Letters

To the Editor: I would like to correct some inaccuracies in an article by Jelinek and Gawler in the December 2008 issue of the Journal about a survivor of disseminated osteosarcoma.1 The article describes a 58-year-old man who was diagnosed in 1974, at the age of 24 years, with histologically confirmed high-grade osteosarcoma of the right femur. He underwent a full leg amputation in January 1975, but metastases recurred 11 months later, in December 1975. The authors of the article misreported a sequence of medically significant events, altering the patient’s actual history. (The correct chronology and early clinical history of the case have been published elsewhere.2,3) The errors and omissions in the article by Jelinek and Gawler, together with the correct sequence of events and relevant inclusions, are outlined in Box 1. In summary, the major errors in the article were as follows: Timeline errors. The authors stated that the patient first saw Dr Meares in September 1976, after chemotherapy had failed. In fact, the patient consulted Meares as a first-line treatment approach on 12 December 1975, and did not consider chemotherapeutic options until September 1976. The authors also stated that the patient had palliative radiotherapy in September 1976. In fact, the patient had only one course of palliative radiotherapy treatment, in February 1976. Vegan diet. The patient never followed a vegan diet. Date of photographs. The photographs in Figures B and C of the article by Jelinek and Gawler were taken on 7 July 1977 (Box 2), not at the time of first contact with Meares, as implied in the article. An appraisal of the patient’s symptoms, combined with an accurate clinical history, reveals a more plausible scientific hypothesis for his remission than the effects of diet and meditation. Although diet and meditation may be adjuncts to a patient’s wellbeing, it is unlikely in this case that they were curative, and certainly veganism was not a relevant factor. Immunotherapy with BCG vaccine treatments, the timing of symptoms and the patient’s eventual diagnosis of tuberculosis could be associated with his remission, as postulated by his radiation oncologist in 1978.6 There is extensive scientific literature about remission of cancer, including osteosarcoma, associated with febrile conditions.5,8-15 The patient’s sporadic visits to doctors meant that metastases were not diagnosed histologically and much of the information reported on his case is anecdotal. Clearly, in this and other cases, unbiased investigative scientific research needs to be undertaken before reporting anecdotes and extrapolations as if they were fact. Teasing apart the errors in Jelinek and Gawler’s story, now on the public record and almost medical myth, is an enormous task, but one that must be done, because correctly reporting the patient’s clinical timeline is crucial in any discussion about the causes of his remission and the flow-on effect to cancer patients and their treating doctors.16 1 Corrections to errors in the article by Jelinek and Gawler1 Errors and omissions in the article Facts, corrections and inclusions December 1975: widespread bony and pulmonary metastases were diagnosed. December 1975: an isolated metastasis in an inguinal node was diagnosed. The patient undertook the Gerson dietary regimen,4 immunotherapy with BCG vaccine,5 and the Meares intensive meditation program.6 September 1976: “[the patient] underwent three cycles of palliative chemotherapy with vincristine, adriamycin, cyclophosphamide and darcarbazine, as well as brief palliative radiation therapy”. September–October 1976: growth of tumours on the sternum increased, and metastases were detected in the left lung. Coughing and haemoptysis were present.6 Experimental chemotherapy (with adriamycin, vincristine and methotrexate)2 was ceased at 10 weeks after December 1976. No radiation therapy was given at this time. Palliative radiotherapy was administered in February 1976, not September 1976. September 1976: “He elected to discontinue these therapies as his condition deteriorated further.” “The patient then consulted prominent psychiatrist and hypnotherapist Dr Ainslie Meares ...”. December 1975: the patient first consulted Meares. In February 1976, he abandoned the Meares meditation program. The 10-month discrepancy between December 1975 and Jelinek and Gawler’s stated date of September 1976 (actual date, October 1976) alters the patient’s medical timeline, implying that it was only after other treatments had failed that meditation began and played a key role in his recovery. Dates of photographs shown in the article: “When Meares first saw the patient, he had visible bony tumours protruding from his ribs, sternum (Figure B) and iliac crest, and was coughing up blood containing small spicules of bone (Figure C).” The article by Jelinek and Gawler implies that the photographs in their Figures B and C were taken around the time when the patient first contacted Meares. The photograph in Figure B was actually taken on 7 July 1977, 19 months after his first contact with Meares. Tumours were not protruding from the sternum when Meares first saw the patient to begin meditation in December 1975, and there were no visible metastases. The coughing up of blood containing bone spicules (Figure C) began in mid 1977, not in the period between December 1975 and February 1976. Vegan diet: “[the patient] adhered faithfully to a vegan diet”. The patient never followed a vegan diet. Veganism involves exclusion of all animal products. The Gerson regimen4 includes dairy foods and calf liver juices. For the following 22 years, the patient’s diet included seafood, dairy products and eggs. First appearance of tuberculosis: “Presumably related to immunosuppression from chemotherapy, he developed pulmonary tuberculosis in June 1978, and was treated for this condition for 12 months.” In 1978, an oncologist diagnosed advanced tuberculosis (TB) dating back to early 1976. (Previous x-rays were examined, showing evidence that TB had been present and undiagnosed for at least 2 years. The patient had very advanced TB by June 1978.6) The suspected cause was BCG vaccine treatments administered in December 1975, possibly exacerbated by chemotherapy and associated immunosuppression in late 1976. 2 Original photographs of patient’s chest taken on 7 July 1977 I am in possession of these original photographs (left), which were dated 7 July 1977 (date enlarged in inset). A copy of page 227 from the original edition of You can conquer cancer7 also confirms the accurate date of the photographs as 7 July 1977 (date enlarged in inset)

Grace O Gawler

In reply: In conjunction with the patient’s memory, and teasing out details, where available, from medical records and investigations of over 30 years ago, we sought to piece together our follow-up story of a remarkable recovery from cancer as accurately as possible.1 We did not attempt to reproduce the original case report in the Journal,2 but rather were highlighting the long-term issues that can be associated with such recoveries. We thank Ms Gawler for attempting to clarify the original timelines. However, based on the medical records and published data, as well as checking further with the patient himself, it seems her letter does little more than muddy the waters in this case. Ms Gawler claims the patient abandoned the Meares meditation program in February 1976. This is factually incorrect and misleading. The patient continued to use Meares’ methods to meditate for 3 hours daily until he recovered, and has meditated at least 1 hour daily since then. The timelines quoted around the photographs in Figures B and C in our original article1 were based on information from Meares’ 1978 article.2 He was somewhat inaccurate, as is Ms Gawler, who claims the photos were taken in July 1977. This is incorrect. Figure B was photographed in July 1976 as chemotherapy was commenced. Figure C was photographed in 2008 and documents bony spicules coughed up during the first half of 1977, collected and retained by the patient. Regarding the use of BCG vaccine treatments, the patient reports that none of the three tuberculosis (TB) specialists whom he consulted gave credence to Ms Gawler’s suggestion that the onset of TB was related to the BCG vaccine. Ms Gawler further postulates that the remission could be linked to a febrile condition associated with TB. The patient did have severe night sweats (which may or may not have been accompanied by fever) over a period of 2–3 weeks in February and March 1976, at a time when he almost certainly had not yet contracted TB, and after which the metastases continued to grow rapidly. After this time, the patient never reported fevers that would make sense of this claim. Ms Gawler claims that the patient’s metastases were not diagnosed histologically and that much of the reported evidence is anecdotal. This is misleading and would surely surprise the involved surgeon, oncologist and other physicians, who used the best available medical evidence at the time and cooperated in the preparation of our original article. The case is documented with a thorough medical history, the patient’s surgeon and other specialists were consulted regularly, and accurate records were retained. Full details confirming the report are available in the patient’s biography.3 The metastases were thoroughly investigated and confirmed by the Peter MacCallum Cancer Centre in Melbourne and regularly tracked via x-ray. The original lesion seen on x-ray was diagnostic for osteosarcoma and the diagnosis was confirmed histologically by biopsy, and again after amputation. The case history is certainly complex and compelling. The message is clear: unexpected recovery from disseminated cancer remains a possibility, and is likely to be influenced by lifestyle factors.

George A Jelinek · Ruth H Gawler

To the Editor: The Between the Flags project of the Clinical Excellence Commission (CEC) is designed to establish a “safety net” in all New South Wales public hospitals, to enable early identification and management of deteriorating hospital inpatients.1 A paediatric advisory group within of the program is currently developing five age-group-specific paediatric observation charts to account for the changes in normal physiological parameters that occur with age in children, and these have been distributed for comment before finalisation. Each chart has specific physiological calling criteria defining when a clinical review or rapid response is required from medical staff (Box). If one or more criteria fall in the “red” zone, the patient requires an immediate, rapid response; if criteria fall in the “yellow” zone, the patient needs a clinical review within 30 minutes. A paucity of data on what represents an abnormal parameter for each age group has also led to a lack of clear triage guidelines for emergency department nurses. For example, the paediatric physiological discriminators of the Australasian Triage Scale include terms such as “mild tachycardia” as a guide for allocating patients to triage Category 3 and “moderate tachycardia” for Category 2.2 We trialled the CEC paediatric inpatient calling criteria to determine whether they could also be used for emergency department triage purposes. We carried out a retrospective review of patients presenting to triage at the emergency department of the Children’s Hospital at Westmead between 1 and 14 March 2010. We assumed that patients who met the CEC’s yellow criteria should be allocated to triage Category 3 (“urgent: review within 30 minutes”) and those who met the CEC’s red criteria should be allocated to at least triage Category 2 (“emergency: review within 10 minutes”). Patient outcomes were classified as “admitted”, “discharged” or “did not wait”. From 1968 presentations, 1885 patients had observations at triage available for review. The numbers of patients in each triage category were: Category 1 (5); 2 (41); 3 (403); 4 (422); and 5 (1014). Only 10 of the 46 patients in Category 1 and 2 would have been flagged by the CEC parameters as needing a rapid response (ie, review within 10 minutes), and none of the three patients admitted to the paediatric intensive care unit would have been identified by the CEC parameters. Of the 403 patients in Category 3 (needing review within 30 minutes), 32 would have been uptriaged to Category 2 by the CEC criteria. Twelve of these 32 patients were in fact discharged home, indicating that the CEC criteria are unsuitable for triage purposes. Of the 1436 patients in Category 4 and 5, 30 would have been uptriaged to Category 2 according to the CEC parameters and, of these, only three were admitted. A further 271 patients would have been uptriaged to Category 3 (181 of these were discharged and 54 did not wait). Of particular note is that 151 of the 271 patients met the yellow criteria because of low respiratory rates that were flagged by the charts but were normal for the patient. At present, the physiological parameters defined in the new CEC paediatric inpatient observation charts are not suitable as a triage tool in the paediatric emergency department, do not replace an experienced triage nurse, and are a poor predictor of disposition. CEC calling criteria* and physiological parameters for children, by age group Calling criteria, by age group Call Physiological parameter < 30 days 1–12 months 1–4 years 5–11 years ≥ 12 years Red† Heart rate (beats/min) Above 180 190 170 160 150 Below 80 80 70 60 40 Respiratory rate (breaths/min) Above 100 65 60 50 40 Below 20 15 15 10 5 Systolic blood pressure (mmHg) Above — — — — — Below 60 50 70 70 80 Oxygen saturation (%) Below 85 85 85 85 85 Temperature (°C) Above 38 — — — — Yellow‡ Heart rate (beats/min) Above 160 170 150 140 130 Below 90 100 80 70 50 Respiratory rate (breaths/min) Above 60 50 50 35 30 Below — 30 20 15 10 Systolic blood pressure (mmHg) Above — 120 120 130 160 Below 70 80 80 80 90 Oxygen saturation (%) Below 95 90 90 90 90 Temperature (°C) Above 37.5 — — — — CEC = Clinical Excellence Commission. * Calling criteria as of March 2010 at the time of this study (the CEC has subsequently revised some of these criteria). Only one “flag” was required to meet a calling criterion. Other calling criteria such as pain, work of breathing and level of consciousness were not measured in our study but will also generate a call. Where no values are present, there are no calling criteria for the parameter. † Red call requires immediate, rapid response. ‡ Yellow call requires review within 30 minutes.

Fenton M O’Leary · Jennifer I Major

To the Editor: Chen and colleagues1 published a risk assessment tool for type 2 diabetes (AUSDRISK) based on the Australian Diabetes, Obesity and Lifestyle Study (AusDiab).2 We tested AUSDRISK’s performance in an independent cohort of 1494 women enrolled in the Geelong Osteoporosis Study (1994–1997; 77% participation),3 comprising an age-stratified sample of women randomly selected from the Barwon Statistical Division and followed prospectively over a decade.4 In 2004–2008, of 1015 surviving study participants aged 25 years or older at enrolment, 800 (79%) returned for follow-up assessment. We excluded 261 women who did not have a fasting plasma glucose (FPG) test result at both baseline and follow-up assessments, and 33 with baseline diabetes. The remaining 506 women formed the cohort on which the AUSDRISK tool was tested. Diabetes was defined by one or more of three criteria: FPG level ≥ 7.0 mmol/L, treatment with insulin or oral hypoglycaemic agents, or self-report. Demographics, ethnicity and lifestyle factors were documented by questionnaire. Participants were described as “active” if they described their mobility as “moves, walks and works energetically, and participates in vigorous activity”; otherwise, they were considered “inactive”. As our baseline questionnaire did not document a history of high glucose levels, we performed two analyses: one assuming no participants had this history, and a second identifying participants with baseline impaired fasting glycaemia (FPG level, 6.1–6.9 mmol/L). The study was approved by the Human Research Ethics Committee, Barwon Health. Using the final AUSDRISK model,1 we allocated points for baseline characteristics according to sex, age, ethnic background, parental history of diabetes, history of high blood glucose (FPG level, ≥ 6.1 mmol/L), use of antihypertensive medications, current smoker status, physical inactivity, and waist circumference. The predictive power of AUSDRISK was determined using the area under the receiver operating characteristic curve (AROC). Using a total AUSDRISK score ≥ 12 as the criterion for prediction of diabetes, we evaluated the performance of AUSDRISK by calculating its sensitivity, specificity and positive predictive value (PPV) in our cohort. Ninety-eight participants had an AUSDRISK score ≥ 12 (or 106 if those with impaired fasting glycaemia were scored for a history of high blood glucose). Statistical analyses were performed using Stata software, version 9 (StataCorp, College Station, Tex, USA). Twenty-eight participants (5.6%) developed incident diabetes during the period of follow-up (13 with FPG ≥ 7.0 mmol/L, 14 receiving treatment with insulin or hypoglycaemic agents, and seven self-reporting the condition). If we assumed that none of the participants had a history of high blood glucose levels, the AROC for AUSDRISK in the Geelong cohort (0.78 [95% CI, 0.72–0.85]) was comparable with that in the AusDiab cohort (0.78 [95% CI, 0.76–0.81]).1 In our study, the sensitivity of the AUSDRISK tool was 50.0% (95% CI, 30.6%–69.4%), specificity was 82.4% (95% CI, 78.7%–85.7%) and PPV was 14.3% (95% CI, 8.0%–22.8%). Recognising baseline impaired fasting glycaemia increased AUSDRISK’s predictive power (AROC, 0.81 [95% CI, 0.74–0.88]; sensitivity, 60.7% [95% CI, 40.6%–78.5%]; specificity, 81.4% [95% CI, 77.6%–84.8%]; and PPV, 16.0% [95% CI, 9.6%–24.4%]). Study limitations were that we only evaluated women, we did not collect data on a history of high blood glucose levels, diabetes was diagnosed in the absence of an oral glucose tolerance test, and criteria for inactivity differed from those used in the AusDiab study. Our population was older than that of the AusDiab study and would probably have had a higher prevalence of diabetes, influencing our PPV result. Not surprisingly, including individuals with impaired fasting glycaemia increased the point estimates for AROC, sensitivity and PPV. In conclusion, our data independently demonstrate the limited predictive value of AUSDRISK for women over a 10-year period.

Julie A Pasco · Mark A Kotowicz · Margaret J Henry · Geoffrey C Nicholson

To the Editor: Evidence is beginning to accumulate on the effectiveness of the low-density lipoprotein (LDL) cholesterol-lowering medicine ezetimibe. While there are no completed trials investigating ezetimibe’s effect on clinically important end points, two recent trials investigating its effect on carotid intima media thickness (CIMT) have both reported disappointing results.1,2 After each of these trials, the Journal has published editorials by Hamilton-Craig, who offers reassurance about ezetimibe and encourages ongoing prescription of this drug to patients who have elevated LDL levels despite maximum-tolerated statin therapy.3,4 Such a sanguine opinion seems at odds with the negative trial evidence, and therefore worthy of debate. Briefly, the ENHANCE (Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression) trial, which compared ezetimibe plus simvastatin with simvastatin treatment alone in 720 patients with familial hypercholesterolaemia, found no significant difference (and a trend in the direction of harm) with respect to the primary end point of CIMT.1 The ARBITER 6-HALTS (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 6 — HDL and LDL Treatment Strategies in Atherosclerosis) trial compared ezetimibe with extended-release niacin in statin-treated patients with coronary heart disease.2 Among 315 patients with available results, the group taking niacin showed a statistically significant reduction in CIMT, but the group taking ezetimibe showed no such reduction. Of concern, increased cumulative exposure to ezetimibe was associated with progression of CIMT (P = 0.05). Although far from definitive, the results of these two trials offer no reassurance of benefit from ezetimibe and, in my view, may portend harm. It may seem counterintuitive that ezetimibe, which significantly lowers LDL cholesterol levels,1,2 could be ineffective or harmful. However, the history of medicine is replete with examples of interventions that improve numerical disease measures without benefit to patients. One recent example was torcetrapib, which, despite increasing high-density lipoprotein cholesterol and reducing LDL cholesterol levels in a promising manner, was found to cause serious adverse events, including death.5 I agree with Hamilton-Craig that we require trials measuring major cardiovascular events to really understand the effects of ezetimibe. Where we disagree is how to manage our patients during the period of uncertainty until publication of the results of these trials. While he argues for continued prescribing of ezetimibe, I suggest we should explicitly share our uncertainty about the safety and efficacy of this drug with our patients by discussing the existing research. Some patients will, like Hamilton-Craig, place their faith in the cholesterol hypothesis and be reassured by an assumption of cardiovascular protection as their LDL falls. Others will choose to wait until we have more robust evidence that ezetimibe is safe and effective. I would wait.

Brett D Montgomery

In reply: I agree with Montgomery that cardiovascular disease (CVD) outcomes are required to determine the role of ezetimibe. The Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial (in which patients with aortic stenosis were treated for 52.2 months with statin plus ezetimibe or statin plus placebo) showed a 4.7% reduction in ischaemic CVD events in the ezetimibe group (P = 0.02; number needed to treat, 23), driven by a reduced need for coronary artery bypass grafting.1 In contrast to previous trials showing regression of atherosclerosis in response to statin therapy, baseline carotid intima media thickness (CIMT) levels in the ENHANCE (Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression) trial were normal, due to previous statin therapy. This is likely to account for the lack of change in CIMT with ezetimibe treatment in the ENHANCE trial.2 As no placebo group was included, neither lack of benefit nor harm from ezetimibe therapy can be inferred.2 Data from animal studies have shown atherosclerosis regression after ezetimibe treatment through multiple mechanisms.3-5 Prospective randomised controlled trials with statins, resins or surgery have independently shown an approximate 1% reduction in CVD per 1% reduction in low-density lipoprotein cholesterol (LDL-C) level. Evidence for the benefits of lowering LDL-C is among the most robust in medicine. Pending the outcomes of IMPROVE-IT (the Improved Reduction of Outcomes: Vytorin Efficacy International Trial, a multicentre study of ezetimibe plus simvastatin versus simvastatin treatment of patients with acute coronary syndrome [http://clinicaltrials.gov/ct2/show/NCT00202878]), or clinical outcome data confirming those of the ARBITER 6-HALTS (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 6 — HDL and LDL Treatment Strategies in Atherosclerosis) trial,6 it seems reasonable to continue to use ezetimibe to lower LDL-C levels in patients who are not achieving LDL-C targets despite statin therapy or who are intolerant to statins. Extended-release nicotinic acid (Niaspan [Abbott Laboratories, Chicago, Ill, USA]) may be an appropriate alternative to statins as second-line therapy, and should be made available under the Pharmaceutical Benefits Scheme for treating patients with dyslipidaemia. (Niaspan has approval from the Therapeutic Goods Administration for marketing in Australia, but is not being imported into Australia at this stage.)

Ian R Hamilton-Craig

To the Editor: National best practice guidelines recognise that accurate data on the health of Indigenous Australians are crucial to improving health service delivery.1 The draft revision of the RACGP Standards for general practices acknowledges the need for improvement and requires that a practice demonstrates how it routinely records, in active patient health records, self-identified Aboriginal and Torres Strait Islander status.2 This is a commendable improvement but should be further strengthened, requiring that Indigenous status be recorded for at least 90% of active patients, the level required for a history of allergies. Improved record keeping in general practice has resulted in the potential to improve Indigenous identification among patients notified with a communicable disease. This enables the documentation of health disadvantage, and allows evaluation of measures aimed at closing the gap in health outcomes between Indigenous and non-Indigenous people. Demographic data in the NSW notifiable diseases database (NDD) were audited for all 258 Hunter New England (HNE) Salmonella infection notifications in 2007 by interviewing patients and their referring general practitioners. Interviews were completed for 83% of patients. Indigenous status was poorly recorded. The NDD listed three patients with salmonellosis as Aboriginal, but showed an unknown status for 87%. Among patients who had attended a GP during their illness (66%), practice records listed two as Aboriginal, but Indigenous status was unknown for 70%. Most GPs (95%) reported using electronic medical records, and 89% completed pathology requests with practice software. Many GPs (60%) requested information on how to appropriately ask about a patient’s Indigenous status. Interviews with patients who had been notified as having had salmonellosis identified 13 as Aboriginal, and no resistance to identification was encountered. The crude salmonellosis notification rates per 100 000 population were 42.2 (95% CI, 19.3–65.1) for Aboriginal HNE residents and 25.5 (95% CI, 21.7–28.6) for non-Aboriginal HNE residents which, while not statistically significant for this small sample, suggests a differential salmonellosis burden, consistent with studies elsewhere.3 The true burden of disease was likely to have been substantially higher, as many infections are not notified.4 The differential burden may also be an underestimate if Aboriginal HNE residents were less likely to be notified than non-Aboriginal residents due to, for example, reduced access to health services. The widespread availability of electronic practice software for generating pathology requests provides a new opportunity to substantially improve Indigenous identification in communicable disease notifications.3 Indigenous status should be routinely recorded by GPs and automatically included on their pathology request forms and subsequent laboratory notifications. There is now a need for a coordinated national approach to ensure consistent inclusion of Indigenous status on all laboratory notification data.

Anthony D Merritt · April R Roberts-Witteveen · David N Durrheim

To the Editor: I refer to the article by Gallego and colleagues in the 19 April 2010 issue of the Journal,1 which stated that (as at the time of writing, in July 2009) Australia had no formal policies for iodine supplementation in pregnant and lactating women. In January 2010, the National Health and Medical Research Council (NHMRC) released a public statement, Iodine supplementation for pregnant and breastfeeding women.2 The NHMRC recommends that women who are pregnant, breastfeeding or considering pregnancy take an iodine supplement of 150 μg each day; and women with pre-existing thyroid conditions should seek advice from their medical practitioner before taking a supplement. The public statement also provides information on the increased need for iodine during pre-pregnancy, pregnancy and breastfeeding, the risks of not having enough iodine and the types of supplement that should and should not be used. The statement was developed in consultation with an expert reference group and was based on a review of recent international scientific literature for the efficacy of iodine supplementation in increasing iodine levels in pregnant and breastfeeding women to levels that mitigate the risks associated with iodine deficiency.3 The public statement and supporting literature review can be found on the NHMRC website.2,3

Warwick P Anderson

To the Editor: We disagree with the opinion expressed by Gallego and colleagues that Australian “women planning a pregnancy and pregnant and lactating women should be advised to take an iodine supplement”,1 and offer two reasons to support our view. First, the data suggesting mild iodine deficiency in Australian women were collected from opportunistic samples of women not representative of the population at large and were obtained before the introduction of mandatory iodine fortification of bread in October 2009. We believe that recommending iodine supplementation in pregnancy without evaluating the effect of mandatory iodine fortification on iodine intake and status of pregnant women in Australia is premature.2 This is supported by a recent report, developed by the Dietitians Association of Australia on behalf of the National Health and Medical Research Council (NHMRC).3 The report clearly shows that the recommended iodine intake for pregnant women (recommended dietary allowance, 220 μg/day) is achievable from foods alone, together with iodine fortification of bread. Second, there are no randomised controlled trials (RCTs) that have examined the effect of iodine supplementation of pregnant women from regions of mild iodine deficiency (as in Australia) on neurodevelopment of the offspring or any other clinical outcomes. Gallego et al state that “iodine-containing supplements consistently benefit the iodine and thyroid status of both mother and newborn”, citing a review of iodine supplementation of pregnant women from populations with mild-to-moderate iodine deficiency.4 In fact, none of the six RCTs included in that review showed a clear effect of supplementation on maternal and newborn thyroid hormone concentrations, which suggests that the maternal thyroid is able to adapt to meet the increased thyroid hormone requirements of pregnancy in areas of mild-to-moderate iodine deficiency.5 Furthermore, Gallego et al cite no evidence to support their statement “Even subclinical hypothyroidism in the mother, occurring as a consequence of iodine deficiency, can cause irreversible brain damage in the fetus . . .”. In our view, major public health recommendations advising routine iodine supplementation for women planning a pregnancy, as well as pregnant and lactating women, should await the results of current RCTs6-8 examining the effect of maternal iodine supplementation on longer-term maternal health and neurodevelopmental outcome of children in regions with mild-to-moderate iodine deficiency, including Australia and New Zealand.

Shao J Zhou · Sheila A Skeaff · Philip Ryan · Maria Makrides

In reply: While Zhou and colleagues disagree with our viewpoint that Australian “women planning a pregnancy and pregnant and lactating women should be advised to take an iodine supplement”,1 we note that they suggest any such recommendation should await the results of their planned randomised controlled trial (RCT) examining the effects of maternal iodine supplementation on maternal health and neurodevelopmental outcome of the offspring. They neglect to mention that the National Health and Medical Research Council (NHMRC) issued a public statement in January this year, with supporting evidence attached, stating that: “The NHMRC recommends that all women who are pregnant, breastfeeding or considering pregnancy take an iodine supplement of 150 μg each day”.2 Similar recommendations, based upon available scientific evidence, have been issued by the World Health Organization, International Council for Control of Iodine Deficiency Disorders, American Thyroid Association and American Endocrine Society. We agree that there is a paucity of RCT evidence examining the effect of iodine supplementation of pregnant women living in mildly iodine-deficient areas, and this is regrettable. Given the overwhelming animal and human evidence that maternal iodine deficiency causes brain damage in the offspring of deficient mothers, we consider there are major ethical issues in conducting such trials where pregnant women would be deprived of iodine and their babies put at risk of brain damage. Zhou and colleagues imply that mild-to-moderate iodine deficiency is not widely prevalent in Australia. This statement ignores the evidence from several clinical studies of pregnant women in New South Wales, Victoria and Tasmania, all showing that mild-to-moderate iodine deficiency is widespread in the majority of the Australian population. Analysis of the data in some of these studies shows between 20% and 40% of women tested are moderately to severely iodine deficient.3 Furthermore, food modelling studies by Food Standards Australia New Zealand (FSANZ) predict between 45% and 75% of Australian women will continue to be iodine deficient after the mandatory use of iodised salt in bread that commenced in October 2009.4 Finally, we disagree with their assertion that the recommended iodine intake for pregnant women can be achieved by the majority of women from foods alone, together with iodine fortification of bread. A trial of bread fortification in Tasmania showed this was not achievable.5 If this were achievable, it is questionable why Zhou and colleagues would even consider conducting an RCT of maternal iodine supplementation in pregnant women in Australia and NZ.

Gisselle Gallego · Stephen Goodall · Creswell J Eastman

In reply: I thank Mountain and colleagues from the Australasian College for Emergency Medicine for their letter.1 Despite their interpretation of our article,2 I think we share many points of agreement. Having worked extensively as a clinician, I agree that patient harm is occurring because of insufficient capacity to treat, and that patients will benefit from more capacity to treat. I also agree that this is an important issue and that approaches to dealing with it should not be subverted. Most importantly, I would also agree that the number of available hospital beds is critical — the unanswered questions are about how many beds, and where they should be provided. I also thank the authors for their acknowledgement that “clinical modelling” is a fundamental driver for their position. Our industry would do well to take its direction in the use of queuing theory from internationally recognised experts in the area, rather than from within the ranks of my fellow doctors. In response to Mountain et al’s call for an 85% bed-occupancy limit as a solution, my call is for more detail about the practicalities of how we would implement this limit, which could start with the provision of clear answers to the following questions: How would compliance with the 85% occupancy limit be monitored? What are the practical measures that bed managers, nurse unit managers, executives and others could use to ensure that compliance occurs? If patient throughput in acute inpatient areas increased, what downstream effects could we expect? How would the application of resources in fixing “access block” compare with the application of the same resources in fixing “exit block”? (And an obvious sub-question: what is the relationship between the two phenomena?) Has a consensus been reached with all specialist groups as to which clinical units in hospitals should have access to extra beds when they become available? Or is it intended that an 85% limit would be applied across the board, irrespective of the differences between patient care needs, lengths of stay, rates of arrival and staffing mixes in different wards? How and when would the effectiveness of such an initiative be assessed? Perhaps another occupancy figure would appear even more efficacious through the lessons learned. I believe these are reasonable questions that ought to be answered by anyone calling for this change. I repeat my group’s call for more, and more informed, investment in health system capacity given this huge problem and the solution being proffered.

Christopher A Bain

To the Editor: In his letter1 regarding Heeley et al’s article on cardiovascular risk perception and evidence–practice gaps in Australian general practice,2 Radford quotes, “no [automated blood pressure-measuring machines] were accurate enough to ... replac[e] a manual sphygmomanometer”. The citation dates from 1973, when oscillometric blood pressure monitors such as the Omron HEM-907 — distributed by the High Blood Pressure Research Council of Australia (HBPRCA) with support from the Servier Foundation — did not exist. In defence of digital blood pressure devices, a cluster randomised controlled trial conducted in Australian general practice has demonstrated their superiority compared with existing manual devices.3

Mark R Nelson

To the Editor: The recent MJA supplement provides an excellent summary of internet interventions for a range of psychiatric conditions, including anxiety, depression and substance misuse.1 However, in highlighting the positive uses of the internet, it is important to remember other aspects of online engagement that can have a negative impact on patients’ mental health. It is useful to ask patients specifically about their internet activities, as they will not necessarily volunteer this information. For example, people can spend a large amount of time accessing pornography online. Negative effects of this may include the impact on existing real-world relationships, the cost, and the risks associated with participation in illegal activities. Some patients may go further, arranging to meet people they have encountered on the internet in person, which entails a risk of physical or sexual assault. The internet provides an opportunity for discreet gambling and, as with other forms of gambling, the effects can be destructive. Excessive participation in online games such as World of Warcraft, to the extent that people spend virtually all their waking hours engrossed in playing games, can also be a problem. Bullying and socially destructive behaviour occurring on widely used social networking sites such as Facebook can cause considerable distress to the victim. Such sites can be used to deliver unwelcome information (eg, ending a relationship by changing one’s Facebook status to “single” and “de-friending” the partner). Privacy can also be an issue, and Facebook provides much information to potential stalkers if users fail to adequately protect their data. Some medical practitioners have allowed patients to become their “friends” on Facebook, which can involve inappropriate access to the doctor’s personal life and a risk of blurring professional boundaries.2 Finally, the internet is increasingly being incorporated into delusions expressed by people with psychotic disorders.3 For example, patients with schizophrenia may have paranoid beliefs that derogatory material about them is being distributed via the internet. Enquiring about patients’ internet activities is therefore a useful addition to the standard mental health assessment.

Cherrie A Galletly

To the Editor: The prophylactic use of inferior vena cava filters (IVCFs) in trauma patients for whom anticoagulation is contraindicated has markedly increased over the past few years. Their need for caval filtration is usually only transient, and once the risk of venous thromboembolism is deemed to be minimal, it would seem appropriate that IVCFs be retrieved. However, a large number of IVCFs remain in situ, due to either failure of retrieval or lack of follow-up. We observed a case that touches on both of these two major problems associated with IVCF retrieval. A 34-year-old man received a prophylactic IVCF after he had sustained severe pelvic fractures, several undisplaced spinal fractures and a splenic laceration in a motorbike accident. He was deemed to be at high risk of venous thromboembolism, and immediate prophylactic anticoagulation was contraindicated because of his pelvic and splenic injuries. The scheduled IVCF retrieval, 8 weeks after insertion, failed due to technical difficulties. A large clot between the struts of the IVCF (Figure) meant further withdrawal attempts were deemed too dangerous. The patient was informed that he had two options: if the filter remained in situ, he would possibly need lifelong oral anticoagulation; or the IVCF could be surgically removed. Soon after this, the patient was discharged with instructions to continue oral anticoagulation. About 5 months later, at a follow-up consultation with the orthopaedic surgeon about his injuries, the patient expressed his concern about the IVCF and especially about the anticoagulation. He was taking it for no other indication than the IVCF. The radiologist who had inserted the IVCF was contacted, and subsequently removed it without any complications. In the case described here, an initial retrieval attempt was thwarted by filter tilt and a large clot burden. After discharge, the patient was lost to follow-up with respect to the IVCF. Fortunately, this was addressed by one of the specialists involved in management of the patient’s other problems. Without this intervention, the patient may have ended up with the filter permanently in situ, with its attendant risks, and an unwarranted lifetime of anticoagulation. When filters have a significant clot burden, anticoagulation can help dissolve this to the point at which retrieval can be effected safely.1 This case highlights the need for appropriate follow-up after IVCF insertion. Various studies have outlined different follow-up strategies, some using a protocol drawn up in a multidisciplinary team setting,2 others designating a key person (usually the clinician who inserted the filter) to undertake this task.3,4 Both strategies have been shown to reduce the number of patients lost to follow-up. The clot, occluding nearly the whole lumen of the inferior vena cava (IVC), is seen as a radiolucent area between the IVC filter struts as the contrast agent passes by.

Dominik Baschera · Jonathan K Sebunya · René Zellweger

To the Editor: We welcome the thoughtful analysis from Elkin and Studdert on international students missing out on internship places.1 Given the impending shortage of available internships in Australia, this is of considerable interest to the over 500 international students who graduate each year. Sydney Medical School (University of Sydney) should be commended for explicitly discouraging international students’ expectations of internship.2 Sadly, this is an isolated example. We agree with the authors that universities have an ethical obligation to ensure this information is adequately conveyed to current and prospective international students. Education policymakers and medical school administrators should be forthcoming with vital information on the future of training for international students in Australia. The Australian Medical Students’ Association is currently developing a comprehensive information booklet, which we will distribute to prospective international students. Among other details, this will clearly outline the issue. However, the issues raised by Elkin and Studdert are not confined to international students. The authors observe that the recent health ministers’ communiqué only guaranteed internship to students in Commonwealth-supported places.3 This not only excludes international students, but also local fee-paying students at private universities and those in state-funded places. The authors argue that international students have no legitimate expectation that they will be provided with an intern place on graduation, given the “clear” statements from the federal government. However, there has been no similar guidance for local private university or state-funded students. Do these students have a legitimate expectation of internship? One could argue that state-funded students do, given the funding bodies are the same ones that will also provide their internships. While Australian permanent residents and citizens currently have first or second priority for internships, depending on their state of study and the state to which they are applying, it seems that in the future these students may miss out in favour of Commonwealth-supported students covered by the health ministers’ guarantee. Elkin and Studdert concluded that Australian courts would be unlikely to find that international students hold a legitimate expectation of internship. It is less certain whether this conclusion might apply to state-funded students or Australian permanent residents and citizens at private universities. At a minimum, these applicants too deserve “full and frank information” about their internship prospects.

Christopher X J Wong · Samuel J Whitehouse · Thomas D Crowhurst · Ross L Roberts-Thomson

To the Editor: Blecher correctly asserts that alarm is not the appropriate reaction to the potential dangers of computed tomography (CT) scans.1 Such alarm risks discouraging patients from having the CT scans they need. Appropriate CT scans are good; inappropriate ones are bad. Blecher is also correct in stating that the linear, no-threshold (no dose is entirely safe however small) model of radiation risk is theoretical.2 However, the advice of all international regulatory radiation protection authorities is to assume that the model is correct. To do so is prudent, even if overly conservative. And while these authorities hold this position, it would be professionally irresponsible to ignore it. Notwithstanding the Health Physics Society statement that the risk of ionising radiation below 100 mSv is negligible,3 the risk is thought to be cumulative. Furthermore, a single CT scan of the chest, abdomen and pelvis may expose a patient to 30 mSv or more, and the risk in children and young adults is considered to be 2–3 times greater than the average.4 The atomic bomb data are based on radiation dose levels as low as 5 mSv,5 with the cohort exposed to doses between 5 and 20 mSv showing an 85% chance that the risk is worse than we think and a 15% chance that it is better than we think. Although not statistically significant at the 95% confidence level, these figures indicate that great care is needed. The dimensions of the risks of low-dose radiation are contentious, but are we willing to ignore the danger of accepting Blecher’s argument? It is a Pascal’s wager. Providing we do not spook patients from having necessary scans (and this requires better communication with patients), our possibly over-cautious approach should result in more appropriate use of diagnostic imaging. The benefits go beyond those of limiting unnecessary radiation. Blecher finds it ironic that concerns about the dangers of CT are rising as radiation doses are falling. Doses may be falling, although that depends on where the baseline is drawn. When multidetector CT scanning was introduced, doses rose,6 but if, since then, doses have been falling, there is nothing ironic about this. Doses are falling because of the concern. Whether a patient undergoes an imaging procedure should be subject to the process of justification mandated in the Australian Radiation Protection and Nuclear Safety Agency code of practice.7 If the potential benefit outweighs the risk, the procedure is justified and the examination should proceed, but optimised to ensure that the lowest possible dose of radiation is used to provide diagnostic images — the ALARA principle (As Low As Reasonably Achievable). In summary: If a CT scan is clinically justified, then it should be performed and we should certainly avoid alarming our patients. If a scan is not justified, it should not be performed. We should adhere to the ALARA principle. Whenever appropriate, a non-ionising alternative to CT scans should be considered, particularly for children and young patients.

Richard M Mendelson · Richard A Fox · Nicholas H de Klerk

To the Editor: Seizures can be precipitated by treatment with praziquantel in patients with underlying neurocysticercosis, but this is rare and has not previously been described in Australia. We describe the case of a patient who developed seizures after antischistosomal therapy. An asymptomatic 23-year-old Burmese man underwent migrant health screening by his local doctor a month after arriving in Australia. His schistosomal serological results were positive (titre, 1:32) and he received three doses of 600 mg praziquantel. Three days later, he experienced several generalised tonic–clonic seizures in short succession, each lasting a few minutes. A magnetic resonance imaging (MRI) scan revealed three ring-enhancing lesions less than 1 cm in diameter, suggestive of neurocysticercosis. He was treated with phenytoin and also received dexamethasone for 1 month. A repeat MRI scan 6 months later showed significant reduction in the size of the lesions, to less than 3 mm. Phenytoin therapy was ceased after 3 months, with no seizures at last review (6 months). In view of the temporal association between the treatment and the seizures in this previously asymptomatic patient, we believe the seizures were precipitated by the praziquantel therapy. Cysticercosis, which is endemic across the developing world, is caused by the helminth Taenia solium. Clinical disease, including neurocysticercosis, is often asymptomatic. Symptomatic neurocysticercosis often presents as seizures, especially as the cysts degenerate, and is the commonest cause of acquired, late-onset epilepsy in the developing world.1 The benefit of treatment remains controversial, especially when there are only a few cysts.1-3 Praziquantel and albendazole therapy accelerate cyst degeneration, and subsequent inflammation may precipitate seizures, which are sometimes pre-emptively managed with corticosteroids.1 There is conflicting evidence on the benefit of treatment for long-term seizure frequency.2,3 Although screening for some parasitic infections in refugees in Australia is recommended,4 this does not include cysticercosis. Serological tests for T. solium cannot differentiate between active and past infections, have limited sensitivity, are not widely available in Australia, and cannot differentiate between neurocysticercosis and cysticercal disease elsewhere.5 The only reliable method for diagnosis is neuroimaging, which is impractical for mass screening. Nevertheless, we advocate a high degree of suspicion for neurocysticercosis in migrants from Taenia-endemic areas. Geographical origin alone is insensitive for identifying an at-risk population. A history of seizures, or the presence of subcutaneous nodules, should prompt investigation with serological testing and subsequent neuroimaging before consideration of treatment. In such symptomatic patients, this will allow the need for anthelmintic therapy to be assessed, along with consideration of adjunctive corticosteroid therapy.

Saliya S Hewagama · Jonathan D Darby · Harsha Sheorey · John R Daffy

To the Editor: “Student medical journals” are a very broad church, encompassing everything from pseudo-magazines to rigorously peer-reviewed publications. In April this year, a national journal of the latter variety was launched here in Australia: the Australian Medical Student Journal (AMSJ).1 The AMSJ accepts research, review and opinion articles from students of medicine or health sciences at Australian universities. The journal’s volunteer staff comprises only medical students, and peer-review is by academics associated with Australian medical schools, or clinicians at Australian teaching hospitals. The inaugural issue could hardly have been more national in its focus, with students from 14 Australian medical schools, covering every state, being represented among the authors. The issue was recently distributed free of charge to thousands of medical students around Australia in both print and electronic formats. After the success of the inaugural issue, we plan to begin biannual production from 2011, continuing in both formats. The AMSJ operates as a not-for-profit student organisation, and printing and other costs are provided for by sponsors, including the Australian Medical Association, Australian General Practice Training, and the Royal Australasian College of Physicians. While it is unique in a number of facets, the AMSJ is not the first publication of its kind. The Australian Medical Students’ Association magazine Panacea began life in 1968 as a journal, albeit not peer-reviewed.2 Several individual Australian medical schools have had their own academic publications for varying periods, such as the Sydney University Medical Journal, which was first published around 1905.3 More recently, our counterparts across the Tasman were well ahead of us, with the New Zealand Medical Student Journal releasing its first issue in 2004.4 Further afield, some of the better known student journals are the McGill Journal of Medicine (MJM) in Canada and the Student BMJ in the United Kingdom. Most student journals fall roughly into one of two categories: those whose focus is primarily instruction and entertainment, with shorter educational or blog-style articles (often written by non-students) having appeal to time-constrained students (eg, Student BMJ); and those that publish academically rigorous student work, perhaps at the expense of reader interest (eg, MJM). The AMSJ has a number of aims (Box), although central to our mission is to transcend this artificial tension and attract student-authored articles that are both thoroughly interesting and academically substantial. The rationale is that anything short of a proper peer-reviewed journal is patronising towards students, but, on the other hand, articles that are not appropriately pitched cause disenchantment. Medical students have played key roles in the history of medicine: notable discoveries made or shared in by medical students include heparin, insulin, the sinoatrial node, the pancreatobiliary sphincter, ether anaesthesia, islets of Langerhans, and spermatozoa.6 We hope that the AMSJ can continue to promote and foster this tradition of student achievement. Aims of the Australian Medical Student Journal5 To provide a medium for Australian medical students to publish their work and share ideas with their peers. To provide a suitable forum for students to make the transition between assignment writing and producing publishable academic work. To inform students about medical topics and issues not typically addressed in core curricula. To facilitate discussion of current issues relevant to medical students. To allow Australian medical schools to showcase the research aspects of their programs. To provide a further incentive for students to produce high-quality work in their studies. To foster the next generation of Australian medical researchers and physician–scientists. To provide an avenue for students interested in a career in medical editing or publishing to pursue this interest as a student staff member.

Matt D Schiller

To the Editor: In February 2009, a 68-year-old man presented to the Royal Victorian Eye and Ear Hospital within hours of developing an itchy, red left eye. The patient, who was otherwise healthy, lived in suburban Melbourne, usually with his pet dogs, but the last of his dogs had recently died. The patient was unsure if all his dogs had been dewormed regularly because he spends about 6 months a year in Europe. General inspection of the eye suggested subconjunctival haemorrhage. However, slit-lamp examination showed a mobile, tightly coiled structure within the subconjunctival blood. It grew increasingly agitated with higher slit-lamp light intensity (Box, A). Assessment of the patient’s visual acuity and the anterior and posterior chambers of the eyes was unremarkable. Blood tests revealed a positive filarial serology and eosinophilia. The patient was transferred to the operating theatre and, under topical anaesthesia, a 5 mm conjunctival incision was made and the mobile structure removed (Box, B and C). The patient was discharged with a prescription for prednisolone acetate 1% and chloramphenicol 0.5% eye drops (one drop four times a day). He made a full recovery. The extracted specimen was reviewed by one of us (D M S). The 150 mm worm was identified as a young adult female filarioid nematode, Dirofilaria immitis (commonly named dog heartworm) after comparisons with laboratory specimens of D. immitis and Pelecitus roemeri. Infection with either P. roemeri (kangaroo and wallaby knee worm) or Loa loa (loiasis) was excluded. Our specimen did not have lateral alae and the distance from anus to tail was shorter than would be expected for the kangaroo worm. In addition, the patient had never been to Africa where loiasis is endemic to several countries. Subconjunctival dog heartworm is rare, but its incidence is increasing in parts of the world.1,2 Dogs are the natural hosts and transmission to humans occurs through mosquito bites of the skin (into which the third-stage infective larva may escape). For an unknown reason, the worm sometimes takes an abnormal migratory route and ends up in the eye of the host. Ophthalmic cases have been reported in dogs.3,4 Careful measures to exterminate mosquitoes and deworm dogs and cats are important in limiting its transmission. Surgical extraction is the definitive treatment and further treatment with systemic anthelmintics is unnecessary.5 Humans are non-natural hosts for this parasite and, therefore, its life cycle cannot be completed within the human body. When a larva does evade the human immune system, as in the case of our patient, the chances of another larva being present elsewhere in an immunocompetent person seems remote. Furthermore, unless the larva becomes clinically apparent, it would be impossible to find. Subconjunctival Dirofilaria immitis infection in a 68-year-old man A: A whitish mobile structure coiled in the haemorrhagic subconjuctival space B: The female Dirofilaria species measuring about 150 mm C: Day 1 after removal of worm and necrotic temporal conjunctiva, exposing bare sclera

Elaine W Chong · Harsha Sheorey · Cheng Hean Lo · David M Spratt · Enrique Graue-Hernández

To the Editor: The medical view, which is repeatedly stated in the literature,1-3 is that up to 100% of those who complete suicide are suffering from a mental disorder. This leaves many doctors feeling they can be held responsible for all those who suicide, including those for whom there is no evidence of mental disorder. A recent High Court of Australia judgment, Stuart v Kirkland-Veenstra,4 illustrates that the medical and legal views of the relationship between suicide and mental disorder are different. In this case, a wife alleged that police officers had failed to provide a duty of care towards her husband, who had been found by the officers in a car with a hose leading from the exhaust pipe into a rear window, but with the driver’s window down and the car engine cold. The officers talked to the husband, who claimed marital problems but that he had changed his mind about suicide and was planning to go home and discuss matters with his wife. The officers felt the husband was rational, cooperative and responsible, with no evidence of alcohol or drug misuse; they offered him assistance (which he declined) and allowed him to leave. Later that day, the husband completed the suicide. He had not told the officers that he was expecting to be served with papers relating to fraud charges that afternoon. The Stuart v Kirkland-Veenstra judgment,4 in favour of the police officers, includes the following statements: Suicide and attempted suicide are seen as reflective of psychological or psychiatric issues which may or may not involve ‘mental illness’ according to established diagnostic conventions . . . Given the complexity and variety of factors which may lead to suicidal behavior, it would be a bold legislative step indeed to sweep it all under the rubric of mental illness, however widely defined. Word limits prevent me from giving more detail about the case, but interested readers will find this accessible judgment valuable. Clinicians dealing with “difficult” (but not mentally disordered) people in difficult circumstances often feel themselves to be in a perilous legal position, able to be held responsible for the actions of all those who choose to end their lives. The Stuart v Kirkland-Veenstra judgment clarifies the legal perspective, that suicide does not necessarily indicate the presence of a mental disorder, and that where mental disorder does not exist, human services personnel will not necessarily be held responsible for the actions of others.

Saxby Pridmore

To the Editor: The current political debate on health reform has made no mention of the 300 000 people who were identified by the National Health and Hospitals Reform Commission as facing “stark health inequalities”.1 We refer to people with intellectual disability, who face a life expectancy 5–20 years shorter than people in the general population, substantial unmet health needs and significant barriers to getting these needs met. A recent review of health inequalities in England states: To reduce the steepness of the social gradient in health, actions must be universal, but with a scale and intensity that is proportionate to the level of disadvantage. We call this proportionate universalism.2 In its health reform initiatives, the federal government has quite rightly included specific funding for the health of Indigenous people and residents of aged care facilities, and for rural health and mental health. Many of these measures are just a start, but they are direct acknowledgement of specific disadvantage. However, the government has taken no such action on the health of people with intellectual disability. In fact, recent changes to Medicare (in May 2010)3 include a step backwards for people with intellectual disability. The merging of intellectual disability health assessment items into four new time-based items means that data are no longer kept on the uptake of intellectual disability assessments. This was the one piece of information on the health of people with intellectual disability that the government collected. Many of the government’s health reforms will have wide community benefit. However, we are long used to people with intellectual disability missing out on the benefits of generic programs. To give one example, funding hospitals on the basis of the “efficient price” of services may create a disincentive to treat people with intellectual disabilities, who need much more time than other patients. To avoid this disincentive, the government needs to create a price-loading for people with intellectual disability, which in turn will require the government to redress the absence of data on hospitalisations of people with intellectual disability. With each plank of its reform, the government at least needs to ask: “What adjustments are needed to make this work for people with intellectual disability?” We are happy to provide the answers.

Nicholas G Lennox · James C Simpson

To the Editor: The recent review by Hayes and colleagues1 does not sufficiently emphasise practical approaches to managing the later stages of Parkinson disease (PD). Nazem and colleagues2 reported active suicidal or death ideation in 30% of patients with PD of mild-to-moderate severity, and an overall rate of major depression of 27.6%. They found that psychiatric symptoms and disorders, especially major depression, rather than PD-related variables, predicted suicidal or death ideation. Only half of the depressed patients were being treated with an antidepressant. Screening for psychiatric disorders should occur on assessment. Skilled counselling is required, and carers need to be well supported, particularly if the patient has intermittent suicidal ideation and a strong wish for the end of life. Clozapine is the only antipsychotic shown to be effective for treating psychosis in patients with PD.3 If the psychosis is schizophrenia-like, with persistent bizarre delusions and florid hallucinations causing agitation, clozapine can be prescribed in Australia by a registered psychiatrist and the patient can be registered with the clozapine monitoring service. If the patient is started on a very low dose (6.25 mg daily) that is only very gradually increased, side effects can be minimised. Successful use of clozapine enables remission of the psychosis and optimal treatment of motor symptoms. Mild hallucinations may be tolerated without specific treatment while the patient retains insight. In an open-label study of patients with mild hallucinations comparing no treatment with quetiapine therapy (or clozapine therapy in a minority of cases),4 the rate of progression to hallucinations without insight, or delusional psychosis, was significantly slowed. Hely and colleagues5 have argued that pathological processes in addition to Lewy body disease may have a role in the appearance of dementia, as age is a better correlate than PD duration. If it is clear that the dementia is a PD dementia, or dementia with Lewy bodies, a cholinesterase inhibitor such as rivastigmine could be prescribed. As rivastigmine is not subsidised on the Pharmaceutical Benefits Scheme in Australia for this indication, a private prescription could be provided in the first instance, and if there was a likelihood of significant Alzheimer disease associated with PD, an authority prescription would be justified. Hely and colleagues pointed out that, in the later disease stages of PD (at 20 years), less than 50% of patients still see their neurologist. However, the quality of life for PD patients in nursing-home care could still be significantly improved by specialist review by members of a multidisciplinary team on an inpatient, outpatient or outreach basis.

David S Tofler

To the Editor: Although Clarke and Fitzgerald’s claim that prices for generic medicines in Australia are high compared with prices in other countries1 is valid, their claim that the Pharmaceutical Benefits Scheme expenditure on statins could be reduced by up to $9.31 billion, by increasing the proportion of generic prescriptions to 100% and paying equivalent prices to those in England, is problematic. For the proportion of generic prescriptions to be increased to 100%, the available generic statins would need to be directly substitutable for currently available statins, including those whose patents have not yet expired (eg, atorvastatin and rosuvastatin). Nicholls and colleagues present the results of a meta-analysis of various doses of atorvastatin, rosuvastatin and simvastatin.2 The findings of the Pharmaceutical Benefits Advisory Committee (PBAC) on the comparative effectiveness of the various statins can be summarised as follows:3 Simvastatin is the benchmark statin; the maximum recommended dose is 80 mg/day. Pravastatin is equivalent to simvastatin on a milligram-for-milligram basis: pravastatin 10 mg is equivalent to simvastatin 10 mg. The maximum recommended dose of pravastatin is 80 mg/day. Atorvastatin 1 mg is equivalent to simvastatin 2 mg: atorvastatin 10 mg is equivalent to simvastatin 20 mg. The maximum recommended dose of atorvastatin is 80 mg/day. It is notable that a simvastatin dose equivalent to atorvastatin 80 mg (ie, simvastatin 160 mg) is beyond the maximum recommended dose of simvastatin. Rosuvastatin 1 mg is equivalent to atorvastatin 3 mg, which would be equivalent to simvastatin 6 mg (ie, rosuvastatin 10 mg is equivalent to atorvastatin 30 mg, which would be equivalent to simvastatin 60 mg). The maximum recommended dose of rosuvastatin is 40 mg/day. It is notable that a simvastatin dose equivalent to rosuvastatin 40 mg (ie, simvastatin 240 mg) is beyond the maximum recommended dose of simvastatin. By applying the therapeutic relativities accepted by the PBAC to the results reported by Nicholls and colleagues, the dose–response curves for rosuvastatin, atorvastatin and simvastatin, all expressed in simvastatin mg equivalents, can be generated as shown in the Box. As seen in the graph, simvastatin (available as a generic) may not be substitutable for atorvastatin or rosuvastatin in patients who need a reduction in low-density lipoprotein cholesterol level of > 45 mg/dL (> 1.15 mmol/L). Although having patients switch to generic prescriptions would reduce expenditure on statins, the possibility that such a switch might be associated with inferior outcomes needs to be considered. Dose–response curves for rosuvastatin, atorvastatin and simvastatin LDL-C = low-density lipoprotein cholesterol.

Liliana Bulfone

In reply: Our recent study1 estimates pharmaceutical expenditure from 2009 to 2019 for various levels of use of off-patent statins, ranging from 25% (close to the current proportion) to 100%. We also show that England has much higher use of generic statins and consequently much lower pharmaceutical expenditure. However, our study does not advocate a particular level of generic use and so it is unclear why Bulfone has chosen to focus on only one of the cases (100% use of generics) presented in our study. We agree with Bulfone’s view that it is important to consider whether the greater use of generic statins has an impact on health outcomes in addition to examining the implications for pharmaceutical expenditure. This is one of the points we have already made: “The key question is whether the health benefits resulting from using statins under patent or combination therapies justify the substantially higher subsidies from the [Pharmaceutical Benefits Scheme].”1 The appropriate framework to use to consider this question would be to examine incremental cost-effectiveness of those statins still under patent (atorvastatin and rosuvastatin) compared with off-patent alternatives (simvastatin and pravastatin). Such an evaluation would be timely, as Australia faces billions of dollars of extra pharmaceutical expenditure over the next decade if we continue to prescribe patented statin formulations at current levels.

Philip M Clarke · Edmund M FitzGerald

To the Editor: We read with interest the article by Cleland and colleagues describing an urban–rural comparison of weight status among women living in socioeconomically disadvantaged neighbourhoods.1 After adjusting for socio-demographic factors, the authors reported no difference in prevalence of obesity, determined using women’s self-reported height and weight, between urban and rural areas. We would like to provide further evidence for the suggestion that obesity might be attributable to sociodemographic composition of areas. We have previously examined the association between area-based socioeconomic status (SES) and different measures of obesity in a randomly selected, population-based female cohort (aged 20–93 years, 77% participation)2 and in a similarly recruited male cohort (aged 20–96 years, 67% participation)3 within the Barwon Statistical Division in Victoria. An inverse association between SES and obesity was observed for both sexes,2,3 and was evident across three different SES indices developed by the Australian Bureau of Statistics (ABS).4 Within our female cohort, we investigated body mass index (BMI) in urban versus rural areas across the SES continuum, for 192 participants aged 20–45 years. We used standard geographical classification5 of 2006 ABS Census data to define participants’ residences as urban or rural (incorporating rural and semi-rural areas). Participants were further grouped according to the 2006 ABS Index of Relative Socio-economic Disadvantage, based on Barwon Statistical Division cutpoints. In our multivariable regression analysis, SES was categorised into the lower 30% (most disadvantaged), mid 40%, and upper 30% (least disadvantaged). Approval for this analysis was obtained from the Barwon Health Human Research Ethics Committee. No differences in unadjusted BMI were observed between participants residing in urban and rural areas (Box). These results were sustained after adjusting for age (data not shown). No interactions were identified between SES and urban or rural residence. No differences in BMI between urban and rural residence were observed for any SES group. These data suggest the lack of difference in BMI between urban and rural residents may be consistent across the SES spectrum. SES was associated with BMI (P = 0.001), while urban–rural residence was not (P = 0.5). Given these data, we suggest that SES is a stronger driving force for BMI than urban or rural residence. In our population, participants in the most disadvantaged group were more likely to be resident in urban areas. This is indicative of Geelong, the main urban centre of the Barwon Statistical Division, being one of the largest public housing areas in Victoria; urban areas provide more low-cost housing options than do rural areas. In contrast, residence in rural areas may be influenced by factors such as the “sea change” movement or prestigious real-estate options, such as the scenic coastal areas located away from the urban centre of Geelong. Mean body mass index (95% CI) of 192 women aged 20–45 years in the Barwon Statistical Division, Victoria, by area of residence Socioeconomic status* Urban† Rural† P‡ Lower 30% (most disadvantaged) 29.5 (26.8–32.1) 37.4§ 0.3 Mid 40% 27.8 (26.1–29.4) 25.3 (21.8–28.9) 0.2 Upper 30% (least disadvantaged) 25.5 (21.2–29.7) 25.5 (24.1–26.9) 1.0 Total population 27.3 (26.3–28.4) 26.1 (23.4–28.7) 0.43 * Defined by the Australian Bureau of Statistics (ABS) Index of Relative Socio-economic Disadvantage of the Socio-economic Indexes for Areas using 2006 Census data, and cutpoints of Barwon Statistical Division for 2006. † Defined by the 2006 ABS Australian Standard Geographical Classification Urban Centres/Localities. ‡ For pairwise difference. § There was only one participant in this category.

Sharon L Brennan · Margaret J Henry · Geoffrey C Nicholson · Julie A Pasco