Letters

To the Editor: I read with interest the article by Grange and colleagues suggesting that vaccination with BCG vaccine or past severe infections may help protect against the development of melanoma.1 They do not mention the work of Coley. Coley was a surgeon at the Hospital for the Ruptured and Crippled in New York, who, after observing the regression of tumours in patients who developed erysipelas involving the tumour site, reported in 1891 in the Annals of Surgery,2 and again in 1893 in the American Journal of the Medical Sciences,3 that injecting Streptococcus pyogenes from erysipelas isolates into the patient’s tumour induced regression. Thus the relationship between neoplasia and bacterial infection has been recognised for 118 years. Coley is considered the father of cancer vaccines.

Michael G E O’Rourke

To the Editor: We report a case of desmoplastic small round cell tumour (DSRCT) in the liver of a 23-year-old woman who presented with a recurrent non-pruritic rash. The woman had a generalised macular rash, predominantly on the back and upper thighs. She reported recurrent similar skin rashes over the previous 4 months that had been treated with intermittent courses of oral antibiotics. She had felt mild fatigue during the 3 weeks prior to presentation. She was otherwise well, but had non-tender hepatomegaly (17 cm) on examination. There was no peripheral lymphadenopathy. Levels of cholestatic liver enzymes were mildly raised (γ-glutamyl transpeptidase, 198 IU/L; alkaline phosphatase, 246 IU/L), but bilirubin and immunoglobulin levels were normal. The serum level of cancer antigen 125 (CA125) was 141 U/mL (reference range, < 35 U/mL). A computed tomography scan of the chest and abdomen showed multiple hepatic lesions (Box 1). A radiologically guided biopsy was taken, and histological examination revealed the typical morphology and immunophenotype of DSRCT (Box 2). Our patient was counselled regarding diagnosis and likely poor prognosis. We did not attempt to preserve fertility, because we felt treatment should not be delayed and that life expectancy was limited. Chemotherapy with alternating VAC (vincristine, doxorubicin and cyclophosphamide) and IE (ifosfamide and etoposide) cycles was started promptly. Molecular testing for EWS1/WT1 (see below) was not performed, as there was insufficient biopsy tissue available. The patient’s rashes disappeared after one treatment cycle, and we postulate that the rashes were paraneoplastic and immune-mediated. Restaging scans after four cycles of chemotherapy demonstrated a partial response. Stem cells were pre-emptively mobilised to store for possible subsequent autologous transplantation. The patient will be reassessed after eight cycles. If there is a significant response, the options of high-dose chemotherapy with autologous stem cell transplantation and/or debulking surgery will be explored. To our knowledge, this is the first Australian report of DSRCT in a woman presenting with recurrent rash. DSRCT is a rare, aggressive tumour that predominantly affects males in early adulthood.1 There is a single Australian report of a 15-year-old boy who died of DSRCT 20 months after diagnosis.2 The histogenesis of DSRCT is unknown, but it exhibits divergent differentiation, expressing epithelial, muscular and neural proteins. It is characterised by the chromosomal translocation t(11;22)(pl3;ql2), formed by fusion of the Ewing sarcoma gene (EWS1) to the Wilms tumour suppressor gene (WT1).3 Patients typically present with non-specific symptoms, and the tumours are usually intra-abdominal. The level of CA125 is often raised, but this does not assist with diagnosis or monitoring.1 Diagnosis is by histology and immunohistochemistry, complemented by cytogenetic identification of an EWS1/WT1 translocation. Patients with DSRCT have a poor prognosis, with a median survival of 15 months. Given the rarity of the tumour, there are no data from randomised phase III trials to guide management. Aggressive multimodality treatment offers the highest chance of disease control and prolonged overall survival.1,4 Palliative debulking can be of benefit if curative resection is not feasible. Radiotherapy is best employed as consolidation treatment after chemotherapy and surgery.1,5 Combination chemotherapy is the backbone of therapy and offers improved progression-free survival. The P6 protocol,6 which uses alternating cycles of VAC and IE with 21 days between cycles, is most widely employed. Subsequent high-dose myeloablative chemotherapy with autologous stem cell support may be beneficial.4 1 Pre-treatment computed tomography scan of the patient’s abdomen, showing multiple hypodense lesions in the enlarged liver 2 Histological sections from a core biopsy of a desmoplastic small round cell tumour (DSRCT) in the liver A: Irregular nests of small round hyperchromatic tumour cells were embedded in a prominent fibrotic stroma (haematoxylin–eosin stain, original magnification ×250). A diagnosis of DSRCT was confirmed by immunohistochemical stains (B–D). B: The muscle marker desmin. C: An epithelial marker AE1/3. D: The Wilms tumour marker WT1. (Original magnification of images B–D ×100.)

Meena Okera · David Moffat · Sudarshan Selva-Nayagam

To the Editor: Over-the-counter herbal supplements to promote weight loss have become increasingly popular. Several of these products contain potentially hepatotoxic substances. We present the first reported Australian case of acute hepatotoxicity associated with the weight-loss product Hydroxycut Hardcore (Iovate Health Sciences, Blasdell, NY, USA). Hydroxycut contains various ingredients, including extracts of the herbs Garcinia cambogia and Camelia sinesis (green tea root), and the chromium salt, chromium polynicotinate. A recent review cites these three ingredients as possible causes of Hydroxycut hepatotoxicity.1 A 23-year-old, previously well, construction worker presented to his doctor with a 2-month history of lethargy and jaundice. Test results confirmed serum liver enzyme derangement, and the patient was advised to stop taking the weight-loss supplement. Results of repeat testing a week later showed worsening liver enzyme levels and he was referred to our hospital. On arrival, the patient denied any symptoms except moderate lethargy and icteric sclera. He was usually well with no relevant medical or surgical history. He weighed 83 kg. He denied drinking alcohol, using prescription or non-prescription drugs, or receiving a blood transfusion. He had had unprotected sexual intercourse 2–3 months earlier. A previously obtained tattoo was being extended by a reputable tattoo parlour. He had been using Hydroxycut Hardcore daily for 10 weeks (obtained from his local outlet of a global nutritional products retailer) in an attempt to lose weight and tone muscle. He claimed to have taken the dosage recommended by the manufacturer (six capsules daily); he was taking no other supplements. Physical examination revealed mild jaundice without other features of chronic liver disease or portal hypertension. However, in addition to abnormal blood levels of liver enzymes, bilirubin and iron, results of the patient’s liver biopsy showed severe acute hepatitis (Box). The abnormal test results were consistent with acute drug toxicity. The patient improved without specific treatment and was discharged 8 days after presentation, with near-normal serum liver enzyme levels. He was well on follow-up at 4 weeks. Two reports from the United States link Hydroxycut Hardcore to acute liver injury in otherwise well young males.2,3 The American Food and Drug Administration in May 2009 advised consumers to stop using the product, based on 23 reports linking it to serious injury, including one case of liver failure leading to death.4 In May 2009, Australia’s Therapeutic Goods Administration (TGA) issued a warning to consumers about the product, although noting that no adverse events had so far been reported in Australia.5 In view of this first reported Australian case of Hydroxycut hepatotoxicity, we advise medical practitioners and consumers in this country to be wary of the product, and call on the TGA to re-examine its continued availability. Investigation results for a 23-year-old man with liver dysfunction after using Hydroxycut Hardcore Investigation Result (reference range) Blood tests Aspartate aminotransferase (U/L) 1182 (12–36) Alanine aminotransferase (U/L) 2950 (5–40) Alkaline phosphatase (U/L) 121 (50–140) Bilirubin (µmol/L) 113 (3–18) Prothrombin time (seconds) 13 (11–15) Iron (µmol/L) 68 (11–30) Ferritin (µg/L) 1897 (30–400) Iron saturation (%) 99 (16–50) Paracetamol Not detected Hepatitis A, B, C Negative HIV Negative Autoantibodies Not detected Epstein–Barr virus, cytomegalovirus, toxoplasma, leptospira, coxiella Negative Haemochromatosis genetic testing No abnormality Other tests Abdominal ultrasound No abnormality Percutaneous liver biopsy Severe acute lobular hepatitis with areas of bridging necrosis; no bridging fibrosis or cirrhosis were seen Hepatic iron index 1.1 (< 2.0)

N Nudrat Rashid · Jason Grant

To the Editor: The editorial by Buchbinder et al suggesting that the effectiveness of vertebroplasty has been determined by the two studies she and her co-authors published1 is misleading. Both studies2,3 contain major flaws. In both, 70% of eligible patients declined to participate. No details of these patients are published, but they may have been the patients with more severe pain. The median duration of pain in the Australian study2 was 9 weeks (compared with 16 weeks in the US study3); only 30% of patients had pain for less than 6 weeks. No information on the need for hospitalisation because of severe pain was given in either study. The average length of hospital stay was not published. In the Australian study, the inclusion criteria were the presence of back pain of less than 12 months’ duration and the presence of one or two recent fractures.2 In this group of patients, whose average age was 74 years, there will be many possible causes of back pain. The fracture may be the main cause of pain, a part-player, or may not be significant. In patients with milder pain and longer duration of pain, non-fracture causes are more likely. In the US study,3 patients were selected on the basis of x-ray unless the fracture “was of uncertain age”. I have performed an audit of my practice and found that in patients with an unequivocal x-ray diagnosis of fracture level, magnetic resonance imaging (MRI) identified another fracture not seen on x-ray in 23 of 63 patients (36%), and in 10 of the 63 patients (16%), a fracture that was presumed acute showed no oedema on MRI. In the Australian study,2 the experience of the radiologists performing the vertebroplasty is not made clear; no details are given about the number of patients they had previously treated. The incidence of osteomyelitis (3.8% at best, 30% at worst, depending on which centre was involved), despite prophylactic antibiotic therapy, is unacceptable. In the US study, injury to the thecal sac in one of 78 patients suggests incompetence. The protocol stated that cement injection was ceased if “cement reached the posterior quarter of the vertebral body or leaked into intraosseous structures”. This sometimes happens after 1 mL of cement has been injected. Experienced operators will perform various manoeuvres to ensure an adequate spread of cement occurs throughout the vertebral body. It would appear this was not done. The volumes of cement injected are not published, except an estimate of “about 3 mL”. The sham procedure was not a true placebo. Injection of local anaesthetic onto the pedicle would likely block the dorsal ramus nerve and provide partial analgesia of the fracture if the fracture extended into the pedicle. Those who perform vertebroplasty regularly see patients who are bedridden, in severe pain, intolerant of analgesics, and who have undergone various procedures including epidural injections or facet joint injections without benefit, and who then respond to vertebroplasty within 24 hours. Efforts should be aimed at refining technique and patient selection, rather than throwing out the baby with the bathwater on the basis of inappropriate studies.

Paul J Graziotti

To the Editor: Clinical trials study a restricted patient group, so their results may not be generalisable to a different population subgroup or the population as a whole. The editorial by Buchbinder, Osborne and Kallmes1 about their recent vertebroplasty studies2,3 concludes that vertebroplasty offers no benefit over placebo. They suggest that, in light of their trials, the decision to list vertebroplasty on the Medical Benefits Schedule will be reviewed later this year. I understood the review to have been part of the original listing on the benefits schedule and not as a result of their studies, and I suggest that their editorial generalises results to a subpopulation of early acute vertebral fractures that they did not study. The duration of symptoms in osteoporotic vertebral fracture is critical, as most fractures heal quickly with a good outcome by 3 months, and only a very small group of patients continue to experience pain.4 A fracture that is still painful months after the event is not a “normal fracture”, and I suggest is less likely to respond to the same management concepts as an acute fracture. In the study by Buchbinder and colleagues, patients had persistent pain and were recruited up to 1 year after their vertebral fracture.2 Nearly three-quarters had significant ongoing pain for at least a month after their fracture, and most for at least 2 months. The study by Kallmes and colleagues also included symptomatic fractures up to 1 year old, with the interquartile range (8–38 weeks) suggesting that they had an even longer period between fracture and inclusion in the trial.3 While vertebroplasty appears to be unhelpful for patients who continue to have chronic pain months after an acute osteoporotic fracture, the authors have not robustly excluded vertebroplasty as improving quality of life and pain management in those who undergo vertebroplasty within days to a month of the fracture. Such an outcome is suggested by Rousing et al, who showed that vertebroplasty within 2 weeks of fracture led to a rapid reduction in pain within 12–24 hours, similar to the result of conservative management at 3 months.4 Any review of the role for vertebroplasty should consider the populations studied and, hence, should define the characteristics of patients in whom to intervene or not intervene.

Kevin D Pile

In reply: The letters by Graziotti and Pile raise spurious issues that in no way threaten the key message of our trials. Participation rates in both trials were better than other controlled trials of vertebroplasty or kyphoplasty.1,2 Eligible patients who declined enrolment in the Investigational Vertebroplasty Efficacy and Safety Trial (INVEST) had similar levels of pain and disability to those who participated.3 Both trials adhered to stringent eligibility criteria, ensuring that only patients with pain due to acute or subacute fractures were included. All operators were trained and experienced, and the low incidence of serious adverse effects in both trials is consistent with the literature. There is no evidence that the outcome of vertebroplasty is influenced by cement distribution or volume.4 Local anaesthetic infiltration of the periosteum of the pedicles, as occurred in one trial,3 is unlikely to have a sustained effect. As Pile points out, most osteoporotic vertebral fractures heal quickly; this implies that most people would be unlikely to benefit from early invasive intervention. Consistent with this, public funding for vertebroplasty in Australia only has interim approval for patients whose pain is not controlled by conservative medical therapy. While duration of medical therapy is not specified, historically, this has ranged from at least 4 to 6 weeks. Thus, both trials included patients similar to those who would qualify for government-subsidised funding of the procedure in Australia. While Pile acknowledges that vertebroplasty appears to be of no value in patients with persisting symptoms (the group most likely to derive benefit), he seems to suggest that it may have a role in early treatment (within days to a month). As well as being at odds with his earlier statement, this is not supported by the available data. Many participants in both trials had short symptom duration (Australian trial, 32% < 6 weeks; INVEST, 20% < 6 weeks and 41% ≤ 13 weeks), and neither trial found evidence that symptom duration was a treatment effect modifier. The trial by Rousing et al reported comparable outcomes from vertebroplasty and conservative treatment in patients with acute symptoms (40 patients, < 2 weeks; 10 patients, 2–8 weeks).5 While no data were presented, the immediate (12–24 hours) benefit from vertebroplasty reported in this open study, like clinical experience, could be attributable to many factors including local anaesthesia, regression to the mean, and expectation bias. The onus remains on proponents of vertebroplasty to prove that any benefits of vertebroplasty outweigh the potential risks.

Rachelle Buchbinder · Richard H Osborne · David Kallmes

To the Editor: In their letter of 5 October 2009, Wong and colleagues highlight the importance of providing training for surgical specialties in the private sector.1 With 64% of surgical activity in Australia now occurring in the private sector,2 and public hospital activity constrained due to ongoing budget imperatives, the Royal Australasian College of Surgeons (RACS) has been actively exploring this idea for some years. The new Surgical Education and Training (SET) program selects trainees into one of nine specialty programs.3 Currently, there are 1254 trainees in the SET program across Australian, New Zealand and overseas positions. Once selected into a specialty program, trainees who succeed in achieving the educational goals will be able to progress through its entirety. Consequently, to enable completion of training in the program, each SET Level 1 post needs to be matched in the public or private sector with more senior training positions to ensure appropriate progression. The RACS has worked with a number of private hospitals and the federal government to identify and fund 50 training positions suitable for surgical education across Australia. The funding has predominantly been provided through the Australian Government’s Expanded Specialist Training Program. This program was established following the release of the Medical Specialist Training Steering Committee report4 to encourage training in settings other than public teaching hospitals. The RACS is keen to have this program substantially enhanced and is attempting to identify models with the federal government that can achieve this. This is where the work by Wong and colleagues1 is so important. The public and private sectors are different. Both can be highly useful for the education of a skilled surgeon. However, all educational environments need enthusiastic supervisors and trainers. The community and our patients also need to be understanding, supportive and enthusiastic for education of surgical trainees to occur. The RACS applauds Wong et al for progressing this discussion and highlighting the benefits that can result from expanding surgical training into the private sector.

Ian R Gough · Ian D Civil · Spencer W Beasley · Bruce H Barraclough · David J Hillis

To the Editor: I note, with a breath of fresh air, your recent column about managing hospital staff rosters1 and, in the same issue, the article by Dietz, calling for a simpler, more resilient health bureaucracy.2 We are stuck in an environment where process seems to be disassociated from outcome and, if the outcome is not what is wanted, then more process is added, thus compounding the problem. Surely it is time to step back a bit and look strategically at bureaucratic processes, and how they work and don’t work? No one would deny that we need good administration — it is one of the very bastions of our way of life. We seem to study most things in an evidence-based manner, or at least try to. Why can’t we have chairs of bureaucratic studies in our universities to rigorously research our bureaucratic processes? Armed with sound evidence, we could develop template systems and other tools to break the nexus in which we find ourselves. Dare I say the spin-off would be greater than just health care. Food for thought.

Robert N Atkinson

To the Editor: We write to encourage policy debate over newborn screening for congenital adrenal hyperplasia (CAH). Classical CAH is a severe, life-threatening disease affecting about one in 15 000 liveborn infants in Australia.1 An inexpensive screening test for newborns is available, but this test is not included in the current newborn screening program in Australia. Three-quarters of children with CAH have the severe salt-wasting type that typically presents with failure to thrive, and progresses to severe hyponatraemic, hyperkalaemic dehydration and shock due to an adrenal crisis within weeks of birth. CAH is the most common cause of ambiguous genitalia in neonates (due to virilisation from adrenal androgens in utero); girls with CAH may be incorrectly assigned as boys unless the diagnosis is made without delay. CAH can be easily detected in neonates before the onset of illness by an established heel-prick newborn screening test that has good specificity and sensitivity, especially when used together with second-tier testing. Screening for CAH has been available for 30 years internationally, and is used in all American states, New Zealand and many countries in Europe, Asia and Latin America. Newborn screening reduces mortality and incorrect sex assignment.2 Case reports from Australia3 and overseas4 have shown that undiagnosed CAH is a cause of apparent sudden infant death syndrome. These deaths could have been prevented if newborn screening was in place. A pilot study in New South Wales showed that newborn screening for CAH prevented salt-wasting crises and their potential long-term consequences.1 The cost-effectiveness of newborn screening is difficult to measure, and there is little published evidence on this subject. Although a recent study suggested that CAH screening is not cost-effective,5 the only outcome assessed was mortality; other benefits of early diagnosis and intervention — including reduced morbidity and psychological impact — were not assessed. Newborn screening for CAH is not expensive; the cost per test within the laboratory is about $2, and the incremental cost per infant is in line with other newborn screening tests. In a recent survey, the Australasian Paediatric Endocrine Group found that 91% of paediatric endocrinologists considered provision of newborn screening for CAH in Australia to be very important. The Newborn Screening Joint Subcommittee of the Human Genetics Society of Australasia unanimously supports the inclusion of newborn screening for CAH in all Australian states. Two Australian parent and patient advocacy organisations — the CAH Support Group Australia, and Caring and Living as Neighbours — also strongly support the proposal for adding newborn screening for CAH to the current screening program. Despite clear predicted benefits and agreement among key stakeholders and expert advisers, no state in Australia currently screens for CAH. It is the state governments — guided by the Australian Health Ministers’ Advisory Council — who decide on funding for newborn screening tests, and who should be accountable for acting against the weight of expert opinion and systematic evidence.

Garry L Warne · Katrina L Armstrong · Thomas A Faunce · Bridget M Wilcken · Avihu Boneh · Elizabeth Geelhoed · Maria E Craig

To the Editor: Our positive experience with insulin pump therapy (IPT) in children without private health insurance contrasts with that of Thong and colleagues,1 who found that IPT did not significantly reduce glycated haemoglobin (HbA1c) levels in uninsured adults. IPT improves metabolic control, reduces the risk of microvascular complications and improves quality of life in children with type 1 diabetes mellitus.2,3 Private health insurance fully rebates the cost of an insulin pump, but many uninsured Australian children with type 1 diabetes are denied access to IPT because their family cannot afford the $8000 purchase price of an insulin pump. The other major impediment to using IPT is the paucity of access to skilled local IPT teams. In November 2008, to improve access to IPT, the federal government introduced a means-tested subsidy (to a maximum of $2500 per child) to be administered through the $5.5 million Type 1 Diabetes Insulin Pump Program.4 By 30 June 2009, the program had subsidised only 31 children for insulin pump purchase (unpublished correspondence from the Hon Mark Butler MP, Parliamentary Secretary for Health, to Mr Darren Chester MP, Member for Gippsland, July 2009). The largest user of this scheme, Gippsland Paediatrics (a private practice in rural Victoria), commenced IPT in 11 of the 31 children. Through local service clubs and other charitable institutions, we raised the funds required to pay the $5500 balance for all 11 children.5 Six other financially disadvantaged Gippsland Paediatrics patients had obtained insulin pumps through grants or community fundraising before the government subsidy program was introduced. Thus we have experience of 17 children, aged between 4 and 18 years (mean, 10.8 years) who were recipients of “donor” pumps. This sample represents about a quarter of the local children with type 1 diabetes and almost two-fifths of the 46 patients we have commenced on IPT. To evaluate the metabolic outcome of IPT for these 17 children, we conducted a retrospective analysis of glycaemic control by comparing the average level of HBA1c during the 12 months before commencing IPT with the most recent HbA1c level. The pre-IPT mean HbA1c level of children using the donor pumps was 9.2% (SD, 1.45%), which fell to 7.6% (SD, 0.83%) (P < 0.001) after a mean IPT duration of 10.2 months (SD, 6.1 months). In children aged 12 years or under (10 patients), the mean HbA1c level fell from 9.0% (SD, 0.94%) to 7.6% (SD, 0.43%) (P < 0.001) after a mean IPT duration of 11.9 months (SD, 7.6 months). In the remaining seven patients, aged 13–18 years, the mean HbA1c level fell from 9.4% (SD, 2.0%) to 7.8% (SD, 1.43%) (P = 0.03) after a mean IPT duration of 7.6 months (SD, 1.4 months). Gippsland Paediatrics uses the RADICAL (Rural Australian Diabetes — Inspiring Control Activity & Lifestyle) model of care.6 The model consists of a collocated multidisciplinary team, including a general paediatrician, diabetes educator and counsellor, with the patient and family receiving proactive emotional support, consistency of personnel, and point-of-contact HbA1c testing. We individualise our approach through regular case conferences and try to match therapy with desired lifestyle. Our study demonstrated that, using this model, IPT improves glycaemic control in uninsured children targeted by government policy — at least in the short term. To improve short-term health and reduce long-term diabetic complications in families who cannot afford insulin pumps, government programs need to make IPT more accessible to those families and support local multidisciplinary IPT teams.2

Peter W Goss

To the Editor: Norovirus, previously known as the Norwalk agent, is a recognised cause of acute diarrhoeal illness in all age groups, but its significance in hospitalised children is poorly described. Noroviruses cause infection worldwide and year-round, with a distinct increase in disease occurrence in colder months.1 Rotavirus has long been recognised as the most important viral cause of gastroenteritis in young children, causing significant morbidity, as well as cost to the community of hospital admission and lost parental productivity.2 In July 2007, two new rotavirus vaccines were licensed for use in Australian infants; their use has reduced severe rotavirus disease requiring hospital admission.3 One difficulty in accurately documenting the role of norovirus in childhood acute diarrhoeal illness has been the limited availability of routine diagnostic testing. Enzyme-linked immunosorbent assay (ELISA) for noroviruses is now available commercially; it has limited sensitivity of 55%–93% but good specificity of 73%–97%. We retrospectively reviewed the frequency of detection of norovirus in the faecal samples taken from inpatients and outpatients with acute gastroenteritis at a tertiary paediatric hospital. We tested stool samples of 3962 children with episodes of acute diarrhoeal illness in a 12-month period (2007) and detected norovirus in 122 (3.1%). Ninety-one of the children infected with norovirus were admitted to hospital; 63 patients had a stay of less than 7 days with a median of 1 day, while 28 patients where in hospital for more than 7 days. The norovirus infection in 30 of the inpatients (33%) was hospital-acquired. Most hospital-acquired infections occurred in patients hospitalised for more than 7 days (19 of 28; 68%), and most of these patients had predisposing medical conditions, predominantly immunosuppression due to treatment for malignancy or other causes. Norovirus is a significant cause of viral gastroenteritis in infants and children. Our findings are comparable with those of other studies, which indicate that norovirus infection causes 20%–88% of viral gastroenteritis in children and is responsible for a significant proportion of hospital admissions of children with gastroenteritis.4,5 With the introduction of universal rotavirus vaccination for Australian infants, the importance of norovirus as a cause of gastroenteritis in infants and children is likely to increase. We recommend that hospitals which admit children consider using norovirus testing to establish the incidence and prevalence of disease, and to inform public health authorities responsible for infection control policy and practices.

Alison M Kesson · Nicola Benwell · Elizabeth J Elliott

To the Editor: Rudkin and colleagues1 remind readers of the importance of detecting congenital glaucoma early to reduce the risks of permanent eye damage, including blindness. The first clinical signs of congenital glaucoma are reported to be blepharospasm, photophobia and excessive tears, all difficult to discriminate in an infant. If the condition is untreated, the cornea progressively loses clarity, and diagnosis becomes more obvious. In giving this account of my personal experience, I remind general practitioners, paediatricians and ophthalmologists that early oedema of the cornea may be detectable before other signs. Our daughter was born uneventfully and without medical problems. Four weeks after the birth, my wife, while gazing into her newborn’s eyes, commented, “Do you think her right eye is . . . more “shiny” than the left?” Looking at all angles, the anxious medical parents were convinced it was. Various medical friends were consulted. “Maybe, possibly”, they indulged us. A call to the senior paediatric ophthalmology registrar at our local children’s hospital was made along the lines of, “Is there such a thing as loss or increase in shine to the eye of a newborn?” In the absence of any other signs, such as inflammation, misery or excessive tears, we were told not to worry. Not reassured, we prevailed upon another ophthalmology registrar who, in a fit-in appointment, confirmed subtle corneal oedema caused by bilateral glaucoma, worse in the left eye. In retrospect, the diagnosis was obvious. “Couldn’t have been anything else”, except the presenting sign was not a cloudy cornea, blepharospasm or misery — it was simply light reflecting off one eye less brilliantly than the other. “It ain’t fine, if it don’t shine.”

Peter J Lewindon

To the Editor: I would like to report the results of a recent survey showing that junior doctors who undertook undergraduate training in a rural clinical school (RCS) felt better prepared for their new role as a doctor than those who did not. In Australia, the potential threat to the quality of clinical training because of increasing numbers of medical graduates justifies an interest in junior doctors’ perceptions of their learning environment and their level of preparedness for hospital work. Factors affecting this potential threat were investigated. In 2008, 428 junior doctors employed in Queensland training hospitals were asked to complete an online survey. Ethics approval was obtained from the Behavioural and Social Science Ethical Review Committee of the University of Queensland. During their undergraduate training, the majority of respondents had not studied at an RCS. The remaining respondents had attended a large university RCS (of about 1600 enrolled students) or a small university RCS (of about 650 enrolled students) in Queensland, or had attended an RCS of unknown size in another state (n = 9). A mixed methods cross-sectional design, based on two validated scales, was used: The Preparation for Hospital Practice Questionnaire (PHPQ) assessed respondents’ perceptions of the adequacy of undergraduate medical training to prepare them for hospital work;1 and The Postgraduate Hospital Educational Environment Measure (PHEEM) measured respondents’ hospital clinical teaching and learning environment.2 Of 167 responses received (a 39% response rate), 33 were incomplete, leaving 134 usable responses. The majority of respondents were women (60%), aged 26–29 years (53%) and graduates of the large university (79%). Forty-eight per cent had chosen to spend a portion of their undergraduate training at an RCS. A univariate analysis (using analysis of variance and analysis of covariance) made comparisons by age, sex, undergraduate university medical program (large or small Queensland university, university in another state) and attendance at an RCS. Overall responses to the PHEEM indicated that there was “room for improvement” in the autonomy, teaching and social support of the hospital learning environment. No significant differences were detected in either the PHEEM or PHPQ subscale scores by age, sex, postgraduate year or undergraduate university. Junior doctors who attended any RCS as part of their undergraduate education scored significantly higher on three out of eight scales of preparedness for hospital work (based on the PHPQ) (Box). A caveat is that confidence and feelings of preparedness do not equate to “competence”, but the study was not designed to assess competence. Confidence is also strongly related to temperament, which could influence self-selection choices such as factors associated with the size of medical school. These findings are congruent with other studies showing that students perceive undergraduate training outside a traditional metropolitan-based program to be of higher quality3 and that the performance of students trained in RCSs is comparable to that of their urban-based peers.4,5 Dispersing smaller cohorts of students to individual clinical schools (similar to the RCS model) may prove a successful strategy to cope with escalating numbers of undergraduate students. In theory, better prepared junior doctors should require less intensive supervision, contribute more to the hospital workload and alleviate the strain on already stretched educational resources in hospitals. In summary, given the imminent increase in medical graduates entering training hospitals, considerable work needs to be done to improve the quality of education provided for junior doctors in order to maintain a high-quality, supportive educational atmosphere. Comparison of Preparation for Hospital Practice Questionnaire (PHPQ) mean subscale scores between Queensland junior doctors who attended a rural clinical school (RCS) as part of their medical training and those who did not* Medical school attended Interpersonal skills Confidence Collaboration Management Science Prevention Holistic care Self-directed learning Any RCS (n = 65)† 3.97 (0.920) 4.00‡ (0.883) 4.28§ (0.735) 4.04§ (0.889) 4.08 (0.838) 4.56 (0.717) 4.56 (0.809) 4.44 (0.643) Large university RCS (n = 42) 3.84 (0.925) 3.82 (0.877) 4.15 (0.772) 3.74 (0.875) 3.95 (0.882) 4.46 (0.737) 4.43 (0.817) 4.36 (0.666) Small university RCS (n = 14) 4.28 (0.897) 4.68‡ (0.770) 4.68§ (0.583) 4.73‡ (0.691) 4.46 (0.692) 5.00§ (0.418) 5.01§ (0.558) 4.71 (0.641) No RCS (n = 69)¶ 3.87 (0.905) 3.58 (0.784) 3.98 (0.853) 3.69 (0.858) 3.88 (0.918) 4.55 (0.726) 4.47 (0.767) 4.43 (0.694) * Figures are mean score (SD). Rating scale of respondents’ perceptions of their preparedness for hospital work: 1 (very inadequately prepared) to 6 (very adequately prepared). † All junior doctors who attended an RCS during their undergraduate degree, including nine non-Queensland RCSs. ‡ Significant at P < 0.001 level. § Significant at P < 0.05 level. ¶ All junior doctors who did not attend an RCS during their undergraduate degree.

Diann S Eley

To the Editor: The general practitioners’ dilemma is acute. Women asking for mammography and/or testing for ovarian cancer; men asking for prostate-specific antigen (PSA) testing for prostate cancer. The debate, fuelled by uncertain knowledge, rages in the general medical journals,1,2 including contributions in the 17 August 2009 issue of the MJA.3,4 The PSA test is, of course, intimately associated with the name of its inventor, Thomas A Stamey. I am, therefore, somewhat surprised that neither of these recent MJA articles mentioned Stamey’s 2004 “recanting” of his proposed value of the test back in 1987: “current evidence from the last 10 years is convincing that the relationship between prostate cancer and serum PSA is tenuous at best, especially with serum PSA less than 10 ng/mL and perhaps even less than 22 ng/mL. This time is not the first we have had second thoughts regarding the usefulness of serum PSA in preoperatively reflecting prostate cancer”. He concludes: “any excuse to biopsy the prostate has an excellent, age dependent chance of being positive”.5 Perhaps the authors could tell your readers why they did not think that Stamey’s 20-year experience of PSA testing and his 2004 conclusions warranted a mention?

Peter C Arnold

In reply: The letter by Arnold highlights the practical dilemma facing busy doctors when communicating with patients about whether to screen for various cancers, prostate cancer in particular. There are no easy answers at present, although presentation of both sides of the argument regarding prostate cancer testing helps doctors and patients make a shared decision.1 We believe the following decision-aid show card, written in plain English, is an excellent resource to assist with this: <http://www.cancer.org.au/File/HealthProfessionals/GPprostateshowcard.pdf >.

David P Smith · Emily Banks · Mark S Clements · Robert A Gardiner · Bruce K Armstrong

To the Editor: In a recent letter by Kowal,1 reference was made to my previous letter2 commenting on an article by Andreasyan and Hoy.3 Kowal questions my suggestion that Andreasyan and Hoy’s work adds evidence to the body of work indicating the health benefits for Indigenous Australians of living in small remote communities. She then suggests that “rather than jumping the gun, we need more research into the effects of outstation life on health and wellbeing”. I think Kowal misses the point. I did not refer to “outstations”. I wrote of the many remote Indigenous communities, most of which have been established in the past 40 or so years, not all of which are called “outstations”. These communities now have their survival threatened by current government policies that support a few selected larger communities at the expense of many smaller communities. The evidence provided by Andreasyan and Hoy, building on other work, does not support policies that are likely to lead to a drift of people away from their homelands to large centralised settlements and the fringes of towns and cities. While the research evidence is not overwhelming, on balance there appears to be more evidence suggesting health benefits from helping people remain on their traditional lands than evidence to support policies that encourage them to migrate to larger settlements and towns. Kowal accuses those who cite this evidence, such as Tom Calma and myself, as jumping the gun. I suggest it is governments that are jumping the gun in imposing policies that are not evidence-based. While there is a need for more research and for careful scrutiny of the research, as undertaken appropriately by Zhao and colleagues,4 the evidence definitely points to concerns that current government policies may have a significant detrimental effect on Indigenous people.

David J Scrimgeour

To the Editor: A timely article by Yelland and colleagues in the 7 September 2009 issue of the Journal1 correctly identifies postnatal depression as a significant public health issue. However, as members of the consortium that developed the 2008 beyondblue National Action Plan for Perinatal Mental Health (NAP),2 we are concerned that the National Perinatal Depression Initiative is being considered by Yelland and colleagues without reference to the NAP, the document on which the federal government based its funding allocation. The NAP recommended not only identifying current depressive symptoms, but also — equally importantly — using a structured method to assess the broader psychosocial risk factors known to affect maternal and infant mental health.2 The NAP also clearly recommended that any psychosocial assessment be accompanied by adequate workforce training and supervision and integrated pathways to care, complemented by community awareness programs. Although Yelland and colleagues1 raise concerns about the potential harm of routine screening for depression in women during pregnancy, none of the participants in a recent Australian study of antenatal screening for depression reported feeling stigmatised, labelled or distressed after using the Edinburgh Postnatal Depression Scale (EPDS).3 Indeed, many reported feeling relieved and supported that additional care was offered. This reinforces the assertion made in the NAP that a well trained workforce is essential for conveying the purpose of routine assessment — that such assessment is not an endpoint nor a substitute for full diagnosis, but the beginning of an ongoing process that helps professionals to be aware of women who may need support and treatment. Multiple studies evaluating the EPDS against structured diagnostic interviews for detecting major depression have shown that the EPDS has very good psychometric properties for scores of 13 or more (indicative of possible depression) in English-speaking populations.4 Yelland and colleagues also express concern that a limited number of interventions will be recommended to help depressed women. In fact, the NAP recommended that the full range of treatment options be offered within an integrated framework of community, primary care and specialist services.2 A first step in a national approach to perinatal mental health is to develop evidence-based clinical practice guidelines for perinatal depression and related disorders. This task is now underway, a clear indication that we are well placed to begin translating knowledge into practice. Research across Australia continues to examine the efficacy of a range of psychosocial risk assessment models,5 barriers to the uptake of referral and treatment options, and the impact of psychosocial assessment on maternal outcomes. This work will help ensure that a national approach to perinatal mental health is embedded in an evidence-based and evaluative framework.

Marie-Paule Austin · Nicole Reilly · Jeannette Milgrom · Bryanne Barnett

To the Editor: The research article by Keogh and colleagues1 on uptake of genetic testing and insurance implications highlights the need to ensure that Australian insurance industry policy in relation to genetic testing does not increase the risk of adverse health outcomes. The authors called upon the insurance industry and the Human Genetics Advisory Committee (HGAC) of the National Health and Medical Research Council (NHMRC) to reconsider the use of genetic information in relation to insurance.1 Another recently published study has also raised concerns about the way genetic information is used in the insurance industry.2 The HGAC has had initial discussions with the insurance industry about: avoiding genetic discrimination in the insurance setting; developing policies and guidelines to ensure appropriate use of genetic test results in insurance underwriting; promoting genetic education and training in the financial industry; and providing support for consumers and health professionals wanting to challenge adverse decisions. Through the HGAC, the NHMRC will encourage the development of an evidence-based process for assessment of genetic tests for use by the insurance industry, to ensure that it meets the required standard for underwriting. This will, in turn, support appropriate, equitable consumer access to optimal health care.

Warwick P Anderson

To the Editor: Congratulations on the 21 September 2009 issue of the Journal, highlighting preventive cardiology in Australia. I believe that the “working class man” of the well known Jimmy Barnes song has trouble affording preventive cardiology care in Australia. Assuming that he is currently employed, he will not be entitled to a Health Care Card and will be paying full price for care in general practice. There will be a gap of $20 to $60 between what he pays and the Medicare rebate per visit. He will have to pay about $30 per prescription. Assuming that he is taking antiplatelet agents, statins, and a blood pressure agent such as an angiotensin-converting enzyme inhibitor, he would be paying about $90 per month for medication. On an average income of $1200 per week1 ($800 after tax), and assuming that he visits his general practitioner monthly, preventive cardiology care might cost him about 4% of his disposable income. If our working class man is earning $900 weekly ($600 after tax), then preventive cardiology care would cost him 5% of his disposable income. Of course, the costs are similar for a wealthy man. However, the costs represent a far smaller percentage of his income than for the working class man. In this regard, the costs of preventive medicine are similar to the poll tax imposed in England in the 14th century. This regressive capitation tax was raised to pay for the imperial wars in France. However, the disproportionate burden it imposed on the serfs resulted in such anger that it led to the Peasants’ Revolt in 1381. Until medicine is funded more equitably, there will be a major disincentive to pursue preventive cardiology care for poorer people, who experience cardiovascular disease at an earlier age than their wealthier counterparts.2 The problem is not which model to use for absolute risk assessment,3 but the money to apply it.

V Michael Jelinek

To the Editor: We describe two liver transplant patients who presented with unexplained dyspnoea and were subsequently found to have unilateral right diaphragmatic palsy, an uncommon complication of orthotopic liver transplantation.1-3 Both transplant recipients were male. One, aged 64 years, had a liver transplant in 2005 for hepatitis C-related chronic liver disease. The other, aged 66 years, had a liver transplant in 2004 for end-stage alcoholic liver cirrhosis. Both patients had presented with exertional dyspnoea several weeks after transplantation. Both were reformed smokers with no prior respiratory symptoms or established respiratory or cardiac condition. Preoperative pulmonary function tests had been essentially normal in both patients (Box 1). Chest x-rays of both patients during the postoperative convalescence period showed unilateral elevation of the right hemidiaphragm compared with the immediate pre-transplant images. (Images for Patient 1 are shown in Box 2.) Fluoroscopic study (the “sniff test”) and a computed tomography scan of the chest confirmed the presence of right hemidiaphragmatic palsy in both patients. Follow-up chest x-rays and pulmonary function tests over 2 years showed no significant improvement. In both patients, the postoperative clinical course over these 2 years was characterised by recurrent hospital admissions with hypoxaemia and intercurrent respiratory tract infections, some requiring supplemental oxygen therapy, non-invasive positive pressure ventilation and invasive ventilation in the intensive care unit. Currently, one of these patients is well, apart from dyspnoea on moderate exertion. The other patient died from a cause unrelated to his diaphragmatic palsy. Unilateral diaphragmatic palsy following liver transplantation is thought to be related to traumatic crush injury to the right phrenic nerve from a clamp placed on the inferior vena cava (IVC) during surgery.1 The proximity of the phrenic nerve to the IVC renders it very vulnerable to this type of injury from side-to-side cross-clamping of the suprahepatic IVC.1,2 In 2008, we modified our technique to avoid cross-clamping of the IVC by performing cavocavostomy, a type of “piggyback” technique that involves “side-biting” (partial clamping) of the retrohepatic IVC away from the diaphragm.4 Unilateral diaphragmatic palsy can reduce exercise tolerance5 and may place additional mechanical stress on ventilation, which could exacerbate hypoxaemia if these patients develop intercurrent pulmonary infections. Reporting on a series of patients with phrenic nerve injury after liver transplantation, McAlister and colleagues1 found right hemidiaphragmatic palsy in 38% of patients after transplantation, but most of the patients recovered their diaphragmatic function within 9 months. In contrast, our patients did not show any signs of recovery for over 2 years, indicating that loss of diaphragmatic function after liver transplantation may be longstanding or permanent. 1 Comparison of pulmonary function tests before and after orthotopic liver transplantation* Patient 1 Patient 2 Pulmonary function test Before transplant After transplant Difference Before transplant After transplant Difference FEV1 (% of predicted) 2.72 L (80%) 1.73 L (51%) – 29% 2.78 L (85%) 1.40 L (47%) – 38% FVC (% of predicted) 3.79 L (87%) 2.41 L (56%) – 31% 3.83 L (92%) 2.17 L (57%) – 35% FEV1/FVC 0.72 0.72 0.73 0.65 TLC (% of predicted) 5.81 L (87%) 4.28 L (62%) – 25% 7.09 L (110%) 5.18 L (86%) – 24% FEV1 = forced expiratory volume in 1 second. FVC = forced vital capacity. TLC = total lung capacity. * Tests were performed while the patients were in a clinically stable condition. 2 Erect chest x-rays before and after orthotopic liver transplantation, Patient 1 A: In 2005, before liver transplant. B: In 2006, 6 months after liver transplant. Note marked elevation of the right hemidiaphragm and presence of bilateral calcified pleural plaques.

H S Subhash · John W C Chen · Libby John · Jeffery J Bowden · Dimitar Sajkov · Peter Frith

To the Editor: There has been considerable debate about whether selective serotonin reuptake inhibitors (SSRIs) can induce suicidal thoughts and behaviour. Using data from the 2007 National Survey of Mental Health and Wellbeing (NSMHWB),1,2 we examined the relationship between SSRI use and suicidality. The NSMHWB was a nationally representative household survey of 8841 individuals aged 16–85 years. Respondents were interviewed face-to-face and they provided information to assess whether they met International Classification of Diseases (10th revision) criteria for a lifetime affective disorder, and had symptoms in the previous year; had experienced suicidality in the previous year; and had used SSRIs (and/or other psychotropic medications) in the previous fortnight (and, if so, whether they had been taking them for < 1, 1–2, 3–5 or > 5 months). We restricted our analyses to the 555 individuals with symptoms of an affective disorder in the previous year, and examined their suicidality over that year. In our first analysis, we compared those who had used SSRIs in the previous 2 weeks and had been taking them for any duration (n = 109) with those who had not used SSRIs in the previous 2 weeks (n = 446 [respondents in this group were not asked whether they had taken SSRIs at any other time]). Secondly, we compared the subgroup who had been taking SSRIs for more than 5 months (n = 80) with the same non-user group we used in the first analysis. In both analyses, SSRI users were no more likely than non-users to have seriously thought about suicide, made a suicide plan or made a suicide attempt (Box). These findings are consistent with two recent systematic reviews of studies of SSRI use and attempted or completed suicide.3,4 Our study results add to their findings because we considered a fuller range of suicidal thoughts and behaviour. Although the reviews concurred with our findings with respect to adults, they found some evidence for SSRI use increasing the risk of suicidality among children and adolescents. The NSMHWB had limitations, including a potential for recall and misclassification bias, and its inability to account for all possible confounders. Importantly, its cross-sectional nature precluded determining whether an individual’s SSRI use preceded or followed his or her suicidality. By restricting our second analysis to SSRI users who had used SSRIs for more than 5 months, we increased the likelihood that SSRI use occurred first, but we could not determine this conclusively. This would have been a problem had we found an association, because we could not infer the direction of causality. However, with no association demonstrated causality becomes a moot point. Our findings support the contention that SSRI use in adults with affective disorders is not associated with suicide risk. Nonetheless, clinical judgement is required in prescribing SSRIs. Suicidality in the previous year among SSRI users and non-users All users* (n = 109) Non-users† (n = 446) χ2 P Long-term users‡ (n = 80) Non-users† (n = 446) χ2 P Seriously thought about suicide 23% 15% 3.20 0.27 20% 15% 0.83 0.58 Planned suicide 9% 5% 1.76 0.31 4% 5% 0.45 0.41 Attempted suicide 8% 3% 5.23 0.10 2% 3% 0.52 0.52 SSRI = selective serotonin reuptake inhibitor. * SSRI use in previous 2 weeks and for any duration. † No SSRI use in previous 2 weeks (use at other times unknown). ‡ SSRI use in previous 2 weeks and for > 5 months.

Jane E Pirkis · Philip M Burgess · Amy K Johnston · Harvey A Whiteford

To the Editor: On behalf of the Australian Medical Council (AMC), I would like to comment on a recent article1 and two letters2,3 in the Journal about the content of the AMC’s Good medical practice: a code of conduct for doctors in Australia (“the Code”)4 and the consultation process used to support its development. The AMC developed the Code on behalf of state and territory medical boards. It was endorsed by the AMC directors and will be recommended to the new Medical Board of Australia, due to be established later this year. The Code was strengthened by a robust consultation process (supported financially by the Australian Government Department of Health and Ageing) and has been supported by members of the medical profession and the community.5,6 Myers2 seems unaware of the make-up of the AMC, which includes nominees of its many stakeholders (including medical boards). He also seems to be unaware that medical boards in Australia (including the Medical Practitioners Board of Victoria) have already issued codes of professional conduct and that the new national Code brings together and builds on the key elements of these existing codes. The core roles of the AMC are the assessment of international medical graduates on behalf of state and territory medical boards and the accreditation of Australian medical schools and medical colleges. It is not the role of the AMC to “evaluate . . . laws and regulations” or to “address the issue of the accountability of regulatory bodies”, as suggested by Myers. Komesaroff and Kerridge1 and Myers2 appear to believe that a code of professional conduct can be legally binding. Although disciplinary tribunals may use the Code as a guide in their task of assessing allegations of unprofessional conduct, the most important role of the Code is to guide doctors about professionally acceptable conduct. Such conduct is based on many elements, but must especially encompass conduct that is consistent with both professional and legal standards developed by the profession and by parliaments, respectively. It would be neither feasible nor useful to develop a code to guide doctors in meeting those standards in their daily work, without reference to the law and to ethical and professional standards. The Code is not designed to enforce particular kinds of outcomes, but does have an educational focus, and we believe it will contribute to informing and enriching practice. Perhaps Komesaroff, Kerridge and Myers would do well to familiarise themselves with the codes of conduct already in place around Australia and to recognise that they have been used for many years by medical boards to assess complaints about doctors’ conduct. The final code is available online.4 It will be interesting to observe how it is used in the years ahead.

Richard A Smallwood

To the Editor: Complementary and alternative medicine (CAM)1 has become increasingly popular, with Australians spending an estimated $1.8 billion on CAM per year.2 We conducted a prospective study to determine the prevalence and patterns of CAM use among Australian patients with osteoporosis and to identify demographic, socioeconomic and disease-specific features that predict its use. A recent Canadian study of 360 patients with osteoporosis showed that 57% used CAM; CAM users tended to be younger than non-users and better educated, but with a lower quality-of-life score for mental health.3 To our knowledge, there have been no similar studies carried out in Australia. We surveyed 202 randomly selected patients of a Sydney tertiary hospital osteoporosis clinic over a 10-month period (March to December 2007). The clinic sees a wide spectrum of people, from healthy postmenopausal women to patients with multiple comorbidities. At their routine clinic visits, participants completed a prospective questionnaire based on previous CAM therapy surveys.3,4 They were asked about use of CAM, reasons for use, cost, perceived benefits, household income, medical insurance status and educational background. Ethics approval for the survey was obtained from the hospital’s ethics review board. The mean age of participants was 68.5 years (SD, 10.9 years); 80% were women; and 56% were born overseas. We analysed responses using firstly a fairly broad “standard” definition of CAM (including all therapies listed in the Box), and then a more stringent definition that excluded hypnosis, multivitamin therapy, tai chi and yoga. CAM use was reported by 104 patients (51%) and 62 patients (31%) based on the standard and stringent definitions, respectively. Comparative popularity of the CAM therapies used by the surveyed patients is shown in the Box. Common reasons for CAM usage were its holistic approach (53%) and the perception that conventional therapy was providing inadequate pain control (29%). Seventy-three per cent of respondents did not consult a physician before starting CAM, and 23% stated that their treating specialists were unaware of their CAM use. Eighty-eight per cent paid for their therapies out of pocket and the mean cost per patient per month was $21. (Given that 2.2 million Australians have an osteoporosis-related condition5 and 51% of these patients use CAM, the estimated annual expenditure on CAM therapies by patients with osteoporosis is $696 million.) CAM users were more likely than non-CAM users to be university-educated (26% v 14%; P = 0.05); to be born in Asia (20% v 13%; P = 0.03); to have a lower lumbar spine bone mineral density T score (mean, − 2.35 SD v − 2.20 SD; P = 0.05); and to make more frequent clinic visits (mean T score, 1.8 v 1.5 visits /12 months; P = 0.03). More than half the respondents (57%) were unable to differentiate between the terms “osteoporosis” and “osteoarthritis”, especially those from a non-English-speaking background (64% compared with 46% of patients from English-speaking backgrounds; P = 0.02) and CAM non-users (57% compared with 41% of CAM users; P = 0.01). The proportion of patients using CAM in our study was comparable to the proportion in a similar Canadian cohort (51% v 57%).3 Patients who resort to CAM for pain relief may be suffering residual fracture pain or coexisting conditions, such as osteoarthritis; patients unable to differentiate between osteoporosis and osteoarthritis may be seeking relief from pain caused by the latter. Given the low rate of patient disclosure of CAM use to physicians in our study and the reasonable chance of interaction between CAM and conventional therapies (17%),3 physicians would be prudent to regularly and clearly discuss concurrent CAM use with patients (using interpreters when necessary) to avoid potentially harmful drug interactions and side effects. At the same time, physicians could recommend appropriate balance-training therapies,6 such as tai chi, which has been shown to improve bone health and prevent falls.7 Proportion of osteoporosis clinic patients who reported using various complementary and alternative medicine (CAM) therapies (n = 104) Therapy No. (%) of patients* Multivitamins 25 (24%) Fish oil 24 (23%) Acupuncture 20 (19%) Tai chi 15 (14%) Glucosamine 14 (13%) Yoga 13 (13%) Chiropractic/osteopathy 12 (12%) Naturopathy 6 (6%) Herbal therapy 5 (5%) Chinese medicine 3 (3%) Aromatherapy 2 (2%) Massage therapy 2 (2%) Homeopathy 1 (1%) Hypnosis 1 (1%) Minerals 1 (1%) Laser therapy 1 (1%) Any CAM (standard definition) † 104 (51%)‡ Any CAM (stringent definition) † 62 (31%)‡ * Percentages total > 100% because patients used multiple therapies. † The standard definition of CAM includes all therapies listed here; the stringent definition excludes hypnosis, multivitamin therapy, tai chi and yoga. ‡ These are percentages of the total sample (N = 202).

Jenson C S Mak · Steven Faux

To the Editor: Robertson and Kerridge1 criticised our article “Patient privacy versus protecting the patient and the health system from harm”2 based on an interpretation that we were advocating notification for all patients with somatisation disorders, but our recommendation for a confidential notification system pertained specifically to factitious disorder. We agree that “ignoring or failing to integrate mental health care in future health planning is to invite a higher burden of morbidity, mortality and cost”.1 Indeed, we do not wish to “[constrain] the patient’s interaction with the health system”, but rather believe that a more complete, accurate and easily available patient history would allow doctors to optimise such patients’ care within the system. Clinically appropriate resource allocation would substitute appropriate psychiatric/psychological and primary care for more costly and inappropriate (potentially harmful) emergency and procedural care, such as numerous cardiac catheterisations. The case described in our article illustrates well the higher burden of morbidity and cost that the patient, and the system, had to endure because of the failure of multiple health providers across a range of acute settings to diagnose and treat the patient’s primary illness.2 Avoidance of truthful disclosure on the part of the patient contributes to this diagnostic failure. An electronic medical record (EMR) notification in this kind of case would allow any given doctor to overcome the otherwise almost insurmountable barriers to collating such a patient’s history, and thus to be aware of, to balance and to manage the factitious disorder diagnosis — a notoriously difficult task.3 Robertson and Kerridge argue there is a lack of evidence for “costly” EMR systems. However, it has been found that “Hospitals with automated notes and records [have] fewer complications, lower mortality rates, and lower costs”.4 A truly private portable EMR should help all patients obtain more appropriate and cost-effective care, by reducing duplication of costly investigations and doctors’ time spent chasing records. Conversely, patients might reasonably abhor a privacy system that inadvertently results in duplicate computed tomography scans — the prior records being “private” and unavailable — when radiation exposure increases the risk of cancer.5 We would be the first to acknowledge the risk of “stigmatisation” and agree with safeguards to mitigate potential consequences, as mentioned in our article.2 However, in the case of this patient and others in a similar situation, we still believe that he, the doctors struggling to provide appropriate care, and the system deserve better, which certainly won’t happen with the status quo.

Dawn E DeWitt · Ravi Bhat · Stephanie Ward

To the Editor: ANZAME (the Australian and New Zealand Association for Medical Education) shares two significant concerns about medical education in Australia that were raised in articles published recently in the Journal.1,2 The first concern is the status of health professional education (HPE) research in Australia. In 2007, the ANZAME Committee of Management investigated the profile of HPE research with the National Health and Medical Research Council (NHMRC) and the Australian Research Council (ARC); both noted they would accept grant applications for such research. At that time, the ARC indicated that they did not have any HPE research expertise among their reviewers. A number of nominations, which included ANZAME members, were made, and the comments of Roberts and Conn1 suggest this has been successful. HPE research was further assisted by an Australian Bureau of Statistics “Field of Research” classification. Professor Brian Jolly was instrumental in achieving this classification code. Fortunately, the code occurs in the education section, as ARC guidelines state they will not fund medical or dental research. At each annual ANZAME conference, educational research is discussed and presented. While Roberts and Conn are correct in stating that other local conferences on education have arisen in recent years,1 this year’s ANZAME conference was the largest ever, and showcased a wide range of research, both completed and in progress. ANZAME also promotes research through seeding grants, by providing particular supports to students who undertake educational research, and by publishing educational research articles in the Association’s journal, Focus on Health Professional Education. The second concern is the need for significant increases in the number of health professional educators to meet the needs of increasing numbers of students and young professionals. Such educators are invariably swamped by the aspects of their work related to program delivery and service requirements, at the expense of research activity. Brooks’ proposal to establish academic centres2 may go some way to overcoming this. However, we need to develop the HPE expertise that will enable new and innovative educational programs to be developed, implemented and evaluated. How are we going to recruit and train HPE academics for these roles? Earlier this year, ANZAME put out a draft position statement to highlight some of the issues and to indicate our support for promoting academic pathways.3 Workshops at the recent ANZAME conference further refined a set of recommendations. It will take vision, time, commitment, and a real increase in funding to ensure we have the trained personnel in place to achieve the required outcomes. HPE in Australia and New Zealand has matured — it now needs support for ongoing research and careful workforce planning to ensure the high quality of health professional educators is maintained.

on behalf of the ANZAME Committee of Management