Volume 195 Issue 3

Earlier concerns put to rest as new evidence confirms their safety and efficacy The three sentinel developments in percutaneous coronary intervention (PCI) have been the groundbreaking use of balloon angioplasty from 1977, the widespread uptake of bare metal stents (BMS) in the early 1990s, and the era of drug-eluting stents (DES) commencing in 2002. DES greatly reduce the incidence of vessel restenosis, and this has allowed the application of PCI to increasingly complex coronary anatomy that had previously been untreatable due to prohibitive restenosis rates. Uptake of this technology was immediate and widespread, with near ubiquitous use (95%) of DES for PCI in the Australian private sector by 2005 despite a fourfold higher cost and uncertain incremental cost-effectiveness over BMS.1 However, the initial unbridled optimism was tempered by case reports of “very late” stent thrombosis, and then shattered by the release of data at the 2006 World Congress of Cardiology in Barcelona suggesting DES were associated with higher mortality rates.2 This dramatically shook confidence in the use of this new technology with an immediate effect on DES use worldwide.3 In early 2007, the widely reported Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial, in which outcomes were similar for medically and percutaneously treated patients with stable angina, further challenged the interventional paradigm.4 Criteria for drug-eluting stent use in Victorian state hospitals6 One or more of: Diabetes mellitus Chronic renal failure Small diameter target vessel (< 2.5 mm diameter) Long target lesion (> 20 mm in length) Ostial lesion Bifurcation lesion Chronic total occlusion Previous coronary artery bypass grafting In-stent restenosis So what was the effect on Australian DES use? In this issue of the Journal, the Melbourne Interventional Group (MIG) present their registry data for DES use in selected Melbourne public hospitals over a 4-year period spanning this crucial time.5 Even though there was already a selective policy in place restricting DES use to patients with lesions at high risk of restenosis (Box), DES implantation fell from a peak of 54% of all stents used between April 2004 and March 2005 to 32% in 2007–2008.5 Even more dramatic falls in DES use (91% to 34%) have been reported in the Melbourne private sector over this period.7 The change in DES use in public hospitals demonstrated by the MIG is revealing, as they have previously reported underuse of DES and calculated that greater than 65% of patients undergoing stent implantation met the criteria for selective use of DES.8 Of further interest is the decrease in the absolute number of patients undergoing PCI, and in particular elective PCI, that is perhaps related to the release of the COURAGE study. It is likely that the change in practice reflects uncertainty over safety of DES at that time. It is therefore reassuring that data reported from the MIG registry affirm the safety and efficacy of DES, with DES use being the only independent predictor of better clinical outcomes at 12 months (driven, as expected, by reduced target vessel revascularisation rates). Given this finding, we would have expected to have seen deterioration in clinical outcomes during the period of low DES use. Surprisingly, this did not happen — the MIG investigators report that the reduction in DES shown by their data was not associated with an adverse effect on overall clinical outcomes. One possible explanation for this is that there was concurrent change in several other variables including referral patterns, stent technologies, implantation techniques, and adjunctive pharmacological therapy (eg, increased use of dual antiplatelet therapy). These changes may have acted favourably on clinical outcomes, masking an adverse impact of reduced DES use. The inability to separate out these confounding influences is one of the limitations of registry data. Following the Barcelona Congress, there was a rigorous reappraisal of the available studies using patient-level data, review by regulatory authorities (including the Australian Therapeutic Goods Administration) and further randomised trials. The safety and efficacy of DES were reaffirmed. Analyses showed they were not associated with an increased rate of myocardial infarction or death, but were associated with a reduction in need for revascularisation of up to 70% compared with BMS.9,10 Moreover, there has been an evolution to “second generation” stent platforms with very low stent thrombosis and restenosis rates,11 and greater understanding of the importance of dual antiplatelet therapy. Indeed, new registry data have provocatively shown a mortality benefit with liberal utilisation of DES.12 So who should receive a DES? If there was no cost difference, it would be appropriate to implant DES in the majority of patients. The main exceptions would be patients unlikely to tolerate 12 months of dual antiplatelet therapy because of increased bleeding risk, an anticipated need for elective surgery, or poor medication compliance. However, a significant cost differential remains and, therefore, rationing to those most likely to benefit (Box) is appropriate. This will, nonetheless, still result in much higher DES utilisation rates than those documented in the MIG registry in 2007. The reassurance that DES are safe has had an effect on practice at our institution, with implantation rates increasing from 43% to 70% over the past 3 years, bringing us back in line with the proportion of patients reported to meet selective utilisation criteria in Victoria.8 The information presented by the MIG gives a fascinating insight into physician behaviour by documenting the local change of practice that followed concerns regarding DES. Confidence has been restored by evidence affirming DES safety, the introduction of “second generation” platforms, and a better understanding of the importance of optimal medical therapy. It would be interesting to see how these more recent developments have affected DES use, and we look forward to ongoing insights from this important local registry.

Christopher J K Hammett MBChB, FRACP, FCSANZ · Peter J Stewart MB BS, FRACP, FCSANZ · John J Atherton PhD, FRACP, FCSANZ

How can implementing a population-wide salt-reduction program be so hard? For most of human evolution, the average daily diet contained a fraction of a gram of salt and our physiology developed accordingly.1 A few thousand years ago, with the discovery that salt could preserve food, average intake started to rise. Now, with salt poured into the food supply, average Australian consumption levels are many times our physiological need.2 Populations eating the level of salt upon which we evolved are now few, but they provide a window into normal physiological processes. One of the most notable findings is that their blood pressure levels do not rise with age.3 Despite recent highly publicised reports,4 there is little debate about the adverse impact of salt on human health.5 The totality of the evidence is convincing and the unbiased findings from randomised trials of salt reduction particularly so. While a number of non-randomised studies have suggested health benefits of salt consumption,4 the publicity they receive greatly exceeds their real significance. Observational nutritional epidemiology is incredibly difficult to do well, and the diversity of findings almost certainly reflects methodological challenges, not discrepant science. Although direct evidence from a single adequately powered mortality and morbidity trial of salt reduction is lacking, the circumstantial evidence remains striking and the likelihood that reduction in salt intake will not reduce vascular risk is small. The strength of the evidence base has persuaded multiple national and international organisations of the need to reduce salt consumption.5 All hypertension guidelines advocate consuming less salt,6 and more than 30 countries now have some form of population-based salt-reduction program in place.7 A series of influential reports has highlighted the large health gains that might be achieved from such national programs and the low costs required to deliver them.8 The issue is no longer whether salt reduction should be a goal, but how it can be achieved. The reason salt reduction presents such a great public health opportunity is that almost everyone eats far more than they need. Average consumption in Australia is between 8 and 10 grams per day,1 with immediate and long-term implications for blood pressure. The early effects occur within weeks and the chronic effects over decades. As shown by Huggins and colleagues in this issue of the Journal,9 and previously noted by the Intersalt study,10 a daily intake 6 grams above physiological need will push up systolic blood pressure by a few millimetres of mercury in the short term and thereafter by about half a millimetre each year. This chronic effect translates into 25 mmHg over 50 years, with enormous implications for individual and population risks of vascular disease. Blood pressure is a leading cause of disease burden in Australia,11 and our strategy for preventing disease attributable to high blood pressure is hypertension control — individuals are diagnosed as hypertensive and treated within the medical system. Hypertension is currently the most frequent reason for a primary care consultation, with annual direct health care costs of more than a billion dollars.12 For those who need and receive it, antihypertensive therapy is a highly effective intervention. Unfortunately, the clinical approach also has some limitations. First and foremost among these is that half of all disease caused by high blood pressure occurs among people without hypertension.13 Risks start to accrue well below the blood pressure level of 140/90 mmHg that generally defines hypertension, and systolic blood pressure levels of 125–135 mmHg are associated with greater risks than a level of 120 mmHg. While more moderate than the risks faced by those with hypertension, these blood pressure levels cause a very large number of adverse events because these are the blood pressure levels of most of the population. The limited coverage achieved by the clinical hypertension control strategy further reduces its effectiveness. Only about half of hypertensive people are identified and treated;14 less than half of these get to target blood pressure levels,14 and almost none achieve a systolic pressure of 120 mmHg or below. Accordingly, clinical management of hypertension in Australia probably prevents only about a 10th of all blood pressure-related disease. A plausible population-wide salt-reduction program that removed salt at the source could within a few years avert a similar proportion of disease burden at an annual cost of just $10–20 million.5 To achieve this, the Australian Government simply needs to set and enforce salt targets for foods, as has been done in the United Kingdom.7 Average salt consumption would fall, mean population blood pressure would immediately follow, and the long-term rise in blood pressure with age would be attenuated. The real question is how this can be so hard. For almost no extra cost and at no risk, there is a high likelihood we could double the proportion of blood pressure-related disease averted within just a few years. With a proven overseas model to follow,7 our failure to take the action required is bordering on negligent. No one is going to lose their parliamentary seat and no one is going to go out of business if they make this happen. There are just going to be a lot of unnecessary strokes and heart attacks while the people pickling us figure this out.

Bruce C Neal MB ChB, PhD, FRCP

Improving health outcomes for mothers, children and families Mental health morbidity associated with the perinatal period — from conception to the end of the first postnatal year — is now recognised as a major public health issue, with depression affecting up to 15% of women during this period.1 It has been reported that 45% of postnatal depression begins in pregnancy,2 and about 38% of women with postnatal depression have a comorbid anxiety disorder.3 About 3% of women experience moderate to severe depression during the perinatal period and 0.2% experience a puerperal psychosis,4 and maternal suicide continues to be identified as one of the leading causes of indirect maternal mortality.5 There is growing evidence of the negative impact of poor mental health outcomes not only for the mother, but also for her child and family.6 The existence of well established maternal and infant health care systems across Australia has provided a unique opportunity for integrating mental health care into mainstream services. Increasingly, the maternal and infant health care sectors are introducing routine, universal psychosocial assessment aimed at detecting women who are at risk of, or suffering from, mental health morbidity. This approach, underpinned by a philosophy of prevention and early intervention, has been developed in the Australian perinatal setting over the past decade through the work and advocacy of leading clinicians and researchers, policymakers and beyondblue: the national depression initiative.7-9 Feasibility of widespread screening for depression in the perinatal period was evaluated in the National Postnatal Depression Research Program (2001–2005).7 It was concluded that screening for depression was feasible in routine clinical settings and acceptable to women and their health care providers (including general practitioners). In addition, maternal mental health morbidity often went undetected and untreated if routine screening was not used. The National Action Plan for Perinatal Mental Health (2008) went on to recommend implementing universal psychosocial assessment, training primary health care staff who administer the assessments, and establishing structures that optimise coordination of, and access to, appropriate services.8 This was followed by the establishment, by the Department of Health and Ageing, of the National Perinatal Depression Initiative (2008–2013), which enabled the introduction of a specific perinatal mental health Medicare stream (under the Access to Allied Psychological Services initiative) and the development of national clinical practice guidelines for depression and related disorders in the perinatal period.9 The clinical practice guidelines are aimed at all clinicians who have a “primary health care” role in detecting possible mental health morbidity in the perinatal period — including midwives, GPs, child and family health nurses, obstetricians and paediatricians. They are underpinned by a systematic literature review that points to a paucity of quality evidence, especially on routine psychosocial assessment and the safety of psychotropic medication in pregnancy. The guidelines recommend routine, universal screening for depression (antenatal and postnatal) using the Edinburgh Postnatal Depression Scale (EPDS)10 and treatment of mild to moderate postnatal depression with evidence-based psychological interventions (eg, cognitive behaviour therapy). Where there is insufficient evidence for recommendations, good practice points (based on lower-quality evidence and/or expert consensus) have been formulated. These include using comprehensive, universal psychosocial assessment (eg, the Antenatal Risk Questionnaire11) in addition to the EPDS, considering mother–infant interaction and risk to infant as integral parts of the assessment, monitoring women with an existing mood disorder closely to reduce risk of relapse, and providing specific advice about the safety of psychotropic medication during pregnancy and breastfeeding.9 While the guidelines recommend routine use of the EPDS in the perinatal period, they emphasise that it should only be used as an adjunct to clinical assessment in the primary care setting. They also highlight that universal psychosocial assessment is an area of debate, has significant resource implications (including training, service organisation and workload requirements), and needs to be closely integrated with access to mental health services. The clinical effectiveness of routine psychosocial assessment remains to be evaluated. A recent randomised controlled trial of early postnatal screening using the EPDS (including supportive counselling where indicated) demonstrated improved maternal mental health outcomes at 6 months postpartum for women receiving the intervention compared with those receiving usual care.12 In a meta-analysis of screening interventions for general depression, screening was found to be beneficial as long as it was integrated with clear pathways to care.13 This is in line with the National Action Plan for Perinatal Mental Health and the clinical practice guidelines — the first steps in translating evidence into practice and developing a broader evidence base. There is now a need to evaluate the effectiveness of combining psychosocial assessment with integrated pathways to care. In addition, an evaluation of the impact of the National Perinatal Depression Initiative on mental health outcomes for mothers is critical if we are to optimise the quality and uptake of services for this vulnerable, yet highly accessible, population.

Marie-Paule V Austin MB BS, FRANZCP, MD · Philippa F Middleton BSc(Hons), GradDipLibSt, MPH · Nicole J Highet DPsych

Objectives: To describe temporal trends in the use of evidence-based medical therapies and management of patients with acute coronary syndromes (ACS) in Australia and New Zealand.Design, setting and participants: Our analysis of the Australian and New Zealand cohort of the Global Registry of Acute Coronary Events (GRACE) included patients with ST-segment-elevation myocardial infarction (STEMI) and non-ST-segment-elevation ACS (NSTEACS) enrolled continuously between January 2000 and December 2007 from 11 metropolitan and rural centres in Australia and New Zealand.Results: 5615 patients were included in this analysis (1723 with STEMI; 3892 with NSTEACS). During 2000–2007 there was an increase in the use of statin therapy, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, and thienopyridines (P < 0.0001 for each). Among patients with STEMI, there was an increase in emergency revascularisation with PCI (from 11% to 27% [P < 0.0001]), and inhospital coronary angiography (from 61% to 76% [P < 0.0001]). Among patients with NSTEACS, there was an increase in revascularisation with PCI (from 20% to 25% [P = 0.004]). Heart failure rates declined substantially among STEMI and NSTEACS patients (from 21% to 12% [P = 0.0002], and from 13% to 4% [P < 0.0001], respectively) as did rates of hospital readmission for ischaemic heart disease at 6 months (from 23% to 9% [P = 0.0001], and from 24% to 15% [P = 0.0001], respectively).Conclusions: From 2000 to 2007 in Australia and New Zealand, there was a fall in inhospital events and 6-month readmissions among patients admitted with ACS. This showed an association with improved uptake of guideline-recommended medical and interventional therapies. These data suggest an overall improvement in the quality of care offered to contemporary ACS patients in Australia and New Zealand.

Bernadette Aliprandi-Costa RN · Isuru Ranasinghe MB BS, MMed · Vincent Chow MB BS · Shruti Kapila MB BS · Craig Juergens MB BS, FRACP, FCSANZ · Gerard Devlin MBChB, FRACP, FCSANZ · John Elliott MBChB, FRACP, FCSANZ · Jeff Lefkowitz MB BS, FRACP, FCSANZ · David B Brieger MB BS, PhD, FRACP

Objective: To evaluate percutaneous coronary intervention (PCI) practice trends and 12-month outcomes in Australia in the era of drug-eluting stents (DES).Design, setting and patients: Prospective study of consecutive patients undergoing 9204 PCIs between 1 April 2004 and 31 March 2008 at seven Victorian public hospitals.Main outcome measures: Temporal trends in baseline characteristics and in-hospital and 12-month clinical outcomes including death, myocardial infarction (MI), target vessel revascularisation (TVR) and composite major adverse cardiac events (MACE), from year to year.Results: Between 2004–2005 and 2007–2008, the mean age of patients undergoing PCI was stable (65 ± 12 years), and comorbidities such as hypertension, hyperlipidaemia, peripheral arterial disease and stroke increased (P < 0.05). There were fewer elective and more urgent PCIs, especially for MI < 24 hours (17.6% in 2004–2005 to 27.2% in 2007–2008, P < 0.01). Overall stent use remained high (mean, 94.6%), but use of DES declined steadily (53.9% in 2004–2005 to 32.0% in 2007–2008, P < 0.01), despite increases in complex lesions. Planned clopidogrel therapy of ≥ 12 months after insertion of DES increased from 54.7% in 2004–2005 to 98.0% in 2007–2008 (P < 0.01). The overall procedural success rate was high (mean, 95.9%), and 12-month rates of mortality (3.8%), MI (4.8%), TVR (6.8%) and stent thrombosis (1.8%) remained low. Selective use of DES was an independent predictor of freedom from MACE at 12 months (odds ratio, 0.68; 95% CI, 0.56–0.81).Conclusions: Use of DES declined steadily from 2004–2005 to 2007–2008, despite increasing patient risk profile and lesion complexity. Procedural success remained high and 12-month adverse outcomes remained low, with increasing use of prolonged dual antiplatelet therapy.

Bryan P Yan MB BS, FRACP, FACC · Andrew E Ajani MB BS, FRACP, MD · David J Clark MB BS, FRACP · Stephen J Duffy MB BS, PhD, FRACP · Nick Andrianopoulos MB BS, MBiostat · Angela L Brennan RN, CCRN · Philippa Loane BSc · Christopher M Reid BA, MSc, PhD

Objective: To assess the relationship between dietary sodium intake, as measured by urinary electrolyte excretion, and blood pressure within a population of older Australian adults.Design, setting and participants: A cross-sectional study of adults enrolled in the Melbourne Collaborative Cohort Study, stratified by sex, country of birth (Italy, Greece, Australia/New Zealand) and age (50–59 and 60–75 years). Blood pressure measurements were taken in 2003–2007 and 24-hour urine collections in 2007–2008.Main outcome measures: 24-hour urinary excretion of sodium and potassium, urinary sodium-to-potassium ratio, and clinic blood pressure measurement.Results: The mean ± SD age of 783 participants was 64.0 ± 6.3 years. Mean ± SD urinary sodium was 155.1 ± 63.1 mmol/day (8.9 ± 3.6 g salt/day), urinary potassium was 82.3 ± 27.9 mmol/day, and urinary sodium-to-potassium ratio was 1.99 ± 0.83. In the 587 participants with blood pressure measurements, urinary sodium and the sodium-to-potassium ratio were both associated with systolic blood pressure in all adjusted and unadjusted models (mmHg change per 100 mmol/day increase in sodium: regression coefficient, 2.3, 95% CI, 0.1–4.6; P = 0.049, adjusted for age, sex, body mass index, country of birth and antihypertensive medication use).Conclusion: This study has demonstrated, for the first time within an Australian population sample of older adults, that sodium intake is positively associated with blood pressure. These results suggest that a population-wide reduction in sodium intake could be effective in reducing blood pressure in adults in Australia.

Catherine E Huggins BSc(Hons), PhD · Sharleen O’Reilly BSc(Hons), PhD, CertHEd · Maree Brinkman BSc(Nutrition), MND · Allison Hodge BSc, GradDipDiet, PhD · Graham G Giles BSc, MSc, PhD · Dallas R English BSC, PhD · Caryl A Nowson PhD, DipNutDiet

Objective: To study patient persistence on therapy for hypertension and dyslipidaemia using a single-pill combination compared with a two-pill approach.Design and setting: Post-hoc observational assessment of Pharmaceutical Benefits Scheme claim records covering the period April 2005 to March 2010.Participants: A 10% random sample of Australian long-term concession card holders was analysed. The patients studied had commenced on either amlodipine and atorvastatin as two individual pills, or a single pill containing both amlodipine and atorvastatin (AA), with neither combined approach having been dispensed to them in the previous 6 months.Main outcome measures: The proportions of patients failing to fill their first repeat prescription after 1 month or failing to persist with treatment at 12 months, and the median persistence time (MPT) were measured.Results: Of 4146 patients prescribed the AA single pill, 11% failed to fill the first repeat prescription and 33% had ceased treatment by 12 months (MPT, 35 months). Of 6204 patients prescribed amlodipine and atorvastatin as two pills, 23% failed to fill the first repeat prescriptions and 59% had ceased treatment by 12 months (MPT, 7 months). In a multivariate model, cessation of single-pill therapy increased by 165% if there was no prior therapy, but only increased by 48%–55% if there was no prior therapy with a calcium channel blocker or statin. MPT on the single pill was 8 months in those without prior antihypertensive therapy, but was ≥ 37 months in those with any prior antihypertensive therapy.Conclusion: A single-pill combination drug is associated with superior long-term persistence compared with two-pill therapy in the management of hypertension and dyslipidaemia.

Leon A Simons MD, FRACP · Michael Ortiz BPharm, PhD · Gordon Calcino BA, GradDipMedStats

The clinical usefulness of laboratory testing of adult patients with venous thromboembolism (VTE) for heritable thrombophilia needs to be critically evaluated. At present, some clinicians use testing to identify patients at higher risk of recurrence (who may benefit from an extended period of anticoagulation beyond the usual 3–6 months) and their relatives at risk of a first VTE episode. As prevalence of heritable thrombophilia is related to age and ethnic origin, the pretest probability of detecting heritable thrombophilia may be low in unselected populations. Interpretation of laboratory results may not be straightforward. Apparent deficiencies of a natural anticoagulant may be due to acute thrombosis and “consumption”, concomitant therapy with heparin and/or warfarin and other clinical factors. The predictive value of recurrent VTE conferred by the most common types of heritable thrombophilia (factor V Leiden and the G20210A prothrombin mutation) is limited. Risk of recurrence associated with deficiencies of a natural anticoagulant is less certain due to their rarity. Clinical risk factors (eg, the presence or otherwise of provoking factor(s) and whether or not the risk factor for VTE is reversible or permanent) appear to be the most important predictors of VTE recurrence. Duration of anticoagulation should be determined by clinical risk factors rather than the presence, or otherwise, of heritable thrombophilia. The benefit of identifying relatives who are carriers of thrombophilia is uncertain, as VTE is a multifactorial disease resulting from the interaction of various risk factors, some well recognised and others as yet unknown.

Wai Khoon Ho MMedSc, FRACP, FRCPA · Graeme J Hankey MD, FRCP, FRACP · John W Eikelboom MSc, FRACP, FRCPA

There is little evidence that public health measures adopted so far have had any impact on the rise in the prevalence of obesity. Weight-loss programs have a very high long-term failure rate. There is emerging evidence that weight is regulated by the hypothalamus and is physiologically defended. There is also a strong genetic predisposition to the development of obesity. The availability and promotion of high-energy foods and the absence of any obligatory need for physical activity compound the problem, but this social change is not easily reversible. One way forward is to focus public health measures on preventing obesity in children while making resources available to treat people who are already obese, including providing funding for bariatric surgery in public hospitals.

Joseph Proietto MB BS, FRACP, PhD

How to ensure a better match between grant applicant and reviewer expertise All researchers have experienced dismay at the failings of peer review.1,2 These include cursory or ill informed reviews from those apparently unschooled in applicants’ disciplines and with superficial understanding of the quality and significance of proposals, publications and achievements being described by aspiring applicants. Only the greenest researchers assume that those who assign papers or grants to reviewers possess Solomonic wisdom in matching the expertise of researchers and reviewers. The reality is very different. Reviewer assigners rely on reviewer databases, particularly for areas beyond their specific expertise. It is here that many problems start. Some names are in these databases by virtue of having previously submitted a grant or paper, regardless of quality or success. Self-chosen research keywords may bear little correspondence to actual expertise. Many relatively inexperienced names appear and searches suggest many who have published little. Grant review panels seek reputable reviewers but reviewer refusal means suboptimal reviewers are often used. No published information is available on grant review refusal rates, but data obtained from the BMJ Publishing Group for 300 866 review requests sent out by 20 journals between 2002 and 2009 show that 32.4% of those asked declined to review.3 Reviewer assigners can then resort to selecting names on the basis of reviewer supplied keywords, without detailed knowledge of the reviewer. Although this can sometimes produce superb reviews, it can also produce those that are confidently written but ill informed. The core problem with current approaches to reviewer selection is that a small number of assessors are involved, typically two or three. Although it would be impractical to involve more people in grant assessments, the rating of track record — typically attracting at least 25% of overall score — could easily break free from the reputational lottery affected by the opinions of a few, sometimes ill informed, people that may affect the fate of a grant application. There is an easily managed, low-cost way of democratising the rating of researcher track record that would end the practice of relying on a small number of sometimes inexpert peers rating applicants’ track records. As part of a project examining the nature of researcher influence, we invited all Australia-based researchers in six research public health fields who had published 10 or more Institute for Scientific Information-indexed publications in the past 10 years to nominate up to five Australian researchers in their respective fields whom they considered to be the most “influential” researchers. Full descriptions of the selection of participants are provided elsewhere.4,5 Participation was high: 83% of invited eligible Australia-based researchers (175/211) completed the rating task, which took about 10 minutes. One hundred and eighty-two individuals across these fields received at least one nomination, producing a distribution of “votes” on researcher influence across these researchers. In five of the six fields, there was impressive consensus on which researchers were most influential, with a long tail of researchers receiving a smaller number of votes, and many none. In all six fields, a large number of researchers (108/182; 59%) received only one vote from all those voting. Of these, 48 (26% of all nominations) were self-nominations. Peer-influence rating generally correlated strongly with four commonly used bibliometric indices of research impact6 (the h, m and q2-indices and the m-quotient).7-10 The traditional approach to track-record ranking involves a small number of researchers being selected as reviewers by an often idiosyncratic process that reflects selector knowledge and preferences and reviewer self-nomination and availability. The existing process lacks transparency and probably provides biased results from an unrepresentative sample of reviewers. Our study demonstrated that the process can be opened up by seeking votes from all research-active peers in each relevant field. Most researchers agreed to participate and found the task unproblematic. We received no critical feedback from those involved. We asked participants to select five researchers they considered to be “most influential” in their fields. The concept of “researcher influence” is arguably wider than that of research track record, but we could have just as easily asked participants to rate the narrower concept of “research track record”. Equally, we could have asked participants to nominate and rank a larger, but non-onerous, number of influential researchers (say, 20), which would have produced a more finely grained distribution of voting, facilitating the overall ranking into quartiles or quintiles that ranged from those considered by many to be influential through to those considered influential by none of their peers. Our proposalIt could be made mandatory for all researchers submitting grant applications to rank the track records of a reasonable number of their peers. Each applicant could be sent a random, computer-generated list of research peers (say, 10) from their respective research fields who where also seeking funding and to rank them as a condition of grant application submission. The generation of these lists could be stratified to ensure that all researchers, regardless of experience, were guaranteed to be ranked by 10 randomly selected peers. Every applicant would thus receive a score of between 100 (if all 10 peers ranked them first) and 10 (if all ranked them 10th). Track record could then be taken as this aggregated raw score. To assist ranking, links could be provided to publications, citations and grant successes. In Australia, the National Health and Medical Research Council now requires all applicants to complete an online track record where all publications and competitive grants are entered into a database which could be linked for this purpose. There are potential weaknesses in this process, although none that are weaker than the approach now operating. Early career researchers would be disadvantaged as they would be unlikely to be competitive with more experienced researchers and would receive lower rankings. This could be addressed by finally dividing all researchers into either “open” or “early career” divisions. Some researchers who challenge research orthodoxies may have the importance of their work discounted by those inhabiting those orthodoxies, and receive fewer votes than their contributions might deserve, but this is already possible under the present system.

Simon Chapman PhD, FASSA · Gemma E Derrick PhD · Abby S Haynes MA · Wayne D Hall PhD, FASSA

A 27-year-old woman was being treated with gastrojejunostomy feeding for severe anorexia nervosa. The position of the gastrojejunostomy tube was checked by fluoroscopy on the day of insertion (Figure, A, arrow). The next day, the patient presented with abdominal pain and “shortening” of the external portion of the tube. Repeat fluoroscopy showed migration of the tube (Figure, B, arrow). Computed tomography showed two segments of jejunojejunal intussusception (Figure, C, arrow and inset, and D, straight arrow) centred around the tube (Figure, D, curved arrow), with an intervening segment of normal jejunum (Figure, D, label J). The patient’s gastrointestinal tract was intact. The intussusceptions were reduced by applying traction on the tube under fluoroscopic guidance, and the patient resumed tube feeding without recurrence.

Uei Pua

A 10-year-old boy from Papua New Guinea with multidrug-resistant tuberculosis and multibacillary leprosy developed acute glomerulonephritis while being treated as an inpatient at Thursday Island Hospital in the Torres Strait, Queensland. This is the first such case to be reported in Australia, where these diseases are uncommon and the combination is extremely rare, and it outlines important learning points regarding the aetiology of renal disease among patients with tuberculosis and leprosy. (MJA 2011; 195: 150-152) Clinical recordA 10-year-old boy from a remote village in Western Province, Papua New Guinea (PNG), presented to Saibai Island Primary Health Centre in the northern Torres Strait, Queensland, with a 4-year history of intermittent malaise, fevers, night sweats, recurrent skin sores and a cough productive of green sputum. He had received treatment for leprosy for 1 month the previous year at Daru Hospital (Western Province, PNG). There was a strong family history of leprosy and tuberculosis among both first- and second-degree relatives. On initial examination, the patient appeared cachectic. There was evidence of recent impetigo on both lower limbs and depigmented areas on his upper and lower limbs. He had thickened ulnar and posterior tibial nerves bilaterally, with normal sensation and motor function on repeated clinical assessments. His lungfields were clear to auscultation, but he had an ejection systolic murmur; he was also found to have hepatomegaly and enlarged inguinal, anterior and posterior cervical lymph nodes. He was transferred to Thursday Island Hospital for inpatient management. Slit skin smears were performed; phenotypic analysis of the right earlobe smear was positive for Mycobacterium leprae, confirming the diagnosis of multibacillary leprosy.1 An initial chest x-ray showed left upper lobe changes consistent with pulmonary tuberculosis; subsequent sputum samples and an aspirate of an anterior cervical lymph node cultured Mycobacterium tuberculosis resistant to rifampicin, isoniazid, streptomycin and ethionamide, in keeping with a diagnosis of disseminated multidrug-resistant tuberculosis (MDR-TB).2 HIV and hepatitis serological tests were negative. On admission, his serum creatinine level was 30 μmol/L (reference range [RR], 46–81 μmol/L). The patient was given intravenous amikacin and oral moxifloxacin, isoniazid, pyrazinamide, ethambutol, pyridoxine and rifampicin; cycloserine, aminosalicylic acid (mesalazine), dapsone and clofazimine were later added. One week after admission, the patient developed acute glomerulonephritis, which manifested as fluid retention (pulmonary oedema, peripheral oedema and ascites), hypertension (maximum blood pressure, 160/112 mmHg), haematuria, proteinuria (up to 9700 mg/L [RR, < 100 mg/L]) and impaired kidney function (serum creatinine level peaked at 69 μmol/L). He was treated with frusemide, nifedipine and prednisolone. There was serological evidence of recent infection with Streptococcus pyogenes (elevated antistreptolysin O and anti-DNAse B titres) and hypocomplementaemia (decreased complement component 3 [C3] concentration with normal complement component 4 [C4] concentration). The nephritic illness resolved slowly over the next few weeks. During this period, the patient developed painful, erythematous nodules over his upper torso and limbs (Box 1). His mother reported that he had experienced several such episodes in the past. The lesions measured 5–10 mm in diameter and were tender to palpation; in association with the cardiac murmur and elevated streptococcal serology there was some initial concern about the possibility of acute rheumatic fever and the patient was commenced on penicillin prophylaxis. However, expert consensus was that the lesions more likely represented erythema nodosum leprosum (ENL) — an immune complex-mediated inflammatory reaction that can occur in both acute and chronic relapsing forms among leprosy patients with a high mycobacterial load. Treatment options for this condition have historically included simple analgesics, steroids, non-steroidal anti-inflammatory drugs, clofazimine and thalidomide. A recent Cochrane review found a paucity of evidence for most treatments of ENL, and only a modest benefit from clofazimine and thalidomide.3 As the patient was already taking clofazimine, thalidomide was not considered to be a practical or necessary option in his case (given its significant side effects, the need for monitoring and the patient’s planned return to PNG); his several subsequent bouts of ENL were treated successfully with oral prednisolone. His renal function remained stable throughout these episodes, and an inpatient echocardiogram was normal. After three negative sputum smears, the patient was removed from isolation and continued treatment with intravenous amikacin. He was discharged home on oral therapy for both MDR-TB and leprosy, with follow-up planned at Saibai Island Primary Health Centre. Unfortunately, at the time of writing, due to unknown patient factors and unforeseen circumstances (such as the closure of the border and cancellation of outreach clinics), the patient has not been seen, nor his medications collected, for almost 6 months. DiscussionThe area encompassed by the Torres Strait and Northern Peninsula Area Health Service District in Queensland includes some of the most remote and isolated communities in Australia, and incorporates the porous maritime border with PNG. Thursday Island Hospital is the main referral hospital for the region and many PNG patients are seen in outer island clinics and treated as inpatients at Thursday Island Hospital. These include a significant number of patients with tuberculosis. Although accurate figures on the epidemiology of infectious diseases in PNG are difficult to obtain, it is likely that the rates of mycobacterial infections such as tuberculosis and leprosy in PNG are both underreported and among the highest in the world. The World Health Organization recently reported an annual incidence of 6.5 per 100 000 for leprosy in PNG,4 with historical prevalence of up to 3% recorded in some remote villages.5 For tuberculosis, PNG has reported an incidence of 233 per 100 000, of which about 25% may be MDR-TB.6 A recent literature review described only isolated case reports and small case series studies of concomitant infection with leprosy and tuberculosis over the past few decades.7 Most of these reported cases were from India, with documented co-infection rates (ie, the proportion of leprosy patients found to also have tuberculosis) in the order of 2.5%–7.7% in India and up to 13.4% in South Africa.8,9 Despite the relative dearth of published accounts of co-infection, it seems plausible that simultaneous infection with M. tuberculosis and M. leprae occurs more frequently than is described in published reports in regions with relatively high rates of both diseases (including countries in sub-Saharan Africa, South America, the Indian Subcontinent, and South-East Asia). Some postulated reasons for why rates of co-infection may nevertheless be lower than expected in high prevalence regions include improvements in the detection rate and treatment for both infections; the WHO’s initiative of providing free leprosy treatment in an effort to eliminate the disease; the effects of BCG immunisation; and the complex, possibly antagonistic interaction between the two strains of mycobacteria.7 Our patient developed acute glomerulonephritis as an inpatient receiving treatment for MDR-TB and leprosy; hence, a number of possible causes of his renal dysfunction were considered. Renal abnormalities occur among most patients with leprosy, particularly those with multibacillary disease (“borderline” or “lepromatous” disease using the Ridley–Jopling Classification of Leprosy), and renal failure is a frequent cause of death in patients with leprosy.10,11 Glomerulonephritis, nephrosclerosis, tubulointerstitial nephritis, amyloidosis and granulomas are the most common renal pathologies found on biopsy or autopsy of leprosy patients.12 Of the glomerulonephropathies, the proliferative glomerulonephritides are the most frequently described lesion among patients with leprosy.11,12 Hypocomplementaemia is a recognised association of renal disease in this setting, particularly among patients with multibacillary leprosy and ENL.12 Typical serum protein profiles seen among patients with renal disease associated with some selected infections are presented in Box 2. The pattern of hypocomplementaemia varies somewhat between the different forms of glomerular disease; low C3 with normal C4 (as in our patient’s case) tends to suggest either poststreptococcal or membranoproliferative glomerulonephritis.13 Evidence of streptococcal infection was found on biopsy from five leprosy patients with renal disease in India; the same case series reported two patients with microfilariae in peripheral blood samples, indicating the possibility of a range of concomitant infections contributing to renal disease in patients with leprosy.14 With respect to drug-induced nephrotoxicity, rifampicin (a common component of the pharmacological regimen for treatment of both leprosy and tuberculosis) has been implicated in acute renal failure, often associated with thrombocytopenia, immune haemolytic anaemia and intravascular coagulation.15 In our patient, however, the combination of oedema, hypertension, haematuria, hypocomplementaemia (in the pattern described), elevated streptococcal serological results and a history suggestive of recent skin infections is strongly supportive of a diagnosis of poststreptococcal glomerulonephritis, which is an uncommon form of renal disease in patients with leprosy. The patient did not undergo kidney biopsy as his condition was clinically improving and it was felt that this highly invasive procedure would not have yielded sufficient additional diagnostic information to make it worthwhile. It is also a moot point whether, given his nationality, this procedure would have been available to him. In summary, our patient had the misfortune to suffer simultaneous infection with multibacillary leprosy and MDR-TB (and may be the first such reported case in Australia), which was complicated by ENL and an acute glomerulonephritis that was probably poststreptococcal glomerulonephritis — a rare form of renal disease in a subset of patients among whom renal impairment is commonly due to other causes. 1 Erythema nodosum leprosum reaction, indicated by red patches 2 Serum protein profiles seen in renal disease associated with specific infections* Serum protein profile Group A streptococcus infection Acute glomerulonephritis Classic diffuse proliferative Decreased C3 Focal proliferative (IgA disease) Increased IgA Mycobacterium leprae infection Acute glomerulonephritis Proliferative forms Decreased C3 Cryoglobulinaemia (ENL) Decreased C3 and C4 Nephrotic syndrome Amyloid Increased AA Mycobacterium tuberculosis infection Nephrotic syndrome Amyloid Increased AA AA = amyloid A. C3 = complement component 3. C4 = complement component 4. ENL = erythema nodosum leprosum. IgA = immunoglobulin A. * The serum concentrations of certain proteins are altered in these conditions.

Lachlan J McIver MB BS, MPHTM, FACRRM · Shaun T Parish MB BS, DTMH, FACRRM · Samuel P Jones MB ChB, DTMH, JCPTGP · Alexander N Kippin MB BS, MPHTM · Timothy J Furlong MB BS, PhD, FRACP

Keith William Shaw served as a pilot in the Royal Australian Air Force from 1942 to 1945, and graduated in medicine from the University of Queensland in 1949. From 1953 to 1984, he was a general practitioner in Kingaroy, Queensland. After he retired, he continued to work intermittently as a locum until he retired fully in 1998. In 1971, Keith became a Fellow of the Royal Australian College of General Practitioners (RACGP). He was Provost of the RACGP Queensland Faculty from 1974 to 1975 and Chair of its Board from 1979 to 1980. From 1980 to 1982, he served as RACGP President. During his presidency, Keith travelled widely throughout Australia in his own “little airplane”. Ably assisted by his wife Anne as his copilot, he crossed the Bass Strait more than once and the Nullarbor several times. As President, he also encouraged the development of reciprocal ties with other colleges in the Asia–Pacific region. In particular, he organised assistance for the conduct of examinations in the Singaporean, Malaysian and Hong Kong colleges. Keith was a great advocate for general practice, especially in rural areas. He was active in the Family Medicine Programme and Australian General Practice Training and taught a generation of students and registrars in his Kingaroy practice, where they learnt about continuing and comprehensive care from an expert. He was also a very strong supporter of the Royal Flying Doctor Service. His contribution to Australian general practice was recognised with honours including Officer of the Order of the British Empire, Life Fellow of the RACGP in 2008, and Fellow of the Australian Medical Association in 1983. Keith died peacefully at his Kingaroy home on 25 March 2011, aged 88 years. He is survived by his wife Anne and three children. Peter R Mudge

To the Editor: Comparing Australian medical school policies regarding conflict of interest (COI) to their United States counterparts, Mason and Tattersall1 conclude that within Australia there is “a need for improved self-regulation”. The authors are applauded for highlighting this important aspect of medical education and organisational practice; however, the comparisons made fail to acknowledge a number of contextual differences that undermine the conclusions drawn. First, significant cultural differences exist between Australia and the US with respect to historical market practices and commercial sponsorship within the tertiary education sector.2 The persistent failure of self-regulation in the US recently culminated in the passing of the Physicians Payment Sunshine Provision, which now mandates transparent disclosure of all (> $10) payments, gifts and sponsorships, and imposes significant penalties for failure to report.3 Arguably, it is this changing legislative landscape that has encouraged US medical schools to develop more robust COI policies, rather than a proactive commitment to manage COI. Second, unlike in the US, most of Australia’s 20 medical schools sit within publicly funded universities, where central policy regulation of COI prevails. Mason and Tattersall’s1 suggestion that each school have its own COI policy without reference to the overarching university’s COI policy is flawed, particularly in a wider academic environment where industry sponsorship of education and commercialisation in research are increasingly encouraged as a desirable strategy to supplement falling levels of Commonwealth resourcing. Third, despite the lack of policies in Australian medical schools, positive performances with respect to COI in the curriculum were noted,1 demonstrating that lack of policy does not necessarily hinder appropriate curriculum content. Finally, on becoming doctors, medical students are bound by their professional codes of practice, codes of ethics, organisational policies and state and federal legislation, which outline the obligation to act within the recognised standards of the profession.4 While medical schools have a significant role to play in preparing future doctors to effectively recognise bias and appropriately manage COI,5 their ability to enforce more rigorous standards than those that apply within the professional community at large is doubtful. The adequacy of current professional codes is a matter for further debate. Medical schools exist within the wider context of the university, the community and the overarching political and legal landscape that governs their resourcing and practices. These factors must be taken into account when judging the actions of medical schools. To present Australian medical schools as lacking1 on the basis of a decontextualised comparison with US schools may be overly simplistic.

Eleanor Milligan · Allan W Cripps

In reply: The medical community in Australia regulates itself through various non-binding codes and guidelines, but these have not been shown to reduce industry influence on doctors or medical students. In contrast, the existence of institutional policies can limit the influence of industry, resulting in medical students and doctors who are less influenced by industry marketing.1,2 University conflict-of-interest (COI) policies must reflect the context in which they exist, but it is unlikely that a general university policy covering all faculties could address the specific challenges presented by medical student education. Policy development, while difficult, is possible, and the University of Melbourne is scheduled to complete a policy framework covering staff and students in health-related degrees this year. Arguably, it was the failure of the medical profession in the United States to self-regulate that led to the legislative changes that stimulated the recent COI policy advances in US medical schools. This could also occur in Australia. Despite the logistical difficulties of developing effective self-regulation within medical schools, there are increasing societal expectations that COI be dealt with effectively. If we ignore this sentiment, we risk the imposition of perhaps excessive and punitive legislation. Medical schools should embrace their influential position, and act now to demonstrate their leadership.

Paul R Mason · Martin Tattersall

To the Editor: In their recent article on unintentional child drowning deaths, Petrass, Blivitch and Finch refer to the “limited detail within both police reports and findings” for South Australian cases of drowning.1 Since 2005, South Australia’s Child Death and Serious Injury Review Committee (CDSIRC), which I chair, has considered the circumstances and causes of all child deaths in SA. The legislation governing the CDSIRC’s work quite rightly precludes the publication of individual details of children’s deaths, but, since 2005, the CDSIRC’s annual report has given a summary of the circumstances and causes of drowning deaths for children in each year. Children drown in a variety of circumstances — in fish ponds, rivers, lakes, dams, buckets of water and in boating accidents — but the greatest number, especially among those under 4 years of age, drown in backyard swimming pools.2 In these incidents, time and again I read about failures of supervision, gate closure and adherence to pool fencing regulations and the maintenance of this fencing. Although the extent and nature of supervision may be of academic interest, the prevention of childhood drowning would best be served by the ongoing promulgation of well researched public health campaigns, such as those delivered by the Royal Life Saving Society — Australia and Kidsafe Australia, and attention to legislative changes that will ensure the regular inspection and maintenance of swimming pool fencing. The CDSIRC’s review of child drownings in SA is based on the detailed information obtained by SA police from witnesses present at the time of the event. This almost always provides a great depth of detail that enables the identification of the key risk factors present in the circumstances of the death. It is unfortunate if this information was not available to Petrass and colleagues, but it is incorrect to infer that such information is not collected in SA. The CDSIRC’s annual reports are available from its website.3 Similar reports are produced by child death review committees or teams in Queensland, New South Wales and Victoria.

Dymphna Eszenyi

In reply: Information made available by South Australia’s Child Death and Serious Injury Review Committee is similar to that in other Australian states that have a Child Death Review Committee; all produce an annual report of circumstances related to child deaths, including child drowning. While we are aware of these reports, for our study of child drowning, individual case details were required that cannot be extracted from compiled summaries in annual reports. By contrast, the National Coroners Information System (NCIS) provides access to original documents for individual drowning cases. Details for South Australian child drownings in the NCIS database were very limited, although at no point in our article did we infer that this information is not collected in SA; rather we stated that that coroners findings were only available for 38.1% of cases in the NCIS, and that autopsy and toxicology reports are not routinely uploaded.1 Further, the recently revised position paper of the National Drowning Prevention Alliance (NDPA) states that neither a single device nor a single solution can prevent child drownings, and recommended that caregivers, aquatic facility owners, managers and operators use “layers of protection” to aid in child drowning prevention.2 We certainly agree that the ongoing promulgation of well researched public health campaigns is an important layer in the prevention of child drowning, although, to date, no published studies have investigated the effectiveness or rigorously evaluated Australian aquatic death prevention campaigns (such as Keep Watch, Kids Alive — Do The Five, SafeWaters and Play it Safe by the Water). However, the NDPA did identify that supervision is the one layer that should be ever-present, regardless of what other layers are used.2

Lauren A Petrass · Jennifer D Blitvich · Caroline F Finch

To the Editor: A review by Harper and Lefkovits favoured increased use of prehospital thrombolysis (PHT) for the management of ST-elevation myocardial infarction (STEMI).1 The acknowledged importance of early reperfusion and the ready application of PHT make this a sound recommendation for settings that are remote from percutaneous coronary intervention (PCI) centres. However, the recommendation of using PHT for patients presenting within 2 hours of symptom onset in metropolitan areas is more controversial. Recent enthusiasm for this strategy has been buoyed by the 5-year data from the randomised CAPTIM study that compared PHT with primary PCI.2 This French study, conducted from 1997 to 2000, was prematurely terminated after recruiting 840 of the planned 1200 patients. There was no difference in the primary composite end point at 30 days. A post-hoc analysis subsequently reported that among the 460 patients randomly assigned to PHT or PCI within 2 hours of symptom onset, there was a trend towards lower mortality among those receiving PHT (2.2% [five patients] v 5.7% [13 patients] at 30 days; P = 0.058).3 By 5 years, an additional eight patients receiving PHT and 12 patients receiving primary PCI had died, resulting in a P value of 0.04 for mortality difference.2 This result reflected one component of a composite end point in a post-hoc subgroup analysis from a prematurely terminated, underpowered trial. Harper and Lefkovits comment that French registry data support the CAPTIM findings. However, data from a more than 10-fold larger Swedish registry do not.4 Important to the successful implementation of PHT is the transport of patients directly to PCI centres where early angiography can be performed if required. However, PCI and fibrinolysis do not make good bedfellows — a lesson learnt through the counterintuitive results of facilitated PCI trials, which showed no benefit and some harm when offering thrombolysis as a prelude to PCI.5,6 This adverse interaction is ameliorated if PCI is deferred for 3 to 24 hours after thrombolysis; however, there is a real risk that early PCI will be overused when STEMI patients arrive rapidly at a staffed PCI facility after receipt of PHT. We need stronger evidence than currently exists to be sure that, in metropolitan settings, the temptation for zealous application of PCI after PHT does not effectively result in over-application of a facilitated PCI strategy, with untoward consequences. In metropolitan regions, the current focus on reducing delays from onset of symptoms to percutaneous revascularisation should remain. Based on the evidence to date, PHT may be a cost-effective but not clinically superior alternative for reperfusion, and should be encouraged as the strategy of choice in circumstances when logistic or resource constraints limit ready access to primary PCI.

David B Brieger

To the Editor: In their article on the decline of infectious syphilis in the Australian Indigenous population from 2005 to 2009,1 Ward and colleagues conclude that it “might be the right time to move toward the elimination of infectious syphilis from remote Indigenous communities”. They note that another previously endemic sexually transmitted infection, donovanosis, has almost completely disappeared from Australia as a result of an elimination program.2 I strongly support their call to action and believe that syphilis can, and should, be next. It is likely that, outside of the small number of communities who have been able to implement a coordinated screening program, the decrease in syphilis in remote areas is an unintended benefit of the use of azithromycin for genital chlamydia and trachoma, and amoxicillin for gonorrhoea. Syphilis is only transmissible to sexual partners for a few weeks during the primary phase (when a chancre is present) and during the secondary phase (when mucocutaneous lesions may be present). Although syphilis is highly infectious during these stages, the relatively short duration of infectiousness partly explains why it is less common than other bacterial sexually transmitted infections. Because the painless ulceration of syphilis is easily ignored by men, or may go unnoticed by women with genital lesions, the diagnosis and treatment of latent (ie, subclinical) disease has been the main focus of syphilis control in remote areas. This approach has had only a limited effect on reducing the incidence of infectious syphilis. Indeed, as latent disease detection and treatment improves, there may be a paradoxical increase in the incidence of infectious cases because latently infected individuals become susceptible to new infection again after treatment.3 Therefore, detection and treatment of all cases of early, infectious syphilis must be the aim of an elimination program, but it will be extremely difficult to achieve this in a remote or rural setting using current diagnostic strategies that almost exclusively rely on serological testing. Serology is still the mainstay of syphilis diagnosis, despite the development of sensitive and specific polymerase chain reaction (PCR) tests for Treponema pallidum. Multiplex PCR tests that can also detect herpes simplex and donovanosis have been used to diagnose genital ulcerative disease in remote areas of Australia,4 but not to screen asymptomatic individuals. The validation of a syphilis PCR test that can be used to identify early, infectious syphilis should be a research priority — one that could be carried out as part of an Australian Government-funded, centrally coordinated but locally implemented, targeted syphilis elimination program.

Francis J Bowden

To the Editor: Recently, Professor Hoy argued for the full inclusion of Aboriginal and Torres Strait Islander people in the Australian Health Survey (AHS), including the measurement of clinical variables and the proposed sample repository.1 Although much of the argument is plausible, several points were overlooked that make it untenable overall. First, the current study design arose with input from at least five Indigenous representative bodies, including the National Aboriginal Community Controlled Health Organisation.2 They identified social and cultural issues as priority areas to be addressed — correctly so, as the underlying causes of health disparity are located in these domains, not primarily in the clinical and biomedical aspects of the AHS. The input from these major national bodies cannot be ignored. Second, yes — there are concerns that “the stored samples and their results might be somehow misused”.1 These concerns are legitimate and well founded in historical and contemporary experiences of Indigenous people. The argument for applying “current scientific and epidemiological knowledge, methods and safeguards”1 to the use of information held in the AHS is correct as far as it goes, but ignores equally important Indigenous knowledge and methodologies, Indigenous intellectual property issues, the principles of “ownership, control, access and possession” of Indigenous information,3 and certain aspects of the United Nations Declaration on the Rights of Indigenous Peoples. This position is therefore inconsistent with the National Health and Medical Research Council guidelines on values and ethics in Aboriginal and Torres Strait Islander health research, particularly as they relate to “survival and protection”.4 Third, denying Indigenous people control over how their health information is used by mainstream research institutions prevents accountability of researchers to communities. Using and publishing this information requires review by relevant experts, in this case Aboriginal and Torres Strait Islander community representatives. Biomedical expertise alone is insufficient to enable effective peer review and, at worst, it risks promoting destructive policies that ignore social, cultural and political realities for Aboriginal people and Torres Strait Islanders. Aboriginal people and Torres Strait Islanders rightly feel that they have been one of the most researched groups in history. And yet, even with this background of decades of being constantly studied, researched and examined, it seems that there is still not enough information being collected. Wellbeing is “grounded in the respect given to people, and the control afforded to them, in their daily lives”.5 Sometimes it’s up to Aboriginal and Torres Strait Islander people to identify what is important in Aboriginal and Torres Strait Islander health: it’s our health!

Kevin G Rowley · Alister H Thorpe

In reply: I thank Dr Rowley and Mr Thorpe for their response.1 It is hard to justify exclusion of any Australian from opportunities to participate fully in important initiatives on the recommendation of bodies whose membership sometimes has no direct link to the persons affected. There is no other population group in Australia to whom this applies. Medical and clinical approaches should complement initiatives to address critical social and cultural issues; they are not in competition nor mutually exclusive. The inclusion of health measures in the adult (but not youth) components of the Australian Health Survey (AHS) acknowledges that there is much to be learned and remediated clinically. Any interpretation of the deliberate exclusion of Indigenous youth from the “measures” elements of the survey is unsettling. There is more, not less, to be learned from this group. Their exclusion deprives policymakers of robust evidence that could improve health status. It condemns enquiry to the current sidestream method of short-term research projects on small pockets of people. These sometimes yield results of dubious generalisability and cause ongoing competition for the impossibly stretched research dollar. Alternatively, is it implied that Indigenous parents are less able to make sound decisions on their child’s participation or that the minors are less likely to cooperate? I suggest that the matter of participation in the AHS be aired through general media channels, as well as those with an Indigenous focus, such as “Living Black” (SBS television) and Imparja television, and through local Indigenous radio stations and community networks. With a developed sampling frame for Indigenous people, dialogue about elements of the examination should at least be conducted with the specific individual tribal groups or communities, if not with the targeted individuals (the preferred option). Subsequently, the whole issue of representation to policymakers in Indigenous health matters might be re-examined on a national basis.

Wendy E Hoy

To the Editor: Although Indigenous males are twice as likely and Indigenous females are half as likely to report being diagnosed with osteoporosis compared with their non-Indigenous counterparts,1 data on the interracial differences in osteoporotic risk factors are limited. Our study of 276 patients attending a tertiary hip fracture unit in Western Australia over a 5-year period is the first to report differences in common risk factors for hip fracture between Indigenous and non-Indigenous patients. Our data showed a lower likelihood of vitamin D deficiency and polypharmacy but higher likelihood of diabetes mellitus, renal disease and alcohol use among Indigenous patients with hip fracture compared with non-Indigenous patients. Using the local orthogeriatric database, we identified 46 Indigenous and 230 randomly selected non-Indigenous patients aged ≥ 45 years who were transferred to a hip fracture unit following surgery for a minimal-trauma fracture at Royal Perth Hospital from July 2005 to June 2010. High alcohol use was defined as alcohol intake exceeding guideline recommendations,2 and polypharmacy as the use of more than five medications. We used a laboratory cut-off of 25-hydroxyvitamin D (25-OHD) < 50 nmol/L to indicate a low vitamin D level. Indigenous status was self-reported during admission. We compared data for Indigenous and non-Indigenous patients using the Mann–Whitney U and Pearson χ2 tests. We used logistic regression (SPSS version 17; SPSS Inc, Chicago, Ill, USA) to examine the association between Indigenous status and the predictor variables. Our study was exempted as a quality assurance activity from formal ethics review by the Royal Perth Hospital Ethics Review Committee and the Western Australian Aboriginal Health Information and Ethics Committee. Risk factors among the two groups are shown in the Box. The most common risk factors among Indigenous patients were antihypertensive use, high alcohol use and diabetes. In the final multivariate model, Indigenous patients with hip fracture were significantly more likely to have diabetes and renal disease and to report high alcohol use, but significantly less likely to have a low vitamin D level and polypharmacy, after adjustment for age, sex and rural residency. These well described risk factors contribute to fracture risk through two mechanisms: falls and secondary osteoporosis. Diabetes-related complications such as visual impairment, stroke and peripheral neuropathy can increase fracture risk.3 In renal dysfunction, osteoporosis is related to cortical thinning and uraemic osteodystrophy.4 Excessive alcohol intake at a young age among Indigenous people may affect peak bone mass.5 The effect of alcohol on liver cirrhosis, cognition, falls due to intoxication and peripheral neuropathy may contribute to fracture risk. Risk stratification will be more robust if these results can be cross-validated in other institutions. Associations between hip fracture and risk factors in Indigenous patients compared with non-Indigenous patients at Royal Perth hospital, July 2005 – June 2010 Variable Indigenous (n = 46) Non-Indigenous (n = 230) P* Crude OR Adjusted† OR (95% CI) Continuous (mean [SD]) Age at hip fracture‡ (years) 81.4 (9.1) 82.3 (9.4) 0.58 0.99 1.03 (0.96–1.10) 25-OHD level (nmol/L) 59.9 (30.2) 40.9 (18.6) < 0.001 – – Categorical (no. [%]) Women 29 (63%) 161 (70%) 0.35 1.11 2.52 (0.51–12.31) Non-metropolitan 42 (93.3%) 38 (16.6%) < 0.001 70.37 70.32 (14.43–342.59) Low vitamin D level§ 15 (38.5%) 142 (69.6%) < 0.001 0.27 0.26 (0.07–0.91) Prior fracture 9 (19.6%) 52 (22.6%) 0.65 0.83 0.42 (0.09–1.90) High alcohol use¶ 19 (41.3%) 10 (4.3%) < 0.001 15.5 13.25 (1.89–92.92) Diabetes mellitus 21 (45.7%) 41 (17.8%) < 0.001 3.87 8.19 (2.02–33.18) Renal disease 16 (34.8%) 21 (9.1%) < 0.001 5.31 6.12 (1.29–29.05) Polypharmacy** 18 (39.1%) 137 (59.6%) 0.01 0.44 0.17 (0.04–0.72) Antihypertensive use 26 (56.5%) 118 (51.3%) 0.52 1.23 2.75 (0.70–10.76) 25-OHD = 25-hydroxyvitamin D. OR = odds ratio. * Mann-Whitney U or Pearson χ2 test. Level of significance: P < 0.05. † Multivariate logistic regression. ‡ Minimal-trauma fracture. § 25-OHD level < 50 nmol/L. ¶ Alcohol intake exceeding guideline recommendations.2 ** > 5 drugs.

Michelle M Y Lai · Nicholas G Waldron

Child care improves behaviour Postnatal depression is known to have adverse consequences for children’s development, but less is known about the effects of maternal depression during toddlerhood. New Australian research used data from a longitudinal cohort study to follow 438 mothers and their children from birth to age 5. The researchers found that recurrent maternal depression when children were aged 2 and 3 was associated with child behaviour problems at age 5. However, as little as half a day of formal child care at the age of 2 quashed the effects of the maternal depression. Informal child care did not produce the same benefits. The researchers suggest that child care may be one way of buffering the effects of recurrent maternal depression. “A modest amount of formal child care for toddlers of depressed mothers is a simple strategy that may have benefits for affected mothers and their children”, the researchers conclude. Pediatrics 2011; 128: e78-e84 Randomised controlled back-pedalling It’s not just politicians who change their mind, according to an analysis of 1 year’s worth of research papers which were published in the New England Journal of Medicine (NEJM). The researchers examined the frequency of “medical reversals”, which they defined as a phenomenon where a new trial — superior to predecessors because of better design, increased power, or more appropriate controls — contradicts current clinical practice. Out of the 212 original articles published in the NEJM in 2009, 124 (58%) made some claim about a clinical practice. Of these, 16 articles (13%) were classified as medical reversals. Medical reversals applied to medical therapies, invasive procedures and screening tests. The authors argue that further study of medical reversals is “necessary and of profound importance”. Arch Intern Med 2011; 11 July (online) NO benefit from Invasive cystic fibrosis test In kids with cystic fibrosis (CF), early pulmonary infection, particularly with Pseudomonas aeruginosa, leads to increased morbidity and mortality. However, it is difficult to detect infection in non-expectorating patients. Oropharyngeal cultures are used widely, despite concerns over their diagnostic accuracy. An alternative test is the bronchoalveolar lavage (BAL), which involves inserting fluid into the lungs under general anaesthetic, and then re-collecting the fluid for examination. Australian researchers randomly allocated 170 infants with CF to either BAL-directed or standard therapy, and followed each child for 5 years. Children in the BAL-directed group underwent BAL before age 6 months when well, when hospitalised for pulmonary exacerbations and if P. aeruginosa was detected. Treatment was prescribed according to the BAL or culture results. At 5 years, infants who underwent the invasive BAL test did not have a lower prevalence of infection with P. aeruginosa or structural lung injury. The test was also linked with mild adverse events, such as worsening of cough. “This study highlights the importance of examining diagnostic and management interventions using appropriately designed randomized controlled trials in a clinical practice setting”, the researchers wrote. JAMA 2011; 306: 163-171 Children inherit battle scars The mental health problems linked to military deployment don’t stop with the military personnel themselves. Previous research has shown that spouses are also affected, and a new study finds that parental deployment takes a mental health toll on children. The US study of more than 300 000 children of military personnel found that those whose parents were deployed to Iraq or Afghanistan were more likely to be diagnosed with a mental illness. The most common diagnoses were for acute stress reaction and adjustment disorders, depressive disorders and behavioural disorders. The researchers also identified a dose-response pattern, such that longer deployment was linked to worse mental health outcomes among children. The analysis determined that an extra 6579 mental health diagnoses among the children were attributable to parental deployment. Arch Pediatr Adolesc Med 2011; 4 July (online) For better or for worse New research adds to our understanding of why marriage seems to decrease the risk of dying from cardiovascular disease. The Canadian study of 4400 patients found that men who were experiencing chest pain due to acute myocardial infarction presented to an emergency department or hospital earlier if they were married or in a de facto relationship than if they were single. The benefit of marriage was not observed for women. The researchers hypothesised that spouses may encourage earlier pursuit of medical care, either directly or indirectly, and that wives may be more likely to assume this caregiver role. CMAJ 2011; 18 July (online)

Sophie McNamara

Med J Aust 2011; 195 (3 Suppl).