Letters

To the Editor: The work presented by Chew and colleagues in setting up and using the Acute Coronary Syndrome Prospective Audit (ACACIA) is an important and influential initiative.1 It has the potential to provide a strong evidence base for the design and delivery of cardiac services in Australia. Their article and the accompanying editorial by Scott2 highlighted the difficulty in determining treatment benefit from uncontrolled observational studies. Among the unreported and possibly significant confounders underpinning the association between acute invasive care and the 47% improved 12-month survival in patients treated for acute coronary syndrome is participation in post-event secondary-prevention cardiac rehabilitation. A contemporary systematic review of randomised controlled trials of cardiac rehabilitation reported a significant relative risk reduction in all-cause mortality of 20% (95% CI, 7%–32%) over a median follow-up of 12 months.3 Despite this evidence and the long-term policy of the World Health Organization that cardiac rehabilitation should be available to all patients with cardiovascular disease,4 this secondary-prevention intervention is largely underused, and those who do attend are generally at lower risk of recurrent coronary events than those who do not.5 Further, secondary-prevention cardiac-rehabilitation programs are cost-effective relative to other coronary interventions6 and, along with proven cardioprotective pharmacotherapy and acute invasive care, should be given priority as part of an optimal treatment and management strategy for secondary prevention. The completion of cardiac rehabilitation or other forms of secondary prevention by ACACIA patients may have favourably impacted upon the marked improvement in 12-month survival seen in the ACACIA cohort. Chew and colleagues identified the fact that patients who underwent invasive therapies were also more likely to be treated according to best-practice guidelines.1 It may be that this same group were also more likely to be referred to cardiac-rehabilitation and secondary-prevention programs. It would be of great interest to know if attendance in cardiac-rehabilitation and secondary-prevention programs was recorded in the ACACIA registry and, if so, why those results were not incorporated.

Leigh D Kinsman · Julie Redfern · Tom G Briffa

In reply: It is often hoped that clinical studies can be “all things to all people”. Yet, in reality, clinical registries are optimally designed to answer a limited number of questions such as use of therapies, current treatment, and reassurance (but not proof) of treatment effectiveness. We decided not to collect data on referral to cardiac rehabilitation in our registry.1 In arriving at this decision, we were cognisant of the fact that, important to exploring the benefits or confounding effects of therapies is the ability to define the intervention accurately, and then adjust for the baseline differences between patients receiving and not receiving such treatment. This is problematic when considering “referral to cardiac rehabilitation”. How should cardiac rehabilitation (inhospital, outpatient, single-day, multi-day programs) be defined? Should one assess referral or attendance (partial or complete)? While the value of rehabilitation is well appreciated, it was not the focus of our study. We are designing future observational studies in this area with more focus on the later phase of patients’ admissions and their posthospital management, including rehabilitation. As we cautioned, the magnitude of benefit associated with invasive management in our study should not be overinterpreted. At best, these studies contribute to the totality of evidence, and offer insights into those patients not currently receiving the benefits of our rich evidence base.

Derek P Chew · John V Amerena · Steve G Coverdale · Jamie M Rankin · Carolyn M Astley · Ashish Soman · David B Brieger

To the Editor: Scott was correct in his recent article to emphasise the need for an Australian registry for percutaneous coronary interventions (PCIs).1 To that end, we report an initiative developed by a voluntary collaborative group of interventional cardiologists in Victoria — the Melbourne Interventional Group (MIG) — which has provided a significant volume of contemporary data on the efficacy and safety of PCI.2 Since July 2004, data on over 9500 coronary interventional procedures in over 7500 patients have been collected into this registry, using data elements and methods based on those of the United States National Cardiac Disease Registry and the Victorian Cardiothoracic Surgical Database.3,4 Methods for data collection and analysis, and the format of data forms have been published.5 The data elements, developed by an MIG working group, have been peer reviewed and are currently under review for publication. MIG has a formal governance structure with a constitution, steering committee and subcommittees that govern data quality, database development, research, publication and funding. Approval for the conduct of the registry has been obtained from the ethics committees of all participating hospitals; all patients enrolled provide informed consent for initial and long-term data collection in a manner similar to that used for the Victorian Cardiothoracic Surgical Database.3 Results from MIG to date show that PCI practice differs between Australia and the US, and that use of drug-eluting stents (DES) is safe and effective in reducing restenosis in patients with appropriate indications, leading to a DES usage rate of 30% in public hospitals.2 The MIG registry may provide an appropriate framework for a national PCI data registry. It satisfies most of Scott’s criteria, and many colleagues in other states have expressed interest in collecting similar data or collaborating in a joint registry. The limiting factor, as always, is funding. We join Scott in supporting the call for appropriate funding to be provided by government and professional societies to allow a national PCI registry to be established.

Christopher M Reid · Andrew E Ajani · David Eccleston

To the Editor: We read with great interest the case report by Barthwal and Herman,1 and agree with many of the points they raise. In-stent thrombosis after cessation of clopidogrel therapy in patients with drug-eluting stents (DES) is a significant problem in Australian medical practice, particularly in the perioperative period,2-4 as the case report by Barthwal and Herman confirms.1 It is often decided to cease clopidogrel therapy during the perioperative period to reduce the risk of bleeding. While clopidogrel given before cardiac surgery has been documented to increase transfusion rates and returns to the operating theatre,5 bleeding risk associated with clopidogrel and non-cardiac surgery remains poorly defined. Greater understanding of the risk of in-stent thrombosis after clopidogrel therapy withdrawal, and the risk of excessive bleeding if it is continued, in individual patients will provide rational perioperative planning and, hopefully, improved outcomes for our patients. Currently, the Cardiac Society of Australia and New Zealand has formed a multidisciplinary committee to create guidelines for the perioperative management of patients with coronary stents. In some instances, clopidogrel therapy may need to be replaced with alternative antithrombotic strategies to prevent in-stent thrombosis. We have proposed such a strategy, with excellent results so far.3,4 The complication of in-stent thrombosis was originally associated with a 50% mortality rate in the first series of cases reported.2 However, we have since reported three patients from Australia with in-stent thrombosis during the perioperative period, all of whom survived.4 We have set up a website (http://www. DESReporting.com) to enable clinicians worldwide to report perioperative management strategies and outcomes for patients with DES in their coronary arteries, and who undergo surgery.3,4 In view of the developing importance of perioperative late stent thrombosis, we strongly encourage reporting through this website. This will enable rapid accumulation of outcomes and associated antithrombotic strategies, with a view to dissemination and publication of the analysed data.

Myles M Conroy · Stephen N C Bolsin

To the Editor: The recent article by Barthwal and Herman highlights the problem of late stent thrombosis in a patient with a drug-eluting stent (DES) undergoing non-cardiac surgery (NCS).1 While the authors stated that clopidogrel therapy was ceased preoperatively and not restarted postoperatively, they did not say whether or not aspirin therapy was continued. In addition, emphasis was not placed on the role the surgical procedure played in this adverse cardiac outcome. Perioperative stent thrombosis as a result of discontinuation of dual antiplatelet therapy has been well described, to such an extent that the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association issued a joint advisory regarding the risk of premature cessation of dual antiplatelet therapy perioperatively.2 A prothrombotic state is well described in the perioperative period, as is a rebound hypercoagulable period following cessation of therapy with antiplatelet agents.3 Preoperative cessation of antiplatelet therapy by interventional teams is common in both routine and emergency procedures; this is sometimes unnecessary and not based on any evidence. Practitioners involved in ceasing antiplatelet therapy for procedures should be aware of the increased risk of major adverse cardiac events in patients with cardiac stents whose antiplatelet therapy is ceased prematurely.2 Duration of antiplatelet therapy following DES implantation is still a contentious issue, but the prothrombotic effect of NCS in addition to the baseline risk of late stent thrombosis in these patients is becoming less easy to ignore.4 Evidence-based guidelines for the perioperative management of patients with cardiac stents undergoing NCS are still to be established. Careful consideration should be given before perioperative cessation of therapy with antiplatelet agents in patients with coronary stents. Undertaking non-emergency surgery within 12 months of DES implantation should be avoided if possible.4,5

Simon J Pattullo · Rohan Jayasinghe

To the Editor: We question the conclusions drawn by Canfell and colleagues1 from their analysis of trends in hormone replacement therapy (HRT) prevalence and breast cancer incidence for Australian women aged 50 years or older. Their ecological analysis lacks individual-level information on HRT use and information on tumour oestrogen receptor (ER) status, and captures only 2 years following the decline in HRT prevalence. This is an inadequate design within which to judge issues of causality; it is at best an hypothesis-generating exercise.2 The examination of only 2 years of breast cancer incidence after the decline in HRT use is unsound because of substantial unexplained annual variability in national breast cancer incidence. This is evidenced, for example, by the graph in Canfell et al’s Box 2, which identifies a fall in 1998–1999 that was not ascribed to changes in HRT prevalence. The lack of data on tumour ER status is another weakness. HRT use increases the risk of ER+ tumours, so any decline in HRT prevalence would be expected specifically to reduce ER+ tumour incidence. We analysed Victorian Cancer Registry data for women aged 50 years or older for the period 2001–2005 — 2 years past the cut-off in Canfell et al’s analysis. Tumour ER status was available for 87% of breast cancer cases in 2001, rising to 90% in 2005. The demographic characteristics of the women for whom these data were available did not change between 2001 and 2005. Over this period, the proportion of all breast cancers that were ER+ increased from 65% to 71%, and the proportion of tumours with known ER status that were ER+ increased from 74% to 79%. Poisson regression analysis of the age-specific incidence rates for both total and ER+ breast cancer for women aged 50 years or older estimated an average annual decline of 1.7% in the total incidence rate (P = 0.0009) and an annual increase of 0.2% in the ER+ incidence rate (P = 0.7). Our findings are illustrated in the Box. Although there was an apparent small decline in total breast cancer incidence in 2001–2003, this trend was reversed in 2004–2005. More importantly, the trend in ER+ tumour incidence was stable across the entire period. Age-standardised incidence* of invasive breast cancer in women in Victoria aged ≥ 50 years, 2000–2005 Vertical bars represent 95% confidence intervals. ER+ = oestrogen receptor-positive. * Standardised to World Standard Population. These Victorian trends, covering a longer time period and including information on the tumour type most likely to be affected by changes in HRT use, provide no support for the hypothesis of Canfell and colleagues.

Graham G Giles · Richard Bell · Helen Farrugia · Vicky Thursfield

In reply: In saying that our work on the effect of hormone replacement therapy (HRT) on the development of breast cancer is “at best an hypothesis-generating exercise”, Giles and colleagues ignore both the preceding literature and the fact that our analysis of Australian data explicitly tested the hypothesis raised by an analysis of United States data. Both the US and Australian analyses showed falling breast cancer incidence from 2001 in women aged ≥ 50 years, but not in younger women, following large reductions in HRT use.1,2 The logic, methodology and statistics presented by Giles et al are unsound. They present data on incident breast cancers for women in Victoria only, a subset of the national data included in our analysis. Not only is it invalid to use a subset of data to retest a hypothesis previously tested on the larger dataset (unless complex statistics are applied3-5), but Giles et al misrepresent Victorian trends. It is clear that in Victorian women aged ≥ 50 years, breast cancer incidence rates fell substantially and significantly by 11.5% between 2001 and 2003 (95% CI, 6.0%–16.6%; P < 0.0001), with no significant change among women aged 20–49 years (P = 0.3) (Box). Giles et al present no data on HRT use. The largest drop in HRT use in Australia occurred between 2001 and 2003, and thereafter use began to plateau.6 It is therefore statistically inappropriate to calculate an “average annual decline” in breast cancer incidence from 2001 to 2005 because changes in HRT use over this time were not linear. In addition, their claim that the “trend was reversed in 2004–2005” is not supported by statistical testing, which shows no significant change in breast cancer incidence in women aged ≥ 50 years in Victoria from 2003 to 2005 (P = 0.4). US data showed that the fall in breast cancer incidence following the drop in HRT use was seen particularly in oestrogen receptor-positive (ER+) tumours.1 As we pointed out,2 the lack of reliable Australian data on ER status means that no conclusions can be drawn about Australian trends in ER+ tumours. Giles et al acknowledge that the Victorian ER data are incomplete and that the completeness has increased over time. This, together with the possibility of differential ascertainment of ER status in women who used HRT over the period of interest, render the trends they present on ER+ breast cancers uninterpretable. Overall, trends in breast cancer incidence in the subgroup of Victorian women cannot be said to differ materially from the national trends. A recent editorial in the Lancet draws attention to the fact that trends in HRT use and breast cancer incidence similar to those we reported have now been observed in many countries.7 The Australian findings add to the accumulating worldwide evidence that, in settings where HRT use was common and breast cancer screening rates relatively stable, a rapid decline in HRT use after 2001 was followed by a fall in breast cancer incidence. Age-standardised incidence* of invasive breast cancer in women in Victoria, 1996–2005 Vertical bars represent 95% confidence intervals. Vertical dotted line indicates commencement of the period over which there was a hypothesised decrease in breast cancer incidence in women aged ≥ 50 years but not in women aged < 50 years. * Standardised to the Australian 2001 population.

Karen Canfell · Emily Banks · Mark Clements · Yoon J Kang · Valerie Beral

To the Editor: There can be little disagreement with Richmond’s assessment that Australia needs more research on the oldest old.1 Certainly, data on centenarians are sparse and unreliable, and there is a need for more thorough and more informed evaluation. The 2006 census was the first recent census to record centenarians’ ages. The 2001 census recorded ages to “100 +”,2 while previous censuses had recorded ages to “99 +”.3 Pre-2006 centenarian percentage age distributions are non-validated “guestimates”.4 Further, the number of centenarians enumerated is questionable5 because of its dependence on age reporting, which suffers inaccuracies from proxy reporting, age exaggeration and rounding. Adjusted population estimates for mid 2007 include 2832 centenarians6 — considerably lower than the 2006 count of 3154 quoted by Richmond.1 Errors in centenarian numbers mean that census tabulations of centenarians’ characteristics (marital status, living arrangements) and derived demographic measures (sex ratios, growth rates) are unreliable. Mortality estimates are also affected. Alternative data, collected through administrative sources or special studies that verify birth and death dates, are needed to reliably estimate mortality in the oldest old and the probability of survival to 100 years and beyond. Richmond’s discussion of the “fastest growing age segment” does not make a clear distinction between growth in the proportion of the population who are centenarians and growth in the number of centenarians. Growth of centenarians as a proportion of total population depends on population structure. Relatively recent fertility declines will have had a similar effect on the proportion of the population aged 60–99 years as on centenarians. Reductions in infant, child and maternal mortality serve to increase the proportion of people who are in younger age groups and thus reduce the proportion who are centenarians. The recent rapid increase in the centenarian proportion is actually the combined effect of larger cohorts reaching old age and increased survival at older ages.7 In Australia, past migration is a major determinant of the relative size of different cohorts. Comparing the cohort aged 100–104 years in 2001 with the cohort of the same age in 2006 (the younger), births data show there were 11 300 more people at birth in the younger cohort.8 Large fluctuations in the difference between the sizes of these cohorts in the age range 25–84 years (from 20 100 to 43 300), calculated from successive population age distributions,9 demonstrate the influence of migration on relative cohort size. Whatever the effects of recent changes in fertility and mortality, historical determinants of population structure significantly influence the number of centenarians from one census date to the next. Two further factors apply to growth in numbers: first, it is easy to achieve a high growth rate for a small group, and second, the 100+ age interval is expanding (whereas younger age groups are of fixed width).

Heather Booth

To the Editor: The pattern of invasive pneumococcal disease (IPD) in Western Australia varies from that described in northern Queensland in a recent article by Hanna and colleagues.1 Their study showed a decline in IPD caused by serotypes included in the 7-valent pneumococcal conjugate vaccine (7vPCV) among Indigenous children and adults after the introduction of the vaccine in north Queensland. Over the same period, there was an increase among Indigenous adults in cases of IPD caused by serotypes not covered by the vaccine. However, the authors reported that there had been no increase in IPD caused by serotype 19A, a non-7vPCV serotype that has been increasingly predominant in other populations.2,3 In contrast to the disease pattern in north Queensland, serotype 19A has become the predominant disease-causing serotype in Western Australia, particularly among non-Indigenous people. Data from the WA Notifiable Infectious Diseases Database show that the incidence of IPD in WA fell from 10.7/100 000 in 2001 (n = 203) to 6.3/100 000 in 2007 (n = 132). In children aged < 5 years, there was a significant drop in overall IPD rate, attributable to the decline in disease caused by 7vPCV serotypes, among both Indigenous children (from 70/100 000 to zero) and non-Indigenous children (from 50/100 000 to 1.6/100 000) (Box). The rate of IPD caused by 7vPCV serotypes also declined among Indigenous and non-Indigenous adults, suggesting a herd immunity effect. From 2001 to 2007, the proportion of IPD cases caused by non-7vPCV serotypes increased among children aged < 5 years (from 19% to 91%) and children ≥ 5 years (from 33% to 72%). Serotype 19A was the only serotype that became more predominant, being responsible for 11 (8%), 14 (10%) and 26 (20%) cases of ICD in 2005, 2006 and 2007, respectively. In 2001, it accounted for 2.5% of cases in children < 5 years (1.6/100 000) and 0.8% of cases in children ≥ 5 years (0.1/100 000). By 2007, these figures had increased significantly to 34% of cases in children < 5 years (7.8/100 000) and 25% of cases in children ≥ 5 years (0.8/100 000). Interestingly, the increase in serotype 19A cases was seen only in non-Indigenous people (particularly children), with the number of cases remaining stable among Indigenous adults and children. Although numerous reports describe increasing prevalence of penicillin-resistant 19A strains,3,4 none of the WA isolates were penicillin-resistant. In summary, after the introduction of the 7vPCV, the rate of IPD caused by 7vPCV serotypes decreased significantly in WA. However, the rate of IPD caused by serotype 19A, a non-7vPCV serotype, increased in non-Indigenous people and in the population overall. These early trends have significant public health implications for vaccine policy. State and territory vaccination programs exist within the framework of the national immunisation program. However, jurisdictional expert advisory groups need local ongoing post-marketing surveillance, coupled with an understanding of historical trends and emerging serotypes, when formulating vaccine recommendations for their populations. Incidence of invasive pneumococcal disease (IPD) caused by serotypes included in the 7-valent pneumococcal conjugate vaccine (7vPCV), by age group and Indigenous status, Western Australia, 2001–2007 * The 7vPCV was funded for Indigenous children from July 2001 and for all Australian children from January 2005.

Carolien M Giele · Anthony D Keil · Deborah Lehmann · Paul G Van Buynder

To the Editor: Needlestick injuries are inevitable during surgery, particularly if operating hurriedly by “feel” in blood-obscured fields, such as in Caesarean sections. The risks associated with these injuries were accentuated by the advent of the HIV pandemic. While working in rural Zimbabwe, an article describing Betadine inactivating HIV in an infected cell culture, with the cells surviving, triggered my interest.1 Betadine (Mundipharma, Basel, Switzerland) is povidone–iodine. Povidone is a polymer — polyvinylpyrrolidone, (C6H9NO)n — with many applications, including past usage as a plasma expander. It is hypoallergenic, has lubricating properties, and forms a loose chemical combination (iodophore) with iodine up to about a 10th of its weight.2 Therefore, a 10% solution of Betadine contains about 1% iodine. The iodophore is usually non-staining, although the iodine retains its chemical properties, such as turning starch dark blue. Povidone–iodine is a powerful antiseptic that kills Staphylococcus aureus and saprophyticus, Streptococcus pyogenes and pneumoniae, Neisseria gonorrhoea, Haemophilus vaginalis, Candida albicans and Trichomonas vaginalis within 30 seconds of contact, and Clostridium tetani spores in 30 minutes.2 In also destroying HIV,1 it may thus be regarded as a self-sterilising solution. Betadine can be applied as a simple protectant in surgical gloves. Before donning, 5–10 mL of Betadine are poured into each glove, with the operator inserting his or her hand and massaging the solution around, up to the gusset, ensuring the digits are liberally coated. Digital sensitivity is unaffected. Betadine’s brown colour (blue-black if the gloves were starch-dusted) makes its presence apparent through the semitransparent latex, and any glove perforation is evident by leakage of the solution (Box, A). Although licensed for topical application only, Betadine has for many years been used internally, as in peritoneal douching, so minor leakage from the gloves into body cavities would be of little consequence. On glove removal after prolonged operating, the skin surfaces of the operator’s hands are stained dark brown by the iodine, except, strangely, the dorsal aspect of the thenar muscles, seemingly because the hotter working digits cause exothermic deliquescence (Box, B). This stain is easily washed off, except for discolouration of the nails, which can be removed with scraping or will otherwise disappear in a day or so as the iodine sublimates. Although this technique needs formal evaluation, using Betadine in surgical gloves has several advantages: It is hypoallergenic, inexpensive, readily available and easy to apply. It provides a powerful additional protective barrier to needlestick injury infection transmission from patient to surgeon and vice versa. It can be used as an adjunct to “scrubbing up”, increasing surgical sterility. It obviates clumsy double gloving, pre-gloving hand drying, and dusting with fibromata-inducing talcs. It has an obvious presence that is psychologically reassuring. Glove perforations are easily detectable, allowing rapid intraoperative re-gloving. Betadine solution in surgical gloves A: Note evidence of a small perforation in the glove over the right thumb. B: Postoperative digital iodine staining, with probable heat-induced deliquescence sparing the thumbs and index fingers despite their being awash with Betadine.

George D S Turner

To the Editor: Petrie and colleagues alert us to some negative effects of “appearance medicine” television programs.1 I agree that participants in television programs on cosmetic surgery should not be induced to have surgery by the offer of a significant reduction or waiving of the fee for the operation on the condition that they expose themselves before, during and after the procedures. Removing the cost component is a significant enticement to undergo cosmetic surgery. However, many procedures need to be repeated and implanted products replaced. If potential patients cannot afford future expenditure, they may be unsuitable for cosmetic surgery. The intense competition between providers of cosmetic surgery procedures leads them to seek media exposure — surgeons and non-surgeons jostle for supremacy and market share. Australian and New Zealand cosmetic surgery websites show a wide array of highly posed, seductive images that promise more than is likely to be possible. In New South Wales, a medical practice amendment on advertising regulation was introduced on 1 July 2008, to provide stricter regulation of “before and after” photographs targeted at patients considering cosmetic surgery.2 However, patients have the right to be informed. A survey, cited by Petrie et al, of first-time patients seeking plastic surgery revealed what I consider a positive side to appearance medicine television programs: patients who regularly viewed such programs believed themselves to be more knowledgeable about plastic surgery, and its issues and risks, than “low-intensity” viewers of such programs.3 The growth of cosmetic surgery has been phenomenal and will continue during the next decade. At present, it is unclear whether patients are enticed or merely educated by appearance medicine television programs. However, it is clear that they are more likely to be knowledgeable because of the information provided to them, and that the knowledge they gain may improve their ability to assess a surgeon’s capability and credibility.

Darryl J Hodgkinson

To the Editor: Type B insulin resistance is an uncommon syndrome characterised by abnormal glucose homeostasis (hypo- and/or hyperglycaemia), the presence of insulin receptor (IRec) autoantibodies, and intact IRec structure. It occurs mostly in African Americans, often with coexisting autoimmune disease.1 We report a case of type B insulin resistance with atypical features. A 44-year-old white male with a 22-year history of poorly controlled diabetes was referred to us with severe Graves ophthalmopathy. His home blood glucose levels ranged from 3.0 to 25.0 mmol/L (reference range [RR], 3.5–5.5 mmol/L) and he required over 800 units of insulin daily. His ophthalmic condition had been diagnosed 18 months earlier and had been observed until its recent deterioration into diplopia. Examination confirmed severe bilateral Graves ophthalmopathy, with 6/6 visual acuity bilaterally, and euthyroidism. Thyroid function tests showed the following levels: thyrotropin-stimulating antibody, 69 U/mL (RR, < 10 U/mL); thyroid-stimulating hormone, 2.3 mU/L (RR, 0.4–4.0 mU/L); and free tetraiodothyronine, 18.5 pmol/L (RR, 10.2–24.5 pmol/L). Routine biochemical and immunological studies were normal. Orbital magnetic resonance imaging showed marked ocular muscle hypertrophy and adipose tissue congestion, consistent with Graves ophthalmopathy. After 3 months of combination immunosuppressant therapy, the patient showed minimal improvement. In view of his diabetes, he was commenced on intravenous immunoglobulin rather than a glucocorticoid. Within 24 hours, he developed marked hypoglycaemia, with a glucose level of 2.1 mmol/L. Despite ceasing insulin treatment, the patient’s home blood glucose levels hovered between 4 and 6 mmol/L for the next 7–10 days. This continued until Day 14, when small doses of insulin were required, escalating to about 800 U/day before the next course of intravenous immunoglobulin. A clinical diagnosis of type B insulin resistance was made. The clinical picture suggested the presence of dual stimulating and blocking autoantibodies in the presence of structurally intact IRecs. At maximal insulin resistance, the IRec concentration is thought to be normal, but probably with reduced affinity. The blocking antibodies are believed to be polyclonal.2 The pathophysiology of the hypoglycaemic phase is unknown, but the antibodies would need to behave as IRec stimulators, possibly via partial agonism and increased IRec numbers.3 The mechanism of the selectivity of intravenous immunoglobulin therapy and its preferential removal of the inhibitory autoantibodies is yet to be unravelled. Proposed mechanisms include suppression of the inhibitory antibody activity and modulation of the immune system in favour of IRec-stimulating (hypoglycaemia-inducing) autoantibodies. Treatments include immunosuppression, plasmapheresis and rituximab therapy.4,5 As far as we are aware, the incidental but favourable response to intravenous immunoglobulin described here has not been previously observed. Our report highlights the atypical characteristics of this fascinating syndrome, including male sex, European ethnicity and a novel treatment modality.

Huy A Tran · Glenn E Reeves

To the Editor: A 50-year-old man presented with gynaecomastia and galactorrhoea, reporting diminished libido and energy over 12 months. Previous medical and psychiatric histories were unremarkable. The patient had a tender increase of the right breast tissue. His testes appeared normal. He had markedly elevated prolactin levels (410 μg/L; reference range [RR], < 15 μg/L) and decreased testosterone levels (5.6 nmol/L; RR, 10–33 nmol/L); results of other biochemical tests were unremarkable. Pituitary magnetic resonance imaging (MRI) showed a microadenoma. Cabergoline 0.5 mg twice weekly was commenced. One year later, the patient had normal prolactin (8 μg/L) and testosterone (14 nmol/L) levels. His libido and sexual function had improved — he claimed his “mates are envious”. MRI demonstrated no changes to the tumour. He was lost to follow-up. Five years after his last review, the patient re-presented with his estranged wife, who was concerned about changes to his behaviour after starting cabergoline. He had engaged in excessive casino and horse-racing gambling, resulting in financial losses (> $100 000), and excessive libido had led to hypersexual activities and divorce proceedings. His prolactin levels were normal (10 μg/L), but testosterone levels were low (8 nmol/L). Cabergoline was ceased. On review 3 months later, the patient’s change in behaviour was dramatic. All gambling and hypersexuality issues had ceased, and divorce proceedings were on hold. His prolactin levels had increased (78 μg/L); testosterone levels were unchanged (8 nmol/L). No changes were seen on MRI. Pathological gambling has been reported in patients with Parkinson’s disease who take dopamine agonists — particularly pramipexole but also cabergoline (4.5% of published cases).1 Most were also prescribed levodopa.1 A minority had concomitant hypersexuality.1 The prevalence of pathological gambling in patients with Parkinson’s disease has been estimated at 6.1%, compared with 0.25% in age- and sex-matched controls.2 There has been one published case report of pathological gambling (but not hypersexuality) following use of a dopamine agonist (cabergoline 0.25 mg weekly) for prolactinoma.3 However, the dose of cabergoline normally used in Parkinson’s disease is higher (0.5–6 mg/day).4 Normalising prolactin levels usually leads to increased libido and vitality, but not pathological gambling and hypersexuality. Our patient had not engaged in these activities before commencing cabergoline, and there was no personal or family history of psychiatric illness. Moreover, his testosterone concentrations during treatment ranged from low to low–normal, never high. His Naranjo score was 6, indicating a “probable” adverse drug reaction.5 No reduction in tumour size was seen, raising the question of a partial non-functioning pituitary adenoma. Cabergoline-induced pathological gambling and hypersexuality are probably under-reported, and physicians should consider screening for these in patients treated with dopamine agonists.

Henrik Falhammar · Jennifer Y Yarker

To the Editor: A 77-year-old woman with a history of idiopathic long-QT syndrome (presumed genetic) presented to hospital with a storm of defibrillator shocks from her implantable cardioverter defibrillator (ICD). She had a single-chamber Guidant Ventak Prizm VR, model 1850, and a Guidant ventricular lead, model 0148 (Guidant Corporation, Indianapolis, Ind, USA) implanted 12 months earlier after an episode of syncope. The lead had been implanted by left subclavian venous access. The patient’s postoperative course and responses to routine questioning indicated that the device was functioning normally. After presenting with device discharges, a 12-lead electrocardiogram showed oversensing suggestive of lead dysfunction. Stored electrograms from the defibrillator showed artifactual signals that were typical of lead disruption. These signals had triggered inappropriate detection of ventricular arrhythmia and subsequent device shocks (Box 1). The pacing threshold and lead impedance were normal. On close examination of the patient’s chest x-ray, a line of radiolucency was detected within the lead between the first rib and clavicle. At reoperation, the lead was extracted with minimum difficulty and the site of the insulation break was detected (Box 2). A new lead was implanted and the patient was discharged home well. Subsequent follow-up was uneventful. Lead failure can occur any time after implantation of an ICD, and should be suspected when patients present with inappropriate ICD discharges.1 This case illustrates oversensing as a result of the lead’s insulation being disrupted by crush compression between the first rib and clavicle. Alternative implantation techniques, such as cephalic vein cut-down or extrathoracic axillary vein puncture, have been suggested for venous access to avoid this complication.2 1 Stored electrograms from the patient’s implantable cardioverter defibrillator showed artifactual signals had triggered inappropriate detection of ventricular arrhythmia and subsequent device shocks (arrow) 2 Implantable cardioverter defibrillator lead after extraction showing the break in the insulation (arrow)

Chin V Hiew · James W Leitch

To the Editor: Accidental ingestion of foreign bodies is common in children. Most pass through the gastrointestinal tract spontaneously,1 but some, such as magnets and batteries, can cause serious problems. We treated three children, aged 4–11 years, who ingested magnets that caused multiple bowel perforations. All three children presented with abdominal pain and vomiting, and were initially treated for gastroenteritis as the history of ingestion was not available. Plain abdominal films were subsequently used to make the diagnosis of foreign body ingestion. The ingested objects were later found to be pieces from magnetic construction toy sets. The first patient was an 11-year-old child with autism. An initial laparoscopy revealed marked dilatation of the small bowel and interloop adhesions. Subsequent laparotomy revealed several magnets (rods, rings and balls) in adjacent loops of the small bowel (Box, A), as well as necrosis and 13 perforations of the small bowel. Segmental resection was performed with a defunctioning ileostomy. During surgery, radiography was performed to ensure that all foreign bodies were removed before closure of the abdomen. The child made a good recovery, and the ileostomy was closed 3 weeks later. The second patient was 4 years of age. An abdominal x-ray revealed a cluster of foreign bodies in the right lower quadrant of the abdomen, with a small gap between the fourth and fifth foreign bodies. A laparoscopy revealed a cluster of magnetic rings (Box, B) perforating the small bowel and the caecum. Two of the rings were on the caecal side and four were on the small bowel side, with an intervening fold of mesentery — the gap on the x-ray. The magnets were retrieved through a minilaparotomy, and the caecal perforation was oversewn. The third patient was a 5-year-old who presented with similar symptoms and x-ray findings. Laparotomy revealed an area of pressure necrosis underlying the magnet and causing perforation of the jejunum, which was repaired by segmental resection and primary anastomosis. As ingestion of foreign bodies is usually not witnessed, a high index of suspicion is required for correct diagnosis.2 Of confirmed cases, 50% of patients remain asymptomatic.3 Fewer than 10% of cases require intervention, and about 1% require surgery.4,5 Ingestion of multiple magnetic objects in children is particularly serious, because of their tendency to aggregate in the bowel and compress intervening tissue, and should be treated aggressively. These cases demonstrate the harmful consequences of magnets in toys. More stringent regulations on the use of magnets in toys — especially in toys for children younger than 5 years — and measures to increase public awareness of this issue are needed. Clusters of ingested magnets in children A: Magnets in loops of the small bowel. B: Magnetic rings perforating the small bowel and caecum, showing intervening fold of mesentery and bowel wall (arrow).

Manjunath B Siddaiah-Subramanya · Peter Borzi

To the Editor: The recent case report by Chow and colleagues raises questions about the causal link between black cohosh use and hepatotoxicity.1 The authors state that the patient had no history of “significant alcohol consumption”, but a presumably related adverse drug reaction report available from the Therapeutic Goods Administration reveals her alcohol use was “3–4 units [of] alcohol per day, [with] 1–2 alcohol-free days per week”.2 Alcohol misuse is a known risk factor for severe liver disease, as is gastric bypass surgery for obesity,3 also in the patient’s history. Unfortunately, because histological examination of the liver 6 weeks after first presentation found no recognisable residual hepatocytes, the diagnoses of alcoholic steatohepatitis, non-alcoholic fatty liver disease and non-alcoholic steatohepatitis cannot be excluded. Without this, the specific conclusion of the liver biopsy that the “Massive hepatocellular necrosis [was] associated with herbal medication”2 cannot be substantiated. The patient “was not taking any other medications, including other herbal preparations”, but the use of multivitamins was disclosed,2 without further information on ingredients, indication, dosage and duration of use. Notably, an overdose of vitamin A can cause severe liver disease. Finally, discontinuation of black cohosh failed to reduce the patient’s bilirubin levels, suggesting ongoing liver cell destruction by the as-yet unknown agent. Chow et al state “Extensive investigations to exclude other causes of acute liver failure gave negative results”.1 It is unclear whether rare liver diseases were excluded, notably herpes infection, which has been reported to cause severe herpetic hepatitis. Nor was polymerase chain reaction testing performed for hepatitis viruses. The authors mentioned other published case reports of hepatotoxicity potentially linked with black cohosh.1 A recent assessment of 42 cases by the European Medicines Agency (EMEA) concluded that most were insufficiently documented, or were otherwise inappropriate for analysis.4 A case in the United States initially described as “probable” (> 1000% of the recommended dosage of black cohosh), based on the report that the patient “did not drink alcohol or use illicit drugs and was not taking any medications”, was later corrected.5 The patient testified under oath that she drank wine regularly and used other drugs, and a US court judged there was no evidence to establish that black cohosh had caused her liver disease.6 There is no apparent credible evidence that black cohosh caused liver failure in the patient described by Chow et al.1 A daily alcohol consumption of 30–40 g should be considered principally in any causality assessment. In addition, idiopathic reasons, rare or unclear liver diseases, and other medications should be considered as possible causes. Even in patients with liver disease who consume little or no alcohol and have no exposure to other toxic agents, the cause of the disease remains unclear in up to 30%. In view of this, reliable and sufficient reporting of adverse drug reactions is a necessary precondition to any reliable assessment of causality.7

Belal Naser · Eckehard Liske

To the Editor: The case reported by Chow and colleagues of liver failure associated with the use of black cohosh1 requires comment regarding causality. The case has also been the subject of an adverse drug reaction report by the Therapeutic Goods Administration (TGA), and a possible causality has been proposed.2 At presentation on 23 May 2006, the patient was aged 50 years (TGA),2 not 51 as stated by Chow et al.1 Her bodyweight was 88 kg (TGA)2 after gastric bypass for obesity.1 She had been taking black cohosh (20 mg daily) intermittently for 3 years. The subsequent temporal course is essential for assessing causality. According to the TGA report,2 the patient increased the dose of black cohosh to 40 mg daily on 31 March 2006 and stopped taking it on 31 May 2006. The case report describes a 2-month history of lethargy, nausea and arthralgia,1 obviously reported at first presentation. Back calculation shows symptom onset around 23 March 2006. Thus, symptoms emerged 1 week before the dose increase, suggesting a lack of temporal, and hence causal, association. The patient had several risk factors for severe liver disease.1 Risky use of alcohol for women is defined as more than seven standard drinks per week or more than three drinks on a single occasion.3 The patient had a daily intake of 3–4 units of alcohol, with 1–2 alcohol free days per week (reported by the TGA),2 rendering her at some risk of alcoholic liver disease. Moreover, gastric bypass with partial resection reduces gastric mucosal alcohol dehydrogenase and consequent gastric ethanol metabolism. In combination with rapid gastric passage of alcohol into the jejunum, this leads to high blood ethanol concentrations, another risk factor for liver disease. Risk factors for possible non-alcoholic steatohepatitis and cirrhosis are obesity and gastric bypass. Other causes were not excluded, including Wilson’s disease (by 24 h urinary copper measurement), hepatitis E, herpetic liver disease and infection by varicella zoster virus, parvovirus B19, parainfluenza virus, adenovirus and cytomegalovirus (by assessing for a change in IgG titre after disappearance of IgM). The marked hepatic mononuclear infiltrate is compatible with some viral infections. Certainly, various herbal products may cause liver disease. A good example is kava,4 but not black cohosh.5,6 The European Medicines Agency examined 42 cases of liver disease with a suspected association with black cohosh, and found that only four patients had some grades of causality.5 Reassessment showed that two of these patients had herpetic hepatitis, one had autoimmune hepatitis, and the fourth was not assessable.6 Further studies are necessary to show clearly whether black cohosh is potentially hepatotoxic.

Rolf Teschke

In reply: Teschke questions the temporal sequence in our reported case1 by raising an ambiguity in dates. We wish to clarify: when the patient first presented on 23 May 2006, lethargy, arthralgia and nausea had been present for only about 3 weeks. This was well after the dose increase in black cohosh in March 2006. As such, the dose escalation definitely preceded the patient’s symptoms and liver failure. To further explore causality would require rechallenge with black cohosh, which we consider dangerous and unethical. Other unlikely causes of liver failure raised by Teschke, although theoretically possible, were not evident. The clinical course and histological findings in the pretransplant biopsy and explanted liver categorically excluded alcoholic cirrhosis and non-alcoholic steatohepatitis as causes of the liver failure. We also reiterate that there was no previous history of liver disease or other medication use. Increasing numbers of case reports are being published showing evidence of hepatotoxicity in patients taking black cohosh. Two well documented cases of seriously deranged liver function in patients taking black cohosh, which resolved on ceasing its use, have just been reported.2 Teschke concedes that four other cases have been reported where some causality between black cohosh and hepatotoxicity was evident.3 Neither Teschke nor Naser and Liske offer any reassurance on the long-term safety or lack of toxicity of black cohosh by referencing any properly conducted safety study. Certainly, there is recent in-vitro and in-vivo evidence in a rat model that black cohosh is toxic to hepatocyte mitochondria and impairs oxidative phosphorylation, resulting in apoptotic hepatocyte death.4 It is notable that, based on available evidence, the Australian Therapeutic Goods Administration requires preparations containing black cohosh to carry a warning of potential liver toxicity, stating that “there appears to be an association between the use of black cohosh and liver damage, but that it is very rare”.5 Furthermore, in the United Kingdom, the Medicines and Healthcare Products Regulatory Agency stated, “Warnings regarding rare adverse reactions in the liver should be added to the product information for black cohosh for both licensed and unlicensed products”.6 Government authorities in Europe3 and Canada7 have raised similar concerns. Long-term studies as well as further animal studies would be welcome in this area.

Elizabeth C-Y Chow · Marcus Teo · John A Ring · John W Chen

To the Editor: The article by Eley and colleagues clearly articulates challenges and solutions for providing quality undergraduate medical education in rural locations.1 Simulation-based education (SBE) also helps meet the challenge of providing quality rural medical education. Simulation is an ethical means of supporting the development of technical and non-technical skills relevant for safe and competent clinical practice. SBE can be used creatively to prepare, supplement and enhance rural clinical placements. Simulation is often used to support learning of clinical events that occur infrequently, such as medical emergencies. These simulations are immersive, placing the clinician in a scenario that reflects the physical, psychological and social fidelity of a real work environment. Similarly, immersive simulations can be used to acquire competence in common examination and procedural skills. Hybrid simulations include combinations of simulators (eg, benchtop models) and actors (simulated patients) in quasi-clinical environments.2 Simulation facilities are increasingly available in rural locations. In Victoria, Gippsland Medical School has a simulation centre with a range of clinical environments including reception, consulting rooms, a fully equipped ward and an emergency room. We provide graduate-entry medical students with an opportunity to develop clinical skills in simulation, aligning scenario complexity, content and context with their learning in real clinical settings. Scenarios are often based on real patients’ experiences, exploring more than just the technical skills the student is learning. Preliminary evaluation suggests this sequencing of skills development, authentic scenario creation and immersive simulations for commonly occurring clinical encounters maximises learning in real clinical settings. We have had strong local community engagement, evidenced by the easy recruitment of simulated patients and support from medical practitioners who teach our students in clinical settings. We are exploring a range of simulated rural clinical placement activities for the remaining years of the curriculum. We believe this approach will relieve some pressure on clinical placements, as students are well prepared to learn in such settings. Additionally, clinical nurse educators have taken on teaching roles in the simulation centre, relieving pressure on medical practitioners. There are limitations to SBE. Specialist facilities are required, teachers and actors need to be trained, and curricula need to be developed and evaluated. However, our experience locally, and the rapid growth of SBE internationally, suggest that this approach to delivering high-quality medical education has relevance in all settings.

Debra F Nestel · Robyn A Hill · George T Somers · Christopher A Browne

To the Editor: We read with interest the article by Griffin and colleagues,1 which provides valuable insight into the practice effects of coaching on medical school selection tests. As senior clinical students, we have watched with more than a passing interest the introduction and growing popularity of coaching courses in recent years. What was once regarded as a costly, unnecessary and potentially disadvantageous exercise has, in recent years, given rise to a flourishing industry. As the authors point out, alternative selection tests such as the Undergraduate Medicine and Health Sciences Admission Test (UMAT) and entry interviews were devised in part to overcome the socioeconomic bias associated with using matriculation results alone.2,3 Ironically, these overpriced coaching courses are often available only to those from higher socioeconomic backgrounds, jeopardising the equity of access that the tests aimed to improve. At many independent high schools, in fact, attendance at coaching courses is now often the norm, in contrast to schools from lower socioeconomic backgrounds. Many students now opt to undertake coaching for fear of “missing out” on what may potentially be an edge obtained by other prospective students. It is the psychological comfort provided to students that they have done some preparation that marketers of coaching courses have been exploiting, as evidenced by the finding from the Australian Medical Students’ Association Medical Education Survey in 2006 that 70% of students felt better prepared for the UMAT as a result of coaching.4 In light of this, data provided by Griffin and colleagues thus provides welcome reassurance that expensive coaching courses may provide little or no benefit in relation to UMAT or interview outcomes. Although their study reported a slight increase in interview scores on the second attempt at entry to medical school, what was not discussed by the authors was the students who undertake coaching before resitting either an interview or the UMAT. While they mention that a proportion of students resit the UMAT, there was also no discussion on the effect of simply repeating the UMAT. Further analysis of the effects of repetition and coaching on candidates who resit the UMAT or interview would circumvent the limitation of directly comparing coached and non-coached groups that are unlikely to be equivalent, given that coaching is voluntary and may be linked with personality, ability and socioeconomic factors. It would be interesting to observe what effect, if any, coaching might have had on these candidates’ results. This might provide further evidence in support of the authors’ findings.

Christopher X J Wong · Ross L Roberts-Thomson

To the Editor: In addition to its well established link with rickets and osteoporosis, vitamin D deficiency has been associated with increased risk of autoimmune, malignant and cardiovascular disease.1 Marginal deficiency occurs at serum 25-hydroxyvitamin D [25(OH)D] levels of 25–50 nmol/L and frank deficiency at levels < 25 nmol/L,2 but there is some evidence that levels < 80 nmol/L3 or even < 110 nmol/L2 could be suboptimal. In Australia, vitamin D deficiency is most frequent in nursing home residents, dark-skinned veiled women, and residents of southern latitudes.2 However, those who are instructed to habitually minimise sun exposure following a diagnosis of skin cancer may also be at particular risk. We recruited patients with a history of non-melanoma skin cancer, who were not taking vitamin D or calcium supplements, from outpatient dermatology clinics at Royal Prince Alfred Hospital, Sydney (latitude, 33° south). Ethics approval was obtained from the Sydney South West Area Health Service and University of Sydney ethics committees, and all participants provided written informed consent. Serum 25(OH)D levels were measured by radioimmunoassay (DiaSorin, Saluggia, Italy)4 in both late summer (February 2006 or 2007) and late winter (August 2006), with participants completing a 2-week diary detailing daily sun exposure and sunscreen application before each measurement. Twenty-five participants (12 men, 13 women; mean age, 64 years; range, 44–78 years) completed both assessments. We found a significant reduction in mean 25(OH)D levels in winter (summer, 69 ± 3.4 nmol/L; winter, 59 ± 6.2 nmol/L; P < 0.05). In summer, all but one participant had 25(OH)D levels > 50 nmol/L, and eight had levels > 80 nmol/L. In winter, 12 participants had 25(OH)D levels < 50 nmol/L, two had levels < 25 nmol/L, and only three had levels > 80 nmol/L (Box). Hence, using the accepted target value of 50 nmol/L,2 12 participants (48%) were vitamin D-deficient at the end of winter, compared with one (4%) at the end of summer. In summer, the mean reported daily sun exposure was 1 hour (range, 10 min–2.5 h), comprising 40 minutes of off-peak (before 11 am or after 3 pm) and 20 minutes of peak exposure. In winter, the mean daily exposure was also 1 hour (range, 20 min–1.5 h), comprising 30 minutes each of both peak and off-peak sunlight. Volunteers reported wearing sunscreen during about 50% of their summer sun exposure and 27% of their winter sun exposure. Despite mean reported daily sun exposure falling within recommended guidelines, half of our participants were vitamin D-deficient at the end of winter, with almost all demonstrating reductions in winter 25(OH)D levels. Our findings suggest that vitamin D deficiency may be much more prevalent than expected in these patients, and that vitamin D supplementation might be indicated for this group, at least during winter. Vitamin D levels in summer and winter 25(OH)D = 25-hydroxyvitamin D.

Anna-Marie McCombie · Rebecca S Mason · Diona L Damian

To the Editor: I read with interest the article by Hardie and Critchley, in which the authors attempted to measure attitudes towards both Australia’s current health care system, and shifts to greater public or private funding of health care.1 The article’s finding that pro-public funding attitudes were greatly favoured over pro-private funding attitudes may in fact be more of a reflection of the leading nature of the authors’ pro-private statements than of the true attitudes of the 800 study participants. Most Australians, regardless of their views on public versus private funding of health care, would be unlikely to support the statements “Australia should adopt a private, user-pays system like they have in the [United States]” and “The very best health care should be available only to those who can afford it”.1 The results are certainly not consistent with the findings from the 2007 Ipsos Health Care and Insurance study2 — a survey with more than 5300 participants and a solid 20-year history, which is supported by governments (Commonwealth and state/territory), private providers and industry associations. This study found that just over half of respondents (52%) supported full government funding of Australia’s health care system, while 42% opposed such a funding approach. In fact, more than 20% of respondents “disagreed a lot” with the proposal that “All hospital and medical costs should be met out of government revenue — the taxes we all pay — people should not have to pay anything directly”.2 The Ipsos results suggest there is still significant diversity of views on how Australia’s health care system should be funded and, importantly, these results do not support the conclusion of Hardie and Critchley that Australians “overwhelmingly favour a more socially responsive public health system, funded by the public purse”.

Michael H Armitage

In reply: We are intrigued by the discrepancy between our findings1 and the 2007 Ipsos study results2 noted by Armitage. We took a psychometrically rigorous approach to measuring the public’s preference for health care systems. If our pro-private statements seem “leading”, then the pro-public statements (“Australia should adopt a collective social health system supported by higher taxes as is done in some Scandinavian countries”, “I would be willing to pay higher taxes to improve Australia’s health care services”) could be similarly construed. Armitage reports that 52% of the Ipsos sample supported (and 42% opposed) full public funding of health care. If we apply this support–oppose dichotomy (ie, per cent above and below the scale mid-point) to our own data, a striking 70% of our sample support (and 30% oppose) greater public funding, while just 7% support (and 93% oppose) more private funding. This is consistent with other Australian studies showing a preference for health and medical research being conducted in public, as opposed to private, settings.3-5 We cannot directly compare our methods and results with the Ipsos survey because, ironically, when we tried to access this research supported by “governments ... private providers and industry associations”, we were advised by Ipsos that the report is not publicly available.

Elizabeth A Hardie · Christine R Critchley

To the Editor: Arnold is correct to question whether the New South Wales reportable misconduct legislation will be effective,1 because it relies on doctors making a judgement about whether a colleague has flagrantly departed from accepted standards of professional practice. Doctors have a high threshold for referring to medical boards, in part because they perceive the system to be adversarial rather than recognising that individual and system factors can combine to create poor professional performance. Also, medical boards have no direct ability to modify the workplace circumstances to make them more supportive of a poorly performing doctor. Poor performance has multiple causes, including mental and physical illness, cognitive impairment, substance misuse, professional isolation, and personality disorders.2 Flagrantly poor performance is rare, but research shows that the prevalence of poor performance is about one in a hundred doctors per annum.2 Many of these doctors are amenable to local remediation, provided there are properly promulgated procedures. The United Kingdom and some states in the United States have developed systems for assessing poorly performing doctors that require directors of medical services to manage complaints locally. In the UK, the National Clinical Assessment Service is available to support medical directors in more complicated cases. Consequently, the number of referrals to the General Medical Council has decreased, but the number of doctors being reviewed has increased to the number that would be expected from research.3 Doctors reviewed by medical boards in Australia do not reach the predicted prevalence levels, and boards’ processes seem slow by comparison with what can be done locally. It is a moot point whether Dr Jayant Patel would have been reported under the new NSW legislation, because some of his colleagues appeared not to have thought that he flagrantly departed from accepted standards. The real problems in Bundaberg were that there were no local mechanisms for health professionals to raise their concerns. For almost 2 years, the director of medical services at the hospital took no direct action.4 Queensland Health is developing local processes that will be administered by directors of medical services supported by a clinical performance support service.5 The evidence against relying solely on medical boards and in favour of local procedures for managing poorly performing doctors is now incontrovertible. Currently, many poorly performing doctors are not being identified and offered remediation, and patients are being left at risk. These are important issues for the National Health and Hospitals Reform Commission.

James A Dunbar · Prasuna Reddy

In reply: The opinion expressed by Dunbar and Reddy that: “The real problems in Bundaberg were that there were no local mechanisms for health professionals to raise their concerns” ignores the many real difficulties (canvassed in my editorial)1 confronting any member of staff who tried to raise their concerns within that institution. Local mechanisms cannot play their part if the institution’s senior staff do not wish to implement them. The ability of and, indeed, encouragement for all staff, regardless of seniority, to report their concerns directly to the medical board, bypasses all local deterrents. Our medical boards have the experience needed to sort out the major from the trivial, the genuine from the frivolous, incompetence from impairment. Dunbar and Reddy continue: “The evidence against relying solely on medical boards and in favour of local procedures for managing poorly performing doctors is now incontrovertible.” This is a straw man. No one, to my knowledge, has made any such suggestion. What I support is: (i) a direct avenue for someone local to report to the medical board; (ii) diligent and sensitive enquiry by the medical board; and (iii) if needed, the cooperative implementation of remediation by the local entity and the medical board.

Peter C Arnold