith Bryant · Graham V Vimpani

Sandy L A Reid Professor, School of Rural Health, University of New South Wales, PO Box 5695, Wagga Wagga, NSW 2650. s.reidATunsw.edu.au To the Editor: Reilly et al draw attention to the lack of research on the impact of the findings of physical examination on patient care, and state that, in the United States, many doctors “do not know how to do it, and do not see why they should”.1 Should we continue to teach these skills in Australia? Experience tells us, even if research does not, that the presence or absence of one or more physical findings may make a crucial difference to patient care. The important thing for teachers is that, while students learn the rituals, we should encourage them to think critically about what they are doing. They focus on passing the next objective structured clinical examination (OSCE), which often requires them to carry out a ritual. They are vaguely aware they will be required to think selectively about real patients and the necessity to make a diagnosis, but have little practice in selecting appropriate physical examination. We who teach them should formally recognise the distinction between ability to perform and ability to choose and interpret physical signs. I learned an inductive process: take a history and perform a complete examination, and then engage the brain. Research would not tolerate such a “fishing trip”! The inductive method has been replaced by a hypothetico-deductive approach. This is criticised, but all doctors take intelligently selected short cuts. We should acknowledge this and critically examine the skill. Students must learn systematic examination. This is the repertoire from which they choose when faced with a clinical problem. OSCEs early in the undergraduate course should assess their competence in this, and students should know exactly what they are to do. Our bedside clinical teaching and later OSCEs should explicitly challenge students to consider the selection of relevant clinical examination required in the light of the history, just as they should consider the value of all other tests, rather than using a blunderbuss approach. Together, history and physical examination have two objectives. One is diagnosis; the other defines or excludes comorbidity. Without them, medical care cannot begin to function effectively or economically. Neither I nor your authors are bewitched; their anecdotes make this clear, and they define the reasons for the lack of research. A focus on considering what can, and cannot, be gained by selective physical examination should reduce our own and our students’ bother and bewilderment.

Sandy L A Reid

Netter’s neurology. H Royden Jones. Teterboro: Icon Learning Systems, 2005 (xxvii + 980 pp). ISBN 1 929007 06 X. Medicine is an art which reaches its highest expression in neurology; form and function follow each other intimately. It is a delight to see a skilled neurologist examine a patient and lay out the neurological signs so that the diagnosis is made apparent (even to a third year medical student). Netter’s neurology combines the great beauty of Frank Netter’s drawings with Royden Jones’ text to give an intricate interweaving of art and science, also a thing of beauty. H Royden Jones Jr has been working with Frank Netter and his drawings since he collated Nervous system, Part 2, neurologic and neuromuscular disorders. Most consultants and many students will have utilised these fabulous drawings at some stage in their careers. Netter’s neurology acknowledges that for many of us clinical learning and its recall is based on both case history and imagery. The text is aimed primarily at medical students or junior doctors, but the images are excellent teaching tools for consultants to demonstrate both pathology and anatomy to patients. The text is not as comprehensive as Adams & Victor’s Principles of neurology, and does not have the number of case reports seen in John Patten’s classic Neurological differential diagnosis, but it wins hands down for the quality of the illustrations. In addition to the illustrations, there are examples of the latest imaging techniques including CT angiography, photomicrographs and updated pictures. There are some annoying typographical errors and some minor editing mistakes. For example, the tumours of the pineal region are reproduced in the atypical Parkinsonian syndromes chapter. Many of the features of this book will be timeless, particularly the first few chapters on the neurological examination and neuro-ophthalmology, as well as the cranial nerves. Netter’s neurology is very weighty, and perhaps inadequate as a text for practising consultants, but it is an excellent textbook for students to borrow from the library (or from a generous consultant). James T HughesNeurologistTamworth, NSW

James T Hughes

Fast facts: obstructive sleep apnea. Barbara Phillips, Matthew T Naughton. Oxford: Health Press, 2004 (74pp). ISBN 1 903734 47 9 Sleep apnoea is extremely common in our community, yet public knowledge is just catching up. Over the last decade, there have been excellent advances in the treatment of sleep apnoea and a growing body of persuasive evidence outlining the harmful effects of sleep apnoea on performance and cardiovascular morbidity. This Fast facts series publication about obstructive sleep apnoea is a concise, up-to-date review of sleep apnoea, written by two extremely knowledgeable authors (of whom one, Matthew Naughton, is an Australian). The handbook is relatively brief but to the point; its strength lies in its clarity. Prevalence, predisposing factors, physiological and cardiovascular effects, and treatment strategies are all addressed. The chapter on medical complications highlights the importance of injury to the cardiovascular system by sleep apnoea. Emerging concepts of sleep apnoea being a form of an inflammatory disease are presented. Breakout boxes summarise important facts in point form. Appropriate diagrams highlight important findings, and examples of sleep studies and treatment devices are included. And, for those seeking further reading, useful references are provided. I believe this is the most up-to-date, concise publication of its type on this topic, providing a very good grounding for medical practitioners in the current approach to sleep apnoea. And, as the language of sleep apnoea is not marred by a lot of jargon, paramedical staff and interested lay people will also be able to digest most of its contents. This handbook would be a good reference publication for doctors who have an interest in the field as well as those new to the area of sleep medicine. It could quite happily sit on a desk in a physician’s office or the resident doctors’ workbench in a hospital ward. Peter SolinRespiratory and Sleep Disorders PhysicianMonash Medical Centre, Clayton, VIC

Peter Solin

Women, sex and hormones It seems that women are likely to remain a mystery for some time to come — at least where sexual satisfaction is concerned. In a study of more than 1000 women, Australian researchers have found that self-reported low libido is not linked to low serum testosterone levels. Further, although women who reported low sexual responsiveness were more likely to have low serum dehydroepiandrosterone sulfate (DHEAS) levels, most of the women with a low DHEAS level did not report low sexual function. All in all, the researchers said no serum androgen level could define the cluster of symptoms that characterise “female androgen insufficiency”. JAMA 2005; 294: 91-96 Men Down Under Most men with erectile dysfunction have not sought medical advice about treatment, according to the Men in Australia Telephone Survey. The survey involved nearly 6000 men from around Australia, aged from 40 to 98 years of age, who were asked via a computer-assisted interview to answer 90 questions about a range of issues, including erectile function, lower urinary tract symptoms and prostate health, as well as their beliefs about male reproductive health. Overall, one in five men reported moderate or severe erectile dysfunction, with higher rates reported in older age groups. Although 90% of all the men surveyed had visited a doctor in the past year, only one in three men with significant erectile dysfunction had spoken to a health professional about it. The researchers say public education campaigns and additional resources will be needed for men to seek medical assistance for reproductive health problems, including erectile dysfunction. Lancet 2005; 366: 218-224 Don’t drive and dial ... If you think you can reduce your risk of having (and getting injured in) a car crash by using a hands-free rather than a hand-held mobile phone when you drive, you may need to think again. Researchers gained the cooperation of 456 mobile-phone owning Australian drivers who had presented at major Perth hospitals after a road crash, as well as their call records from major networks. They then compared mobile phone activity just before a crash with the drivers’ phone activity during other time periods (also while driving). Use of either type of mobile phone device, hands-free or hand-held, 10 minutes before a crash was linked to a fourfold increase in the odds of crashing. BMJ Online First (www.bmj.com) Stop seizures easily Buccal midazolam is not only more likely to be easier and less embarrassing to administer to a child having an acute seizure than rectal diazepam — it may also be more effective. A randomised controlled study conducted in UK hospital emergency rooms compared these two strategies in 177 children older than 6 months of age, finding that more stopped seizing within 10 minutes if they received buccal midazolam rather than rectal diazepam. Further, fewer children experienced recurrence of the seizure within the next hour. Lancet 2005; 366: 205-210 Unexpected deaths declared Doctors have been warned by the US Food and Drug Administration (FDA) and Health Canada that atypical antipsychotic agents, such as risperidone and olanzapine, may lead to an increased risk of death when used in patients with severe dementia. An FDA advisory described 17 trials involving more than 5000 patients with dementia taking either placebo or one of four atypical antipsychotic agents. Although the trials averaged only 10 weeks in duration, mean mortality in the treatment groups was 4.5% compared with 2.6% in the placebo groups. Deaths were largely due to cardiovascular events or infection. The CMAJ report suggested that education of families and staff and specialised dementia wards may be more preferable ways of managing behavioural disturbances in patients with severe dementia than the use of atypical antipsychotic agents. CMAJ 2005; 173: 252 Care for a coffee? Looking for a reason to justify that extra coffee? According to a systematic review, a higher daily consumption of coffee is linked to a lower risk of developing type 2 diabetes. The reviewers analysed data from 15 epidemiological studies conducted around the world, including in Europe, the US and Japan. Irrespective of geography, trial participants who drank the greatest number of cups of coffee a day — six or seven or more — were about 35% less likely to develop diabetes than those who only drank up to two cups a day. Unfortunately, for the coffee connoisseurs among us, the reviewers say it would be premature for us to start telling our patients to drink more coffee. The connection between coffee and glucose metabolism is not fully understood; and, as always, any potential health benefits of coffee drinking need to be weighed against the possible harms. JAMA 2005; 294: 97-104

Ann Gregory