Letters

To the Editor: A recent editorial in the Journal suggested that blood could be sent overseas for genetic testing for maturity onset diabetes of the young (MODY).1 We are pleased to be able to point out that genetic testing, including clinical and laboratory support with full gene sequencing for both MODY1 and MODY3 and for neonatal diabetes (mutations in SUR1 and Kir6.2), is available in Australia. Testing for MODY2 and for a number of other disorders of the pituitary–adrenal and pituitary–gonadal axis in children is also available. We are happy to receive specimens and referrals from clinicians who would prefer to use an Australian clinical laboratory accredited by the National Association of Testing Authorities. More information is available via: http://www.mater.org.au/Home/Services/Pathology.aspx.

Mark F Harris · Ivan N McGown · David M Cowley

To the Editor: A recent MJA Supplement discusses prognostic and end-of-life communication for health professionals on the basis of a systematic literature review and an expert advisory panel.1 It is usually the case that malignant disease is diagnosed after biopsy, and this is usually undertaken by a surgeon. In a consecutive series of 100 patients presenting with a lesion in a bone with no past history of malignancy, the lesion was the presenting feature of systemic malignancy in 44 of those patients.2 Hence, it is usually the surgeon’s role to advise the patient (and caregivers) that the patient has a terminal disease and, in some cases, the prognosis can only be measured in weeks. It will be obvious that this can be a significant shock to all, particularly when there was no prior indication that malignancy was a possibility. I note that not one of the 35 experts was a surgeon. I also note that surgery as palliation is given virtually no role other than a brief mention in Box 11, despite the well documented role of surgery.3 It has been my experience that the most common question asked by patients with the diagnosis of a terminal malignancy is about the role of surgery; the question “Why can’t you just cut it out?” is a universal feature. This has not been addressed. It is my sincere hope that further expert advisory panels addressing this area become truly multidisciplinary and include perhaps the most relevant discipline — surgery.

Mark T Clayer

In reply: We agree that the content area of these guidelines is very relevant for surgeons, as for all health professionals involved in the care of adult patients with advanced life-limiting illnesses and their caregivers. Surgical representation on our expert panel would have been very useful. We agree that surgery has an important role in terms of palliative treatment options that may be available for certain clinical circumstances. The issue of how to respond to the question “Why can’t you just cut it out?” is an important one. We believe that the principles outlined in these guidelines would be relevant when responding to this question, but would welcome specific suggestions from Clayer and other surgeons about how they respond to such patients. We would hope to include these suggestions along with other input from surgeons in any future update of these guidelines.

Josephine M Clayton · Karen M Hancock · Phyllis N Butow · Martin H N Tattersall · David C Currow

To the Editor: In their recent Snapshot, Sharma and colleagues reported an interesting case of a woman presenting with prolonged fever and inflammation of external ears, nose, and throat.1 On the basis of negative antineutrophil cytoplasmic antibodies (ANCAs), a diagnosis of relapsing polychondritis was made and the possibility of Wegener’s granulomatosis “ruled out”. Corticosteroid and azathioprine were given to the patient accordingly. However, patients with Wegener’s granulomatosis can present with limited otolaryngological symptoms with or without positive ANCAs.2,3 As a rule, ANCAs are present in 90% of patients with the generalised form of the disease, but in only 60% of those with the limited form.4 Conversely, some cases of relapsing polychondritis can have a positive test result for ANCAs.4 A case has been reported of a Wegener’s granulomatosis patient with otolaryngological manifestations that led to an initial diagnosis of relapsing polychondritis, but who subsequently developed pulmonary and renal involvement.3 While a routine biopsy to exclude Wegener’s granulomatosis in patients with inflammatory otolaryngological symptoms may not be practical, with a limited period of follow-up, a diagnosis of relapsing polychondritis should be made cautiously and only provisionally. This is true even in cases such as the patient described by Sharma and colleagues with 6 months of illness and 7 months of follow-up, as pulmonary and/or renal manifestations could take years to follow. We believe that negative ANCAs should never be used to rule out Wegener’s granulomatosis, especially in its limited form.

Weekitt Kittisupamongkol · Wanla Kulwichit

To the Editor: Scott and colleagues have shown that Australia is no different to the rest of the world in applying evidence-based treatment predominantly to patients at lower risk.1 They suggest that therapy may be withheld from high-risk patients because of over-estimation of the risk of treatment, under-estimation of the actual absolute risk of non-treatment, and consideration of cost-effectiveness and social inequalities. I suggest that their data support the concept that the patient at highest risk who misses out on evidence-based treatment may in fact be being managed with kindness and wisdom. Such a patient is old, has comorbidities, can be frail, and may be taking 10 pills or more per day, so questions of optimal prognostic therapy must be balanced against quality-of-life factors. There is abundant evidence that patients at highest risk do not receive the maximum amount of therapy. I suspect the kindness and wisdom factor is underestimated in clinical decision making. What we need now is some good qualitative data — market research — to help explain this phenomenon before we intensify the evidence-based mantra.

V Michael Jelinek

In reply: Jelinek rightly draws attention to the need, when caring for patients with acute coronary syndromes, to distinguish disease-related risk from age-related risk arising from frailty, comorbidity, physical disability, cognitive impairment, depression, social isolation, age–treatment interactions, and quality of life. All these factors affect treatment goals in older patients and may, as we conceded, justify withholding certain treatments in individual cases. However, even after accounting for “wise compassion”, under-treatment is still likely because: our treatment eligibility criteria excluded patients with advanced comorbidity or who declined treatment; population-based studies of risk–benefit trade-offs argue for more intense treatment use in patients ≥ 75 years,1,2 in whom absolute risk reductions exceed those in younger patients by as much as 10%;3 and all four key treatments at discharge (aspirin, β-blocker, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, and statins) can be administered as once-daily, single tablet formulations, which are usually well tolerated. Given that a third of patients presenting with acute coronary syndromes are aged 75 years or older, for whom 30-day risk of death or myocardial infarction exceeds 20% and who account for 60% of all deaths related to myocardial infarction,4 we recommend, similar to expert bodies,4,5 judicious (not mantra-driven) use of evidence-based treatments in all eligible older patients.

Ian A Scott

To the Editor: We refer to the study reported by Correa-Velez and colleagues, which found lower hospital utilisation rates among patients from refugee-source countries compared with the Australian-born population in Victoria.1 As noted by the authors, there is a dearth of evidence on the use of health services by refugees. Their 6-year investigation stands as a singular study of its kind in Australia, and we recognise its potential to inform policy on refugee health care. However, we argue that the authors’ conclusion that “the Refugee and Humanitarian Program does not currently place a burden on the Australian hospital system” cannot be drawn from the data collected in the study. Refugee groups have health needs related to histories of torture and trauma, and associated somatic symptoms.2 Furthermore, refugees have often been exposed to diseases that are infrequently encountered in the general Australian population. Considerable time is required to train health professionals to diagnose and treat such complex clinical presentations. In addition, adequately servicing the special needs of this patient group requires the provision of appropriately qualified interpreters. When an interpreter is required during a clinical consultation, additional time is often needed to gain clarity. Interpreters can also be difficult to source, which places added time and resource pressures on health care administrative staff and budgets. Correa-Velez et al do refer to the “multiple barriers that prevent refugees from adequately accessing health care services”. Further research is required to comprehensively assess the reasons why, given the complexity of their health care needs, refugees are not accessing the hospital system at the same rate as other Australians. The authors suggest that reasons for an increase in service utilisation by refugees in recent years may include an increased level of familiarity with services, or poorer health status of recently arrived refugees. Previous reports have indicated that refugees tend not to utilise health care services where fundamental issues of access, such as language barriers and lack of education about the availability of health care services, have not been addressed.2,3 Since Correa-Velez and colleagues’ data were collected, several states, including Victoria, have developed primary health care programs for refugees, with varying degrees of success. As the Queensland Government considers a new statewide model for refugee health,4 it is essential to ensure adequate resources are allocated for refugee and staff education programs and interpreting services.

Joy L Mendel · Claire E Brolan

To the Editor: We report two cases of previously well male bodybuilders who presented with severe extrapyramidal reactions after intramuscular injection of the antipsychotic fluphenazine decanoate, in the mistaken belief that it was an anabolic steroid. The first patient, aged 31 years, obtained fluphenazine decanoate from a gym contact. He injected 50 mg intramuscularly on alternate days (Days 1, 3 and 5) to a total of 150 mg, then presented to two local hospitals on Days 7 and 11 with difficulty swallowing, generalised muscle stiffness and lethargy. He withheld the history of fluphenazine use, and was diagnosed with tonsillitis. On Day 14, he presented to our emergency department (ED) with marked dystonia, immobility, and inability to speak or swallow food. On examination, he was afebrile and haemodynamically stable. He was given a trial dose of benztropine 2 mg, but improvement was slight and, given the absence of relevant history, benztropine was not repeated. The neurology team raised the possibility of a conversion disorder, but the psychiatry team, noting the patient’s attempts to speak and an absence of recent stressors, believed that further investigation into an organic cause was required. When the patient’s wife learned that he had used fluphenazine and alerted the neurology team to this use, he was started on regular benztropine and his condition improved over the next 3 days. The dose of benztropine was reduced on discharge, but his dystonia recurred and required readmission to hospital for further treatment. The second, unrelated patient, also aged 31 years, openly admitted purchasing fluphenazine decanoate from “a friend of a friend”. After injecting two 50 mg depots, he had multiple presentations to three EDs, where he was treated for dystonia with immediate doses and then regular low doses of benztropine. On admission to our hospital 19 days after injection, he was afebrile and haemodynamically stable, with marked dystonia. His initial creatine kinase level was elevated (553 U/L; normal, < 204 U/L), but subsequently normalised and was not accompanied by autonomic dysfunction. His condition improved with regular oral diazepam and benztropine, but symptoms recurred when he inappropriately reduced his benztropine dose after discharge. On subsequent review, both patients’ dystonia was resolving, but they had significant akathisia. Inadvertent and inappropriate use of a long-acting phenothiazine not only required prolonged anticholinergic therapy for these men, but we believe placed them at risk of neuroleptic malignant syndrome. We have found no previous similar reports in the medical literature, but are aware anecdotally of at least one other case of a patient treated recently at a district hospital. The anabolic steroid nandrolone decanoate is referred to colloquially on numerous websites and by our patients as “deca” (from the Organon brand name Deca-Durabolin). We believe our patients and their supplier(s) have mistaken the “decanoate” in fluphenazine decanoate for the pharmacologically active component of the drug.

Elizabeth A S Giugni · Rachel S Boddy · Natalie G Limet

To the Editor: The introduction of indoor smoking restrictions in Western Australian pubs, clubs and nightclubs1 has been championed as a public health success and an advance in tobacco control. But how well is it being observed, and is the current legislation adequate? Although smoking in Australia is declining, a report showed that one in seven 16–17-year-olds had smoked cigarettes in the previous month.2 Peer pressure has an important influence on smoking uptake,3 and alfresco hospitality settings, being exempt from the smoke-free restrictions, constitute important risk environments for young people. Moreover, 85% of adults in WA do not smoke, but continue to be affected by second-hand smoke drifting from alfresco balconies, beer gardens and street cafes. Indeed, the legislation risks turning these popular and highly visible entertainment areas into nicotine classrooms4 for the young, and “no-go” zones for health-conscious non-smokers. We set out to evaluate compliance with the smoke-free legislation, and its impact on smoking in licensed premises. Twenty medical students were recruited to monitor smoking in 93 Perth hotels and nightclubs on two Friday evenings during November 2006. Entertainment areas were classified as indoor (smoke-free), semi-outdoor (smoke-free, failing to meet exemption criteria) and alfresco (smoking allowed), in accordance with the new legislation. Average observation times were 20 minutes, 17 minutes and 15 minutes respectively. Indoor compliance with the legislation was high, with smoking noted in only five (5%) of the 93 premises. Whether by default or design, 58 premises (62%) had alfresco areas and there was smoking activity in those areas in 56 (97%) of these premises. Forty premises (43%) also had semi-outdoor areas where, contrary to the legislation, smoking remained prevalent (23 premises; 57.5%). Overall, smoking was observed in 69 of the 93 premises (74%). In 35 of these premises (51%), smoking was visible to the passing public. These results demonstrate the inadequacy of the new smoke-free legislation in restricting smoking, protecting the health of non-smokers and strengthening tobacco control. The legislation has been well accepted, but smoking (legal and illegal) remains prevalent in licensed premises. This presents a serious challenge to tobacco control and efforts to reduce smoking by young people. A key lesson from the history of tobacco control is that partial bans achieve partial results.5 A complete ban on smoking, both inside and outside licensed premises and restaurants, is urgently required.

William J Patterson · Michael M Daube · Stephen L G Hall · Denitza Moronova

To the Editor: Bajorek et al1 did not address two aspects of compliance that may be an issue in community care of patients with atrial fibrillation taking warfarin: time of dose, and point-of-care testing. There is no pharmacological reason requiring warfarin administration in the evening. This practice arose to facilitate dose adjustment on the day of testing, initially in hospitals, and subsequently flowed on to community care. We know that compliance is better with once-daily administration re-gimens, and this patient group invariably needs other medications, such as diuretics, that require morning doses. Concomitant morning administration of warfarin would be logical. In addition, it would reduce attendances by domiciliary nurses to cognitively impaired patients, who may otherwise require twice-daily visits for administration of medications. This would alleviate a significant burden on this stretched resource. The implementation of point-of-care testing at the general practitioner’s surgery by a registered nurse can be of great benefit in the liaison required to manage therapy, and facilitates instant dose adjustments by the doctor, who has comprehensive knowledge of the patient’s pharmaceutical and health circumstances.2

Peter W Ford · Angela Close

In reply: I thank Ford and Close for highlighting additional points regarding the optimal management of anticoagulants in general practice. Indeed, neither of these points was raised by our study participants. Regarding the timing of doses, for medication safety reasons, in many hospitals the warfarin dose is listed for mid-evening administration; the recently introduced National Inpatient Medication Chart (NIMC), which incorporates a designated “warfarin section”, nominates 16:00 as the time. In the hospital setting, this timing is necessary to enable the treating medical team (rather than after-hours staff) to review the day’s blood test results, and subsequently prescribe the appropriate dose. The process ensures that treatment is optimally managed by those most knowledgeable about the patient’s regimen, prevents dose omissions, and reduces the time to dose stabilisation (and potentially, time to discharge). Ford and Close appropriately point out that this timing may not always be convenient for patients once they are discharged to the community setting. The optimal regimen should facilitate the patient’s adherence to treatment, and therefore should coordinate with the rational use of existing support services. This needs to be more carefully considered in discharge planning when warfarin therapy is involved. Point-of-care testing is an efficient mode of monitoring anticoagulation therapy, but we were unable to expand on this in our previous discussion (due to word limits). Internationally, point-of-care testing underpins many comprehensive monitoring services, whereby allied health professionals (eg, trained nurses or pharmacists) perform the blood tests, monitor results, adjust doses, and/or prescribe therapy, as well as educate patients, under the guidance of a medical officer. Such services are conventionally offered on an outpatient basis (eg, the Antithrombosis Center, University of Illinois Medical Center, Chicago, Ill, USA) or within the general practice setting, and are effective and safe models of care. Patient self-management using point-of-care testing devices has also been studied overseas,3 with reports of good control of international normalised ratio (INR) and high patient satisfaction. Locally, point-of-care testing has been trialled within community pharmacies. In a Sydney-based study, trained community pharmacists monitored INRs using point-of-care testing, reviewed doses according to standardised nomograms, and subsequently liaised with GPs regarding dose adjustments. The results showed that collaborative management effectively maintained INRs within the therapeutic range.4 There is scope to develop such models further, and we are currently investigating GPs’ preferences for models of care, as well as opportunities for mobile anticoagulation services.

Beata V Bajorek

To the Editor: In a recent article,1 Scrimgeour showed the differences between death rates in Aboriginal people and in the general Australian population. He used the Accessibility/Remoteness Index of Australia (ARIA)2 to show that Aboriginal people in remote areas generally had higher death rates than those near major health facilities. However, this widely used tool is inaccurate when applied to some health facilities. Cherbourg Aboriginal community (population about 2600) is located in the South Burnett district of south-eastern Queensland, 260 km by road from Brisbane. It has a 10-bed hospital with two resident doctors. There are several small towns (population 1000–3000) in the district. Two have hospitals with no full-time medical staff. The main centre is Kingaroy (population about 12 000), 50 km from Cherbourg. It has a 60-bed hospital with resident staff, but no specialists or consultants. There are general practitioners but no medical specialists in the district, although some specialists visit for a day or so per month. Most patients needing specialised services go to public hospitals in Brisbane (220 km away [from Kingaroy]), Toowoomba (170 km away) or Nambour (140 km away), where waiting lists are long. Children go to children’s hospitals in Brisbane, either by road (a 3-hour journey) or by helicopter. The ARIA index ranges from 0.0 (major city) to 12.0 (very remote area). Cherbourg (classed with Murgon, 5 km from Cherbourg) has an index of 2.9 and Kingaroy, 2.6. The cities of Darwin, Cairns and Townsville, all with major hospital and health facilities, have an ARIA index of 3.0, while Alice Springs, which also has a major hospital and specialists, has an ARIA index of 6.0. Clearly, the remoteness index is not a good indicator of the availability of local specialist health services. The ARIA classification is widely used. The anomaly of the South Burnett and Cherbourg Community may (or may not) be the only problem with the index. Until such anomalies are corrected and ARIA is validated, any results derived using the index should be treated with caution.

Alan E Dugdale

To the Editor: The Guidelines for the management of acute coronary syndromes 20061 state: “Enoxaparin may be used in conjunction with fibrin-specific fibrinolytic agents in patients under the age of 75 years, provided they do not have significant renal dysfunction. An intravenous bolus dose of 30 mg followed by a 1 mg/kg subcutaneous injection every 12 hours in combination with tenecteplase is the most comprehensively studied therapy.”1 In Australia, enoxaparin is not licensed for intravenous use (Tony Hall, Team Leader, High Risk Medications and Systems, and Christine Maclean, Associate Director, Safe Medication Practice Unit, Queensland Health, personal communication) and there is no recommendation for the intravenous use of enoxaparin in the drug product information.2 Are the authors recommending “off-label” use of intravenous enoxaparin, or do they wish to modify the guidelines to reflect what the management should be if clinicians are unable to use intravenous enoxaparin?

Mark Little · Chris Johnstone

In reply: The guidelines were published to provide clinicians with the most contemporary information on the management of acute coronary syndromes based on the international literature, and may include treatments which are not currently available, officially licensed or available through the Pharmaceutical Benefits Scheme in Australia. In the context of adjuvant therapy for patients with ST-segment-elevation myocardial infarction (STEMI), the guidelines recommend that antithrombin therapy should be used with fibrin-specific fibrinolytic agents.1 Based on the best evidence available at the time, the guidelines mention two antithrombins, unfractionated heparin and enoxaparin, to be considered for use in this setting. The recommendation for enoxaparin is based on comprehensive evidence of clinical benefit with the regimen of an initial intravenous (IV) bolus dose followed by subcutaneous injections every 12 hours. It is up to individual practitioners to determine whether the IV dose should be provided “off-label” or omitted, based on the evidence and the circumstances of the individual patient and setting. The issue of superiority of enoxaparin over unfractionated heparin as adjuvant therapy for patients with STEMI is currently being evaluated in light of recent evidence,2 and will be included in a future update of the guidelines.

Constantine N Aroney · Philip Aylward

To the Editor: I read with great interest the recent updated review of amoebiasis by van Hal and colleagues1 and their previous letter2 describing three cases of locally acquired amoebiasis due to Entamoeba histolytica in Australian men who have sex with men (MSM). These articles should alert clinicians to the emergence of invasive amoebiasis and the possibility of person-to-person transmission of E. histolytica through oral–anal or oral–genital sex among MSM in developed countries. The same phenomenon has been reported in Taiwan3 and Japan.4 The prevalence or incidence of intestinal amoebiasis among people at risk may have been underestimated in the past, as microscopy of stool specimens has lower sensitivity and specificity than E. histolytica antigen detection methods for diagnosing the disease.1,5 Cases of amoebiasis may evade detection using the diagnostic algorithm proposed by van Hal and colleagues,1 which suggests using microscopy of stool specimens to detect E. histolytica complex followed by confirmation with specific antigen detection methods or molecular methods. To increase diagnostic sensitivity and specificity, I suggest revising the diagnostic algorithm for intestinal amoebiasis in developed countries to include more accurate first-line detection methods. For example, specific antigen detection methods or polymerase chain reactions, as proposed by Tanyuksel and Petri,5 could be incorporated.

Chien-Ching Hung

To the Editor: van Hal and colleagues deserve congratulations for their lucid, concise and timely review of the complex problem of human amoebic infection and its diagnosis.1 Not surprisingly, however, their article raises more questions than it answers. To me, the gist of their message was as follows: what was in the past diagnosed as Entamoeba histolytica infection, based on the microscopic identification of organisms from faeces, culture or histological sections, actually may have been caused by other species, viz. E. dispar (a recently described non-pathogen) or E. moshkovskii (known for a long time from sewage samples, but only recently found to infect humans). Because these species are all identical morphologically, they can be distinguished reliably only by sophisticated molecular techniques. To complicate matters further, despite E. dispar having been virtually defined as the “non-invasive form” of Entamoeba, most true E. histolytica infections are still asymptomatic.2 Not only the parasite, but also individual host factors (perhaps including genetics), determine pathogenicity. Thus, not all people infected with the same pathogenic strain will manifest symptoms or signs of invasive disease. Given their biology and evolution, it is conceivable that, eventually, invasive strains of even E. dispar will be discovered! Furthermore — and this seems not to have been investigated yet — mixed infections involving different species and strains of these parasites almost certainly occur (not to mention the “traditional” non-pathogenic amoebae, which frequently do occur in mixed infections). The authors advocate treatment of even asymptomatic E. histolytica infections, but how would these be detected outside epidemiological surveys or healthy population screening programs? Given the difficulty and expense of specifically identifying the infective organism even in symptomatic cases, and the relative cheapness of treatment, surely it would be sufficient simply to treat on the basis of clinical presentation plus the identification of E. histolytica-like parasites, with or without objective evidence of histopathology. Anything more could be justified only within the context of a well funded and carefully designed research program and/or epidemiological study.

Paul Prociv

In reply: We agree with Hung that molecular and antigen testing methods are more sensitive for Entamoeba histolytica detection than microscopy and that reliance on microscopy alone would result in under-detection. Our algorithm1 was presented the way it was for several reasons. Firstly, both molecular and antigen testing are significantly more expensive than microscopy. Secondly, as these tests can currently only detect a single pathogen, they would not replace microscopy. Most patients, especially men who have sex with men (MSM), have multiple intestinal parasites, so the more specific methods would remain an adjunct in parasite detection.2 Thirdly, the positive predictive value of any test is dependent on the prevalence of the disease. The prevalence of E. histolytica in Australia, based on current data, is less than 1% in high-risk populations, including MSM. Thus, at present, molecular and antigen tests would be more likely to give false positive than true positive results. However, we agree that our algorithm could be modified as suggested if prevalence rates were between 5% and 10%. Finally, as seen in the MSM population in Taiwan, this is not a static situation, and ongoing local surveillance is required.3 We agree with Prociv that, before the introduction of molecular techniques, E. histolytica prevalence would have been overestimated. We also agree that specific host factors and/or undefined parasitic virulence factors can lead to invasive disease. However, given the extensive molecular work that has been undertaken, we believe it unlikely that invasive strains of E. dispar will be discovered.4 Furthermore, recent studies show that mixed infections are common.2,5 In symptomatic patients, empirical amoebicidal therapy is warranted. However, to ensure that alternative diagnoses (eg, inflammatory bowel disease) that require different treatment are not overlooked, all attempts to accurately speciate Entamoeba complex should be undertaken. We acknowledge that speciation using the polymerase chain reaction is beyond the means of most laboratories, but this is not the case for enzyme immunoassay testing of stool samples, which is rapid, sensitive and relatively cheap. For asymptomatic patients who are carriers of E. histolytica cysts, the World Health Organization recommends treatment.5 However, in areas of low prevalence such as Australia, Entamoeba cysts are more likely to be non-pathogenic E. dispar or E. moshkovskii species than E. histolytica.3 Thus, in Australia, treatment would be unnecessary in a high proportion of patients. Furthermore, therapy requires a luminal agent (paramomycin), which is difficult to obtain. The most practical solution is to either give no treatment or to treat only those patients who have tested positive for E. histolytica.

Sebastiaan J van Hal · Damien J Stark · Debbie Marriott · Jock L Harkness

To the Editor: Two recent articles in the Journal touch on the current plight of medical academics. Hays emphasises the need to reassert the role of teaching in academic medicine — otherwise, “our aim to produce safer, more efficient doctors will be under threat”.1 Joyce and colleagues outline the projected increase in the number of graduates from Australian medical schools, although their concern is more for the post-graduate careers of these young doctors than for their initial clinical training.2 In 2006, Van Der Weyden warned that not only do new ways of teaching medical students need to be rapidly explored but also that more skilled teachers must be found and trained.3 Medical students themselves believe that more clinical teachers are required to ensure that the increasing numbers of students are taught effectively.4 From personal experience we know that, while many full-time clinicians are both willing and inspiring teachers at undergraduate level, a core of permanent academics is needed to direct teaching during these clinical years. But why would anyone choose to be a medical academic today? Certainly not for the money — a recently qualified obstetrician/gynaecologist, starting at senior lecturer level after about 15 years of training, is looking at an income of less than half that of a staff specialist at the same level, and a quarter of that possible in private practice. One day of private practice per week does not help — obstetrics is a full-time commitment, and even in gynaecology the need to pay practice and indemnity costs outweighs any financial benefits. Is it the kudos? Adjunct academic titles are easily gained by non-academics: hospitals are awash with adjunct associate professors and lecturers. The adjunct appointment system often lacks regular and critical appraisal, and in some cases titles are used to the professional or financial gain of the recipient, with little reciprocal input into teaching at the institution concerned. (However, there are indications of attempts to crack down on such practices.)5 The lifestyle then? Academics may have a less frenetic clinical schedule, but the continuing pressure to produce quality research and to jump increasingly higher hurdles to obtain grants can mean that the limits of the working week are much less defined than for our staff specialist colleagues. We have seen many colleagues depart academia in the past few years for the more verdant pastures of full-time clinical practice. While we are in agreement with Hays about the need for more research into how best to design medical education, we believe that, unless there are urgent improvements in the remuneration, career structure and professional regard for clinical academics, the core workforce of skilled teachers so clearly needed for incoming students will just not be there to deliver that education.

Ajay Rane · Caroline de Costa

To the Editor: Like Haley’s father,1 I too lament the fact that Latin terms have fallen out of use in medical terminology. I also think it retrograde that Latin is being taught to fewer and fewer of our secondary students, as they are missing out on an opportunity to learn so much more about our own language, let alone terms that they might use later in their clinical practice. However, I do not think that it was Latin that helped the young teacher out of a difficult predicament in the 1950s. I can assure Haley that “pseudocyesis” is all Greek to me.

Peter Piazza

To the Editor: Thank you for the charming letter about “non-pseudocyesis” published in the 19 March issue.1 It reminded me of the Brander Matthews quote: “A gentleman need not know Latin, but at least he should have forgotten it.” This is particularly apt, as the term “pseudocyesis” is from Greek.

James Mitchell

To the Editor: The tale told by Katherine Haley’s father about his clever advice on how to protect the privacy of a young pregnant woman makes a good story.1 However, while “non” is a Latin word, “pseudocyesis” is very good Ancient Greek (ψευδοκύησις). Queen Mary I (“Bloody Mary”), who was believed for many months to be with child but ultimately returned to court childless, may have suffered from pseudocyesis. I agree with Dr Haley’s opinion about the lamentable decline in the use of both Latin and Greek terms in medical practice. I take the time to teach my students, residents and registrars enough Latin and Greek to render classical plurals correctly (eg, fistulae, diverticula, carcinomata). Whether they take any notice of this classical teaching is another matter.

William E M Renton-Power

To the Editor: I was both delighted and a little perturbed to read the recent letter by Katherine Haley about her general practitioner father who outsmarted the Department of Education by a medical sleight of hand, stating that his patient had “non-pseudocyesis”.1 However, it was not Latin, but Greek, that did the trick. Despite Dr Haley’s background in Latin, he, like all physicians, had unwittingly used Greek during his medical course. I was fortunate to do a year of Ancient Greek during my undergraduate medical course and, like my late GP father, also did Latin for matriculation. It is unfortunate that Greek is no longer taught in Queensland schools, and Latin only in a few. I believe that we are the poorer for this, and it shows in all sorts of ways, including a general decline in literacy even at the tertiary level. A classical grounding demands scholarship and precision. I have found that knowledge of both Greek and Latin has enriched my knowledge of English literature and Western philosophy, as well as French. Such a grounding also trains the mind in analytical and ordered thought and provides greater insight into the workings of syntax and grammar and a greater facility with words — the building blocks of our language, many of which are derived from Greek and Latin. At the risk of stating the obvious, I will remind readers that anatomical words in medicine are predominately Latin or Greek and that the names of nearly all symptoms and diseases are Greek (with some exceptions, such as “angina pectoris”). In Dr Haley’s time, it was common for potential doctors to receive an arguably more “polished” education that embraced one or two languages, including Latin and, in some private schools, Greek. Alas, the current system of medical student selection favours those “idiots savants” who excel in mathematics and science and not the arts. With respect, I would like to point out that in the term “non-pseudocyesis”, the only Latin component is “non”, the rest being Greek (ψευδής, false; κύησις, pregnancy). For both the enthusiast and the non-classicist, may I recommend my father’s 5th edition of Gould’s medical dictionary (1943), which contains the etymology of every medical word.

Roger K A Allen

To the Editor: The recent article by Venn et al reported that childhood overweight carries through into adult overweight and obesity, but that most obese young adults in their study were “healthy” weight as children in 1985.1 As demonstrated by National Health Surveys, age is one of the strongest predictors of overweight,2 with body mass index (BMI) increasing as we grow older. However, there are two additional time-related components influencing obesity. Since 1985 (when Venn et al reported the prevalence of overweight and obesity in children was less than 10%), the environment appears to have become more obesogenic — a 2004 survey in New South Wales showed that 26% of children were overweight or obese.3 It is not only children who are vulnerable — the percentage of overweight adult Australians increased for almost all age groups from 1990 through 2001, and the mean BMI at which Australians enter adulthood has increased with each subsequent survey. For example, for women aged 20–24 years, mean BMI increased from 22.1 kg/m2 (1990) to 22.5 kg/m2 (1995) to 23.2 kg/m2 (2001) to 23.3 kg/m2 (2004). As the heights and weights were self-reported in these surveys, true BMI values may be even higher. We recently reported that year of birth (birth cohort) also predicts prevalence of overweight and obesity, independent of age and survey period; the prevalence of overweight and obesity in adults increased progressively with birth cohorts born since 1960.4 This birth span includes the cohort in the study by Venn et al.1 While obesity begins in childhood for only a small proportion of adults, the so-called healthy weight children now have a higher mean BMI, giving little margin for the seemingly inevitable increases in weight with ageing, before the population mean BMI reaches the cutpoint for overweight and later obesity. The 2004–2005 National Health Survey showed that men reached the overweight cutpoint at 25–29 years and women reached it at 30–34 years.5 Given increasing child and adult obesity, the need for allocation of public health resources to improve dietary and physical activity habits is undisputed. However, these data1,4 indicate that efforts should be directed to the hard-to-reach group, young adults, to prevent weight gain at this point. This will pose considerable challenges, because this group has minimal contact with health services, and perceives the threat of chronic illness as irrelevant. However, swift intervention is required, not only for their own health and that of their children as they become parents, but also because they will become overconsumers of health care for chronic diseases within a generation.

Margaret A Allman-Farinelli · Lesley King · Adrian E Bauman

In reply: Allman-Farinelli et al make an important point about the influence of age, survey period and cohort effects on the prevalence of overweight and obesity. While age and cohort effects could not be clearly separated in the 1985 Australian Schools Health and Fitness Survey, the prevalence of overweight and obesity increased with age in 7–15-year-olds.1 Our data collected from 4571 of the individuals in that survey at follow-up about 20 years later also showed an increase in the prevalence of overweight and obesity with age, although these findings were not presented in our report.2 In the Box, we show the distribution of body mass index (BMI) values for men and women in three age groups (24–27 years, 28–30 years and 31–34 years). Mean BMI values across the age groups were 25.2 kg/m2, 25.6 kg/m2, and 26.5 kg/m2 in men and 23.5 kg/m2, 24.2 kg/m2, and 24.6 kg/m2 in women. The prevalence of obesity (BMI ≥ 30 kg/m2) increased with increasing age as follows: age 24–27 years — men 12.2%, women 9.9%; age 28–30 years — men 12.3%, women 12.0%; and age 31–34 years — men 15.6%, women 14.6%. Distribution of body mass index values for men and women in three different age groups* * 24–27 years, 757 men and 854 women; 28–30 years, 767 men and 807 women; and 31–34 years, 673 men and 691 women in the 20-year follow-up of the 1985 Australian Schools Health and Fitness Survey.

Alison J Venn · Russell J Thomson · Michael D Schmidt · Verity J Cleland · Beverley A Curry · Hanni C Gennat · Terence Dwyer

To the Editor: O’Leary and colleagues1 rightly point to the need for better evidence on whether low to moderate maternal alcohol intake affects the fetus. Evidence to date is weak and inconsistent, largely because alcohol consumption in pregnancy is generally poorly documented,2 and few studies have recorded data on factors that could potentially modify fetal exposure. Evidence could come from large pregnancy cohort studies, usually designed to address other issues, but there are no published guidelines on how to collect information relevant to fetal alcohol exposure during gestation. There is, therefore, a great need to define a core dataset for research studies, as well as one that is sufficiently simple to use in routine pregnancy care settings. We have identified a number of issues that need to be addressed. To stimulate discussion, the Box shows our suggested core dataset. Maternal alcohol intake: Alcohol questionnaires have largely been designed to identify women who are heavy drinkers, misuse alcohol or are alcohol-dependent.3 Questionnaires are needed that capture information on alcohol intake across the range, from minimal to heavy drinking, as well as information on drinking patterns and alcohol intake at different periods of gestation. Factors that may modify the relationship between maternal intake and fetal alcohol exposure: For a given maternal intake over a given period, maternal blood alcohol level and hence fetal alcohol exposure may vary according to maternal size and body composition. Other factors can affect maternal alcohol absorption and elimination, such as whether alcohol is taken with food,4 and possibly maternal genotype.5 This information is rarely reported in pregnancy studies. Factors that may modify effects of alcohol on the fetus: There is animal evidence that maternal micronutrient supplementation may protect the fetus against some of the adverse effects of gestational alcohol exposure.6 We need to consider recording supplement use and measures of maternal nutritional intake or status. In well resourced studies, fetal genotype could also be considered.6 Researchers with expertise in the field need to reach consensus and provide guidelines on the best way to assess fetal alcohol exposure, so that pregnancy researchers and clinicians with little experience of alcohol research do not need to create their own. Better data should provide better evidence on which to base advice to women who are (or may be) pregnant. Good studies may also provide explanations for the apparently variable link between maternal alcohol consumption and adverse sequelae in the offspring. Suggested core dataset for studies of maternal alcohol intake during gestation and outcome of offspring As a basis for discussion, we suggest the folllowing dataset: Baseline Weeks of gestation at pregnancy recognition, or expected date of delivery and date that pregnancy was recognised (to allow calculation) Height For specific periods of gestation (eg, from date of start of last menstrual period until pregnancy recognition; from pregnancy recognition to 12 weeks’ gestation; from 13 to 28 weeks; and from 28 weeks to term) Body weight (eg, at 12 and 28 weeks) Alcohol intake — we suggest: Average number of standard alcoholic drinks per week; Average number of days per week on which alcoholic drinks are taken; and Maximum number of drinks on one occasion. Whether alcohol is taken with or soon after food (never, sometimes, usually or always) Dietary intake of fruit and vegetables Use of nutritional supplements

Ruth Morley · Jane L Halliday · Susan M Donath