Letters

Jeremy J N Oats,* H David McIntyre† (on behalf of the Australasian Diabetes in Pregnancy Society, in conjunction with the Women’s Health Committee of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists) * Clinical Director, Department of Women’s Services, Royal Women’s Hospital, Carlton, VIC; † Director, Department of Endocrinology, Mater Health Services, South Brisbane, QLD. jeremy.oatsATrwh.org.au To the Editor: Consensus guidelines for the management of gestational diabetes mellitus (GDM) were prepared by the Australasian Diabetes in Pregnancy Society in 1997–1998 and subsequently published in the Journal.1 Since that time, there have been two minor revisions to these guidelines. The first, in relation to the recommended frequency of follow-up testing of women identified as having GDM, was detailed in a letter to the Editor in 2002.2 The second concerns the timing of delivery of women with GDM. At the request of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG), the original recommendation that “continuation of the pregnancy in uncomplicated GDM to 10 days beyond term is acceptable provided that indications from fetal monitoring are reassuring” has been modified by replacing “10 days beyond term” with “full term” to bring this into line with current practice. The initial guidelines were arrived at by consensus of Australasian practitioners involved in the care of women with GDM. The Australasian Diabetes in Pregnancy Society recognised, both at the time and subsequently, that the level of evidence available to guide clinical decision-making fell well short of that necessary for a definitive statement on the timing of delivery. It is noteworthy that no international consensus exists concerning the optimal timing of delivery in pregnancies complicated by GDM. The American Diabetes Association, in its Clinical Practice Guidelines, recommends delivery “during the 38th week . . . unless obstetric considerations dictate otherwise”.3 The European Association of Perinatal Medicine does not make a recommendation, instead stating that “the optimal time of delivery and need to induce labour are still controversial.”4 There is currently a paucity of quality evidence on which to confidently base recommendations. We hope that current studies, such as the Australian Carbohydrate Intolerance in Pregnancy Study and the Hyperglycemia and Adverse Pregnancy Outcome Study,5 will provide this evidence.

Jeremy J N Oats · H David McIntyre

T C K Brown Former Director of Anaesthesia, Royal Children's Hospital, Flemington Road, Parkville, VIC 3052. tckbrownATnetspace.net.au To the Editor: The epidemic of recreational use of γ-hydroxybutyrate (GHB; also known as γ-OH) is a cause for concern, as it is a basal anaesthetic agent (ie, it renders the patient unconscious, with analgesic supplementation required for surgery). It is not surprising that people taking too much of it are becoming unconscious.1 GHB was introduced in France as a basal anaesthetic agent by Laborit about 1960. It has a slow onset of action (up to 10 minutes when given intravenously, thought to be due to conversion to an active metabolite, γ-butyrolactone).2 It causes bradycardia, sometimes requiring atropine administration to maintain cardiac output, and raises blood pressure. Respiration is slow and deep, so that alveolar ventilation is not reduced. Trials of GHB as an anaesthetic were conducted in Melbourne by Dr William Cole and myself in the late 1960s,3-5 and it was used for microlaryngeal surgery for several years. Its major problems were prolonged sleep (1–3 hours after 40–100 mg/kg in children) and a high incidence of postoperative vomiting, adding the danger of aspiration in unconscious patients. GHB was also tried as an anaesthetic in Dunedin, New Zealand, where it was found that the sleep time could be reduced by intravenous administration of physostigmine.6 The fact that this drug is a basal anaesthetic needs to be more widely publicised.

T C K Brown

Geoffrey M Forbes,*† Matthew J Zimmerman, † Brendan J Collins,† John T Edwards† * Head, † Gastroenterologist, Department of Gastroenterology and Hepatology, Royal Perth Hospital, Perth, WA. geoff.forbesAThealth.wa.gov.au To the Editor: The editorial by Viiala and Olynyk on screening flexible sigmoidoscopy (FS)1 is a welcome reminder that there are alternative colorectal neoplasia (CRN) screening strategies to the Australian National Health and Medical Research Council’s preferred option of annual faecal occult blood testing. The availability of tests for CRN screening raises the issue of whether screening tests should be dictated by government or professional bodies, or requested by the consumer. FS and colonoscopy remain potential alternatives to faecal occult blood testing in Australia, as reflected by US screening guidelines2 and recent local data.1,3 However, it is unreasonable for Viiala and Olynyk to compare the risks of screening FS (generally diagnostic only) in average-risk subjects (perforation rate, 1/50 000) with the risks of colonoscopy (both diagnostic and therapeutic) in Western Australian tertiary hospital outpatients with symptoms or other risk factors for CRN (perforation rate 1/1000). Firstly, it is important to recognise that the perforation risk associated with screening FS comes not just from the diagnostic screening test (1/50 000), but also from follow-up colonoscopy and subsequent polypectomy in patients with distal adenomas seen on FS. Secondly, in the WA tertiary hospital cohort,4 the estimated perforation rate for diagnostic colonoscopy is about 1/2800 (and about 1/420 for colonoscopy accompanied by polypectomy). Asymptomatic subjects having screening colonoscopy are likely to have a lower risk than patients with symptoms or other significant comorbidities having investigative colonoscopy. Recent data from colonoscopic screening programs (which include subjects having polypectomy) have shown an overall perforation rate of less than 1/3000.5 Medical practitioners arranging colonoscopy, and people having this procedure, should be informed about the risks involved and, importantly, be aware that these risks are likely to vary according to the setting in which colonoscopy is performed.

Geoffrey M Forbes · Matthew J Zimmerman · Brendan J Collins · John T Edwards

Darryl J Hodgkinson Director, Cosmetic and Restorative Surgery Clinic, Double Bay Day Surgery, 20 Manning Road, Double Bay, Sydney, NSW 2028. dr_hodgkinsonATbigpond.com To the Editor: I would like to congratulate Peters et al on their strong stance against elective surgery in patients who smoke.1 The plastic surgery community became aware in the last two decades of the problems of healing in smokers. When patients claimed that they gave up cigarette smoking before surgery, we often found that the serum cotinine levels on testing were elevated, indicating that they had not given up smoking. Patients who are smokers and who develop a healing complication, in breast reduction, mastopexy, abdominoplasty or a facelift, often attribute the complication to the surgical technique rather than their own habit. Many of these patients have gone on to litigate successfully. Voracious plaintiff lawyers attribute only a small amount of blame to the patient whose smoking has, in fact, contributed significantly to their complication. In our plastic surgery practice, we have a non-smoking policy, and my malpractice insurer will not cover me for patients on whom I operate and who develop a complication associated with smoking. Hence, all patients who are smokers who wish to have elective surgery are referred to a smoking-cessation program and have to have given up smoking for at least 2 to 4 weeks before surgery. I prefer not to operate on smokers at all, as serum cotinine tests often confirm that their cessation attempt has been incomplete. In the United States, where patients pay for their own health insurance, their premiums are adjusted for lifestyle. In Virginia, in the 1990s, a “Healthy Virginian policy” existed where premiums were reduced for non-smokers. My suggestion would be that the Medicare levy also be either reduced for individuals who do not smoke or increased for those who do.

Darryl J Hodgkinson

Nicholas A Tonti-Filippini Medical Ethicist, 15 Alburnum Crescent, Lower Templestowe, VIC 3107. ntf-dslATkeypoint.com.au To the Editor: Some time ago, I was approached by a general practitioner who had been trying for more than 12 months to arrange surgery for a patient who was suffering from intermittent claudication. The indications for surgery seemed compelling. The man was in great pain and disabled by the condition. The vascular unit at a major metropolitan hospital refused to operate on him while he remained a smoker. The man had been an alcoholic, but had managed to beat that addiction and had been “dry” for the entire 12 months. With the patient’s permission, and at the request of the GP, I contacted the surgeon. The surgeon explained to me that his refusal to provide elective surgery was on the grounds that the patient smoked, which would increase recovery time and the risk of complications. After discussion of the ethical and legal situation, an early appointment for surgery was arranged with the patient. Peters and colleagues, authors of a recent editorial on smoking cessation and elective surgery,1 would do well to attend to the terms of the Commonwealth Disability Discrimination Act 1992. It is unlawful for a person who provides services, or makes facilities available, to discriminate against another person on the grounds of the other person’s disability. It seems legitimate to consider the effects of smoking on success rates as part of deciding whether elective surgery is likely to be safe and effective for an individual patient. However, the editorial suggests that patients be denied surgery, such as joint reconstruction, as a resource-allocation decision, even if the surgery would be in their interests. It is important that smoking is recognised as an addiction. Some groups, such as the mentally ill, are particularly prone to it. A study by the Harvard medical school found that people with mental illness are twice as likely to be smokers, and nearly 45% of all smokers in the United States are people with a “mental disorder”.2 To the extent that it is an addiction, smoking needs to be considered as a medical condition in much the same way as alcoholism is referred to as a medical condition. A doctor who did not provide a needed treatment to a smoker on the grounds that the patient was a smoker would be in violation of that person’s fundamental human right to healthcare and his or her right not to be discriminated against because of a disability. In fact, the doctor would be in breach not only of the Hippocratic oath, but of the Australian Medical Association’s Code of Ethics 2004,3 which states “. . . refrain from denying treatment to your patient because of a judgement based on discrimination”.

Nicholas A Tonti-Filippini

Matthew J Peters,* Lucy C Morgan,† Laurence Gluch‡ *Head, Department of Thoracic Medicine, †Thoracic Physician, ‡ Surgeon, Department of Breast and Endocrine Surgery, Concord Repatriation General Hospital, Hospital Road, Concord, NSW 2137. matthew.petersATcs.nsw.gov.au In reply: The rigid way in which Hodgkinson has addressed risk reduction in plastic surgery seems reasonable, as long as there is open disclosure and access to smoking-cessation services is assured. It is an unfortunate fact that our healthcare system cannot provide everyone with what they want, or need, in a clinically appropriate timeframe. Resources are finite. In his own case example, and without considering the legal or ethical basis of his intervention, once Tonti-Filippini arranged for a patient at high risk of complications to have surgery, someone else was immediately prevented from having hospital care that was necessary for them. If complications developed, extending hospital stay, more than one patient might have been adversely affected. Let me extend Tonti-Filippini’s case a little and imagine that a similar patient with peripheral vascular disease who was moved further down the vascular surgery waiting list as a result of the smoker’s surgery being expedited was an ex-smoker who had taken advice and ceased smoking to reduce risks and improve the surgical outcome. Then, in the period of surgical delay, the affected leg became acutely ischaemic and amputation (rather than vascular reconstruction) was required. Are there not ethical implications that follow? Reading more deeply into the Australian Medical Association’s Code of Ethics, one finds that we should work to increase standards and the quality of and access to medical services in the community, and make available our special knowledge and skills to assist those responsible for allocating healthcare resources. These are important obligations. Most smokers are addicted, and this is a medical problem that needs to be consistently identified and addressed; the issue of smokers with mental illness was highlighted in the editorial. If a clinical decision is made not to perform surgery in the context of continued smoking, it is not made because the person is a smoker, or because they have an addiction, but because the ongoing smoking has major, adverse consequences that we are unwise to ignore. The distinction is subtle but important.

Matthew J Peters · Lucy C Morgan · Laurence Gluch

B E Christopher Nordin,* Allan G Need† * Physician, Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA; † Head, Division of Clinical Biochemistry, Institute of Medical and Veterinary Science, Adelaide, SA. christopher.nordinATimvs.sa.gov.au To the Editor: The article by Seeman and Eisman on treatment of osteoporosis1 not only neglects the pathogenesis and prevention of this condition, but also fails to appreciate the profound differences between the three main types of fragility fracture (peripheral non-hip, hip and spine). To say that adults lose bone with age because the “volume of bone resorbed is greater than the volume replaced” is a spectacular but common tautology which simply describes what would be expected from an external negative calcium balance. The common postmenopausal bone loss can generally be accounted for by the rise in calcium requirement due to a fall in calcium absorption and rise in obligatory calcium excretion.2-4 This can be corrected with hormones or compensated for with a calcium supplement, which is known to suppress bone resorption.5 In 20 trials of calcium therapy completed up to 1997, the loss of bone in 855 postmenopausal women treated with calcium was 0.3% per annum, compared with 1.0% per annum in 635 untreated control women (P < 0.001).6 In older women, this relative calcium deficiency is complicated by a decline in vitamin D status caused by reduced exposure to sunlight and progressive thinning of the skin. It has been known for 30 years that vitamin D deficiency is common in patients with hip fracture,7 for 20 years that this was also true in Australia,8 and for 12 years that vitamin D with calcium can reduce the hip fracture rate by 43% in 18 months in women in residential care.9 When it comes to established osteoporosis (the combination of low bone density with fracture), treatment needs to distinguish between the three main types of fracture referred to above. In hip fractures, surely the first priority must be to give adequate vitamin D and calcium. Most non-hip peripheral fractures occur in women with bone densities in the normal range,10 so the need for treatment is debatable unless bone turnover is very high. Vertebral fractures are a different matter. Unlike peripheral fractures, they do not “heal” in the usual sense — the deformity remains and often causes local pain and mechanical dysfunction. The recurrence rate is very high, because all the vertebrae have much the same bone density, and the osteoporotic collapse of one indicates that the others are ready to follow. This condition is notoriously difficult to manage and should almost be regarded as a medical emergency that requires full investigation — not least to exclude myeloma — and rapid, effective treatment. It is in the secondary prevention of these fractures that the remedies advocated by Seeman and Eisman probably have their main role and are most cost-effective. In fact, although the authors place great emphasis on prevalent fracture as a risk factor for further fracture, the reference they quote deals with prevalent vertebral fracture, not with prevalent non-hip peripheral fracture, where the evidence of benefit from bisphosphonates and raloxifene is very much weaker. We are arguing for much greater emphasis on the prevention of osteoporosis with adequate calcium after the menopause and adequate vitamin D in the elderly, and the use of appropriate investigation and selective treatment in the management of the condition when it is established.

B E Christopher Nordin · Allan G Need

Ego Seeman,* John A Eisman† * Professor of Medicine and Endocrinologist, Austin Hospital, Studley Road, Heidelberg, VIC 3084. † Professor of Medicine, and Director, Bone and Mineral Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney, NSW. egosATunimelb.edu.au In reply: Our article concerned a discussion of evidence-based treatment for the prevention of osteoporotic fractures. Prevention of osteoporosis per se is important, but the approaches chosen must be evidence- based. Calcium supplementation may diminish, but not abolish, bone loss by reducing remodelling rate.1 Any association of a lifelong diet high in calcium appears to be with peak bone mass, not rates of bone loss,2 and may be attributable to differences in protein intake or physical activity. Despite opinion, meta-analysis of prospective, randomised, double-blind, placebo-controlled studies does not support a role for calcium supplementation in reducing fractures.3 Later rather than earlier intervention avoids needless exposure to treatment for large numbers of individuals at low absolute risk of fracture (ie, those who are unlikely to sustain a fracture even without treatment).4 Vitamin D is of course indicated in vitamin D deficiency. However, there is no evidence for anti-fracture efficacy of vitamin D in ambulant community dwellers.5

Ego Seeman · John A Eisman

John M N Hilton Associate Professor, Department of Pathology, University of Sydney; and Consultant in Forensic Medicine, PO Box 45, Katoomba, NSW 2780. kornhilATiinet.net.au To the Editor: Byard’s succinct dissertation on the Clark case1 omits one crucial aspect in redressing this miscarriage of justice. Without the vigorous and persistent efforts of a vocal and well directed support group, which included Mrs Clark’s legal team, their scientific and medical advisors, the Law Society of England, and her family, she would still be serving a life sentence in jail. An Australian example of the effectiveness of such a support group in combating injustice is afforded by the Lindy Chamberlain case.2 Historically, Sir Arthur Conan Doyle spearheaded the efforts — sustained over nearly 20 years — to exonerate Oscar Slater,3 an unfortunate German–Jewish immigrant to Glasgow who was condemned to death after a conviction for murder based largely on identification evidence given by one of the probable perpetrators. Slater was granted a reprieve from the death sentence at the last moment, only to serve some 17 years in a grim Scottish penitentiary. Less fortunate was Timothy Evans,4 who was convicted and hanged for murdering his wife and daughter on the evidence of one of London’s infamous mass murderers, John Christie. Evans was eventually pardoned — unfortunately, too late to save his life — largely thanks to a very active support group headed by the journalist Ludovic Kennedy. In contrast, those who lack such a support group are exemplified by Ziggy Pohl,5 who was convicted, despite rather than because of the evidence, of killing his wife in Queanbeyan, NSW. He served more than a decade in prison, only to have the true perpetrator confess after Pohl was released on parole. Byard highlights evidentiary shortcomings in one recent English case. How many other people have suffered the ignominy, distress and dire consequences of unjust convictions because they lacked the support of an individual or a group prepared to question the propriety of the conviction process?

John M N Hilton

Jessica H Ford,* Annette J Dobson† * Research Assistant, † Professor of Biostatistics, School of Population Health, University of Queensland, Herston Road, Herston, QLD 4006. A. DobsonATsph.uq.edu.au To the Editor: Helping pregnant women to stop smoking and not to resume after their baby is born is a key target for smoking prevention. Pregnancy (or trying to become pregnant) is a time when women are motivated to stop smoking for the sake of the baby and they are in contact with healthcare professionals who can help them do so. We have calculated the impact of smoking during pregnancy in terms of deaths, hospital separations and costs to the healthcare system, and estimated the extent to which these effects could be reduced through interventions initiated by healthcare professionals as part of routine clinical contact. We considered the following conditions: pre-eclampsia (which is less common among smokers), low birthweight (including hospital costs for the mother and the baby, and infant deaths), premature rupture of membrane, spontaneous abortion, ectopic pregnancy, placenta praevia (including infant death), and sudden infant death syndrome (SIDS). We used estimates of relative risks (RRs) for these conditions for women who smoke during pregnancy (or, for ectopic pregnancy, for women who might become pregnant) from meta-analyses.1-3 We obtained data on deaths,4 hospital separations,5 and costs to the healthcare system6 for 2001–02. The prevalence of smoking among pregnant women of all ages in New South Wales since 1994 has been in the range 17% to 22%.7 The prevalence of smoking among all women of child-bearing age in 2001 was about 28%.8 From these data, we calculated attributable fractions1,2,9 for average values (using point estimates for RRs and 20% for prevalence of smoking in pregnancy) and extreme values (using the 95% confidence limits for RRs and 17% and 22% for smoking prevalence). In summary, the average number of adverse events attributable to smoking each year in Australia are: infant deaths, 78 (extreme values, 66–87); hospital separations, 6890 (extreme values, 4130–9450); costs to the healthcare system, $23 million (extreme values, $16–$29 million). A Cochrane review of behavioural (not pharmacological) interventions for stopping smoking in pregnancy showed an absolute reduction of 6% (95% CI, 4%–8%).10 Thus, if the prevalence of smoking during pregnancy were reduced from 20% to 14%, we calculate that there would be 20 fewer infant deaths, 1600 fewer hospital separations, and a saving of $5 million to the Australian healthcare system per year. (Details of the calculations can be obtained from the authors.) These gains could be realised by increasing community awareness of the risks of smoking in pregnancy and helping health professionals to use smoking prevention strategies in their routine encounters with pregnant women.

Jessica H Ford · Annette J Dobson

Michael C Kennedy Research Associate, Department of Clinical Pharmacology and Toxicology, St Vincent’s Hospital, Darlinghurst, NSW 2010. drmkennATozemail.com.au To the Editor: Since the Sydney Olympics in 2000, many developments have occurred in drug use and the rules regulating drugs in sport. The most significant regulatory development is the acceptance by the Olympic Federation, and many other sports bodies, of the World Anti-Drug Agency’s World Anti-Doping Code.1 Caffeine and pseudoephedrine have been removed from the Prohibited List, and an in-competition monitoring program is under way to detect any changes in the patterns of use of caffeine, pseudoephedrine and other drugs not on the banned list. Had this code been used in 2000, the Romanian gymnast Andreea Raducan would have retained her gold medal, lost after she inadvertently used a cold preparation containing pseudoephedrine. Precise in-competition limits on blood and breath alcohol have been introduced in sports such as archery and modern pentathlon. β-Blocking agents and diuretics are completely banned in specific sports. A new category of “specified substances” now exists: . . . the prohibited list may identify specified substances which are particularly susceptible to unintentional anti-doping rule violations because of their general availability in medicinal products or which are less likely to be successfully abused as doping agents. These substances include cannabinoids, probenecid, glucocorticosteroids and ephedrine. Doctors treating athletes should advise them to inform their relevant sporting authority of drugs prescribed. If necessary, athletes can apply to the Australian Sports Drug Advisory Committee for a therapeutic use exemption for a banned substance. Notifiable substances can be documented on an Abbreviated Therapeutic Use Exemption form held by the national sporting body. There can be no doubt of the need for drug testing to ensure a level playing field. Drug use to enhance performance is unabated since the Sydney games, with scandals occurring around the world. The Bay Area Laboratory Corporation scandal, involving the anabolic steroid tetrahydrogestrinone, is the most prominent. This has ruined several sporting careers and led to criminal charges against company directors.2 Other anabolic steroids continue to be widely used, including nandrolone, which causes problems because of contamination of dietary supplements and some foods.3 One of the “holy grails” for drug cheats over the past 4 years has been to enhance oxygen transport and delivery. RSR13 (efaproxiral), an allosteric modifier of haemoglobin, is in clinical trial as a radiosensitising agent. It has been shown to increase Vo2max in dogs and hence has been of interest to endurance athletes. The manufacturer’s collaboration with the Olympic Analytical Laboratory of the University of California (Los Angeles) resulted in an analytical method now being available for detection of the drug in sport.4 Haemoglobin- and non-haemoglobin-based oxygen carriers are now available commercially. There are few scientific data about their use in sport, but it is likely they are misused by some athletes.5 Recombinant human erythropoietin is widely used in cycling and other endurance sports. A detection method developed from Australian research will limit its use, at least at the Olympic venue.6 Genetic manipulation is unlikely in 2004, but its potential is foreseen. This technology is also prohibited in the new code.1 Unfortunately, drugs will continue to be misused. The opportunity for Olympic winners to gain huge financial rewards will fuel their use.

Michael C Kennedy

Anton Y Peleg,* Wendy J Munckhof† * Infectious Diseases Registrar, Alfred Hospital, Prahran, VIC 3181; † Specialist in Infectious Diseases and Microbiology, Infection Management Service, Princess Alexandra Hospital, Brisbane, QLD. A. PelegATalfred.org.au To the Editor: Infection with community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is emerging in many countries, including Australia.1 We report the first case of fatal necrotising pneumonia caused by CA-MRSA in Australia. A previously well 21-year-old Aboriginal man presented to the emergency department with fever and a productive cough. He had no known risk factors for sepsis (such as immunosuppression, diabetes, HIV infection, alcoholism, asplenia or recent influenza) and no history of hospitalisation in the previous 12 months. Chest x-ray revealed left mid-zone consolidation. He was prescribed amoxycillin–clavulanate and discharged. Two days later, the patient re-presented, with rigors, haemoptysis and agitation. Examination revealed a respiratory rate of 38 breaths per minute, oxygen saturation of 79% breathing room air, temperature of 38.7°C, sinus tachycardia (135 beats per minute), and a systolic blood pressure of 80 mmHg. Respiratory examination revealed diffuse coarse crepitations. No other source of infection was identified. The patient required intubation, mechanical ventilation and inotropic support. Sputum and blood samples were taken for culture, and empirical treatment was begun with intravenous ceftriaxone, erythromycin and a single dose of gentamicin and rifampicin. Initial investigations showed leukopenia (2.3 × 109/L; reference range [RR], 3.9–12.7 × 109/L), acute renal failure with a serum creatinine level of 0.18 mmol/L (RR, 0.06–0.11 mmol/L), and severe metabolic and respiratory acidosis (pH, 7.19; RR, 7.38–7.43). The following day, blood and sputum cultures showed gram-positive cocci resembling staphylococci, and intravenous flucloxacillin was added to the antibiotic regimen. Repeat chest x-ray revealed bilateral necrotising pneumonia. Despite resuscitation efforts, the patient died 48 hours after admission. Susceptibility testing of blood and sputum isolates subsequently confirmed MRSA. The isolate was sensitive to erythromycin, clindamycin, gentamicin, ciprofloxacin, tetracycline, vancomycin, rifampicin and fusidic acid. Methicillin resistance was confirmed by detection of the mecA gene by polymerase chain reaction (PCR). Further PCR testing of the isolate revealed the Panton–Valentine leukocidin (pvl) gene, an important virulence factor that has been associated with necrotising pneumonia2 and death,3 and is rarely found in methicillin-susceptible S. aureus or hospital-acquired MRSA isolates.1,2,5 Typing of the isolate by pulsed-field gel electrophoresis showed that it was the recently described “R” pulsotype of CA-MRSA, or “Queensland clone”.4 This clone was first noted in the white population in south-east Queensland in 2000, and is uncommon in Aboriginal people.4 Most CA-MRSA infection in Aboriginal people is caused by WA-MRSA, which may be less virulent than the Queensland clone of CAMRSA as it lacks the Panton–Valentine leukocidin.5 This is the first reported case of fatal necrotising pneumonia caused by CA-MRSA in Australia and illustrates the invasive nature of this infection. Thus far, CA-MRSA has predominantly caused skin and soft tissue infections, but the incidence of life-threatening sepsis is increasing. The first case of severe pneumonia caused by CA-MRSA in Australia was reported in early 2003.6 Fatal cases of necrotising pneumonia caused by CA-MRSA have also been described in the United States3 and France,7 and this presentation is becoming a particular feature of this organism. Clinicians should consider the possibility of CA-MRSA in any patient presenting to hospital with severe staphylococcal sepsis or pneumonia and should consider including parenteral vancomycin in the initial empirical therapy, particularly in geographic locations where CA-MRSA has been reported and in ethnic groups at increased risk.

Anton Y Peleg · Wendy J Munckhof

Lloyd K Morgan General practitioner (retired), PO Box 150, Lorne, VIC 3232. lloydmorganATiprimus.com.au To the Editor: O’Leary et al1 are pessimistic about the value of antibiotic treatment for leptospirosis, based on an inconclusive Cochrane review2 and no proven mortality decrease. Yet we can be more optimistic, given the efficacy of prophylactic doxycycline (soldiers in Panama were 95% protected by 200 mg once-weekly3), the susceptibility of leptospira to various antibiotics in vitro (especially penicillin, but not erythromycin4), and the existence of a Herxheimer reaction with penicillin,5 which indicates in-vivo activity. The Cochrane review2 was of randomised controlled trials of confirmed cases. It included 75 patients given antibiotics and 75 given placebo. Penicillin (61 patients) and doxycycline were not compared. The time from symptom onset to starting antibiotics was stated in only two trials (9 and 2 days). Nevertheless, the review concluded that penicillin or doxycycline may do more good than harm. In the spirochetaemic phase of leptospirosis (Days 4–7), vasculitis causes multiorgan failure. Successful treatment with antibiotics seems likely if commenced within 2 days of symptom onset, before generalised vasculitis is irreversible. Unfortunately, early diagnosis and efficacy assessment is difficult because symptoms are protean and non-specific, no rapid laboratory test exists, the condition is mild and self-limited in most cases, and mortality varies from zero to 7%. A high index of suspicion is essential so that antibiotics can be commenced empirically. The consensus is that antibiotics should be commenced within 4 days. In one study, starting antibiotics within 7 days was associated with shorter illness, and if antibiotics were started within 2 days the shorter duration was highly significant (P = 0.006).6 Another trial showed penicillin commenced on Day 9 was beneficial, but antibiotics had been used before entry to the trial.2 Various penicillins and tetracyclines have seemed useful, but only oral doxycycline and intravenous benzylpenicillin are recommended. These are the first and second preferences, respectively, in Therapeutic guidelines antibiotic.7 In the case described by O’Leary et al,1 antibiotics were commenced on Day 3, but the penicillin dose was only half the recommended daily dose for leptospirosis. The vasculitis was probably terminal before the patient was transferred to Concord Hospital.

Lloyd K Morgan

Marianne E Jauncey,* Paul K Armstrong,† Emily L Morgan,‡ Jeremy M McAnulty§ NSW Public Health Officer, Public Health Training and Development Branch; † Medical Epidemiologist, § Director, Communicable Diseases Branch; NSW Health, North Sydney, NSW. ‡ General Practitioner, Ballina West Medical Centre, Ballina, NSW. Marianne.jaunceyATyahoo.com.au To the Editor: In 2003, severe acute respiratory syndrome (SARS) became the first pandemic of the 21st century. Despite spreading to 29 countries, a rapid and coordinated international effort led to its containment. Here, we examine Australia’s only laboratory-confirmed case, and the investigation of possible subsequent transmission. In June 2003, the World Health Organization (WHO) notified Australian health authorities of a 26-year-old tourist in whom SARS-coronavirus-specific antibodies had recently been detected. She was part of a retrospective serological survey of people who stayed at the Hotel Metropole, Hong Kong, on 21 February,1 the same time a SARS source case infected at least 14 other hotel guests.2 On 22 February, the 26-year-old tourist travelled to Australia and 4 days later developed myalgia, lethargy and cough. On 6 March, 6 days before the first WHO global alert on SARS, she saw a general practitioner (GP) in northern New South Wales, to whom she also reported nausea, vomiting, nocturnal fever and pronounced lethargy. On examination she was afebrile, pale, unwell, with a cough and clear chest on auscultation. She declined further investigations and hospital admission; her condition gradually improved, and she left Australia 6 days later. She reported close contact with only three people during her Australian visit — her partner, the GP, and the GP’s surgery nurse. None reported subsequent illness and all tested negative for SARS-coronavirus antibody by direct immunofluorescence, a highly sensitive and specific method.3 Australia was fortunate that the tourist was not particularly infectious. The Hotel Metropole case was identified as the source case for four national and international clusters of SARS.2 The resulting human and economic cost was substantial.4 Without specific treatments, basic public health measures proved the only effective means to contain SARS. These included rapid case detection and isolation, contact tracing, handwashing and the correct use of personal protective equipment.5 Many GP practices and some hospitals in Australia do not have isolation facilities or infection control resources to effectively contain diseases like SARS. In the event of local transmission of SARS, infection may well have occurred in Australian healthcare workers. In the wake of SARS and, more recently, avian influenza, GPs must develop infection control plans to protect their own health as well as that of their patients. These should include obtaining a history of travel to outbreak-affected areas, reserving an area for patient isolation, and using appropriate infection control precautions during such outbreaks. Clinicians in other healthcare settings also need to review current infection control practices. If Australia is to remain the “lucky country” with regard to communicable diseases, basic public health measures aimed at preventing transmission of infection in healthcare settings is essential.

Marianne E Jauncey · Paul K Armstrong · Emily L Morgan · Jeremy M McAnulty

Jennifer W Majoor,* Joseph E Ibrahim† * Associate Professor, Department of Psychiatry, Alfred Hospital, Prahran, VIC; † Monash University Professor of Aged Care Medicine, Peninsula Health, Frankston, VIC. J. MajoorATalfred.org.au To the Editor: We applaud the Journal’s new series to improve the standard of teaching within the medical profession.1,2 However, it seems ironic that a profession that relies so heavily on an experiential, apprentice-based model of learning should be running such a series. Since the early nineties, we have seen a paradigm shift with regard to improving the quality of healthcare. However, this recent managerial preoccupation with systems, processes and outcomes has largely ignored the relationship between effective teaching and patient care. Clinical service work is given priority over training and education activities, and it is likely that, if it weren’t for the clauses in our employment contracts, all training, conferences and educational activities would occur out of work hours. Although we have seen a number of structural interventions to promote ongoing education, such as the introduction of Continuing Medical Education programs, the idea that “any” education will do, and that “anyone” can teach, remains pervasive. The danger of promoting “teaching on the run” is to reinforce the view that teaching is not a specialised discipline that requires specific skills and training. It is astounding that no formal qualifications in education are required for teaching at the most senior level, whereas to be taken seriously as a researcher requires an MD or PhD. It is a rare gifted teacher who instinctively performs well without formal training. High-quality teaching requires formal training, just as high-quality research does. Do we allow anyone in medicine to simply do “research on the run”? Would we ever consider a series called “Research on the run”? In medicine, we recognise that people are drawn to particular specialties because of their different knowledge, skills, interests and temperaments. This is not always the case in teaching, and names on a tutorial roster are too often allocated without regard for the style or ability of the teacher. Lake points out that the majority of problems with teaching are related to the traditional culture of medical practice and health service delivery.2 Similarly, Quadrio has observed that “career advancement in medicine . . . depends primarily upon research productivity, less upon clinical work and teaching . . .”.3 In our view, medicine requires another paradigm shift towards competency assessment and promotion of our teachers in academic settings. Furthermore, the allocation of appropriate resources is paramount and is justified because of the likely spin-offs for improved quality of patient care. We look forward to the day when medical education is rewarded as a highly valued endeavour, rather than a burden for busy clinicians and academics. We eagerly await further instalments of this well intentioned series on teaching, and hope that it goes some way towards effecting a “Kuhnian revolution”.4 (US scientist Thomas Kuhn proposed that scientific knowledge proceeds according to popular paradigms that, every now and then, undergo “intellectually violent revolutions . . . in each of which one conceptual world view is replaced by another . . .”.)

Jennifer W Majoor · Joseph E Ibrahim

Fiona R Lake Associate Professor in Medicine and Medical Education, Faculty of Medicine and Dentistry, University of Western Australia, Nedlands, WA. flakeATcyllene.uwa.edu.au In reply: As noted by Majoor and Ibrahim, teaching and learning, as a mission, are not well regarded when compared with research. Not only that, but changes in healthcare are making it harder to teach. Shorter patient stays and more complex patients result in “survival” learning by junior staff, rather than in-depth learning.1,2 Experts in medical education will be increasingly important in teaching, guiding curricula, and assessing trainees.2 However, professional learning occurs while doctors immerse themselves in clinical practice. “On the run” teaching doesn’t mean substandard teaching, but relates to doing it while delivering patient care.3 Although there is room for improvement, many clinicians teach well. Most are keen to teach and would like to have formal training,4 and evidence suggests that, with support, they can improve.2,3 How much support? Short workshops have been shown to have an impact, as has the provision of a few simple educational ideas.5 By not supporting our clinicians/teachers in ways that could be very simply put into practice, we risk losing in-context learning and wasting an enormous resource. Along with focusing on the teacher, I believe we need an important shift in the way health services recognise (provide time for) and reward (see as important) the mission of teaching and supervision alongside their mission of excellence in delivery of care.

Fiona R Lake

Chin-Pin Yeo,* Melissa J Gillett,† Samuel D Vasikaran‡ * Chemical Pathologist, † Biochemistry Registrar, ‡ Head, Core Clinical Pathology and Biochemistry, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847. gptycpATsgh.com.sg To the Editor: In about 2% to 5% of patients with subclinical hypothyroidism, the condition progresses to overt hypothyroidism each year.1 It is currently recommended that thyroid function tests should be repeated at 6- to 12-month intervals to monitor improvement or worsening in level of thyroid-stimulating hormone (TSH).1 Testing for thyroid peroxidase antibody (TPOAb) is also common practice in subclinical hypothyroidism, as it has been shown that individuals with raised TSH and TPOAb levels have a 40-fold increased risk of developing overt hypothyroidism.2,3 We audited the management of patients who had a result indicating subclinical hypothyroidism from our hospital laboratory, focusing on follow-up thyroid function and TPOAb tests. In December 2003, we retrospectively inspected clinical case notes of patients who had been reported in November 2002 with a TSH level of 4.1–9.9 mIU/L (normal reference interval, 0.4–4.0 mIU/L) and a free thyroxine (FT4) level within the reference range of 10–23 pmol/L (subclinical hypothyroidism). We also contacted the patients’ general practitioners (GPs) for further information when necessary. There were 72 patients with results suggesting subclinical hypothyroidism. Of these, we excluded 29 from other hospitals and three whose GPs were not able to be contacted. Of the remaining 43 patients, 18 had no previous history of thyroid disease (8 men and 10 women; age range, 24–90 years). Six patients were seen in the emergency department, four in the outpatient clinics, and eight in the wards. All the laboratory reports of subclinical hypothyroid results were accompanied by a comment advising repeat thyroid studies at a later date and thyroid antibody tests. However, only three of the 18 patients (17%) had TPOAb tested. Only seven of the 18 patients (39%) were followed up with repeat thyroid function tests, at intervals ranging from 3 days to 7 months. One patient, with a TSH level of 9.8 mIU/L, was started on thyroid replacement therapy. The GPs of 10 of the 11 patients who did not have follow-up testing were not informed of the initial TSH results. The low rate of follow-up of hospital patients with a first-time diagnosis of subclinical hypothyroidism is of concern. While the increase in TSH level in some of these patients may have been related to sick euthyroidism, this can only be confirmed by normalisation of TSH level on repeat testing. TPOAb testing can be deferred until confirmation of persistently raised TSH level. Better strategies, such as a computerised system for selective copying of results to GPs whenever relevant, and inclusion of treatment advice dependent on TPOAb status in the reports,4 may be needed to improve follow-up.

Chin-Pin Yeo · Melissa J Gillett · Samuel D Vasikaran

Adam P Morton* * Endocrinologist, Mater Hospital, South Brisbane, QLD 4101. AmortonATmater.org.au To the Editor: I appreciated the recent comprehensive review of androgen deficiency and replacement therapy in men by Handelsman and Zajac.1 I ask their opinion of the importance of obstructive sleep apnoea as a cause of secondary hypogonadism, and also of the safety of androgen replacement in men with hypogonadism who have obstructive sleep apnoea but are intolerant of continuous positive airway pressure (CPAP) treatment. In my practice, obstructive sleep apnoea is one of the most common associations, if not indeed causes, of hypogonadotropic hypogonadism. Several studies have shown that obstructive sleep apnoea is associated with secondary hypogonadism, which is partly or completely reversed by both CPAP treatment and uvulopalatopharyngoplasty.2-4 Secondary hypogonadism is also a feature of several conditions in which there is a high prevalence of obstructive sleep apnoea, including chronic spinal cord injury and cardiac failure. Of concern, studies have shown that androgen replacement may precipitate or worsen obstructive sleep apnoea.5,6 Similarly, a study of women with endogenous androgen excess caused by polycystic ovary syndrome found they were 30 times more likely to suffer from sleep-disordered breathing than control women.7 A single case report describes resolution of obstructive sleep apnoea in a non-obese woman after removal of a benign testosterone-producing ovarian tumour.8 Thus, I would value Handelsman and Zajac’s comments as to whether they consider obstructive sleep apnoea to be an important cause of secondary hypogonadism, and whether symptoms of this condition should be sought before initiating androgen replacement therapy.

Adam P Morton

David J Handelsman,* Jeffrey D Zajac† * Director, ANZAC Research Institute, Concord Hospital, Hospital Road, Concord, NSW 2139; † Head, Department of Medicine, Austin Hospital, Melbourne, VIC. djhATanzac.edu.au In reply: We thank Morton for his thoughtful comment that, in addition to monitoring for obstructive sleep apnoea precipitated by testosterone therapy, it may be worthwhile screening for this condition before starting treatment. Symptoms to be sought include daytime sleepiness and partner reports of loud and irregular snoring, especially among overweight men with large collar size. Obstructive sleep apnoea rises steeply in prevalence with age and causes mild hypogonadotropic hypogonadism, which is rectified by effective continuous positive airway pressure (CPAP) treatment.1 Obesity, depression, cardiovascular disease and other conditions that become more common with age have similar effects. Together, they contribute to the lower blood testosterone levels found in unselected older men, in whom testosterone remains an unproven treatment.2 This condition differs from classical hypogonadotropic hypogonadism caused by hypothalamic or pituitary disorders, which routinely requires lifelong testosterone replacement, and (occurring in a younger population) is rarely associated with obstructive sleep apnoea. The prevalence of obstructive sleep apnoea precipitated by testosterone treatment remains unclear. A case precipitated by injectable testosterone has been reported,3 while testosterone has potential adverse effects on sleep in older men.4 Clinical experience suggests that, among younger hypogonadal men, obstructive sleep apnoea is a rare idiosyncratic reaction to testosterone, which, like polycythaemia, may be particularly related to supraphysiological blood testosterone levels. However, the prevalence may be higher among older men. Hence, we agree that pretreatment screening is wise (rather than proven) for older men starting testosterone treatment, but is not routinely necessary for young men with classical hypogonadism.

David J Handelsman · Jeffrey D Zajac

A Rod MacQueen Clinical Director, Drug and Alcohol Services, Mid Western Area Health Service, Bloomfield Hospital, Forest Road, Orange, NSW 2800 rod.macqueenATmwahs.nsw.gov.au To the Editor: The article by Martyres et al on drug-seeking behaviour by young heroin users,1 leading to the deaths of 202 people over 5 years, leads to an inescapable conclusion. Too often, the medical profession is part of the problem rather than the solution, and as a result young people die. Here is an issue where the admonition primum non nocere should be foremost in our practice. After working with drug users and prescribing methadone for 22 years in a variety of settings, my experience is that drug users use drugs! Whether it is logical, safe or appropriate, or not, this group seeks drugs to modify or modulate their state of being. They often have serious medical and mental health issues, but have sadly decided on their preferred treatment without much knowledge of the diagnosis or of alternative interventions. They are often very skilled in obtaining drugs. So, we must perform our role equally well. Doctors are not drug dealers. Our duty is not to promote or support intoxication, or even relaxed happiness if that increases the risk of misadventure. It is to promote and support health. It is difficult to see how a prescription for 50 benzodiazepines to a young person (or even an older person) can ever be construed as healthcare. To do it again next day, next week, on and on, is almost unbelievable, yet the data indicate that is exactly what is happening.1 Even publicans have rules prohibiting serving intoxicated patrons. That one was “offering the customer what he asked for”, a common excuse for this sort of prescribing practice, would not be a suitable defence in the Coroner’s Court if insulin, digitalis, or even vitamin A, had been prescribed on request. But appeals to good practice and commonsense, along with current regulatory strategies, are apparently not sufficient to protect this vulnerable group. Kamien points out that data from the HIC could be used to provide immediate information to doctors about whether a patient is a “doctor shopper”.2 The data are already collected and could easily be made available if the will existed. Potential prescribers could at least gain accurate and timely information on which to base their decisions. There would be less excuse for “convenience store” prescribing, and more chance of ethical behaviour. At present these data remain largely useless in preventing avoidable deaths. But, surely, learning nothing from the deaths of 202 young Australians is not an option?

A Rod MacQueen

John M Hart General practitioner, Swan Medical Centre, 280 Great Eastern Highway, Midland, WA 6056 swanmedATiinet.net.au To the Editor: I write to share my concerns about the “doctor shoppers” in our community.1 The large medical group in which I practice has long been tormented by the demands of a constant stream of drug addicts, and I feel that we have now lost a very useful tool for dealing with these patients. I refer to the loss of access to the “Doctor Shopping Hotline”. This has resulted in increased aggravation for both staff and doctors. The problem is compounded by our practice being open at weekends and public holidays, when these patients arrive with the familiar story of not being able to get their benzodiazepines and opiates because their own doctors are not available. The Health Insurance Commission recently notified me about a patient who had attended our surgery, and many others, during a 3-month period last year. During this time, he saw more than 30 doctors and was prescribed more than 300 Pharmaceutical Benefits Scheme (PBS) items (6000 benzodiazepines and more than 2000 opiates [Panadeine Forte]). I strongly feel that the hotline should be reinstated — for the benefit of the doctors and the patients, and to help reduce a totally unwarranted drain on the PBS.

John M Hart

Jeff Whalan Managing Director, Health Insurance Commission, PO Box 1001, Tuggeranong, ACT 2901 medicare.enqAThic.gov.au In reply: I note the concerns expressed by Hart in relation to the discontinuation of the Doctor Shopping Hotline, and his call for the reinstatement of such a service. The Doctor Shopping Project, which was funded to the end of June 2002, focused on a limited selection of nervous system medications. It has been replaced by the Prescription Shopping Project, which is much broader in scope, as it encompasses all medicines on the Pharmaceutical Benefits Scheme (PBS). The new project aims to reduce the number of patients obtaining PBS medicines in excess of therapeutic need, and provides the opportunity for more informed prescribing across all categories of PBS medicine. The Health Insurance Commission (HIC) recognises the value of an information service for medical practitioners under the Prescription Shopping Project. An independent researcher has been engaged to explore the reactions and attitudes of medical practitioners and consumers to implementing such an information service. The research also aims to gain insight into medical practitioners’ intentions of using such a service, and their expectations of the scope and delivery of the service. Findings were presented to the HIC in early July 2004. The HIC will now convene a forum of relevant peak bodies to consider the scope and delivery of an information service in light of the findings. The HIC looks forward to working with the profession to establish an information service for medical practitioners under the Prescription Shopping Project.

Jeff Whalan

Paul Prociv Honorary Research Consultant, School of Molecular and Microbial Sciences, University of Queensland, Brisbane, QLD 4072. p.procivATmailbox.uq.edu.au To the Editor: In their brief review of water and public health, Leder et al1 uncritically attributed the Palm Island “epidemic” of 19792 to algal toxicity, commenting that it was the only recorded manifestation of this phenomenon in Australia. The original report described a hepatitis-like illness (associated in many with dehydration and bloody diarrhoea) in 138 children and 10 adults of Aboriginal and Torres Strait Islander descent living on Great Palm Island, northeast of Townsville, Queensland.2 No causative agent was actually identified. My investigation in the early 1980s of Toxocara pteropodis, a parasite of flying foxes, excluded it as a likely aetiological agent in the Palm Island outbreak, and compelled a critical reanalysis of other possibilities, which led me to conclude that subacute copper toxicity was the most plausible explanation. My rationale was published as a hypothesis.3 Sadly, discretion (to protect local technicians) compelled me to withhold critical information that explained how the community had been inadvertently exposed to excessive levels of copper in its water supply. Now that water management is becoming a major societal concern and algal blooms seem to be increasing in frequency, the issue needs to be resolved — and sufficient time may have elapsed for details to be revealed without impugning individuals. In 1985, having concluded that copper poisoning was the most likely explanation, I contacted the environmental health personnel who had overseen the mixing of algicide into the Palm Island water supply in 1979. They were aware that the actual volume of water to be treated had probably been grossly overestimated, because Solomon Dam’s water level was very low at the time. This meant that an excessive dose of copper sulfate was added to the dam, but it was assumed that this would be “erring on the safe side”. Further, the copper sulfate was not distributed uniformly through the water in the dam: a local resident with a dinghy had been contracted and instructed to spread the bags of copper salt around the dam, but had instead dumped it all at one place — immediately over the outlet pipe which carried the island’s drinking water. This would readily explain how the community encountered a sustained pulse of high copper levels in its tap water. While chronic copper poisoning can lead to infantile hepatic cirrhosis,4 acute gastrointestinal symptoms (as manifested during the Palm Island episode) are also well documented.5,6 In the absence of laboratory confirmation of copper toxicity, the cause of the “Palm Island mystery disease” must remain speculative. However, in any future similar outbreaks, copper poisoning should be excluded before attributing the cause to algal toxicity.

Paul Prociv

Christine B Phillips,* Suzanne Manning† * Senior Lecturer, Academic Unit of General Practice and Community Health, Australian National University Medical School, PO Box 254, Jamison Centre, Jamison, ACT 2614; † Intern, Department of Psychology, Australian National University, Acton, ACT. christine.phillipsATcalvary-act.com.au To the Editor: Since 1999, most asylum seekers in Australia who have been detained and subsequently found to be genuine refugees have been issued temporary protection visas (TPVs). Missing from much of the debate about management of asylum seekers has been the impact of the provisions of TPVs on children. A comparison of the entitlements of refugees on permanent and temporary protection visas is given in Box 1. To estimate the proportion of TPVs issued to children under 18 years of age, we analysed data provided by the Department of Immigration and Multicultural and Indigenous Affairs (DIMIA). The denominator population was drawn from data on numbers of temporary and permanent protection visas issued between June 1999 and June 2002.1,2 Numerator data were drawn from information provided by DIMIA on request.3 As shown in Box 2, we found that between October 1999 and June 2002, 23% of all TPVs were issued to children under the age of 18. Some of these children are now over 18 years of age. However, as children born to TPV holders in Australia are also given TPV status, more children will be recruited into this visa category. Australia is a signatory to the UN Convention on the Rights of the Child, which enshrines key rights for children, such as the right to health and safety.4 However, we believe that several of these basic rights are undermined by the lack of provisions afforded to TPV holders: they are prohibited from sponsoring family members, and they have limited access to settlement services for refugees (Box 1). Withholding of family reunion provisions increases the risks for children, as it makes it more likely that parents will take their children with them when they undertake hazardous travel to seek asylum. This is in contrast to the traditional model of families sending an index person, who then sponsors other family members. The lack of a comprehensive settlement package for TPV holders, and the temporary and indeterminate nature of the visas, is likely to compound the psychological distress experienced by both adult and child refugees. Children who have experienced ongoing adversity are vulnerable to developing psychological disorders.5 The children of TPV holders must also live in families where the parents bear an ongoing burden of fear and destabilisation. The effects of TPVs are borne by large numbers of children. There is a need for concerted advocacy by health professionals to ensure that the health consequences of TPVs for children are recognised and addressed. Addendum 13/07/04. While a recent federal government initiative will allow current Temporary Protection Visa holders to apply for permanent Australian residency, we urge ongoing review of refugee visas. 1 Comparison of entitlements of refugees on permanent and temporary protection visas Services funded by the Australian Government Refugees with permanent visas Refugees with temporary protection visas Settlement services Translating and interpreting service Eligible Not eligible Accommodation support Eligible Not eligible Assistance from Migrant Resource Centre Eligible Not eligible Early health and intervention service Eligible Eligible Torture and trauma counselling Eligible Eligible English language tuition Free tuition for adults and children Adults not eligible. Children eligible from July 2002 Family reunion May apply to sponsor family members Not eligible Employment Access to all assistance programs Not eligible except for most basic services Income support Eligible for full range of social security benefits Restricted entitlements Medicare Eligible Eligible Education Primary and secondary education Eligible Eligible Tertiary education Eligible for HECS Must pay upfront fees Travel Right of return if holder travels overseas No right of return if holder leaves country HECS = Higher Education Contribution Scheme. 2 Proportion of temporary protection visa (TPV) holders who were children when visa was granted (1999–2002) Years* No. of TPVs granted No. (%) < 18 years when TPV granted 1999–2000 871 108 (12.4%) 2000–01 4456 907 (20.3%) 2001–02 3196 952 (29.8%) Total 8523 1967 (23.1%) * Financial years.

Christine B Phillips · Suzanne Manning

Kim Hoe Chan,* Murugasu Segasothy† * Medical Registrar, † Associate Professor of Medicine, NT Clinical School of Medicine of Flinders University, Alice Springs Hospital, PO Box 2234, Alice Springs, NT 0871 m.segasothyATnt.gov.au To the Editor: A recent review suggests that acute rheumatic fever, osteoarthritis and systemic lupus erythematosus account for most rheumatic disease in Australian Aboriginals, and comments on the rarity of gout.1 Although the increased prevalence of hyperuricaemia in Aboriginals compared with non-Aboriginals has been described,2 clinical attacks of gout in Aboriginals have so far been extremely rare.1,3 This is in sharp contrast to various Polynesian and other indigenous populations, including Mäori in New Zealand, Filipinos in Hawaii and Alaska, Chamorros and Carolinians in the Marianas Islands, and Taiwanese aborigines. In these populations, increased prevalences of both hyperuricaemia and gout have been documented.4,5 In an extensive literature search, we found only one report of confirmed acute gouty arthritis in an Australian Aboriginal with normal renal function,3 although there have been several Aboriginals in the “Top End” with crystal-confirmed gout in association with chronic renal impairment.1 Between January 2001 and April 2004, we identified seven new cases of acute gouty arthritis in Aboriginals (Box), confirmed by joint aspiration revealing monosodium urate monohydrate crystals. Three of these patients had confirmed acute gouty arthritis without renal impairment. This series also includes the first reported cases of gouty arthritis in Aboriginal women. Our findings suggest that the prevalence of acute gouty arthritis in Australian Aboriginals is much higher than previously reported. Discussion with physicians at Alice Springs Hospital revealed that they too have encountered gouty arthritis in Aboriginals, but whether this was confirmed by joint aspiration is not known. It appears that gout has been misdiagnosed or under-reported, or both. Further epidemiological studies should be undertaken to confirm this hypothesis, and we must have a higher index of suspicion for gout when an Aboriginal patient presents with an arthropathy, as gout is a potentially disabling and yet easily treatable condition. Aboriginals with acute gouty arthritis, Alice Springs Hospital, January 2001 – April 2004 Age (years) Sex UA level (mmol/L) Site of joint aspiration Possible precipitating factors Joints involved 46 M 0.37 Right knee Alcohol Right knee 44 M 0.45 Right knee Acute renal failure, alcohol Right knee, left first metatarsophalangeal joint, left ankle 65 M 0.23 Right knee Renal transplant, cyclosporin Right knee, right foot 64 F 0.50 Right knee Chronic renal impairment Both ankles and first metatarsophalangeal joints, right knee 61 F N/A Right knee Acute-on-chronic renal failure, alcoholism Right knee 51 M 0.48 Left knee None identified Left knee 35 M 0.54 Right knee None identified Both ankles, right knee UA = uric acid. Reference range, 0.20–0.45 mmol/L. N/A = not available.

Kim Hoe Chan · Murugasu Segasothy