Letters

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

Alexander S Gallus

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

Ian Hamilton-Craig

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

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

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

Caroline F Finch

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

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

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

Sandy L A Reid

To the Editor: One of the great privileges in practising obstetric medicine is to support a couple through a successful confinement when they have previously been advised against attempting pregnancy because of pre-existing maternal disease. However, in some cases, pregnancy carries a substantial risk of morbidity and mortality to both the mother and infant. Indeed, many maternal deaths in Australia are still preventable,1 and underlying cardiac disease is an important cause.2 Recently, I was consulted for preconception counselling by a young woman with dilated cardiomyopathy. Based on the limited evidence in the literature, her risk of dying as a result of pregnancy would be greater than 25%.3 Similarly, I was recently involved in the care of a young woman with Eisenmenger syndrome who elected to terminate her pregnancy due to the 50% mortality associated with pregnancy with this condition.4 Pregnancy in young women with moderate renal failure carries a significant risk of permanent decline in renal function, along with a high risk of intrauterine growth retardation and prematurity for the baby.5 Organ transplantation offers the best hope for women in this situation, as pregnancy outcomes are excellent after solid organ transplantation (with the exception of lung transplantation). However, many women have organ dysfunction severe enough to compromise pregnancy outcome, but not to warrant transplantation.6 Pregnancy in the presence of maternal disease may also pose a substantial cost to the community. A 2001 study in the United Kingdom estimated the mean cost of pregnancy care for five mothers with severe cardiac disease to be £23 000, not including the cost of neonatal care.7 One mother and one baby died. Options for couples with pre-existing maternal disease are limited. In Queensland, they are excluded from adopting a child because they are not infertile and because of the mother’s medical condition. Altruistic surrogacy would allow them to have a child that is genetically their own without risking the mother’s and infant’s health. However, legislation on surrogacy varies significantly between Australian jurisdictions (Box),8 and, in Queensland, all surrogacy arrangements — both commercial and altruistic — are illegal. Thus, my patient with dilated cardiomyopathy faces prosecution if she were to attempt surrogacy anywhere in Australia while a Queensland resident, whereas it would be freely available to her if she moved 80 km south and became a New South Wales resident. I believe altruistic surrogacy should be available for women in whom underlying medical conditions result in a significant risk of morbidity or mortality associated with pregnancy. Legislation on surrogacy arrangements in Australia* Queensland: The Surrogate Parenthood Act 1988 (Qld) makes all arrangements relating to surrogacy illegal in Queensland, imposing criminal penalties on all parties involved in both altruistic and commercial surrogacy arrangements. Tasmania: The Surrogacy Contracts Act 1993 (Tas) makes it an offence to make or receive a payment or to publish any advertisement in relation to a surrogacy contract. All surrogacy contracts are void and unenforceable. South Australia: The Family Relationships Act 1975 (SA) makes it an offence to enter into a surrogacy contract for valuable consideration, and contracts are illegal and void. Australian Capital Territory: The Parentage Act 2004 (ACT) does not prohibit non-commercial surrogacy, provided no advertising or intermediaries are involved, and payments to cover expenses are allowed. Victoria: The Infertility Treatment Act 1995 (Vic) prohibits commercial surrogacy, and has complex criteria regarding eligibility of surrogate mothers. * New South Wales, Western Australia and the Northern Territory do not have surrogacy legislation.

Adam P Morton

Comment: Morton feels that women for whom pregnancy poses a substantial risk should be offered altruistic surrogacy, so that they can still have a child that is genetically their own. The suggestion is commendable but opens a hornets’ nest. First, “genetic ownership” is a bit of a fiction at best, given that the only item genetically owned by the mother is an egg with 23 chromosomes and some cytoplasm. Admittedly, Morton refers to couples rather than to women, but few are the men who have incontrovertible evidence of any genetic stake in their alleged offspring,1 and, given the rate with which partnerships change, thousands willingly care for children in whom they know they have no genetic stake at all. After implantation of the fertilised embryo, the carrier of the pregnancy owns whatever there is to be owned, irrespective of where some of the genes came from. At birth, genetic ownership changes again, and the child becomes its own “genetic owner”. So, how much “genetic ownership” of a child can there be? Second, who would qualify for altruistic surrogacy? It seems reasonable that women with Eisenmenger syndrome should not embark on a pregnancy given the high mortality associated with it. But how do we know that collecting ova and all it entails, and the subsequent years caring for a baby/toddler/child/teenager, would not be an even greater challenge to the woman’s health than pregnancy? Third, where will these surrogates come from (especially for women without sisters or other suitable family volunteers), and how do we ensure that they will be happy to hand back the child to its “genetic owners”? How will we protect these altruistic women in subsequent years against potential law suits for alleged failures in duty of care to the child that they carried (for example, by exposure to toxins during the pregnancy)? Fourth, is there not a far easier and more logical solution to this problem, provided that egg collection does not endanger the woman’s health? Why not preserve the woman and her partner’s frozen embryos until the woman’s medical condition is sufficiently stable to both sustain a pregnancy and care for the child that hopefully results from it? If the woman’s health cannot be restored sufficiently to achieve this, these couples could then show some altruism of their own by donating the embryos to infertile couples who desperately want a child irrespective of whether they can claim “genetic ownership”. Thus far, there is little evidence that altruistic donation and genetic ownership are even half way to meeting each other.2 However, Morton should be commended for drawing attention to a national problem in women’s health. The disparities and discrepancies between the Australian states and territories in almost anything that relates to reproduction2-5 is an utter disgrace. Reproductive health should be equitable among all Australians.

Marc J N C Keirse

To the Editor: Osteonecrosis of the jaw, recently reported in patients treated with bisphosphonates, may be analogous to the historic occupational disease “phossy jaw”.1,2 Phossy jaw was osteonecrosis of the jaw caused by exposure to white phosphorus during the manufacture of matches. “Lucifer” strike-anywhere matches were first produced in 1833. They were made by dipping the match ends into a mixture containing white phosphorus.3 Workers were exposed to fumes from the white phosphorus during mixing and spreading of the dip material, and dipping, drying and boxing of the matches.3,4 The first case series, comprising 22 cases, was reported in Vienna in 1845.5 About 11% of those exposed developed the disease.5 The average period from first exposure to diagnosis was 5 years.4,5 Occasionally, this period was as short as a few months.5 The mandible and maxilla could be affected, the mandible in 60% of cases (Box).3 Dental decay was considered a prerequisite, and preventive measures included dental surveillance and treatment within the factories.4 In that pre-antibiotic era, phossy jaw was fatal in about 20% of cases, usually because of septicaemia or meningitis.5 Donald Hunter, British doyen of occupational medicine, commented: “It was the most distressing of all the occupational diseases because it was very painful and was accompanied by a foul fetid discharge that made its victims almost unendurable to others. It was obstinate and chronic, the treatment was agonising and the final result was a distressing disfigurement. It was this disfiguring effect plain to every observer that made phosphorus poisoning so notorious and led to determined efforts for its abolition in every civilised land.”5 In 1906, several European countries banned the manufacture and importation of white phosphorus matches at the Berne Convention.4,5 A safe substitute, sesquisulfide, had been discovered by a French chemist and successfully used for manufacture of strike-anywhere matches in 1898.4,6 In the United States, John Andrews published a report in 1910 of 150 cases of phossy jaw from 15 of 16 match factories then in operation.4,6 The Diamond Match Company, which held the American patent rights for sesquisulfide, waived their rights, thereby allowing the entire US match industry to use this alternative.6 Congress then passed the Esch law, which imposed a prohibitive tax on white phosphorus matches and banned their import and export.4,6 Eventually safety matches were developed that used amorphous red phosphorus, which did not have the toxic properties of white phosphorus.5 Phosphorus necrosis of the jaw A Deformity resulting from excision of entire lower jaw in a case of phosphorus necrosis. (Case of Dr John P. Andrews, The Occupational Diseases, W Gilman Thompson, D Appleton & Co, New York, 1914). B Phosphorus necrosis of entire lower jaw excised by Mr McCarthy in 1884 (London Hospital Medical College Museum).

A Michael Donoghue

Peter W Holmes,* David Armstrong,† Nicholas Freezer‡ * Deputy Director, Adult Respiratory Medicine, † Director, Paediatric Cystic Fibrosis Unit, ‡ Director, Adult and Paediatric Respiratory Medicine, Department of Respiratory and Sleep Medicine, Monash Medical Centre, Locked Bag 29, Clayton, VIC 3168. peter.holmesATsouthernhealth.org.au To the Editor: We congratulate Lam et al1 for identifying the major problems in transferring adolescents from the Royal Children’s Hospital, Melbourne, to adult care. The article and the accompanying editorial2 address a difficult problem relating to the transfer of adolescent patients from a stand-alone paediatric hospital to adult services. Lam et al conclude that there needs to be a change of attitude among adult physicians, and recommend the provision of additional resources to enhance the smooth transition to adult care. As long as paediatric services remain geographically separated from their adult counterparts in stand-alone hospitals, these problems will continue, regardless of any increase in resources. In New South Wales, tertiary paediatric services have now been incorporated onto the same campus as tertiary adult hospitals in shared-site arrangements. This facilitates the transition process, as adult physicians are more closely linked to their paediatric colleagues via shared clinical and research infrastructures. Such close cooperation allows paediatric and adult physicians to share their care during transition and provides the adult physicians with full access to the patients’ medical records and radiology, microbiology, laboratory and pulmonary function data. At Monash Medical Centre, we have taken this further by totally incorporating our adult and paediatric services into one single Department of Respiratory and Sleep Medicine. This arrangement allows an integrated approach to childhood, adolescent and adult care. The combination of services generates trust between all members of staff (an issue raised in the editorial2) and gives adult physicians a greater understanding of the needs of adolescents with complex health problems. One solution to the difficult problem of transition to adult care is to phase out stand-alone paediatric services with their own costly management infrastructure. A shared campus arrangement allows greater integration of the full range of tertiary paediatric and adult services and offers many advantages in providing a seamless transition to adult care.

Peter W Holmes · David Armstrong · Nicholas Freezer

Robert D Henderson,* Pamela A McCombe* * Neurologist, Royal Brisbane and Women’s Hospital, Herston Road, Herston, QLD 4029. Robert_HendersonAThealth.qld.gov.au To the Editor: We read with interest the recent article by Kiernan.1 Many patients with motor neurone disease (MND) are also taking complementary therapies, with the potential for drug interaction with riluzole. A recent patient highlighted this. A man in his 50s with progressive MND commenced riluzole at the time of diagnosis. Initial liver function tests performed after starting the drug gave normal results. Eight months later, with disease progression, he began taking low-dose naltrexone 50 mg dissolved in 50 mL of water, of which he took 4 mL a day. Three months later, he began to feel nauseous, with debilitating lethargy, and developed jaundice. Liver function tests showed: alanine aminotransferase level, 3030 U/L; and asparate aminotransferase level, 2074 U/L. On stopping taking both drugs, his symptoms resolved and the liver function test results gradually became normal. No other contributing cause for the hepatotoxicity was found. From the temporal profile, the hepatotoxicity in our patient was possibly due to the combination of riluzole and naltrexone, although either drug alone could be implicated, or there may have been another mechanism. Riluzole is predominantly metabolised by cytochrome P450 enzymes (CYP1A2), but there is considerable patient variability, and the hepatotoxicity mechanism is largely unknown2 (see also MIMS Online: http://www.mims.hcn.net.au). In recent months, low-dose naltrexone has become popular with patients who have MND, although there are no published data of efficacy. Hepatotoxicity caused by naltrexone is dose-dependent and uncommon.3 Naltrexone is metabolised by glucuronidation in the liver to an active metabolite, but a direct interaction with riluzole through cytochrome P450 enzymes appears unlikely.4 There have been no clinical studies to evaluate interactions with other drugs of either riluzole or naltrexone (apart from opiates).3 This case highlighted for us that patients may be taking other therapies for MND, and that clinicians should be aware of the possibility of serious drug interactions when riluzole is prescribed.

Robert D Henderson · Pamela A McCombe

In reply: Henderson and McCombe describe a patient to highlight an issue raised in a recent editorial:1 that patients with motor neurone disease (MND) may develop abnormal liver function tests for reasons other than riluzole therapy. In their patient, riluzole was prescribed for a year and liver function test results remained stable. Deterioration in liver function coincided with the introduction of naltrexone. Ultimately, riluzole, an established MND therapy, had to be ceased. Naltrexone is an authority medication, prescribed in the setting of alcohol or opioid dependence. MEDLINE searches failed to find any study or indication for naltrexone in the treatment of MND. An internet search, however, revealed a number of personal anecdotes, with a curiously Australian emphasis, suggesting an immuno-modulatory role for naltrexone in MND. A few further clicks of the mouse and the naltrexone ordering site with costings appeared. Patients with incurable diseases commonly seek “alternative” treatments2 at great personal financial cost, calculated at thousands of dollars per patient with MND.3 Often there is insufficient, or, as with naltrexone, no evidence that these treatments are effective.4 Most patients with MND will consider alternative therapy, irrespective of their educational background5 or understanding of disease pathophysiology. How each physician approaches the use of complementary and alternative therapies by their patients may develop into an important issue in the therapeutic relationship. Certainly, being aware of the possibility may prove critical. In the patient described by Henderson and McCombe, an unfortunate outcome of irreversible liver failure in a patient with NMD was averted through conventional monitoring of liver function.

Matthew C Kiernan

To the Editor: Forder et al conveyed that trials without allocation concealment have the potential to mislead.1 However, it is not true in any meaningful sense that “Without exception, allocation concealment is achievable in all randomised clinical trials. In contrast, it is not always possible to blind people to study treatments received.” Rather, “Masking may be defined as either the process (researchers not revealing treatment codes until the database is locked) or the result (complete ignorance of all trial participants as to which patients received which treatments). A masking claim indicates only the former . . . If masking is possible only some of the time, then clearly reference is being made to the result, and not the process. To be fair, then, one would have to ask if the result of allocation concealment is always possible . . . only the process of allocation concealment, but not its result, can be ensured.”2 Forder et al also state that certain methods (including sealed envelopes) are considered to be adequate concealment methods. Sadly, this is true, but only if the emphasis is on the word “considered”, because sealed envelopes are both imperfect at preventing direct observation of future allocations and useless at preventing the prediction of future allocations, even without direct observation. Because the extent of prediction depends on the specific restrictions used on the randomisation,3 allocation concealment is not even a binary phenomenon, and so to truly assess allocation concealment in a given trial, one must ask how much prediction is possible in that trial. Allocation concealment is perfect if no observation or prediction is possible, and only partially effective if some prediction is possible. Many trials use randomised blocks, and smaller block sizes tend to allow for substantial prediction.3-5 So, while methods aimed only at preventing the direct observations of future allocations may be considered to be adequate, it is clear that in reality they are not. That the authors failed to use this opportunity to set the record straight indicates their implicit agreement with the incorrect statement that methods aimed only at preventing the direct observations of future allocations are not only considered adequate, but actually are adequate. Pretending that allocation concealment is binary, and hence that it suffices to use methods aimed only at preventing the direct observations of future allocations, represents ignorance that may be bliss, but certainly is not harmless.

Vance W Berger

To the Editor: In their article on controlled trials, Forder et al1 described the trial by Karlowski et al on vitamin C and the common cold2 as an example of how patients’ or investigators’ preconceptions about the value of the treatment may affect a trial’s results. However, their presentation of this trial is misleading in two respects. Firstly, the Karlowski et al trial was reanalysed and the “placebo-effect explanation” of the original authors was shown to be erroneous.3 For example, their subgroup analysis of “blinded” and “non-blinded” participants excluded 42% of all episodes of colds, even though the subgroups were presented as complementary; numerous further problems are detailed elsewhere.3 Thus, the trial by Karlowski and colleagues cannot be seen as an example of the placebo effect in action. The concept of large and omnipresent placebo effects can be traced back to an early article by Beecher, who chose “15 illustrative studies” covering such conditions as, “severe postoperative wound pain, cough, headache, seasickness, etc.”4 Beecher calculated that the “average placebo-effect” was 35.2% (SE, ± 2.2%). However, these studies did not use a control group. The comparison was “before–after”, which is affected by the regression to the mean phenomenon as most of these conditions are self-limiting. Thus, Beecher’s studies did not measure the “effect” of placebo. A recent meta-analysis of 114 trials comparing a placebo group with a no-treatment group found no evidence of placebo effect on binary outcomes, and only a rather small effect on pain, thus disproving Beecher’s notion of great and universal placebo-effects.5 This empirical evidence was disregarded by Forder and colleagues. Although there are reasons to use placebo whenever practicable, the bias caused by the absence of a placebo control should not be exaggerated, and the “placebo effect” should also not be misused to support investigators’ own preconceptions.3 Secondly, the trial by Karlowski et al was focused on the effect of vitamin C on the common cold,2 and thus the “placebo effect explanation” in this particularly influential trial is crucial to the biological question. A recent meta-analysis of 55 placebo-controlled trials found that regular vitamin C supplementation had no effect on the incidence of colds in the general population (relative risk [RR], 0.98; 95% CI, 0.95–1.00), but reduced the incidence of colds in people exposed to substantial physical or cold stress (RR, 0.50; 95% CI, 0.38–0.66).6 Also, regular vitamin C intake reduced the duration of colds in adults by 8% (95% CI, 3%–13%) and in children by 13.5% (95% CI, 5%–21%). Although further studies are needed to evaluate the practical significance of these findings, it is evident that the interpretation by Karlowski and colleagues that the effect of vitamin C on the common cold may be explained by the break in the double blind2 is false and should not be reiterated.

Harri Hemilä

Peta M Forder,* Val J Gebski,† Anthony C Keech‡ * Statistician, † Principal Research Fellow, ‡ Deputy Director, NHMRC Clinical Trials Centre, University of Sydney, Locked Bag 77, Camperdown, NSW 1450. enquiryATctc.usyd.edu.au In reply: Allocation concealment refers to ignorance of future treatment assignment before randomisation whereas masking or blinding is most commonly used to refer to the concealment of treatment assignment after randomisation.1 There are two criteria for successful concealment of allocation: (i) physical concealment of the process of random assignment to treatment, and (ii) concealment of any pattern of consecutive assignments. Successful concealment of the process must prevent unauthorised access to randomisation lists, envelopes or algorithms; the best way is to use a centralised or remote service for randomisation, whereby an independent party other than the clinician or investigator accesses a secure sequence list or a secure computer system to generate the next allocation.2,3 Successful concealment of the pattern of random assignments prevents investigators from predicting a future treatment assignment on the basis of pattern recognition of allocations to date. Identifying a pattern of previous allocations can occur in open-label trials, in which all parties are aware of allocated treatments after randomisation, or if the blinding of patients and investigators has been compromised. The likely success of concealing the allocation process can reasonably be judged by its description in most trial reports (usually found in the Methods section). However, it is usually more difficult to assess the likelihood that investigators could have predicted future allocations. Unsuccessful concealment of treatment assignment after randomisation (masking or blinding) should be detailed in the trial report. In circumstances where the blinding has been substantially compromised, exploring the results of treatment separately among participants who were unblinded and those who remained blinded, should be considered, although these are no longer randomised comparisons. In the study by Karlowski et al,4 the placebo did not match the active treatment in taste, which alerted the investigators to the likely occurrence of significant unblinding within the study. To their credit, the investigators sought to quantify the extent of unblinding by means of a questionnaire at study close-out, and reported their findings by results of these responses. The particular grouping of responses, however, has been the subject of some discussion,5,6 and while the interpretation of a possible placebo effect has been challenged, it has not necessarily been disproven. (The absence of a placebo effect could be proven only if information concerning perceived benefits of vitamin C related more to cold frequency than cold symptoms. Biologically, it is far more plausible for a placebo effect to result in fewer cold symptoms reported than fewer colds reported.) This trial highlights the impact of compromised blinding in the reporting of trial results, emphasising the importance of maintaining adequate blinding for reliable and unbiased trial results. Good quality reporting of trials, in accordance with the CONSORT statement,7 includes describing the processes in enough detail to assure readers that any pattern of randomisation is not predictable. Authors should report issues relating to allocation concealment, blinding (where appropriate) and randomisation sufficiently to convey the message that these essential trial principles were successfully achieved.8

Peta M Forder · Val J Gebski · Anthony C Keech

H Patrick McNeil,* Michael C Grimm† * Associate Dean (Medical Education), South Western Sydney Clinical School, † Associate Professor of Medicine, St George Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2052. p.mcneilATunsw.edu.au To the Editor: We read with interest the article by Koczwara and colleagues proposing a national exit examination for all Australian medical school graduates.1 It is refreshing to see interest in educational outcomes, a distinctly different trend from earlier reforms that shifted curricular focus from content to the learning process, exemplified by problem-based learning (PBL). Although the early process-focused programs were based on sound pedagogy current at their time, their educational outcomes have been relatively disappointing, with marginal or no demonstrable improvements in knowledge structures, clinical skills, or generic capabilities such as self-direction.2 Rather than an indictment of PBL, the results may reflect what was missing in those programs: explicit focus on educational outcomes, alignment of assessments with outcomes, and attention to the learning environment. There is widespread agreement on the outcomes desired by medical schools. They include teamwork, effective communication, critical evaluation and reflective practice, as well as more traditional outcomes.3 Unfortunately, assessment methods have been slow to match curricular reforms, as these outcomes require new approaches, such as group and assignment work, peer assessment and portfolio examination, which are only now emerging in Australia.4 A national exit examination for Australian graduates is unlikely to adequately measure this range of outcomes. While Koczwara and colleagues recognise that a national examination “might need to include a clinical component” and “would necessarily entail the explicit statement of professional values and expectations”, they support a multiple-choice question examination, suggesting such performance “can correlate well with clinical skills and future performance in multiple disciplines”.1 While this might “complement rather than replace” other medical school assessments, the message sent by its failure to address personal and professional attributes would be invidious. In recognition of the limitations of multiple-choice questions, national examinations in North America now include a clinical component.5 This has major resource implications and, like all high-stakes assessments, uses relatively reliable, but much less valid measures — standardised or simulated clinical encounters. This is at odds with current initiatives in medical schools, which are moving to clinical assessments with higher face validity, such as the mini-CEX (mini-clinical examination exercise).6 It would be near impossible to adequately measure generic outcomes, such as teamwork, communication and reflection, in a single national examination. Koczwara et al recognise that insufficient attention has been paid to ensuring that achievement of educational outcomes is embedded in reform of medical curricula. Their solution is overly simple for a highly complex set of issues.

H Patrick McNeil · Michael C Grimm

Christopher Lawson-Smith Surgeon, and Surgical Examiner, Australian Medical Council, 1/10 McCourt Street, Leederville, WA 6007. lawsmithATbigpond.net.au To the Editor: Foreign medical graduates sitting for the Australian Medical Council (AMC) examinations are expected to achieve a standard comparable to that of Australian medical students. If we do not measure the level of knowledge and problem-solving ability nationally, there is no reasonable basis for presuming that the AMC examination is fair. A uniform examination-based assessment should be passed by all potential medical practitioners before registration in Australia. I would be in favour of a national exit examination.1

Christopher Lawson-Smith

To the Editor: The recent article by Koczwara and colleagues proposing a national exit examination for medical students1 prompted me to recall a 1970 trial of a national examination in surgery.2 Seven of the then eight medical schools participated. Interstate differences were wide for some questions; separate analyses of the 15 teaching hospitals showed variation to be even wider within a university than between universities. Do local differences still undermine the validity of a national examination? It is still uncertain what is actually tested by questions on paper. Context-free, standardised questions and answers assume clinical teaching and practice are standardised. However, clinical teachers writing examination items know well that many colleagues choose the “wrong” answer. Consensus may be imposed on those who differ. Teachers then forget their disparity, but expect candidates to choose only one “true” answer! Clinical performance is interactive, multifaceted, situation-specific and value-laden. Complex judgement and decision-making cannot be measured by ticking predetermined boxes. Clinical experts develop personal subsets of specific evidence, and seek different data for diagnosis and management. But separate, context-free tasks, as in an objective structured clinical examination (OSCE), naively assume they do not.3 OSCE even standardises scoring; examiners become recorders rather than assessors. Reductionist standardisation reflects a pseudoscientific attempt to apply objectivity, consistency and precision to complex human interactions around incomplete evidence and uncertainty, approximations, judgements, trade-offs and locally-determined decisions.4 Internal consistency of measuring instruments does not confer external validity in real world clinical practice. The inexorable growth of medical knowledge and technological opportunities continuously expands “what every doctor should know”. Medical learning today embraces a mix of science-based, problem-based and work-based learning experiences, with community-based experiences5 increasingly included. In their recent article, Koczwara and colleagues identified gaps in oncology education,2 a field ranging from molecular processes to euthanasia. Is oncology managed and taught consistently across different medical schools and hospitals across Australia? Which facets would you test in a national exit examination?6 Clinical performance today includes patient/person management, case management, health system management and self-management. Clinicians can judge student performance consistently. However, formal clinical examinations lack the range of cases and open-ended time that allow examiners to observe all the patient-care skills espoused by today’s curricula.7 Assessment of performance in case management and procedural skills within hospital practice can be conducted simpy by paired examiners.8

Ken Cox

In reply: We appreciate the insightful responses to our proposal.1 Lawson-Smith alludes to one of the most significant justifications for a national examination — fairness. One cannot expect foreign medical graduates to attain a standard comparable with that of Australian graduates if we do not measure this standard. We propose that we owe fairness not only to foreign graduates coming to Australia, but also to Australian medical students who have a right to confidently expect an education that will lead to similar knowledge, skills and attitudes, irrespective of which university they choose. And finally, we owe fairness to society, which would also expect the same standards of graduates irrespective of where they come from. Unless we consider what are acceptable standards, we operate within an environment where standards of outcome differ from place to place and as we do not measure outcomes uniformly, we do not know how they differ nor have a system to address potential deficiencies. McNeil and Grimm point out that medical education has focused less on outcomes and more on process, and raise concerns that assessment methods lag in the sophistication necessary to assess outcomes. We wonder whether the reason for this lack of sophistication lies in the relative lack of interest in this field, and also in the lack of agreement on what constitutes acceptable outcomes. The process of outcome assessment is indeed complex, and the first step is national consensus on appropriate outcomes to be uniformly achieved. McNeil and Grimm also point out that some of the desirable outcomes, such as teamwork, effective communication, critical evaluation and reflective practice, may be harder to test than medical knowledge. While this is certainly the case, reliable assessment methods do exist, such as the Moral Judgment Interview2 and Rest’s Defining Issues test.3 The mini-CEX (mini-clinical examination exercise) that McNeil and Grimm refer to, allows testing of judgement, professionalism, communication, organisation and efficiency.4 Cox questions whether a written examination can test the complex judgement and decision-making process that is better tested in the clinical setting by experienced clinicians. We propose that the national examination is not meant to replace clinician-based assessments and ongoing learning and feedback. Furthermore, a national examination does not need to be conducted only in the written form. Specialty exams already conducted nationally incorporate a clinical element and are conducted in multiple locations. The main objective of a national examination is to ensure the comparison of outcomes against agreed acceptable national standards. This objective should not impose specific limitations on the structure of the examination. Cox warns of the risk of “reductionist standardisation” and asks whether oncology is taught consistently across different medical schools in Australia. We acknowledge that uncertainty is ever present in medical decision-making, but remain hopeful that there exist core knowledge, skills and attitudes that patients can expect and that can provide a foundation for national standards. Oncology is not taught consistently across different medical schools in Australia today. While its mode of delivery may differ, we propose that its outcomes should not. And we hope that agreement on national outcome standards and a national process of assessment of these outcomes will be a first step in achieving that objective.

Bogda Koczwara

To the Editor: GP-Psych Support is a national advice service on mental health management that links general practitioners (GPs) with psychiatrists by phone, fax or email within 24 hours. The service is federally funded through the Better Outcomes in Mental Health Care Initiative, and began operating in March 2004. Over the first 6 months of operation of the phone/fax arm, there were 726 case discussions between GPs and psychiatrists. A third of the GPs were rurally located, and 17% used the service twice or more. Most GPs (94%) accessed the service through the 1800 freecall number, rather than by fax. Three-quarters identified no other suitable, accessible source of urgent psychiatric advice. Two-thirds of cases involved female patients, and 80% were aged 19–65 years. In only 14% of cases was another mental health service provider involved (a psychiatrist in 2%). The primary diagnoses are shown in the Box. The most common topic discussed was medication (77%), with less demand for discussions of general management principles (12%) or diagnosis (7%). However, cases were discussed broadly, and referral to another mental-health care provider was recommended in a third of cases, including to a psychiatrist in 8% of cases. An evaluation survey with 450 randomly selected GP service users received 129 replies. Although the survey response was low (29%), the feedback was very positive, with over 99% of respondents indicating that they would consider using the service again. Over 95% of respondents reported satisfaction with the service in terms of ease of use, helpfulness of advice and ease of interaction with the psychiatrist. Compared with other sources of mental-health care advice, over 85% rated GP-Psych Support as better in regard to accessibility, reliability and the appropriateness of the advice given. Over 70% stated that contact with the service had increased their knowledge about the management of mental disorders and their confidence in managing mental health problems, and had improved the quality of care they provided to their patients. Fifty-three per cent of GPs reported an increased willingness to manage more complex mental health problems. From these data, it appears that psychiatrist telephone support has been well received and adds significantly to the resources available to GPs working in mental health care. The 10 most common primary diagnoses among 726 patients discussed in GP-Psych Support Diagnosis Percentage of patients Depression 45.9% Mixed anxiety and depression 12.6% Chronic psychotic disorder 8.8% Anxiety disorder 8.6% Acute psychotic episode 5.2% Bipolar disorder 5.1% Organic or cognitive disorder 3.6% Drug or alcohol use disorder 2.5% Somatoform disorder 1.5% Eating disorder 1.2%

Stephanie E Bradstock FRANZCP · Andrew J Wilson FRANZCP · Matthew J Cullen FRANZCP · Katie L Barwell RN

Ashwin Swaminathan,* Iain B Gosbell,† Nicholas A Zwar,‡Mark W Douglas§ * Infectious Diseases Registrar, † Director and Associate Professor, § Infectious Diseases Physician, Department of Microbiology and Infectious Diseases, Liverpool Hospital, South Western Area Pathology Service, Locked Bag 7090, Liverpool, NSW 1871; ‡ Director and Professor of General Practice, Sydney South West Area Health Service General Practice Unit, Fairfield Hospital, Sydney, NSW. Iain. GosbellATswsahs.nsw.gov.au To the Editor: Infestation with the sandflea Tunga penetrans, or “chigoe flea”, is rarely encountered in Australia, but has been noted in children recently arrived from Central–East Africa. There have been only two previous Australian case reports of this parasitic infection, both in adult travellers returning from Africa.1,2 Several families who had been living in crowded refugee camps in Tanzania underwent routine screening for infection within 2 weeks of arrival in Australia. Four of 14 children examined had cutaneous lesions on their feet — mainly on the toes, nail beds and interdigital spaces (Box). These lesions were papular, less than 1 cm in diameter, pale yellow with dark centres, and were variably painful and/or itchy. Chronic, adjacent skin and nail bed changes were evident, as were small, loosely attached seed-like objects. Papules could be lifted with a sterile needle, leaving a small, non-bleeding cavity. Tunga penetrans, with numerous attached eggs, was identified by microscopy. Tungiasis occurs when an impregnated female sandflea burrows into the unprotected skin of a warm-blooded host. There is a predilection for the feet, although the perineum, buttocks and arms may also be infected.3 The head of the sandflea breaches the upper dermis to feed on blood vessels, while the abdomen traverses the epidermis, with its posterior components (anus, genital opening and respiratory spiracle) reaching the surface, forming a papule. Over several weeks, the flea releases hundreds of eggs before dying. After hatching, the larvae thrive in dust, soil and sand; they are found on beaches and in animal stockyards of tropical countries.3,4 Infection of pigs and other livestock, the usual host reservoirs, has led to significant problems in the livestock industry.1,4 Apart from pruritis and pain caused by local inflammation, morbidity results from ulceration and secondary bacterial infection, including tetanus and gas gangrene.1,2,4 Fleas can be removed using a sterile needle and forceps, and secondary complications prevented with tetanus prophylaxis, and antibiotics as appropriate. Successful outcomes with antiparasitic agents, such as ivermectin and thiabendazole, have also been recently reported.5 Tungiasis is indigenous to Latin America and the Caribbean, but was introduced to Africa, where it is now endemic, and to parts of South Asia.4 Given the current influx of African refugees into Australia, including the tropical north, the obvious concern is whether Tunga penetrans could establish itself here. We encourage medical practitioners dealing with newly arrived African refugees to examine for tungiasis in their screening evaluation. If, as suspected, this condition is prevalent, national infection control guidelines aimed at preventing establishment of the disease in Australia may be needed. Lesions caused by Tunga penetrans, the “chigoe” sandflea A characteristic Tunga penetrans lesion (thick arrow), with pale-yellow papule and dark centre, and a less obvious lesion (thin arrow) with surrounding chronic skin changes and multiple, loosely attached eggs.

Ashwin Swaminathan · Iain B Gosbell · Nicholas A Zwar · Mark W Douglas

Raymond F Raper,* Elizabeth Fugaccia,† Yahya Shehabi‡ * Board Member, † Member, ‡ Chairman, NSW Regional Committee, Joint Faculty of Intensive Care Medicine, 117 Alexander Street, Crows Nest, NSW 2065. yshehabiATozemail.com.au To the Editor: We are writing in response to the pejorative, unhelpful and somewhat misleading editorial “The shortage of kidneys for transplantation in Australia”.1 There are many possible reasons for lower organ donation rates in Australia. Several Australian initiatives have led the way in reducing the incidence of severe, traumatic brain injuries. These include the compulsory wearing of seat belts and helmets, random breath testing, and a zero blood alcohol limit for inexperienced drivers. Intensive care medicine is better structured and organised in Australia and New Zealand than in most of the countries cited by Mathew et al, with higher organ donation rates. Intensive care outcomes in Australia are world-leading. So the donor rate may be lower because patient outcomes are better. A comprehensive chart audit of donor potential in New South Wales carried out under the supervision of the Organ Donation Network NSW/ACT, identified very few missed donors (T Wills, Manager, Organ Donation Network NSW/ACT, personal communication), and a Victorian audit has suggested that the donor pool may be much lower in Australia than previously estimated.2 Similarly, organ donation rates will appropriately vary considerably among hospitals. To improve outcomes, critically ill patients are transported to centres with specific experience and expertise, resulting in a preponderance of potential donors in hospitals with trauma and neurosurgical services compared with hospitals lacking these. The intensive care community supports these life-saving initiatives, notwithstanding the effect they may have on organ donation potential. In fact, the principal “barrier” to organ donation in Australia appears to be the consent rate. From 2000 to 2004, 44% of families declined organ donation when faced with an actual rather than a hypothetical request.3 The intensive care community represents the interests of critically ill patients and their families. We will continue our best endeavours to improve both the survival and quality of life of patients suffering devastating brain injuries (our performance standard). When all brain function ceases, despite our best efforts, we will continue to facilitate organ donation, in discussion with the family, and in consideration of the patient’s known or projected wish. The intensive care community has led the way in developing organ donation-related practice guidelines4 and in related education. Australian Donor Awareness Program — Training (ADAPT) workshops are now a compulsory component of Fellowship of the Joint Faculty of Intensive Care Medicine training. The editorial implication of poor performance and lack of commitment is inaccurate and offensive.

Raymond F Raper · Elizabeth Fugaccia · Yahya Shehabi

Timothy H Mathew,* Randall J Faull,† Paul L Snelling‡ * Medical Director, Kidney Health Australia, GPO Box 9993, Adelaide, SA 5001; † Nephrologist, Royal Adelaide Hospital, Adelaide, SA; ‡ Nephrologist, Royal Prince Alfred Hospital, Camperdown, NSW. tim.mathewATkidney.org.au In reply: We regret that Raper et al have misinterpreted our editorial on the shortage of donor kidneys in Australia.1 We are particularly concerned and indeed mystified by their last statement, where they state that we implied that “poor performance and . . . lack of commitment” were to blame. This was in no manner our message. Rather, we sought to emphasise that all possibilities to optimise local donation rates should be explored, so desperate patients seeking grafts from potentially dangerous overseas sources need not expose themselves to serious potential morbidity and mortality. We consider that our intensive care colleagues perform superbly under the most difficult of circumstances when managing potential organ donation. We understand they are often unsupported with managing potential donations while they must at the same time deal with the grieving family, and the immediate demands of treating other seriously ill patients. We simply suggest that problems within the system (for example, differences between states in the number of intensive care beds per head of population or in the provision of specifically funded donor coordinators) that might hinder increasing organ donation should be carefully examined. We believe it is unhelpful to suggest that the South Australian experience should simply remain unexplained. In the article by Opdam and Silvester (cited by Raper et al), of 112 potential donors, 46 were considered medically suitable unrealised potential donors, and their estimated maximal potential donor rate was 30 per million,2 remarkably similar to the rates seen in Spain (the country with the highest organ donor procurement rate) and South Australia. We agree with the conclusions of Opdam et al that “an increase in the organ donation rate may be possible through increasing consent and the identification and support of potential donors”. As they also state, this would require substantial changes in clinical practice, with resource and ethical complications We did not mean to offend our intensivist colleagues. We merely suggest that we all need to assess the systems in which donation occurs and attempt to improve donation rates, for the sake of the many desperate people awaiting organ transplants in this country.

Timothy H Mathew · Randall J Faull · Paul L Snelling

To the Editor: The article by Senanayake and Ferson1 on detention for tuberculosis included two case histories. In the case of “Patient 2”, we believe the details published were misleading and unnecessarily disclosed potentially identifying information. This case was presented in sufficient detail to allow identification of “Patient 2” by including date of admission, personal details, city of admission and details regarding his past history of alcohol addiction and attempts to self-discharge. All this information was not necessary and did not take into account all the relevant medical complicating factors. We were surprised that, as the primary treating team involved in this patient’s care over the inpatient stay of 3 months and the following 6-month outpatient follow-up, we were not informed of the authors’ plans for publication, nor requested to comment on the facts of the report. We were also surprised to read details of the article in The Sydney Morning Herald on the day of the article’s publication in the Journal.2 An individual’s right to privacy is a fundamental human right. It is unfortunate that the careful consideration that had been given to his detention was not extended to publishing his case details. As Senanayake and Ferson point out, “Patient 2” recognised that his human rights were being “infringed” because he was being held in a “jail cell”, which was a temporarily modified isolation room in a public hospital under 24-hour guard. In law, information provided to a medical practitioner by a patient becomes subject to a statutory duty to protect the patient’s privacy and a common-law duty of confidence is owed by the treating medical practitioner to the patient. The NHMRC Guidelines approved under Section 95A of the Privacy Act 1998 indicate that, when a patient history is published, an important principle is that a patient may not be identified or held up to ridicule.3 Furthermore, public access to medical journals on the Internet has allowed increased availability of such reports to the general public and increases the chance of family members and others identifying individuals. The principle of protecting patient privacy has previously been respected by the Journal. An article published in 1994 reported a 1979 outbreak of tuberculosis in medical students who attended an autopsy of an immunosuppressed patient with unsuspected active tuberculosis.4 A report of the incident was not published contemporaneously, mainly to protect the privacy of the students involved. As the report by Senanayake and Ferson suggests, our patient was socially disadvantaged, and several aspects of his behaviour were probably attributable to a Jarisch–Herxheimer reaction in conjunction with acute alcohol withdrawal. Although we recognise the need to serve the public interest in health service management activities, this must be balanced against the requirement for patient privacy regardless of social class. We suggest that the publisher has an obligation to ensure that patient consent is obtained, and that the primary treating team has been involved in the review of case details so that misleading and potentially identifying information is not released inappropriately.

Medical Registrar · Respiratory Physician

Ruth M Armstrong,* Martin B Van Der Weyden† * Deputy Editor, † Editor, The Medical Journal of Australia, Locked Bag 3030, Strawberry Hills, NSW 2012. medjaustATampco.com.au In reply: We concur with the principle that patient privacy should be protected in case reports. As recommended by the International Committee of Medical Journal Editors,1 measures in place at the Journal include asking authors to obtain patient permission for publication where possible, and directing authors to remove potentially identifying patient information. The article in question was not a case report. Case details were given to exemplify the circumstances that might lead to detention of a patient for public health reasons in New South Wales, and dates and some details were retained to illustrate the temporal flow of the story. We agree that this may have made the patient identifiable, if not to the general public, to himself or his family. We regret this editorial lapse, and have reworded the patient details in the electronic version of the article.2 Although chastened by our anonymous colleagues’ observations, we are somewhat puzzled as to why, given their concern about their patient’s privacy, they are determined to draw further attention to the exposing details. We assume that, in this case (as in the cases of detaining patients for treatment of tuberculosis), public interest prevails. We also agree that case reports of detailed clinical histories require the input of the primary treating team, but the question of authorship should be determined by the involved parties, not the Journal. Be that as it may, as the article was a public health report (and thus not meant to be a detailed clinical exposition), we do not believe that the input of the treating team was required.

Ruth M Armstrong · Martin B Van Der Weyden