Letters

To the Editor: We report a patient with spontaneous intracranial hypotension (SIH), which is now an increasingly recognised syndrome. Orthostatic headache with typical findings on magnetic resonance imaging (MRI) are the keys to diagnosis. When correctly diagnosed, SIH management is easy and highly effective in most cases. A 38-year-old woman presented to our hospital after having daily headaches for 3 weeks. The acute onset of severe headache occurred initially when she bent down and tried to lift her 16-month-old child. The headache began as a sharp pain over the right side of her occiput and rapidly spread to her frontal area. The headache was particularly bad in the morning and while standing, and was relieved by assuming a recumbent posture. Apart from nausea, she had no other associated symptoms. General and systemic examination findings were normal. MRI of the brain showed diffuse dural enhancement and smooth thickening of the dura (Box, A) and a total spinal magnetic resonance image showed fluid in the posterior soft tissues at C1/C2 level (Box, B). These findings confirmed the leak of cerebrospinal fluid that accounted for the intracranial hypotension and orthostatic headache. Initial treatment with bed rest, increased fluid intake and non-steroidal anti-inflammatory drugs relieved her symptoms marginally. After a failed lumbar epidural blood patch, 10 mL of autologous blood was injected at the site of the cervical level leak. The patient’s symptoms resolved, and she was asymptomatic and had had no recurrence at follow-up at 4 months. Also known as Schaltenbrand syndrome, SIH is very rare, with a prevalence of about 1 in 50 000 population, and a female preponderance of 3:1.1 Patients with connective tissue diseases2 or Chiari malformation may be more susceptible to SIH. Orthostatic headache is the cardinal feature of this syndrome. Headache is usually holocranial, although it might be localised to the frontal or occipital regions. Patients may have other symptoms such as diplopia and photophobia. MRI with gadolinium is critical in diagnosing this syndrome. The condition of most patients improves with conservative therapy (bed rest, increased fluid intake and caffeine). Epidural autologous blood patch is effective in relieving low intracranial pressure headaches.3 Surgical repair of the leak is rarely used and should be used only if medical therapy fails.4 Magnetic resonance images of the patient’s brain and cervical spine A: Diffuse dural enhancement and smooth thickening of the pachymeninges. B: Fluid in the posterior soft tissues at C1/C2 level.

Mohamed Asif Chinnaratha · Ronald A Criddle · Paul J Graziotti

To the Editor: Recent studies provide evidence that having a low serum vitamin D level is a risk factor for autoimmune disease, including type 1 diabetes mellitus (T1DM).1,2 Available data come from northern hemisphere countries where sunlight exposure levels and the genetic background of the population are different from those in Australia. We compared vitamin D levels in stored serum from Brisbane children and adolescents with T1DM who attended the Mater Children’s Hospital clinic with local historical control data from a previous study.3 Levels of 25-hydroxyvitamin D (25-OHD; the major circulating form of vitamin D) were lower in those with T1DM than in the control group, with no difference in levels of 1,25-dihydroxyvitamin D (1,25-[OH]2D; the biologically active form). Children and adolescents with T1DM were more than three times as likely to have vitamin D deficiency4 as those in the control group. There was a trend towards seasonal variation in 25-OHD levels, with mean levels (95% CI) being 53.8 nmol/L (47.0–60.6 nmol/L) in summer, 61.4 nmol/L (54.9–67.9 nmol/L) in autumn, 56.4 nmol/L (51.7–61.0 nmol/L) in winter and 64.7 nmol/L (58.8–70.6 nmol/L) in spring (P = 0.06), but no difference in seasonal variation between T1DM and control groups (P = 0.73). There was no difference in the ages or proportions of males and females in the two groups (Box). There were no differences in vitamin D levels between the sexes in either T1DM or control groups, nor any correlation with duration of diabetes. These observations support previous reports. One found low 25-OHD levels in 459 Swedish patients aged between 15 and 34 years who were newly diagnosed with T1DM compared with age-matched and place-matched controls.1 Another found low 25-OHD levels in 88 newly diagnosed children and adolescents.2 Understanding the nature of low vitamin D levels in people with diabetes is important because it potentially clarifies the mechanisms of autoimmune β-cell destruction, and may lead to interventions for preventing or delaying insulin dependence by using vitamin D or its analogues. Vitamin D probably acts by modifying the autoimmune response, as 1,25-(OH)2D modulates dendritic cell function to promote tolerogenic T cells. It may be relevant that we have recently found low blood dendritic cell counts in children and adolescents with T1DM.5 Vitamin D levels in our Queensland sample of children and adolescents were lower overall than those found in the subjects of the Swedish study, (mean 25-OHD levels [± SEM] were 96.7 ± 2.7 nmol/L for the control group and 82.5 ± 1.3 nmol/L for those with T1DM); this is unexpected given Brisbane’s latitude (29°S) compared with that of Sweden (about 55–65°N). These differences might be explained by differences in dietary intake, sun avoidance behaviours promoted in Queensland, or differences in the assays used, as the Swedish group used the Nichols chemiluminescence assay (Nichols Institute, San Juan Capistrano, Calif, USA) and we used the DiaSorin radioimmunoassay (DiaSorin Inc, Stillwater, Minn, USA). The observation in the Swedish study that the deficit in 25-OHD level did not resolve over time after diagnosis concurs with our finding of low levels in children and adolescents several years after diagnosis. While our pilot data cannot support causal inference, and is limited by being retrospective and our lack of information about history of sunlight exposure, dietary vitamin D intake, cultural factors such as sun avoidance or veiling, skin tone, and not having contemporaneous controls, it strongly supports the case for prospective clinical studies of vitamin D in T1DM. Comparison of clinical characteristics and vitamin D levels in healthy children and adolescents and those with type 1 diabetes mellitus Variable Control group Type 1 diabetes mellitus group P No. of children and adolescents 94 47 Age (range) 13.2 years (12.5–13.8 years) 13.6 years (12.6–14.6 years) 0.47* No. of males/females 44/50 21/26 0.81† Mean duration of diabetes (95% CI) — 4.7 years (3.9–5.5 years) Sample collection period July 2000 – December 2001 June 2001 – July 2006 Mean 25-OHD level (95%CI)‡ 64.6 nmol/L (61.3–67.9 nmol/L) 54.7 nmol/L (50.3–58.9 nmol/L) 0.0005* Mean 1,25-(OH)2D level (95% CI)‡ 126.7 pmol/L (115.8–137.6 pmol/L)§ 127.6 pmol/L (114.8–140.4 pmol/L) 0.92* Proportion 25-OHD-deficient (≤ 50 nmol/L) 18% (17/94) 43% (20/47) 0.002† (OR,¶ 3.4; 95% CI, 1.5–7.3) Proportion with 1,25-(OH)2D level below reference range (40–150 pmol/L) 0 (0/84) 4% (2/47) 0.13** (OR,¶ 9.3; 95% CI, 0.4–197.6) * t test. † χ2 test. ‡ DiaSorin radioimmunoassay double antibody assay (DiaSorin Inc, Stillwater, Minn, USA), performed by Queensland Health Pathology Services. § 84 controls; insufficient serum for analysis in 10. ¶ Odds ratio for deficiency in type 1 diabetes mellitus. ** Fisher’s exact test. 25-OHD = 25-hydroxyvitamin D. 1,25-(OH)2D = 1,25-dihydroxyvitamin D.

Ristan M Greer · Meredith A Rogers · Francis G Bowling · Helen M Buntain · Mark Harris · Gary M Leong · Andrew M Cotterill

To the Editor: I read with interest the excellent review article on the metabolic syndrome by Chew et al in the 16 October 2006 issue of the Journal.1 In their article the authors claim there is a lack of data about the relationship between hyperinsulinaemia and changes in free testosterone levels. As part of the Kuopio Ischaemic Heart Disease (KIHD) Risk Factor Study, an ongoing prospective epidemiological study of 2682 middle-aged Finnish men investigating risk factors for chronic disease, our research group has shown an association between the presence of metabolic syndrome at baseline and a change in sex hormone levels at follow-up after 11 years.2 In our study, men who met the World Health Organization criteria for metabolic syndrome both at baseline and at 11-year follow-up were at 2.6-fold increased risk of developing hypogonadism (serum total testosterone concentration < 11 nmol/L) during the study period compared with men who did not have metabolic syndrome. There was also a non-significant trend for men with metabolic syndrome to develop hypogonadism as defined by calculated free testosterone levels of < 225 pmol/L at 11-year follow-up.2 In the same cohort, we also reported a reverse association — that is, hypogonadism predicting metabolic syndrome.3,4 However, as the question posed by Chew et al was whether hyperinsulinaemia affects free testosterone levels, I examined the KIHD data further for evidence of such an association. I found that subjects grouped in ascending baseline fasting serum insulin quartiles had baseline mean free testosterone levels of 316 pmol/L (SD, 72 pmol/L), 312 pmol/L (SD, 77 pmol/L), 299 pmol/L (SD, 74 pmol/L) and 271 pmol/L (SD, 79 pmol/L), respectively (P < 0.001 for trend). At 11-year follow-up, mean free testosterone levels for subjects in each quartile were 248 pmol/L (SD, 64 pmol/L), 242 pmol/L (SD, 68 pmol/L), 229 pmol/L (SD, 70 pmol/L) and 216 pmol/L (SD, 67 pmol/L), respectively (P < 0.001 for trend). The proportional drop in free testosterone levels over 11 years was approximately the same in each quartile, ranging from 20% to 23%. On the basis of these data, it seems that hyperinsulinaemia is associated not only with a fall in serum total testosterone levels but also with a fall in free testosterone levels in a general population.

Tomi-Pekka Tuomainen

In reply: We thank Tuomainen for his interest in our review article, and for sharing with us his data showing an inverse association between fasting serum insulin levels and calculated serum free testosterone levels. We were cautious in our statement about the relationship between hyperinsulinaemia and free testosterone levels, as there are conflicting data in the literature regarding this,1,2 and few studies that directly measure free or bioavailable testosterone. Moreover, there is ongoing controversy about the calculation of free testosterone levels using total testosterone and sex hormone-binding globulin concentrations, with the validity and assumptions of some of these widely used estimation equations being called into question.3,4 We also echo the concerns of Allan et al5 about the potential pitfalls of diagnosing hypogonadism based on testosterone levels only. As the presence of low total (and even calculated free) testosterone in obese men may not necessarily reflect deficient androgen action, the diagnosis of androgen deficiency should only be made in the context of supportive clinical features. Furthermore, in abdominally obese men with the metabolic syndrome, levels of sex hormone-binding globulin and both total and calculated free testosterone can increase following weight loss,6 thereby obviating the inappropriate use of testosterone supplementation in such patients.

Gerard T Chew · Seng Khee Gan · Gerald F Watts

To the Editor: The recent article by Miller and colleagues regarding adverse drug events (ADEs) in general practice highlights the high frequency and considerable morbidity associated with ADEs in the general community.1 The authors identified recognised side effects, drug sensitivity, and allergy as responsible for most ADEs. The contribution of the patient’s genotype to drug response, via altered metabolism or responsiveness to pharmaceuticals, is increasingly recognised as potentially responsible for a significant proportion of ADEs. The science of determination of the genetic contribution to an individual’s response to drug action is referred to as pharmacogenomics,2 and represents a potentially beneficial diagnostic tool to aid in the prevention of ADEs. Treatment with warfarin, one of the most frequently prescribed drugs in Australia, has been estimated to account for up to15.1% of all severe ADEs, manifest as minor and major bleeding.3 We have recently determined the presence, frequency and laboratory sequelae of genetic variants (single nucleotide polymorphisms) in two genes responsible for the metabolism (cytochrome P450 2C9 [CYP2C9]) and potency (vitamin K epoxide reductase complex, subunit 1 [VKORC1]) of warfarin4 in an Australian population. In our study of 120 patients in an anticoagulation clinic, the frequencies of allelic variants of the CYP2C9 and VKORC1 genes responsible for altered warfarin activity were 31%5 and 59% (unpublished data), respectively, in keeping with previously published studies.4 Detection of these variants was associated with increased induction international normalised ratio (INR) readings compared with controls, and reduced overall warfarin requirements.6 These findings support previous studies,7 and suggest that genotype determination may be of benefit in identification of patients with increased sensitivity to empiric induction phase warfarin dosing schedules. This may allow for a reduction of induction doses of warfarin, decreasing the risk of excessive INR and bleeding sequelae, commonly observed with induction of warfarin treatment. Furthermore these benefits may aid in reduced time to stabilisation. Additional cost–benefit analysis8,9 will enable determination of the economic viability of genotype determination as an adjunct to management of warfarin dosing. The high population frequency of genetic variants associated with warfarin response emphasises the significant contribution genetic factors can play in patient reaction to drugs and highlights their involvement as potential causes of ADEs.

Keith A Byron · Anthony E Dear

To the Editor: V-shaped pillows (“tri-pillows”) may cause suffocation of an infant left to sleep between the two arms of the pillow when he or she slips into the crevice between the arms, or beneath the pillow. The deaths of two infants who died in this manner were reported in South Australia in 1997, and a third death was the subject of a coronial inquiry.1,2 In 1998, the SA State Coroner recommended that “a public warning be issued against the use of tri- or U-shaped pillows by infants under two years of age for sleeping”.2 This message has also been issued in subsequent safe-sleeping campaigns, with a statement in the SIDS and Kids national “Safe sleeping” brochure that “tri-pillows are too soft and can cover baby’s face”, and a statement on the SA Child and Youth Health website that “. . . babies should not be left in these pillows while they are sleeping”.4 Despite these clear messages, deaths continue to occur in SA,5 and V-shaped pillows are still being sold in the foyer of a local obstetric hospital. Although the pillows are being promoted to assist breastfeeding, infants who have been left to sleep on them will be exposed to the risk of suffocation. Deaths of infants in shared sleeping situations may also occur due to suffocation from “overlaying”. However, parents are still being advised by health advice telephone enquiry services to sleep in the same bed with their children. This was the unequivocal message given to one of the authors (G C) when she recently telephoned for advice following the birth of her first child. No mention was made of the potential danger of suffocation if parents are physically large, intoxicated, sedated, or simply exhausted, or if the infant is placed between the parents under bedcovers. It appears, despite clear evidence that certain sleeping situations are potentially dangerous for infants, as well as the widespread dissemination of this information in safe-sleeping literature, that certain organisations or individuals continue to give a contrary message. What hope do parents have of understanding these issues and making informed decisions to optimise the safety of their infant’s sleeping environment if they are exposed to such conflicting messages and advice? Perhaps another question to ask is, “What responsibility do organisations and employees bear if an infant dies as a result of parents following such advice or purchasing equipment such as a V-shaped pillow?”

Roger W Byard · Glenda Cains · Helen Noblet · Maxine Weber

To the editor: Bairnsdale ulcer is known by the eponyms Buruli in Uganda, Kakerifu in Zaire, Kumusi in New Guinea, and was formerly referred to as Searls’ ulcer in Australia. In the original 1948 article describing the causative organism,1 MacCallum and colleagues acknowledged assistance from Drs Alsop, Clay and Searls, in that (alphabetical) order. In sending material to Melbourne for examination, these doctors of the Bairnsdale Clinic described the ulcers, and also commented on the similarity of their appearance in the first three patients. J R Searls, after whom the ulcer was originally named, was regarded as an excellent general practitioner. He died in 1971.

Derek H Meyers

“What’s in a name? That which we call a rose By any other name would smell as sweet.” — William Shakespeare, Romeo and Juliet; II, ii, 1-2; circa 1595 Comment: In 1948, MacCallum and colleagues published an article reporting a new mycobacterial infection in man,1 and later named the causative organism Mycobacterium ulcerans. In their article, they described six patients, five of whom came from the Bairnsdale district in Gippsland, Victoria. Three Bairnsdale general practitioners, Drs Alsop, Clay and Searls, had initially recognised a novel disease in their region and submitted pathological specimens to Melbourne University for diagnosis.2 Subsequently, the same disease was described in many different areas, mostly in Africa (“Buruli ulcer”). Each new outbreak tended to give rise to a new name; of all these, perhaps the most colourful is “Sik belong Sepik”, describing the infection as it occurs along the Sepik River in Papua New Guinea. In Victoria, where most Australian cases of M. ulcerans infection occur,3 we have continued to use the term “Bairnsdale ulcer” even though the main endemic areas are now the Bellarine and Mornington Peninsulas near Melbourne.3 Medical eponyms have a place for diseases that are poorly understood or have unknown causes, but it could be argued that the terms “Bairnsdale ulcer” and “Buruli ulcer” now belong in the annals of medical history. However, there are other considerations. In 1998, the World Health Organization launched the Global Buruli Ulcer Initiative.4 This successful advocacy raised the profile of this neglected disease and facilitated major improvements in diagnosis and treatment. For better or worse, “Buruli ulcer” has become the internationally recognised term for M. ulcerans infection, and we propose that we should now also adopt this name in Australia. While this should come as a relief to the good citizens of Bairnsdale and the Bellarine peninsula, what about those of Buruli in Uganda? Fortunately, their county has been renamed and is now known as the Nakasongola District.5

Paul D R Johnson · John A Hayman

To the Editor: Recent articles in the Journal referred to clinical characteristics of lesions caused by Mycobacterium ulcerans in Australia, and to recommendations and challenges in their management.1-3 Brazil may also be an endemic area of this devastating neglected but treatable disease. In developing countries, cases of Bairnsdale or Buruli ulcer (BU) can be misdiagnosed or underreported because neither the general public nor health care workers have sufficient knowledge about the disease, and because affected people usually have little contact with the health care system, or do not seek prompt treatment.4 Expensive tests like the polymerase chain reaction are not available to confirm all suspicious cases, and smears can give a low diagnostic yield; there are often minimal histopathological changes and absence of bacilli, particularly in patients with long-standing lesions previously treated with effective antimicrobial drugs.4 We report the case of a 65-year-old Brazilian woman with a 2-year history of BU in her extremities coexistent with osteomyelitis in the fourth cervical vertebra (Figure 1), and evidence of inadequate nutrition. Although she had received BCG vaccine as an infant, mycobacteria osteomyelitis developed in the site of an arthrodesis performed in 1998 to treat an accidental fracture.4,5 This patient had lived in a poor riverside rural area with a humid, hot climate. As in descriptions of Australian cases, our patient was much older than the age (5–15 years) at which most cases of M. ulcerans infection are reported in tropical and subtropical regions.1,2,4 Before her disease was characterised through positive cultures for M. ulcerans in samples from skin and bone lesions, the main differential diagnosis was ulcers resulting from fungal infection and leishmaniasis,4 conditions that are frequently seen in the region where she lived. The earlier skin lesions had appeared in May 2004 as papules and nodules, and evolved as painless, chronic, indolent ulcers with undermined edges.2,4 Despite treatment in another hospital that included surgery as well as medical therapy with rifamycin, aminoglycoside and quinolone antibiotics, the disease recurred. On admission to our hospital in August 2006, she had an extensive ulcer on her left arm in addition to scars on the right inner thigh (Figure 2). After nearly 2 months of hospitalisation, the patient was discharged to continue antimicrobial therapy with outpatient follow-up. Despite this, the lesions are healing very slowly. 1: X-ray image of osteomyelitis (arrows) affecting the body of the fourth cervical vertebra. 2: Extensive ulcer on the left arm (arrows; A) and brown pigmented scars on the inner right thigh (B).

Vitorino M dos Santos · Flávio L Noronha · Érica C Vicentina · Camila C Lima

To the Editor: In 2000, the United Nations Millennium Summit produced an agenda for reducing global poverty. It listed eight Millennium Development Goals (MDGs) and was signed by 189 countries. Improving maternal health (with the aim of reducing the maternal mortality ratio by three-quarters between 1990 and 2015) is the fifth and perhaps the core health-related MDG if we consider the centrality of mothers in social development and health.1,2 Globally, the number of maternal deaths remains high at 529 000 per annum.2 Ensuring maternal survival demands functional health care systems with skilled health care workers. However, migration of health care workers (mostly to wealthier English-speaking countries) is a major threat to achieving the MDGs.3-5 Here, I estimate the associations between maternal health and physician migration and human resources for health. I used recently updated physician migration3 and global health workforce data4 to look at correlations between physician migration and two core maternal health indicators — the maternal mortality ratio, and the percentage of births attended by skilled personnel.1,2 I also explored the associations between these maternal health indicators and human health care resources. Migration was measured as the number of physician émigrés working in Australia, the United Kingdom, Canada, and the United States during 1999–2002, per 1000 population of their source countries.5 Physician migration density values for all four countries combined, and for each country individually, were determined (Box). Human health care resources included current densities of health care workers remaining in the source countries (Box). I calculated the Pearson’s correlation coefficients between these variables and the two core maternal MDG indicators. The Box shows that countries with better maternal health are likely to have higher physician migration and more human resources for health care. For example, higher migration to Australia is seen from countries with lower maternal mortality (r = − 0.29; P = 0.011) and more births attended by skilled staff (r = 0.25; P = 0.037). I acknowledge that, like most health system and global health analyses, these correlations are based on an ecological (cross-country) design which does not lend itself to causal inference. These findings are therefore descriptive and require further exploration. Furthermore, the two maternal health indicators used here (which are the core maternal health MDG indicators used by the United Nations) could be viewed as indicators of health system and population health progress. Although physicians and other health care workers play major roles in maternal survival, especially in pregnancy, they cannot be seen as the only requirements for better maternal health. Physicians’ roles can also be substituted by other health care workers in many situations in resource-poor settings. However, less-poor source countries often have higher capacities than poor nations to turn out skilled workers who subsequently migrate. Contrary to conventional wisdom, Australia, the UK, Canada, and the US draw substantially more migrant physicians from countries with higher health care worker capacities. Many countries may be losing physicians just when they should be reaping the benefits of their improving fortune. Given the patchy progress towards achieving the MDGs,1 health care worker shortages may impede many countries’ progress in improving health standards if migration rates exceed workforce replacement in the face of changing but increasingly complex health care needs.1,2,4 Physician migration must be taken seriously if the global target of reducing maternal mortality by three-quarters between 1990 and 2015 is to be realised and sustained. Australia and other Western countries must partner with source countries to develop strong political commitment and scaled-up investments in human resources for health. Correlations between source countries’ core maternal Millennium Development Goal indicators and (A) physician migration to Australia, the United Kingdom, Canada and the United States and (B) human health care resources* Maternal Millennium Development Goal indicators in source countries (A) Physician migration to Australia, the UK, Canada and the US No. of source countries† Mean physician migration density‡ (SD) Maternal mortality ratio¶ P Births attended by skilled health care staff** P Total migration 141 0.094 (0.224) − 0.45 < 0.001 0.34 < 0.001 Migration to Australia 75 0.007 (0.040) − 0.29 0.011 0.25 0.037 Migration to the UK 117 0.017 (0.072) − 0.27 0.003 0.17 0.072 Migration to Canada 116 0.008 (0.027) − 0.47 < 0.001 0.45 < 0.001 Migration to the US 124 0.061 (0.158) − 0.55 < 0.001 0.43 < 0.001 (B) Human health care resources Mean density of health care workers§ (SD) Physicians 141 1.655 (1.426) − 0.84 < 0.001 0.67 < 0.001 Nurses 141 3.636 (3.544) − 0.81 < 0.001 0.72 < 0.001 Public and environmental health care workers 64 0.114 (0.169) − 0.56 < 0.001 0.54 < 0.001 Health management and support workers 71 1.488 (2.222) − 0.73 < 0.001 0.51 < 0.001 * Data are those available for 1999–2002, and each variable was transformed into its natural logarithmic form for analysis. † Top 10 source countries losing physicians (per 1000 population) to the four destinations combined (in decreasing order): Ireland, Saint Lucia, Lebanon, New Zealand, Jamaica, Iceland, Malta, Dominican Republic, Israel, and Cook Islands. Top 10 source countries for Australia: New Zealand, Ireland, Singapore, Fiji, Malta, Sri Lanka, South Africa, Slovakia, Bahrain, and Hungary. Top 10 source countries for the UK: Ireland, Malta, Barbados, Jamaica, New Zealand, Sri Lanka, Libya, Greece, Iraq, and Iceland. Top 10 source countries for Canada: Ireland, Jamaica, Kuwait, Lebanon, South Africa, New Zealand, Barbados, Bahrain, Saudi Arabia, and Iceland. Top 10 source countries for the US: Saint Lucia, Lebanon, Ireland, Iceland, Dominican Republic, Jamaica, Cook Islands, Israel, Belize, and the Philippines. ‡ Number of source country’s physicians working in Australia, the UK, Canada and the US per 1000 source country’s population (based on average year-2000 population). § Number of health care workers remaining in home/source country per 1000 population. ¶ Correlations between the number of maternal deaths per 100 000 live births and (A) physician migration density and (B) human health care resources. ** Correlations between the percentage of births attended by skilled health care staff and (A) physician migration density and (B) human health care resources.

Onyebuchi A Arah

To the Editor: In reference to the letter by Kennedy et al, reporting two patients who tested positive to human T-lymphotropic virus I/II (HTLV-I/HTLV-II) antibodies after administration of the intravenous immunoglobulin, Octagam (Octapharma Australia, Sydney, NSW),1 the Therapeutic Goods Administration (TGA) would submit that: This product was accepted for review by the TGA at a time when plasma products sourced from overseas had to demonstrate superiority over the local product. This requirement was fulfilled by Octagam on grounds that included pathogen safety issues. HTLV-I and HTLV-II are entirely cell-associated viruses and are thus irrelevant to the safety of plasma derivatives. They are in a group of pathogens for which risks, implied by epidemiological factors, apply to cellular but not to plasma products. Another common example is malaria. The Australian plasma pool includes donations from individuals who are at risk of transmitting malaria, so their cells are not used but their plasma is used for fractionation. This situation is well understood and managed by regulators, none of whose standards internationally include the need to test plasma donors for HTLV-I/HTLV-II infection. As the bulk of Australia’s fractionation pool is derived as a by-product of whole blood, blood is tested for HTLV-I/HTLV-II in this country, but it is not a mandatory requirement in Australia or anywhere else. The exclusion of antibody from the plasma pool, as occurs for HTLV-I/HTLV-II in Australia, may actually lead to the loss of potentially protective antibodies, which may well have a therapeutic effect in protecting patients from HTLV-I/HTLV-II infection.2 Such considerations apply, for example, in the requirements of the Food and Drug Administration in the United States for source plasma for fractionation. The requirements take care to allow the inclusion of antibody-positive units for some viruses that would be excluded from blood transfusion. The incident referred to by Kennedy et al was appropriately reported to the TGA’s Adverse Drug Reactions Unit, which concluded that this was not an adverse event. A Northern Territory Government document on HTLV reports: “In Central Australia the prevalence of HTLV-I is estimated to be up to 14%, compared to 4.7% in the Northern Territory cattle country . . .”3 The residual risk of transmission of HTLV-I/HTLV-II infection, while low,4 clearly varies across the potential donor population, and comparisons that are irrelevant in relation to the safety of specific products would appear to be unwise. It is recommended that practitioners seeking to assess causality in putative infectious disease transmission by plasma products follow rigorous scientific processes, such as those recommended by the German regulatory authority.5

Albert Farrugia

To the Editor: Growth charts are important tools in assessing the physical development of infants and children. Understanding and comparing the derivation and applicability of the new World Health Organization Child Growth Standards1 and the Centers for Disease Control and Prevention (CDC) growth charts2 is essential. Arguments for and against the standard use of the new WHO growth charts are being discussed on the basis of differences in study designs used and growth patterns found.3,4 The WHO charts show the growth of breastfed infants on the basis of data from about 8500 children from widely different ethnic backgrounds and cultural settings (Brazil, Ghana, India, Norway, Oman and the United States); these children were from selected populations in which no health, environmental or economic constraints on growth existed.1 In contrast, the CDC charts represent the combined growth pattern of artificial-formula-fed and breastfed infants in the United States, where about 50% of infants are never breastfed and only around 33% are breastfed for 3 months or longer.2 Is it possible to misdiagnose breastfed infants who are growing normally as failing to thrive if the CDC growth charts are used? The simplest common definitions used for failure to thrive are a drop below the 3rd or 5th percentile for weight, or when growth deviates from an established growth curve for 3 consecutive months.5 By the CDC growth charts, the normal growth pattern described by the WHO Child Growth Standards for a 15th percentile, breastfed, female infant at 18 months would meet all three definitions of failure to thrive. The clinical response to this perceived failure to thrive may be to provide additional energy in the form of energy-dense foods or supplements (eg, artificial formula). This would at best be unnecessary, and at worst might contribute to the development of overweight and obesity. So, where to from here? We recommend that all health professionals who use growth charts be cognisant of which chart they are using and its application, especially for breastfed infants. There is also a need for Australian national and state governments to debate which growth charts should be used and in what contexts. Finally, irrespective of the choice of growth charts, it must be recognised by practitioners and the general public that these charts are guides only, and should be used as part of a holistic approach to infant growth assessment and management.

Barbara Radcliffe · Jan E Payne · Helen Porteous · Simone G Johnston

To the Editor: Single case reports of “meth mouth”, similar to that recently published in the Journal,1 exaggerate the dental problems surrounding the use of methamphetamines. Evidence that methamphetamines cause grinding and wear of teeth,2 xerostomia,3 and cravings for sweet drinks is weak. The drug use reported by Shetty was intravenous or intranasal, not oral. While systemic effects may contribute to dental problems, local oral effects associated with acidity of methamphetamines would be minimal with intravenous or intranasal drug use. A more plausible explanation for dental disease may be the years of neglect, trauma and poor diet experienced by many people who use drugs.4 Many drug users begin using as early as 14 years of age and consume multiple illegal psychoactive and legal antipsychotic and antidepressant medications associated with xerostomia. A comprehensive drug-use history is required before dental problems are attributed to one drug. Advising treating dentists to avoid the use of analgesics is misinformed and potentially leaves patients in severe pain unnecessarily. People affected by methamphetamines are unlikely to seek dental or medical treatment. A more likely scenario is presentation because of pain between methamphetamine binges, or presentation when they are taking stock of their health problems. At such times, they are unlikely to be affected by methamphetamines, which generally have short half-lives. At these times, non-steroidal anti-inflammatory drugs, nitrous oxides, narcotics (including codeine) or increases in methadone dose may be needed to manage pain. Analgesic depressants are not contraindicated unless other illicit or licit depressants are being used concurrently, as depressants work on different receptors and areas of the brain than amphetamine-type stimulants. Careful discussion with the patient and the patient’s general practitioner or alcohol and drug specialist is critical in balancing the need for pain relief with the potential for drug interactions and even overdose, if the patient is taking other depressants (legal or otherwise). Practitioners can contact a 24-hour drug information line for health professionals for information of this kind in most Australian states and territories (Box). Drug information contact numbers Service Contact number DACAS (VIC) 1800 812 804 DACAS (TAS) 1800 630 093 DACAS (NT) 1800 111 092 DASAS (NSW) 1800 023 687 or (02) 9361 8006 ADIS (SA) 1300 131 340* CAS (WA) 1800 688 847 or (08) 9442 5042 ADIS = Alcohol and Drug Information Service. CAS = Clinical Advisory Service. DACAS = Drug and Alcohol Clinical Advisory Service. DASAS = Drug and Alcohol Specialist Advisory Service. * Clinicians should ask to be put through to the duty doctor service.

Anne-Marie L Laslett · John N Crofts

To the Editor: Perusing your long-needed issue on men’s health,1 I was struck by the absence of any mention of obstructive sleep apnoea. As an anaesthetist in private practice, I see three or four middle-aged men with previously undiagnosed obstructive sleep apnoea each week. Usually, I also see at least one man who has had the diagnosis confirmed, but has not persisted with treatment because his wife has become used to his snoring or has moved to another bedroom. Advising the undiagnosed men of the importance of a sleep test, I refer them back to their general practitioner for follow-up, and suggest a couple of respiratory physicians who could perform the test. On a somewhat random follow-up, I have been disappointed with the results, as the following comments were reported back after men’s GP consultations: “Most blokes over 50 snore”; “Your wife will get used to it”; and “Surgery doesn’t work”. Men who have been diagnosed but haven’t persisted with treatment (together with their wives) are often totally unaware of the health risks; they believe that they are only managing the unacceptable noise of their snore! I would have thought that some of the articles in the issue would have mentioned the contribution of obstructive sleep apnoea to hypertension, atrial fibrillation, erectile dysfunction and sleep disturbances, with resulting poor performance during the day, particularly in the workplace. This is an extremely important health issue (and not only in men) that appears to be sadly neglected, still.

Kenneth W Sleeman

In reply: We thank Sleeman for his astute comment. In the men’s health issue,1 our intention was to highlight several major areas relevant to men’s health rather than attempt comprehensive coverage of the field. Sleep apnoea was indeed one of the potential topics we identified when we planned the issue. We anticipated that sleep apnoea would be discussed within some of the key contributions to the issue. Although this did not eventuate, we acknowledge the importance of sleep apnoea in general medical practice, and plan to revisit the topic in future issues of the Journal.

Ann T Gregory

To the Editor: With the proposed formation of the Australia New Zealand Therapeutic Products Authority (ANZTPA), the recent viewpoint article1 and accompanying editorial2 on systems of evaluating medicines were timely. Both reports provided interesting comments on existing systems and proposals for improving these in the future. However, I would like to comment on some omissions and errors in these articles. In their viewpoint article, Kelman et al stated that “there are as yet no overseas examples of ‘routine’ medicines monitoring”.1 This is not correct. The New Zealand Intensive Medicines Monitoring Programme (IMMP) has been undertaking routine monitoring of selected medicines since 1977. The IMMP collects nationwide prescription data to form cohorts of patients who are subsequently monitored for adverse events.3 These patient cohorts provide accurate denominator populations, which, as noted by Kelman et al,1 is important for risk quantification by measurement of incidence. The IMMP uses prescription-event monitoring (PEM) methods to perform active postmarketing surveillance of new medicines in New Zealand, and has been successful in identifying numerous new signals of adverse drug reactions and in quantifying risk.4 The IMMP has developed ways of enhancing PEM methodology by linking records with national morbidity and mortality databases.3 This methodology was recently successfully applied in a study of the safety and usage of atypical antipsychotic medicines in a nationwide paediatric population.5 In their editorial, Stanley and Meslin commented that none of the health care data linkage systems in England, Scotland, the United States or Canada “are nationwide or have the routine ability to link health care records with drug prescription data”.2 As described above, the IMMP has both these abilities. It was somewhat surprising that, although discussions regarding pharmacovigilance in the ANZTPA are now well underway, current systems in New Zealand were not mentioned in either of these Journal articles. I would encourage Australia to develop pharmacovigilance systems similar to those established in New Zealand. Of course, these will need to be adequately funded to achieve the expected outcomes. The formation of the ANZTPA is a great opportunity to improve pharmacovigilance in both countries.

Mira L Harrison-Woolrych

To the Editor: In his article on research misconduct,1 Marcovitch cited my article on institutional corruption in medicine, which was published in the BMJ in 2002.2 He states: Readers of the MJA will have to find the paper version in their libraries, as the electronic version has been replaced on the BMJ’s website . . . with the bald statement that it has been removed for legal reasons. In case any of your readers are concerned that the article has been retracted, I would like to point out that the article was removed from the website on 10 June 2004, when Dr Richard Smith was editor of the BMJ. Dr Smith cited my article in his own article on research misconduct in 2006.3 He would not have done so if the article had been retracted. Neither would Marcovitch.1 My article described how some senior individuals in British academic medicine had concealed misconduct for a decade. The article had an editorial footnote stating: “Documentary evidence corroborating this article was made available by Dr Wilmshurst to the BMJ.” It was cleared for publication by the BMJ’s lawyers. An “Editor’s Choice” column entitled Corruption in medicine accompanied my article online.4 That column has also been removed from the website. It stated: “The article by Wilmshurst has its origins in a seminar he gave to the BMJ in 1996. For years he had been informing us of misdemeanours. Fear of libel stopped us from publishing.”4 Ironically, it was fear of libel actions that caused the BMJ to remove the article from the website. Soon after publication, the BMJ received threats of libel actions from academics and their institutions. Dr Smith and I spent considerable time working with lawyers to counter these challenges. None came to court, but the legal costs for the BMJ’s insurers mounted. It was pointed out that a libel action must be started within 1 year of publication. Because the article was on the website it was constantly being republished. If it was removed from the website there could be no more threats of litigation after 1 year. Therefore, the insurance company that covers the BMJ against libel insisted that the article be removed from the website. If readers are unable to get a copy, they can email me and I will send a PDF version.

Peter T Wilmshurst

To the Editor: A further reason for the differences in antenatal Down syndrome screening rates between urban and rural women, reported by Coory and colleagues,1 is likely to be the relative difficulties many Queensland women face in accessing abortion services. We are aware of several Queensland public hospitals that provide excellent antenatal screening services — testing for chromosomal abnormalities as well as providing the 18–20-week ultrasound scan for structural abnormalities. However, these hospitals do not offer subsequent counselling or abortion for women who make the difficult decision to terminate a pregnancy at this gestation, instead directing them to the private system. Some of these women are undoubtedly among the many Queensland women who travel interstate for abortions each year.2-5 First-trimester abortion is difficult to access for women in rural areas throughout Queensland. This is probably an important factor in women making the decision not to have early screening and/or chorionic villus biopsy, and possibly also a factor in doctors not offering it. Having to travel several hundred kilometres for the test, with the possibility of a further journey for an abortion, is beyond the resources of many rural women. We are in agreement with Coory et al that a majority of the population would support equity of access to services and equal choices for all women in the matter of antenatal screening for fetal abnormality. In fact, amniocentesis for chromosomal abnormalities has been available, with little controversy, for more than 30 years. If early antenatal screening is made available to all women, then it is reasonable to expect that appropriate counselling and access to safe, affordable abortion is also provided.

Caroline M De Costa · Cait Calcutt

To the Editor: Women of the remote Indian Ocean Territories (Christmas Island and the Cocos Islands [see map]) regularly question why their comprehensive obstetric service, allowing deliveries on the Islands, ceased in 1998. A study in 20051 aimed to provide answers for these women. There is one general practitioner on the Cocos Islands and two on Christmas Island. Previously, procedural GPs attended to most deliveries. Now, pregnant women must leave the Islands 4 weeks before their expected delivery. The financial, physical, emotional, and cultural costs of this are substantial. Reports published in 20022 and 20043 identified community concerns, but resisted recommendations to resume on-Island birthing, because of perceived low birth numbers and difficulty sustaining the skills of clinicians. Both studies relied on external birthing data, as the Indian Ocean Territories Health Service (IOTHS; administered by the Department of Transport and Regional Services) had not documented numbers of deliveries. The Alberton Report,3 extrapolating from Australian Bureau of Statistics (ABS) data, assumed that the population of children aged less than 1 year in a census year equalled the number of deliveries the year before. The ABS has a system to protect the confidentiality of small isolated populations and purposely does not report these numbers. The Bath Report2 relied on data from the Western Australian Midwife Notification System (MNS). The MNS reported 136 births to Island women from 1995 to 2004, while our study (Western Australian Centre for Remote and Rural Medicine)1 recorded 326 births. Thus, the MNS attributed only 41% of known births to Island women during 1995–2004, and only 23% during the period considered by the Bath Report. We believe that the MNS data shortfall occurred for two reasons. Firstly, women frequently provide their temporary mainland address on the MNS form for practical reasons. Secondly, one in seven women leaving the Islands to deliver their babies choose to give birth in a state other than Western Australia to be closer to family, and these births are not attributed to women from the Islands. The methods used by the Alberton Report, the MNS and the Bath Report result in underestimations of the number of confinements for Island women by up to 77%. It is regrettable that this situation has not been previously recognised or acknowledged, and that recommendations for the resumption of obstetric services by the IOTHS have repeatedly been based on incomplete data. If records of the numbers of births for Island women had been collected and considered by the IOTHS, Island families might again enjoy a comprehensive on-Island delivery service for low-risk pregnancies.

Susan Downes · Sally M Roach

To the Editor: We report an exceptional case of a woman who underwent emergency “finger fracture valvuloplasty” (FFV) in 1954 to treat rheumatic mitral stenosis and required no further surgical intervention for 51 years. The woman presented in 1954 with pulmonary oedema due to mitral stenosis during the first trimester of her second pregnancy. She underwent FFV at Lewisham Hospital in Sydney. She had a prolonged convalescent period, was discharged after 5 months, and delivered a healthy child. She was one of two pregnant patients reported in the Medical Journal of Australia by Hall and Windsor.1 She remained well and active until 2005, when she presented with New York Heart Association Class III symptoms of dyspnoea on exertion, and ultimately underwent mitral valve replacement that year. She made a good recovery postoperatively and remains well. In the 1920s, 10 patients with mitral valve stenosis were treated surgically.2 In 1923, Cutler and associates from Boston operated on seven patients using a cardiovalvulotome (through the left ventricle) and, in the same year, Duff and Evarts from Washington used a cardioscope (through the left atrium) on one patient. In 1925, Soutter from London and Pribram from Germany used a “finger fracture method” and a valvulotome, respectively, on one patient each. However, of the 10 patients, only two survived, one of Soutter’s and one of Cutler’s. The procedure was subsequently successfully revived in 1948 by Harken in Boston, Bailey in Philadelphia, Blalock in Baltimore, Brock in London, and others, who performed various procedures including valvuloplasty and commissurotomy. However, the so-called FFV (Harken) became the favoured procedure. It evolved from using the forefinger, to using the little finger, to eventually using a knife. Most surgeons had difficulty in using the mitral knife to divide the medial commissure and thus developed their own instrument.2 There are few successful case reports of FFV in pregnancy. In the United Kingdom, Brock reported three, Logan and Turner, six, and Marshall and Pantridge, 18.3 Hall and Windsor in Sydney performed FFV in two of seven pregnant women who were being considered for FFV, including our patient. One of the other five, who were managed conservatively, died.1 In 1963, Windsor said, “Eleven years’ experience in the surgery of the mitral valve has brought with it a great respect for the ability of the mitral commissures to resist finger, knife and dilator”. He reported follow-up of 90 patients who underwent FFV. No more than 40 patients (45%) obtained good results. Sixteen patients in this group have since been reoperated upon by the more effective transventricular route using a mechanical expanding dilator.4 It should be noted that mitral stenosis in young women is rarely accompanied by calcification, and this may allow a more complete and successful valvuloplasty. All the procedures mentioned above occurred before the development of cardiopulmonary bypass and open heart surgery in 1954. Early pioneers in surgery faced many challenges and disappointments, as well as condemnation, criticism and ridicule from colleagues. Some, like Soutter and Bailey (the latter nicknamed the “butcher of Hahnemann Hospital [Philadelphia]” after his first four FFV patients died) lost their practices.5 We would like to pay homage to all surgical pioneers and conclude with a comment from Harken: “He who would not learn from the past is condemned to relive it”. Finger fracture mitral valvuloplasty technique (Hall and Windsor1)

John S Murala · Hugh D Wolfenden · George S Youssef · Daniel Friedman

To the Editor: Systemic ototoxicity secondary to the use of aminoglycosides is well known in clinical medicine, and appropriate monitoring measures to prevent vestibulo-cochlear ototoxicity are routinely performed. Less well known is the potential for topical ear drops, particularly the aminoglycoside group, to cause both vestibular and cochlear damage when introduced through a patent grommet or tympanic membrane perforation for the treatment of infection.1 Although the incidence of aminoglycoside ototoxicity with ear drops is uncommon (for cochlear toxicity, in the order of one in 10 000 patients treated2), individual susceptibility and patient compliance problems may lead to inner ear damage. Concerns with the potential ototoxicity of aminoglycoside ear drops has led to American,3 British4 and Canadian5 expert committees providing guidelines on the use of potentially ototoxic ear drops in patients with tympanic membrane perforations or patent grommets. The Consensus Panel of the Australian Society of Otolaryngology Head and Neck Surgery (ASOHNS) unanimously agreed on the recommendations shown in the Box, which are based on the American guidelines. Broadly speaking, the Consensus Panel recommends avoiding the use of ototoxic ear drops in patients with perforated tympanic membranes where possible. The Australian National Aboriginal Community Controlled Health Organisation study showed that the non-ototoxic fluoroquinolone drops were more effective than commonly used ototoxic ear drops.1 An application to the Therapeutic Goods Administration for introduction of ciprofloxacin drops to the ear has recently been approved, and has been placed on the Pharmaceutical Benefits Scheme as an authority prescription for Aboriginal and Torres Strait Islander children with chronic suppurative otitis media as of February 2007. However, clinical circumstance may dictate that potentially ototoxic agents need to be used if culture/sensitivity testing suggests that fluoroquinolone drops would not be appropriate, are unavailable, or if previous treatment with fluoroquinolone ear drops failed. The Consensus Panel did not believe routine auditory/vestibular monitoring was warranted by the risks of ototoxicity, provided the treatment was short (5–10 days). The full document outlining the Consensus Panel’s recommendations is available from ASOHNS. Recommendations of the Consensus Panel of the Australian Society of Otolaryngology Head and Neck Surgery on ototoxic ear drops and tympanic membrane perforation Non-ototoxic eardrops are preferable in the presence of tympanic membrane perforations or grommets. If potentially ototoxic antibiotic ear drops are used, they should only be used in infected ears and discontinued immediately the infection has resolved. If potentially ototoxic antibiotic ear drops are prescribed for use in the open middle ear or mastoid, the reason for their use and a warning to the patient/parent of the risk of ototoxicity should be given and documented. If potentially ototoxic antibiotics are prescribed, the patient should be specifically instructed to return to the doctor if he or she develops vertigo, hearing loss or tinnitus. If the tympanic membrane is known to be intact and the middle ear and mastoid are closed, then the use of potentially ototoxic preparations presents no risk of ototoxic injury.

Robert J Black · Vince C Cousins · Peter Chapman · Zoran Becvarovski · Harvey L C Coates · Stephen J O’Leary · Christopher F Perry · Brian J Williams

To the Editor: Coiera accurately described some lessons from the United Kingdom’s experience with health information technology1 that should be noted by potential “fast followers”, such as Australia’s National E-Health Transition Authority (http://www.nehta.gov.au). The debate about the merits of the “opt-in” versus the “opt-out” approach highlights a need for further discussion about the optimum consent model to achieve the aims of a shared electronic health record (EHR), combining patient-controlled health records with a tool for clinical decision making, and research and planning.2 Informed consent and ethical approval are vital for publication of evaluation findings. The 2007 National statement on ethical conduct in human research3 recognises that consent processes do vary, depending on the context and type of research. Opt-in is an active process and is believed to build consumer confidence and reinforce a strong privacy message.2 Opt-out is more passive, assuming that most people are willing to share their health information for clinical and/or research purposes. Our own experience with opt-in is that less than 0.4% of patients approached decline to participate in data extraction projects.4 With opt-out, there is little evidence to show that it is in any way harmful for initial patient contact. On the other hand, opt-in has been associated with a poor response rate and a biased study population in medical record research,5 in research in screening clinics,6 and in a pilot study of patients with angina.7 Because recruiting unbiased patient samples with high response rates is essential for scientific rigour, opt-out should be the default recruitment strategy for studies with a low risk for participants. The most appropriate consent model for all situations, in an ethical and secure electronic environment, is one that allows patients and providers to make their own decisions about giving expressed or implied consent within an opt-in or opt-out approach. The participants in the process must be sure that consent has in fact been granted. The health record (paper or electronic) must demonstrate that the consent process has taken place and document the outcome. We have developed software to enable use of this flexible consent protocol, permitting context-sensitive and ethical access to personal health information if patients, clinicians and researchers have given their consent. The literature and our experience suggest that this flexible approach, based on the choices of patients and providers, should lead to good participation rates and allow the objectives of a shared EHR to be achieved in a cost-efficient manner.

Siaw-Teng Liaw · Douglas I R Boyle

To the Editor: The editorial by Coiera and Westbrook1 and indeed the letter by Fox2 tended to use the term “clinical software” in a broad sense. In Australia, doctors who use clinical applications are in fact using electronic medical records. The major functionality provided is one of information storage, with the ability to produce a range of documents that were previously handwritten. To accept that the currently available applications offer decision support is a very generous, and possibly naïve, interpretation. The common example of decision-support tools used in Australia is the humble prescription writer. Current vendors offer a variety of prescription writers and, as Coiera and Westbrook1 assert, they check for drug–drug interactions and dosage errors and provide various alerts. Coeira and Westbrook go on to question whether appropriate testing is being performed on the large number of applications available. At first glance this question may seem to be somewhat invalid, as most of the software packages in Australia use either the AZDex (a proprietary internal drug database used by Medical Director) or MIMS (a pharmaceutical database of products currently available in Australia by CMPMedica Australia) drug databases. These two highly regarded sources of drug information provide the developer with an easy-to-implement set of tools that effectively ensures “quality” information is provided to the doctor preparing the prescription. The problem is that, although we have quality databases, there is little or no compliance testing to ensure that the applications that use them are developed to an equally high standard. For example, there is no mechanism to inform end-users which parts of the database have been used, and there is no testing to ensure the end-user is presented with accurate information. While many Australian doctors have moved to computerised clinical records, their ability to use these data for improving clinical care is being curtailed by a lack of standards and coding of conditions. Computers are not efficient in dealing with the free text that is traditionally used in clinical notes, and even data such as drug prescriptions are difficult to analyse because of the lack of a standard method of drug naming or coding. I look to a future when true clinical support tools are available. To this end, the development, coordination, and facilitation of a series of standards by the National E-Health Transition Authority should be supported.

Ian D Williams

In reply: At the heart of much debate on patient consent for access to electronic data are two conflicting desires — many consumers wish to minimise access to their record, and many clinicians have genuine concerns that such restriction may lead to patient harm. In some cases, privacy is paramount (eg, psychiatric or sexual health history). In others, such as emergency presentations, patient wellbeing may override such concerns. This has led many to conclude that there is no “one size fits all” model for e-consent.1 The current debate between the boundary cases of “opt-in” and “opt-out” is misleading because many specialist services of necessity will have local consent processes, crafted to meet the need of their patients and their clinicians. Yet, many health information technology initiatives do not seem prepared to consider this complexity, and opt-in or opt-out are all that is on offer. Liaw and Boyle’s concerns about dropout rates under an opt-in system affecting secondary use of patient data for research purposes are no doubt real, but it is hard to draw too strong a comparison between patient recruitment for research and patient permission to store data for their own care. Williams correctly points out in his letter that decision support remains a small component of the software to support clinical practice that most Australian general practitioners now use. However, anyone using a prescription program that suggests doses, checks interactions, or generates alerts is using decision support. We can say so confidently because research repeatedly shows that such functions change clinical decisions. Indeed, something as simple as accessing research articles and guidelines using the Internet is a form of decision support, because it changes clinical decisions significantly, and sometimes negatively.2 Consequently, it is perhaps naïve to await “true” decision support using artificial intelligence before we worry about how software affects clinical behaviour. If the intervention was a drug and serious patient harm resulted from infrequent side effects, everyone would quickly agree some controls might be needed. Somehow, we still don’t seem to get as excited about the harm that may come from using bread-and-butter clinical software, but we should.

Enrico W Coiera

To the Editor: Whatever the method used to select medical students (whether academic, psychometric, or interview), the basic problem in assessing the method’s predictive capability is that only candidates who perform at the higher levels in the assessment will be admitted. The only way to test the predictive validity of an assessment is to admit candidates from a much wider band of performance, creating a much less compressed score range for comparison. By definition, candidates with lower scores are excluded, thus making this analysis impossible. The study by Groves et al had an overall response rate of 13.6%,1 a rate at which no conclusions could, or should, be drawn. Entry to medicine remains a highly charged and emotional subject. It is unfortunate that the press has drawn conclusions from a study from which conclusions cannot be drawn.

John E Marley