Volume 193 Issue 3

Blood lead levels in children in Mount Isa are substantially elevated, and a purported lack of knowledge of the lead source is no longer tenable Environmental lead levels and blood lead concentrations in children at Mount Isa, in north-western Queensland, are substantially elevated compared with background values1-3 and, as a consequence, there is a public health risk. This problem is exacerbated by the reluctance of stakeholders, including Xstrata Mount Isa Mines Ltd, operator of Mount Isa Mines (MIM), and Queensland environmental and health authorities to acknowledge and respond effectively to the fact that the main environmental lead source is mining and smelting activity.1,2 It is frequently claimed that the lead source is natural surface mineralisation;4-6 this is not the case. Mount Isa city, located immediately adjacent to MIM, is a major lead, zinc and copper producer, and Australia’s largest atmospheric emitter of sulfur dioxide, lead and other metals.7 The emissions are likely to have had an impact on the blood lead level (BLL) of a significant proportion of the city’s population of about 21 000. The causal link between smelter lead emissions and an increased risk of adverse health effects has been convincingly documented elsewhere,8 and responded to, albeit with varying degrees of urgency, at smelting sites around Australia (Box).9 In Mount Isa, the link has been routinely questioned and remedial action delayed. In recent decades, considerable evidence has emerged showing lifelong negative health, intellectual and sociobehavioural effects associated with childhood BLLs above 10 μg/dL, the level widely regarded as the threshold above which intervention is necessary. However, there is emerging evidence of adverse effects occurring at 5–10 μg/dL, and even at levels as low as 2 μg/dL.8-11 In 2008, Queensland Health reported that Mount Isa children aged 1–4 years had a mean BLL of 5 μg/dL, with 37% having levels > 6 μg/dL and 11.3% having levels > 10 μg/dL.3 Recent data from Fremantle, Western Australia, an urban centre with no major industrial lead source, showed a mean BLL in children of 1.8 μg/dL, with no individual readings exceeding 10 μg/dL.12 This is similar to the mean BLL of 1.9 μg/dL (with only 1.6% of readings ≥ 10 μg/dL) for children aged 1–5 years in the United States in 1999–2002.10 Compared with these figures, BLLs remain substantially elevated in many of Mount Isa’s children and, as shown by numerous studies elsewhere, the level of lead exposure is likely to correlate with neurocognitive impairments.8-11 Lead exposure places children on an abnormal developmental trajectory that may result in reduced social and educational achievement and unmet life potential. Assuming that the Mount Isa BLL data are representative of all 1–4 -year-olds in the city (of whom 27% were sampled),3 then, on average, every nine days a child will exceed the BLL threshhold of > 10 μg/dL. Research commissioned during a Queensland government-led inquiry a decade ago,1 as well as subsequent peer-reviewed studies,2 have unequivocally demonstrated widespread contamination of soil and airborne dust in and around Mount Isa, as a result of both historic and ongoing mining and smelting activity by MIM. Contaminants include lead, copper and other metals and metalloids. Frequent claims that natural mineralisation of soils is the main cause of increased lead levels4-6 are incorrect, and have stymied an appropriate response to the Mount Isa lead problem. The “gossans” (ridges of lead-bearing surface rocks) initially discovered west of Mount Isa are now largely covered by mining operations, and cannot be a major source of environmental lead. Furthermore, there is no substantial natural exposure of copper ore, which was discovered “accidentally” during deep drilling. These observations are supported by data published by several of MIM’s own geologists over the past 60 years.13 Numerous soil profiles in and around Mount Isa show that it is usually only the surface layers that are contaminated with lead and copper.1,2 Concentrations of these metals correlate significantly with each other and are up to 20 times higher at 0–2 cm depth than at 10–20 cm depth. This shows that (1) soil contamination with both lead and copper can only have come from particles emitted into the atmosphere from MIM, as there is no other common source for both metals, and (2) that the surface soil metal enrichment can only have come from aerial deposition of contaminated particles. Lead isotope fingerprinting, used as a tracer, shows that surface soil — but in most cases not deeper soil — contains lead from the Mount Isa lead ore body due to aerial deposition.1 The capture by MIM of smelter fumes (sulfur dioxide and associated metal-bearing particles) is inefficient, as shown by the ongoing high emission levels that, for some compounds, have been rising in recent years.7 The Queensland Government’s air quality data for Mount Isa14 show 10 breaches of the guideline level for sulfur dioxide between September 2009 and February 2010, and that lead concentrations in air increased substantially during these breaches. However, the current legal standard for lead concentrations in air in Mount Isa is higher than the Australian national lead-in-air standard of 0.5 μg/m3, and therefore was not breached.15,16 More importantly, the current Mount Isa standard is an order of magnitude greater than the recently revised US lead-in-air standard,8 which was lowered by the US Environmental Protection Agency after assessing about 6000 studies related to the health impacts of lead exposure.8 The lower standard was deemed necessary to properly protect the health and wellbeing of children.8 The evidence is clear. There is a single primary source of environmental lead in Mount Isa: the historic and ongoing mining and smelting activity. Acceptance of this patent fact by all stakeholders will lead to a more targeted remedy to the lead problem, and better health and environmental outcomes for the community of Mount Isa. A purported lack of knowledge of the lead source is no longer a tenable response and provides no long-term resolution for Xstrata, the government or the children of Mount Isa whose futures are at risk. Australian mining- and smelting-related blood lead levels and government and industry responses9 Port Pirie, South Australia Early 1980s: high blood lead levels (BLLs) confirmed 1984 onwards: decontamination and demolition of residences, slag dumps covered, emissions controlled 2004: BLLs decreased but remain elevated Broken Hill, New South Wales Early 1990s: high BLLs confirmed 1994 onwards: land and home evaluation and remediation 2006: BLLs decreased but remain elevated Boolaroo, NSW Early 1990s: high BLLs confirmed 1991 onwards: emissions controlled 1997: lead abatement of homes 2003: smelting operations ceased 2005: BLLs decreased substantially after smelter closure Mount Isa Mines, Queensland 1994: high BLLs confirmed 1997: Mount Isa lead emission limits set above Australian national limits (national limits written into law in 2009, to apply in Mount Isa from 2012) 2000: partial emission capture 2007: Xstrata Mount Isa Mines “lead pathways” study initiated (not completed June 2010) 2008: BLLs lower than in 1994 but remain elevated 2009: Queensland government lead management report 2010: highest lead emissions in Australia

Niels C Munksgaard PhD · Mark P Taylor BSc(Hons), PhD · Alana Mackay BEnvMgt

New guidelines are timely but miss an opportunity to emphasise early intervention for all young people There are few mental health issues of greater concern to the wider community than the management of young people with depressive disorders. Consequently, the new draft clinical practice guidelines from beyondblue: the national depression initiative1 are timely. The previous National Health and Medical Research Council Clinical practice guidelines: depression in young people were produced in 1997 and rescinded in 2004, and a variety of other international perspectives are now available.2,3 Internationally, the limitations of the clinical trial database, such as small and non-representative or restricted trial samples, and exclusion of more severe cases or patients with suicidal ideation, are widely recognised. Hence, the authors rely very heavily on “good practice points” that are said to be “based on lower quality evidence, expert opinion and current good practice”. Importantly, the new draft guidelines recognise that appropriate services are still not provided to about 75% of Australian young people with depression. They suggest there is a lack of clear evidence for primary (or universal) prevention and give qualified support for pre-emptive psychological strategies for those at high risk. Recent systematic reviews of school-based prevention and early intervention programs for anxiety and depression, however, support a more optimistic view (reporting effect sizes of 0.11–1.37 for anxiety, using data from 20 programs;4 and 0.21–1.40 for indicated depression interventions, based on 28 programs5). These effect sizes were often clinically important and support the notion that school-based programs should be pursued more assertively. Other key issues covered by the guidelines include the challenges associated with engaging young people with our health care systems, the lack of focus on improving long-term outcomes, and the fact that more severe bipolar and psychotic disorders emerge against the background of earlier depressive disorders. In Australia, surveys of young people have highlighted attitudinal and knowledge barriers6 and the clinical reality that under-recognition of and lack of access to evidence-based psychological therapies are still common.7 Unfortunately, the guidelines overemphasise and reinforce stereotypes of young people who are reluctant to seek care, parents who are unaware of the nature of the disorder, the complexity of clinical assessment and lack of access to specialist mental health services. These are artefacts of the current failure to respond to youth mental health as a salient public health issue. We would encourage the authors to take full advantage of the opportunity to add depth to the emerging field of youth psychiatry and to support the development of enhanced models of empowering, collaborative and youth-focused clinical practice.8 The most novel outcome in the new draft guidelines is the Expert Working Committee’s decision to focus on the age range of 13–24 years, rather than a more restricted focus on 12–18 years. This is consistent with current understanding of the continuities in brain and social development,9 the pattern of incidence of mental disorders and the changing sociology of adolescent and early adult development.10 There is clear evidence of multiple transitions in both the genetic and environmental determinants of depressive disorders from the onset of puberty right through to the early adult period.11 The key developmental processes in the brain — synaptic pruning and maturation of the white matter tracts — are continuous throughout these years.9 However, in key areas, the guidelines fall back on the traditional divide between adolescents (13–18 years) and young people (19–24 years). While this reflects the reality that most treatment studies have used a 13–18-years age range, it ignores the fact that the division at 18 years is based on legal and educational boundaries rather than clinical, developmental, neurobiological or cultural considerations, and thus is not soundly based. What is desperately needed in both clinical research and service development12 is a shift away from this artificial divide to the more inclusive age range of 12–25 years. Short-term treatment recommendations are spelt out in the guidelines, at least for those under 18 years of age. Specific psychological therapies are the preferred first-line intervention for most patients, while new antidepressant drugs are reserved for those with more severe disorders or those who fail to respond to psychological interventions. The small risk of increased suicidal ideation in young people commencing newer antidepressant drugs (4% for active treatments versus 2% for placebo13) is appropriately re-emphasised. Previously, wide media coverage of United States Food and Drug Administration warnings about antidepressant drugs resulted in major changes in clinical practice in the US.14 Clearly, the authors expect a similar outcome in Australia, suggesting that these new guidelines may even lead to “a net saving in the area of pharmacotherapy”. This is inconsistent with the more serious emphasis that the rest of the document puts on providing evidence-based care for many more young people. Importantly, it has been suggested that the fall in antidepressant use in the US was associated with an increase in suicides in young people.14 Previous population-based data have indicated a positive relationship between exposure to antidepressants and reduction in suicides. In those under the age of 18 years, most suicide attempts occur in the month before treatment and then decline sharply once treatment has commenced.15 We need to move beyond endless debate about the appropriate threshold for providing active care — the real treatment issue is one of appropriate sequencing of treatments. Wherever possible, clinical care should start with engagement of the young person and his or her family and then be linked with active provision of relevant information and evidence-based psychological therapies. A clinical staging model16 combined with appropriate stepped care may therefore offer a useful clinical approach. In a basic stepped-care model, those presenting with early or less severe forms of illness are initially offered appropriate non-pharmacological interventions. If the condition is more severe, the clinical situation worsens or the young person fails to respond to psychological therapies, then antidepressant therapy may well have a crucial role to play. The guidelines fail to emphasise the emerging importance of early intervention services. What is really required in Australia is a fundamental commitment to increase access to evidence-based care systems for young people from 12 to 25 years of age. While various state and national planning documents and the recent Council of Australian Governments decisions on health reform point the way for future service reforms, we still lack the real investment and commitment to turn these treatment guidelines into accessible and responsive clinical services systems.

Ian B Hickie AM, MD, FRANZCP · Patrick D McGorry PhD, FRCP, FRANZCP

Evidence concerning the safety of rosiglitazone continues to evolve In February 2010, the United States Senate Committee on Finance released a report on the safety of rosiglitazone.1 The report concluded that there were possible cardiac risks associated with rosiglitazone and that the manufacturer, GlaxoSmithKline (GSK), was aware of this well before it became public. The authors further stated that, rather than warn patients and regulatory authorities promptly, GSK executives chose to intimidate independent physicians who publicised the possible risks, minimise the impact of adverse findings, and downplay the possibly beneficial cardiovascular effects of the other available drug in the class, pioglitazone.1 A week before the Finance Committee report was released, an editorial by Steve Nissen, lead author of the meta-analysis that first raised cardiovascular concerns regarding rosiglitazone in 2007,2 was published online.3 The editorial related to an article on the increased risk of heart failure, a recognised adverse effect of glitazones, found in the Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycaemia in Diabetes (RECORD) trial.4 However, it was more a detailed account of the sequence of events surrounding rosiglitazone’s possible adverse cardiovascular effects, starting with its US approval in 1999. The editorial viewed the RECORD trial (the main results of which were published mid 20095 but not considered in the Finance Committee report) as underpowered, despite demonstrating that rosiglitazone was non-inferior to metformin or sulfonylurea for the primary endpoint of cardiovascular hospitalisation or death. Although there were no new safety concerns or efficacy data in either the Finance Committee report or Nissen’s editorial, there was a prompt media response. The New York Times, for example, highlighted a suggestion by the Finance Committee that if every diabetic patient in the US taking rosiglitazone was given pioglitazone instead, 500 heart attacks and 300 cases of heart failure would be averted every month.6 There was also a quick response from GSK, which categorically rejected the findings of the Finance Committee and the assertions of the New York Times in separate media statements, and published a point-by-point response to Nissen’s editorial.7 More recently, the results of a retrospective analysis of US Medicare data for older patients8 and an expanded meta-analysis from Nissen’s group,9 both suggesting adverse cardiovascular effects of rosiglitazone, have contrasted with a post-hoc analysis of data from the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes study, in which rosiglitazone was found to be of significant benefit in patients with established coronary artery disease.10 At present, rosiglitazone remains approved for use in Australia as monotherapy or as part of dual oral combination therapy with metformin or a sulfonylurea,11 although only the combination therapy is subsidised by the Pharmaceutical Benefits Scheme. The product information contains a boxed warning for patients with known ischaemic heart disease, particularly those taking nitrates, and highlights the increased risk of myocardial ischaemia found in pooled short-term clinical studies.11 In the US and Europe, rosiglitazone remains available despite the recent media reports. The US product information has similar warnings to those of the Australian version, while the European version has the general recommendation that the drug not be used by patients with ischaemic heart disease and/or peripheral arterial disease. One possible reason why rosiglitazone was not withdrawn in 2007 is that the statistical methods used in the original meta-analysis2 were questionable. Alternative reasonable approaches can yield increased or decreased risks that are either statistically significant or not significant for both myocardial infarction and cardiovascular death.12 As there are no trials with cardiovascular events as the primary endpoint showing benefit of pioglitazone over other therapies, the most compelling evidence for its apparently better cardiovascular profile comes from a similar meta-analysis to that for rosiglitazone.3 A cardiovascular disease outcome study of rosiglitazone versus pioglitazone is, therefore, justifiable and in progress (Thiazolidinedione Intervention with Vitamin D Evaluation [TIDE]; ClinicalTrials.gov NCT00879970). Nevertheless, TIDE might become a casualty of the recently reactivated controversy before it reports in 2015, as the Endocrinologic and Metabolic Drugs Advisory Committee of the US Food and Drug Administration (FDA) continues to review the ethical and clinical implications of the available rosiglitazone safety data. Although the debate about the safety of rosiglitazone has centred on cardiovascular risk, a further potential concern is fracture.13 The deleterious effects of glitazones on bone emerged in animal studies dating back to 1996. Unfortunately, despite knowledge of these data, neither glitazone manufacturer included prespecified bone loss parameters and endpoints in any clinical trial. However, retrospective analyses of data from blood glucose-lowering efficacy trials involving rosiglitazone and pioglitazone, reported in 2006 and 2007, respectively, confirmed an increased fracture risk in humans.13 Given that these drugs have been available in Australia and most other countries for only 10 years, their long-term effect on fracture rates is worrying, especially in postmenopausal women. Glitazone therapy can improve glycaemic control in patients with type 2 diabetes, but patients should be selected according to drug-specific contraindications and warnings, the glycaemic effect should be reviewed after at least 3 months to confirm response, and adverse effects including weight gain, fluid retention and reduced bone density should be monitored during continued use. The recent adverse publicity regarding rosiglitazone highlights issues that can arise when drugs are approved and marketed without definitive efficacy and safety data. There is a need for pharmaceutical companies, academia and regulatory authorities to use preclinical and early phase clinical data to identify, through careful phenotyping, the patient population with the most potential for benefit and the least potential for harm when new drugs are being evaluated for registration. One important consequence of the rosiglitazone controversy is that adequately powered Phase IV cardiovascular safety studies are now required by the FDA when new therapies for diabetes are registered.3 The promise of the glitazones was that they targeted one of the central pathophysiological defects in type 2 diabetes, namely insulin resistance, and improved markers of cardiovascular risk including serum C-reactive protein and microalbuminuria. Unfortunately, based on a variety of clinical trials and observational studies, they do not appear to have a consistent cardiovascular advantage over established blood glucose-lowering agents, including metformin and sulfonylureas.

Timothy M E Davis MB BS, DPhil, FRACP · Johannes B Prins MB BS, PhD, FRACP

I was happy in my retirement and living on the old-age pension with my husband when I had a call in early 2009 from Curtin University requesting a meeting to discuss cultural safety in Aboriginal health. You can imagine my surprise! Here I was, a 70-year-old retiree, content in the knowledge that I had worked and studied my way up from being a housewife and mother to being a respected Doctor of Philosophy, writer, and promoter of Aboriginal issues through my writing. I was full of curiosity to know the reason for this out-of-the-blue telephone call. Arrangements were made to meet with Associate Professor (now Professor) Sandra Thompson to discuss her proposition. I was to work as an Associate Professor for Cultural Safety in the Faculty of Health Sciences at Curtin University’s Centre for International Health, which had recently added Indigenous Health to its program. I started work there in April 2009. The cultural safety for indigenous health movement began in New Zealand during the 1980s when a Maori student nurse, Irihapeti Ramsden, queried hospital policy on standard nursing practices by saying “You people talk about legal safety, ethical safety, and safety in clinical practices and a safe knowledge base, but what of cultural safety?”1 Clearly, cultural safety was not on the nursing agenda. Irihapeti Ramsden instigated the cultural safety movement in New Zealand. Although the Treaty of Waitangi recognised the Maori as being the first people of their country, Maori nurses knew that the Treaty was not being honoured in the nursing fraternity.1 Maori nurses and patients were being isolated from mainstream nursing practices and treated as second-class citizens because of their cultural differences. Maori nurses wanted to be acknowledged and treated as equals in the workplace. The Maori nurses and patients had strong cultural ties and began to question why they should maintain nursing practices that were contrary to their own cultural beliefs and customs. Gradually the concerns of Maori nursing staff and patients in hospitals were recognised, and cultural safety is now embedded in most schools of nursing in New Zealand. The Nursing Council of New Zealand has amended its standards for registration to include safe cultural practices.1 Now the concepts of cultural safety, including cultural awareness and cultural competence, are being introduced into the Australian nursing system through the universities. Unfortunately, it is taking longer to change the colonial mentality and inherent racist attitudes towards Aboriginal people in this country than in New Zealand. We have over 200 years of invisibility and exile to overcome before Aboriginal people can attain the ideal status of equality. After joining the Centre for International Health at Curtin University, my interest in cultural safety grew and I realised that it was the solution to many health problems facing Aboriginal people. They needed to feel worthy as individuals and not be denigrated for being Aboriginal, with all the negative connotations that that image conjures up. If medical, nursing and other health organisations could forget the policies of the past and accept Aboriginal people as equals instead of patronising them and treating them as children, the health and hospital systems would have a better chance of reducing morbidity and mortality rates among Aboriginal people. As my own awareness of the cultural safety issues grew, I remembered the past and the government policies I had lived through over the years. Before the 1967 referendum,2 Aboriginal people were wards of the state governments and had no authority over their own lives. They were subject to laws and policies that enabled state governments to monitor their movements and enforce those laws if Aboriginal people dared to show initiative by making their own decisions. They were a subjugated people. However, due to the United Nations policy on indigenous rights, attitudes were slowly changing towards indigenous peoples worldwide. The Universal Declaration of Human Rights was adopted and proclaimed on 10 December 1948 at the General Assembly of the United Nations.3 All countries were to give citizenship to their indigenous people, and Australia was no exception. But the Aboriginal people of Australia did not know about the Declaration, and it was not until almost 20 years later that they were made citizens of this country. The 1967 referendum, in which Australians voted 90.77% in favour of Aboriginal people becoming citizens in their own country,2 was an important landmark for us because it meant we were no longer wards of state governments but were free citizens. Improvements to the living conditions of Aboriginal people living on reserves in Western Australia began by providing the basic necessities of life, such as having easy access to tap water (instead of carrying water in buckets from public taps) and having ablutions blocks with laundry, bathing and toilet facilities. Two-bedroom wooden-slab housing was erected (with no electricity) to replace tin shacks, tents and bough sheds. But no one thought about Aboriginal health except Aboriginal people themselves, when they needed medical and nursing attention. The health and wellbeing of Aboriginal people were in a sorry state. On the positive side, teenage Aboriginal children were being sent to Perth to further their education and obtain training in different careers. I was one of those children. However, it wasn’t until March 1956, when I began training as a nursing aide at Royal Perth Hospital, that the issue of Aboriginal health was brought to my awareness. Training Aboriginal girls as nursing aides (a new program implemented by the state government of Western Australia) had only begun two months previously. But I found that while the hospital system accepted Aboriginal patients, the health personnel were indifferent to Aboriginal needs. In fact, at this time, native hospitals were situated in many country towns, and Aboriginal people with chronic illnesses were mainly admitted to these hospitals. The treatment they received was passable, but there was a definite paternalism that hindered quality patient care. Being an Aboriginal nursing aide in the mainstream hospital system was difficult at times, and I experienced racism from staff and patients. For example, one time when I was working in a country town after completing my training, I needed to have my appendix removed. On the morning of the operation, I had a shower and considered myself clean. But, according to the ward sister, I hadn’t washed the navel area clean enough for her liking, so she sent me back to scrub myself again. What can I say? I was 18 years old and gauche, and arguing with the ward sister was out of the question. In retrospect, I realise that my personal hygiene was being called into question. I felt degraded, because I always showered every morning. Other examples of racism occurred with patients in other hospitals — some didn’t want me to touch them when I had to bed-bathe them or see to their personal needs. When I told the ward sister, she berated these patients, but it was horrible to know that many of these people judged me by the colour of my skin and not my work ethic. These days, racist attitudes have become more covert, and are a subtle mixture of paternalism, arrogance and the assumption of white privilege. But there is an even more serious lack of cultural safety for Aboriginal people when receiving nursing care (as patients) or giving care (as staff). My own cultural upbringing made it very hard for me to tend to the personal needs of Aboriginal men who were hospital patients. I felt uneasy when they needed assistance with their bed-baths or toilet needs. It was embarrassing for both parties because, as a woman, it was culturally taboo for me to be tending to a man’s personal needs. It was a matter of cultural protocols gone awry. Knowing and understanding Aboriginal protocols would be a starting point for many who work in the hospital system. Nevertheless there are many fair-minded Australians who want to improve Aboriginal health and the hospital system through introducing cultural safety to those who have the power to implement change. It needs to be widely recognised that achieving cultural safety in health programs for Aboriginal people will advance good health practices and boost positive health statistics through the acceptance of Aboriginal people for their differences from mainstream Australians. In other words, we are the first peoples in Australia — people in our own right, with our own cultures, customs and protocols. At the Centre for International Health, we intend to implement programs in the curriculum that will include Aboriginal studies and protocols for cultural safety in all schools of health. Talking to Aboriginal students in high school is also on the agenda because it is important for students to think about training for a career in health. Knowing and understanding Aboriginal protocols would be a starting point for many who work in the hospital system. I remember when my father was sick just before he passed away in 1992. The staff at Sir Charles Gairdner Hospital, in Perth, let members of the family visit him regardless of the time limit on hospital visits or the number of family members present. This was at a time when cultural safety was unheard of, but the hospital staff had the common decency to realise that my father had a large family and we all wanted to say goodbye. The human kindness shown by the hospital staff is remembered with gratitude and proves that cultural safety for Aboriginal people can be attained. In this instance, the nursing staff chose to show respect for a grieving family rather than passing negative judgement on us because we were Aboriginal people. The number of workshops and seminars teaching cultural awareness is increasing, but making people aware does not mean they are culturally competent or that they understand cultural safety as a health practice. People working in remote areas generally have more knowledge and acceptance of Aboriginal people than those who live in the cities and suburbs, although there are exceptions, as the above example of my family’s experience shows. Urban and foreign medical and nursing staff working in city and country hospitals should take a crash course in Aboriginal studies and protocols, as many have had no contact with Aboriginal people, let alone experience with treating them as patients. Aboriginal people themselves must change their attitudes to ill health, and understand the necessity of maintaining the treatment that medical and hospital personnel advise. For instance, diabetes sufferers should follow appropriate diets, have regular exercise and remember to take their medication. It is very important that Aboriginal people take responsibility for their own health, provided they are not too old, too young or too infirm to do so. They need to work with medical staff to find mutually acceptable solutions to combat their own or their family’s health problems. Working with medical and nursing practitioners would enhance the practice of cultural safety. Finally, to the question posed in the title of my essay: “Cultural safety in health for Aboriginal people: will it work in Australia?” — I believe it could work. Attitudinal changes of medical and nursing staff will change the status quo of Aboriginal health, and changing antiquated images of a past era is a step in the right direction. We can alter the negativity associated with Aboriginal people and their cultures by recognising their unique value to Australia’s past, present and future. If implementing and maintaining cultural safety for Aboriginal people means improving their wellbeing and survival, then it should be compulsory in all spheres of health practice in this country.

Rosemary van den Berg PhD

Objective: To estimate the cost of the extra time worked by Australian workers due to their co-workers’ alcohol drinking.Design, setting and participants: A secondary analysis of data obtained from 1677 Australian workers aged 18 years or older collected as part of a broader national study into the third-party harms of alcohol. Computer-assisted telephone interviews were conducted between October and mid December 2008.Main outcome measures: Self-reported measures of the time spent covering for other people at work because of their alcohol drinking; measures of other impacts from co-workers’ alcohol drinking; and self-reported income.Results: Around a third of Australian workers have experienced negative effects from their co-workers’ alcohol drinking, with 3.5% of workers reporting having to work extra hours to cover for others. The total annual cost to the Australian economy of this extra work is estimated to be $453 million.Conclusions: The results of this study suggest that Australian workers are significantly affected by other people’s alcohol drinking, at considerable cost. This finding highlights the significant cost to the workplace of alcohol consumption, extending previous work which has focused only on alcohol-related absenteeism.

Caroline E Dale BA, MSc · Michael J Livingston BAppSc, BInfTech, BA(Hons)

Objectives: To determine the extent to which children with a hospital admission related to assault or maltreatment or to a notified sexually transmitted infection (STI) have contact with the Western Australian Department for Child Protection (DCP), and to investigate injuries and conditions often associated with child maltreatment and subsequent contact with the DCP.Design, participants and setting: Retrospective cohort study using de-identified, record-linked child protection and hospital morbidity data to identify all children aged 0–17 years in Western Australia between 1 January 1990 and 31 December 2005, and a subcohort of children born in WA between these dates, admissions of these children to public and private hospitals in WA, and their contact with the Western Australian DCP.Main outcome measures: Annual trends in notifications and substantiations of child maltreatment; proportion of children with assault-related and maltreatment-related hospital admissions resulting in notifications, substantiations, or out-of-home care.Results: Most children admitted for maltreatment-related reasons (90%) had contact with the DCP, with 81% of these children being notified, 68% having maltreatment substantiated, and 50% entering out-of-home care. Specific injuries and conditions were associated with children who had greater contact with the DCP, including retinal haemorrhage, rib fractures, multiple injuries, STIs at under 14 years of age, and malnourishment.Conclusions: The health system effectively identifies and notifies real cases of maltreatment, and a high proportion of these are substantiated. Health data play an important role in improving maltreatment surveillance, providing opportunities to make valid comparisons over time and between jurisdictions, as well as to monitor conditions and injuries associated with child maltreatment.

Melissa O’Donnell GradDipEd, MPsych, PhD · Natasha Nassar BEc, MPH, PhD · Helen M Leonard MB ChB, MPH · Richard P Mathews BPsych, MA · Yvonne G Patterson BSc, MPsych, MBA · Fiona J Stanley MB BS, MSc, MD

Objectives: To describe the health service attendance patterns of urban Aboriginal and Torres Strait Islander (Aboriginal) Australians and make comparisons with those of the general Australian population.Design and setting: General practitioner-completed survey of all attendances over two separate 2-week periods in 2006 at an urban Aboriginal health service in Canberra, which provides services for about 3500 patients per annum.Main outcome measures: Standardised attendance ratios (SARs) for a range of health problems, using patients attending Australian general practice for the same reasons as the reference population.Results: Patients attending the Aboriginal health service were significantly younger than the Australian general practice patient reference population. The most common conditions managed were psychological, encompassing substance misuse; psychological problems accounted for 24% of all attendances. Patients attending the Aboriginal health service had higher rates of attendance for psychological conditions (SAR, 2.14; 95% CI, 2.01–2.28), endocrine conditions (SAR, 2.44; 95% CI, 2.29–2.60) and neurological conditions (SAR, 2.90; 95% CI, 2.71–3.09), as well as for circulatory, digestive and male and female genital conditions, than the reference population. Patients attending the Aboriginal health service had significantly lower attendance rates than the Australian population for respiratory illnesses, and conditions related to eyes or ears.Conclusions: At this urban Aboriginal health service, attendance patterns reflected complex health care needs that are different from those expected of a population of this age. Urban Aboriginal health service attendance appears to reflect significant ill health among the patients, aligning more with Aboriginal health statistics nationally rather than health statistics for urban non-Aboriginal Australians.

Karen M Flegg MB BS(Hons), FRACGP, MIPH · Christine B Phillips MB BS, MPH, FRACGP · Anne L Collins BA, BSc · Peter G Sharp MB BS · Meetali Kanagasundaram BSc(Hons), BBiomedSc, MB BS · Ray W Lovett BN, BHSc, MAppEpi · Marjan Kljakovic MB ChB, FRNZCGP, PhD

Objective: To implement and evaluate a multimodal intervention to improve osteoporosis treatment in patients with a fragility fracture.Design, setting and participants: Strategies to improve the management of patients discharged from an emergency department after presentation with fragility fracture were implemented prospectively in a large tertiary public hospital. Patients were surveyed by post to assess their awareness of osteoporosis and of the need for treatment. General practitioners and hospital clinicians completed an online questionnaire about their attitudes to osteoporosis and its management. A simplified consensus guideline was developed for local use. Our study was conducted between 1 October 2007 and 31 October 2008.Main outcome measures: Rates of referral of patients for osteoporosis review; rates of investigation and treatment.Results: Although most GPs (259/306 [85%]) accepted that it was their responsibility to assess and treat their patients and inform them of their osteoporosis risk, only 35/87 patients (40%) indicated awareness of their risk. After implementation of our project, the rate of bone mineral densitometry investigations improved from 6/200 (3%) to 39/87 (45%) (P < 0.05). The number of patients receiving calcium and vitamin D supplementation increased from 24/200 (12%) (for both supplements) to 29/87 (33%) and 32/87 (37%), respectively (P < 0.05). Initiation of specific treatments increased from 12/200 (6%) to 26/87 (30%) (P < 0.05). Referral of eligible patients to the Fragile Bone Clinic for osteoporosis review improved from 20/500 (4%) to 51/194 (26%). After being contacted by a fracture liaison nurse, 84% of these patients presented for osteoporosis review in the clinic.Conclusions: A major key to improving osteoporosis management is to actively identify all patients at risk and proactively engage and encourage them to seek assessment and management. A multimodal strategy involving a dedicated fracture liaison nurse may offer the greatest potential for improving education and patient follow-up and treatment.

Charles A Inderjeeth MB ChB, MPH, FRACP · Denise A Glennon MB BS, FRACP · Kate E Poland MB BS · Katherine V Ingram MB BS, FRACP · Richard L Prince MB BS, MD, FRACP · Victoria R Van BHSc · C D’Arcy J Holman MB BS, MPH, PhD

Objective: To examine the impact of a national current affairs television program about the association between osteonecrosis of the jaw and bisphosphonates on subsequent prescription use, fractures and deaths.Design and setting: National Pharmaceutical Benefits Scheme prescription data for 9 months after the television program were used to estimate the impact of reduced bisphosphonate use on fractures and mortality.Main outcome measures: Prescription rates, fractures and deaths.Results: The estimated reduction of 29 633 in the number of bisphosphonate prescriptions may have resulted in 70 hip fractures, 60 other fractures and 14 deaths that would otherwise have been prevented over the 9-month period of the study.Conclusion: Although it is important for patients to be informed of the risks of medication, media coverage that does not present a balanced view has the potential to do more harm than good.

Philip N Sambrook MD, LLB, FRACP · Jiang S Chen PhD · Judy M Simpson BSc, PhD · Lyn M March PhD, FRACP

Cystic fibrosis (CF) carrier testing can be used to inform reproductive decision making, allowing carriers to avoid having a child with CF. A government-funded, population-based CF carrier screening program would allow greater equity of access to this test. The setting in which CF carrier screening is offered significantly affects the extent to which participants make well informed, voluntary decisions to accept or decline testing. Screening offered before pregnancy and in non-clinical environments better promotes participant autonomy than screening offered in the prenatal consultation.

Lucy J Modra MB BS(Hons), BMedSci, GDipArts(Phil) · R John Massie MB BS, FRACP, PhD · Martin B Delatycki MB BS, FRACP, PhD

Objective: To identify factors associated with psychiatric morbidity and hazardous alcohol use in Australian doctors.Design, setting and participants: Cross-sectional postal survey of 2999 doctors (including all major specialty groups, trainees and general practitioners) insured with an Australian medical insurance company. The potential for psychiatric morbidity was measured by the General Health Questionnaire (GHQ), and the potential for hazardous alcohol use by the Alcohol Use Disorders Identification Test (AUDIT). The survey was conducted in 2007.Main outcome measures: Demographic, work-related and personality factors associated with a GHQ score > 4 and an AUDIT score ≥ 8.Results: Factors significantly associated with psychiatric morbidity in doctors were: having a current medicolegal matter, not taking a holiday in the previous year, working long hours, type of specialty, and having personality traits of neuroticism and introversion. Factors significantly associated with potentially hazardous alcohol use were being male, being Australian-trained, being between 40 and 49 years of age, having personality traits of neuroticism and extroversion, failing to meet Continuing Medical Education requirements, and being a solo practitioner.Conclusions: The mental health of medical practitioners is crucial to the quality of care their patients receive. Doctors should reflect on their hours of work and need for holidays. Involvement with medicolegal processes, such as lawsuits, complaints and inquiries, is a stressful part of medical practice today. Doctors need to be educated about these processes and understand how the experience may affect their health, work and loved ones.

Louise M Nash MB BS(Hons), BA, FRANZCP · Michele G Daly BSc(Hons), MSc · Patrick J Kelly BMath(Hons), PhD · Elizabeth H van Ekert BADipEd, MMedHum · Garry Walter MB BS, PhD, FRANZCP · Merrilyn Walton BA, MSW, PhD · Simon M Willcock MB BS, PhD, FRACGP · Chris C Tennant MD, MPH, FRANZCP

Concerns have been raised about the capacity of the health workforce to meet increasing future health care demands. Strategies aimed at improving workforce supply, at least in Australia, are focused heavily on education (ie, increasing the number of training places in key health professions) and recruitment (ie, recruiting overseas-trained health care professionals). Data from the 2006 Australian Bureau of Statistics census of population and housing indicate that while many Australians hold health professional qualifications, many are either not in the workforce or not employed within the health occupation they hold qualifications for. Some immediate solutions for increasing the health workforce are to attract qualified health professionals who are either not in the workforce or are working outside the health occupation back into their occupational role; to increase worker retention for those still working within the occupations they trained for; and to explore strategies for better retention of new graduates.

Matthew J Leach BN(Hons), ND, PhD · Leonie Segal BEc(Hons), MEc, PhD · Esther May BAppSc(OT), PhD

Older people living in residential aged care facilities (RACFs) are at considerably higher risk of suffering fractures than older people living in the community. When admitted to RACFs, patients should be assessed for fracture risk to ensure early implementation of effective fracture prevention measures. Routine or regular determination of calcium and phosphate serum levels in institutionalised older people is not indicated. Opinion is divided about the value of routine measurements of serum concentrations of 25-hydroxyvitamin D, parathyroid hormone and bone turnover markers. The non-pharmacological approach to fracture prevention includes multifactorial programs of falls prevention and the use of hip protectors. Vitamin D supplementation is recommended for all patients in RACFs. Dietary calcium intake should be optimised (1200–1500 mg per day is recommended) and supplementation offered to those with inadequate intake. The decision to prescribe calcium supplements should be guided by patients’ tolerance, whether or not they have a history of kidney stones, and emerging data about its cardiovascular safety. Bisphosphonates are the first-choice pharmacological agents for fracture prevention in older persons at high risk. Intravenous administration is as efficient as oral and has the significant advantage of better adherence. Use of strontium ranelate has not been tested on people in RACFs, but evidence in the “old-old” (those aged 75 years and older) suggests it could be a therapeutic option for fracture prevention in this setting. In general, teriparatide should not be considered as a first-line treatment for fracture prevention, particularly for people in RACFs.

Gustavo Duque MD, PhD, FRACP · Jacqueline J Close MD, FRCP, FRACP · Julien P de Jager FRACP · Peter R Ebeling MD, FRACP · Charles Inderjeeth MB ChB, MPH, FRACP · Stephen Lord PhD · Andrew J McLachlan PhD · Ian R Reid MD, PhD · Bruce R Troen MD · Philip N Sambrook MD, FRACP

Charles Bonnet syndrome (CBS) is a disorder in which psychologically normal people, often with vision impairment, experience complex visual hallucinations. The hallucinations are purely visual and do not occur in any other sensory modality, and people with CBS have full insight into the unreal nature of the hallucinations. This report describes the case of a CBS sufferer who experienced a distressing change in the nature of her visual hallucinations following a stressful event — the Black Saturday bushfires of February 2009. Clinical recordA healthy and alert 80-year-old woman presented for an orthoptic consultation in September 2009. The patient was legally blind (ie, her best corrected visual acuity was less than 6/60), with diagnosed age-related macular degeneration and closed-angle glaucoma. She had a known 4-year history of Charles Bonnet syndrome (CBS), a condition that caused her to have complex visual hallucinations, usually triggered when she was in unfamiliar surroundings. She reported that the nature of her hallucinations had changed significantly. Previously, the patient had experienced images such as “an elephant walking down the street with a child on its back” and intricate blue designs when looking at white plates or coloured carpets. While the patient was aware that the images were not real, occasionally her insight was delayed if the hallucination fit into the surrounding environment. For example, she would see a truck while travelling as a passenger in a car and, upon alerting the driver that they were about to collide with the truck, would be informed that it was a letterbox by the side of the road. When the hallucinations had first appeared, the patient had thought “there is something going on in my head” and reported her symptoms to her husband and then to her ophthalmologist, who explained the benign nature of the disorder. Since that time, she had not been troubled by the hallucinations, explaining “usually I can laugh at it”. Initially, the patient’s experience with CBS followed the typical pattern — she experienced hallucinations weekly that usually lasted only for several seconds. The patient’s hallucinations became atypical on “Black Saturday”, 7 February 2009, a day of intense heat and bushfires in the southern Australian state of Victoria. Bushfires raged in 14 regions across the state, resulting in 173 deaths.1 The patient lives in an area affected by the fires and was evacuated from her home on Black Saturday. That day and subsequently, she experienced hallucinations that were horrific in nature to her, such as seeing a prickly coat on her short-haired dog, spiral wire-like hair protruding from the heads of bald family members, and their faces beginning to melt, “like wax dripping”. She saw people’s legs covered with curly, black, wiry hair. Despite her visual impairment, the patient is a talented artist and has drawn her disturbing hallucinations (Box 1). The hallucinations that commenced on Black Saturday persisted for days, rather than seconds, and the images frightened the patient for the several days during which she experienced them. She reported experiencing great stress during the bushfires and also recalled earlier distressing episodes with significant fires as a child, while living in London: a chimney caught fire in her home; she witnessed the burning of the Crystal Palace in 1936; and she was present during the “Blitz” between September 1940 and May 1941, when London was subjected to intense aerial firebombing. She reported that these stressful episodes relating to fire increased her fear on Black Saturday and explained that “fire has a particularly bad effect on me”. Following discussion about CBS and her experiences, a review was not considered necessary from an orthoptic point of view, but she was encouraged to make contact as necessary if symptoms changed. She was also instructed to continue seeing her ophthalmologist and her psychologist. DiscussionThis case demonstrates that a stressful life event can change the nature of hallucinations experienced in CBS, with an accompanying change in emotional experience (from non-distressing to distressing). In general, hallucinations can result from false sensory input to the brain and occur in the absence of external stimuli. When a person presents with visual hallucinations, an underlying psychiatric disorder, neurological abnormality or drug intake can be suspected.2 Visual hallucinations can also occur as a result of lesions in the visual system, from the cornea to the cortex. The occurrence of complex visual hallucinations, as reported in this case, was first described by Swiss philosopher, naturalist and lawyer Charles Bonnet in 1760, after whom the disorder was later named. CBS is characterised by vivid, elaborate and recurrent visual hallucinations in psychologically normal people, who have full insight into the unreal nature of the hallucinations.3,4 The hallucinations are purely visual and do not occur in any other sensory modality. Images of complex patterns and people are most common, and the hallucinations often fit into the surrounding situation. They can appear for several minutes every week, and can continue to occur for 12 months or more. Often CBS occurs upon waking, but not exclusively so.5 Key features of CBS are listed in Box 2. Two theories have been proposed to explain CBS: the “release” and “sensory deprivation” theories. The release theory postulates that a lesion at any level of the visual pathway leads to the release of defective electrochemical impulses, thereby causing visual hallucinations. The sensory deprivation theory proposes a similar mechanism, except that it is reduced sensory input to the brain as a result of an ocular lesion that causes spontaneous discharge of neurones at the level of the retina or cortex.6,7 Triggers for the onset of CBS have not been clearly identified, and the circumstances the person finds themselves in at the onset of an episode can vary. It is possible that this patient suffered with acute stress disorder, as she had a past history of exposure to fire-related trauma and reported distressing recollection of the bushfires, but she did not report other symptoms of acute stress disorder.8 The change in nature of her hallucinations may represent interplay between CBS and an acute or post-traumatic stress disorder. The number of cases of CBS in Australia is not known. Reticence to discuss symptoms of CBS out of fear of being labelled insane is common. Most people only tell a family member about their symptoms and very few discuss the problem with a medical professional.5 Further, the symptoms of CBS are probably not always recognised and therefore correctly identified. As in this patient, CBS is usually associated with vision impairment, and it is important for clinicians to be aware that these types of hallucinations may occur in patients with advancing age and early vision impairment. The prevalence of CBS in people with impaired vision has been reported to be between 10% and 40%, with a much lower prevalence in Asian populations (< 1%).9-13 It is estimated that almost half a million Australians have vision impairment,14 and the prevalence of CBS hallucinations among these patients has been found to be 17.5%,5 suggesting that about 85 000 people in Australia may have CBS. However, while there is an association between CBS and loss of vision, it can also occur in individuals with no obvious ocular abnormality. There is no treatment of proven effectiveness for CBS, but the use of selective serotonin reuptake inhibitors has been associated with a reduction in hallucinations.15 Sporadic reports of effective medications can be found in the literature, but no controlled clinical trials have been published. Some sufferers indicate that closing their eyes or blinking may make the hallucinations stop.5 This case report highlights the limited knowledge about the underlying causes and triggers of CBS and the need for further investigation into this disorder. 1 Patient’s drawings of her disturbing hallucinations following the Black Saturday bushfires Family members with melted faces and spiral wire-like hair on their heads and legs, and a prickly coat on the patient’s short-haired dog. 2 Key features of Charles Bonnet syndrome Vivid, elaborate and recurrent visual hallucinations3 Experienced by psychologically normal people who have insight into the unreal nature of the hallucinations3 Risk factors include vision impairment, old age, hearing impairment, living alone, and female sex5 Reported prevalence is 10%–40% of the vision-impaired population; prevalence is skewed by non-reporting of the hallucinations for fear of being labelled with a psychiatric disorder5 Hallucinations typically last for several minutes and commonly occur upon waking5 There is no treatment of proven effectiveness6

Meri Vukicevic BOrth, PGDiplHlthResMthds, PhD

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

To the Editor: A recent article by O’Donnell and colleagues1 claimed contradictory results to a previous study which found that compensation was associated with worse health and return-to-work outcomes after injury.2 Their findings were similar to those of the previous study until they excluded a group of non-compensable patients because they had accessed private health insurance. The authors argued that “private health insurance was similar to other compensation agencies in that patients in this group had their health care costs met”. Using this argument, all patients would be compensable, as Australia has a universal health care system in which all Australians have their health care costs met. There is no precedent in the literature for such an exclusion. Compensation bodies provide additional payments beyond health costs, including payment for pain and suffering and income replacement. They also involve patients in a complex process with many features thought to influence outcomes (eg, the adversarial nature of making compensation claims and delays in receiving payments). We believe that the exclusion of private patients from the non-compensable group in the study by O’Donnell et al was incorrect and reduced the already small study sample, limiting the capacity to identify differences across groups. Furthermore, O’Donnell and colleagues found that compensable patients had higher anxiety levels at 24 months, until a supplementary analysis showed that, after controlling for stressful interactions with compensation agencies, compensation itself became non-significant. Surely stressful interactions are one of the mechanisms by which any compensation effect might be mediated. To say that an association is not significant once the mechanism of the effect is allowed for is akin to stating that smoking is not carcinogenic once the carcinogens are allowed for. O’Donnell and colleagues appear to be stating that simple access to compensation is not harmful, with which we agree, but fail to consider the complexities of compensation involvement. Both studies1,2 share a common limitation — that of comparing victims of transport-related injury with victims of other injury types. A recent study confirmed compensation and lawyer involvement as predictors of worse outcomes in a study of compensable and non-compensable transport-related trauma.3 A true understanding of the effect of compensation requires comparison of patients of comparable injury circumstances (eg, road trauma) and different compensation systems. Studies are clearly needed to establish a better understanding of the complexities of compensation delivery and the impact on outcomes. O’Donnell and colleagues’ conclusions have the potential to mislead compensation authorities and other stakeholders who should be focused on addressing this issue.

Belinda J Gabbe · Ian A Harris · Alex Collie · Peter A Cameron

To the Editor: In their recent study, O’Donnell and associates1 examined the effect of compensation, and the clinically vexing problem of interaction with insurance companies, on recovery after hospitalisation for trauma in Victoria. They concluded that access to compensation might not be associated with a poor outcome per se. We agree that the relationship between compensation and health outcomes is complex, but believe there are a number of conceptual and methodological issues that undermine their findings. First, as they note, this sample of injured people might not be representative of those making an insurance claim. In an earlier study of motor vehicle accidents in New South Wales,2 less seriously injured victims who only attended their general practitioner or spent less than a day in hospital comprised as much as 70% of those seeking compensation. Furthermore, the article by O’Donnell and colleagues provides no description of any differential attrition with respect to factors that may be associated with poorer psychosocial outcomes (such as previous psychiatric disorders), other than sex and acute hospital factors. The outcome measurement characteristics change in the course of the analyses, potentially undermining power to detect any differences. For example, the quality-of-life and disability measures become dichotomised using norms in the population for the modelling, rather than as scores in the baseline characteristics as in Boxes 2 and 3. This approach has the potential to conceal true differences between the groups because of regression to the mean and baseline differences in both groups. The main problem relates to the possibly post-hoc exclusion of privately insured subjects from one group. We do not believe that private health insurance can reasonably be considered to be “compensation”. It can provide money to cover the cost of inpatient treatment and very limited outpatient services, but provides no more recompense and retribution for injury than Medicare. Older and wealthier Australians disproportionately hold private health insurance. This group is likely to differ on a number of factors, many of which are associated with better psychosocial outcomes. Although the authors have evaluated some demographic factors, this is likely to have introduced some potentially significant confounding. Thus there is little justification for the removal of this group from the non-compensable group alone. We would be interested to see an analysis after the removal of subjects with private health insurance from both groups. This would allow a more rigorous examination of the effect of one factor — actual insurance compensation — on recovery outcomes.

Nicholas S Glozier · Matthew Large

To the Editor: O’Donnell and colleagues seek to extend and improve on previous research into the relationship between compensation status of injuries and medium-term health outcomes.1 Improvements are needed because much of the empirical analysis in this area has had major methodological limitations.2 Their analysis uses an impressive array of mental health measures to probe the “compensation effects”. However, several aspects of the study design raise questions. First, with very few exceptions, the transport accident compensation scheme in Victoria covers all injuries arising from transport accidents. It is therefore unclear how a quarter of patients in the non-compensable group could have suffered injuries due to motor vehicle accidents (MVAs) yet have fallen outside the scheme. Second, the purpose of control variables in a multivariate model is to address potential confounders of the relationship between the predictor of interest (MVA compensability) and the outcomes (measures of health status at 24 months). Using significant univariate differences between the predictor of interest and other covariates as the basis for selecting control variables is statistically inappropriate, and this approach may have affected the results of the regression analyses. Third, a key study finding is that significant differences in health outcomes were detected between MVA-compensable and non-compensable patients at 24 months after injury. These then “all but disappeared” when the non-compensable group was altered by shifting three patients who had accessed Transport Accident Commission compensation over to the MVA-compensable group and dropping 54 patients who had accessed “other forms of compensation”. The result casts the spotlight on the removed group. It suggests that their mean health status at 24 months was relatively high. But who were they? Little information is provided, other than that nearly two-thirds (36/57) had private health insurance and were dropped for this reason. (In our view, private health insurance should not be construed as compensation, because policies tend to be highly selective about services covered and generally do not provide payment for lost income or non-economic losses.) Another possible explanation, not addressed, is that with only 88 patients left in the non-compensable group, the multivariate analyses lacked power to find differences. The relationship between compensation availability and injury recovery is complex. Policy interest in the relationship looks set to increase in the next few years, as the federal government explores the merits of a national disability scheme.3,4 In this environment, the need for rigorous research and reliable findings will be greater than ever. O’Donnell and colleagues’ welcome contribution to the evidence base should stimulate further debate about how best to disentangle the effects of injury compensation systems on the health outcomes of Australians who call upon them.

David M Studdert · Harold Luntz · Genevieve Grant

To the Editor: As noted by O’Donnell and colleagues,1 there is a growing body of evidence suggesting that provision of compensation is associated with poor recovery after injury. Most of this evidence arises from international workers compensation jurisdictions. However, two recent Victorian studies have examined health and work outcomes in compensable and matched non-compensable groups after transport injury.1,2 Despite examining broadly similar patient groups and using broadly similar outcome measures, the two articles reach very different conclusions. There has been substantial community reaction to these findings. Gabbe and colleagues’ suggestion that compensation is associated with poor recovery2 provoked public criticism of its methodology from the Law Institute of Victoria, and a prominent plaintiff legal firm released a public statement3 3 days after publication of the study by O’Donnell et al. There is a disconnection in conceptualisation of this issue between the research community and those involved in compensation regulation and policy. Researchers are focusing on the question “Does compensation lead to poor health outcomes?”, while the more nuanced policy question attracting the attention of many injury compensation regulators is “Which, if any, aspects of the compensation scheme have a positive or negative impact on health, vocational and social outcomes?”. Close inspection of the published literature suggests that there are individual components of compensation systems that may have a negative impact on outcome, including the provision of payments for pain and suffering4 and the provision of income benefits.5 There are also examples of compensation organisations acting to improve outcomes via their broader remit as government regulators. For example, the Transport Accident Commission was a major driver of the reorganisation of the Victorian state trauma system, which has resulted in a significant reduction in mortality after road trauma.6 O’Donnell and colleagues1 note the complex relationship between compensation and health outcomes, with particular reference to patient characteristics. The compensation schemes themselves are also highly complex. However, there has been very little research effort directed towards identifying the impact of specific scheme components on patient outcome. In Victoria, the two major injury compensation regulators have funded the Institute for Safety, Compensation and Recovery Research to address this issue. This level of interaction between policymakers and researchers is needed to improve outcomes for those injured in transport- and work-related accidents.

Alex Collie · Niki Ellis

In reply: We thank the authors of the above letters for their comments. Our response will focus only on the major themes raised. We note the concerns about excluding people with private health insurance. The issue here is not whether having health care costs met by private health insurance is the same as having motor vehicle accident (MVA) compensation entitlements. Rather, it is whether access to private insurance payments for health care is the same as not having any compensation at all. We argue that injury patients with private insurance have access to a broader range of health care services and providers than those in the public system, and can access these services more quickly because they avoid long public sector waiting lists. The suggestion that patients who are dependent on public health care in the 2 years following injury (non-compensable patients) receive the same health care as those who have private insurance is unjustified. Most studies to date have not considered other schemes such as private insurance, ignoring the potential impact they may have on health outcomes. We recognise that there may be demographic differences between patients who are involved with other schemes such as private health insurance, and these factors may contribute to outcomes. In noting the inherent limitation in this approach, we nonetheless argue that there are also limitations to including these patients, and therefore an analysis that excludes privately insured patients is a valid addition to the literature on compensation. In response to the point raised by Gabbe and colleagues, we note that our analysis showing that “stressful interaction with the compensation agency” accounted for variance in anxiety scores was designed to investigate potential mechanisms that may explain why anxiety was higher in the MVA-compensable group. We did not conduct the analysis to argue that this group was not more anxious than the non-compensable group. They were more anxious. Glozier and Large were concerned that differential attrition may affect comparisons between the two groups. To clarify, there were no significant baseline differences between completers and non-completers on any measure. Their second issue relates to the removal of patients with private health insurance from the analyses. To clarify, we removed anyone who indicated at 24 months that they had accessed private or other forms of compensation, regardless of their original compensation classification. Studdert and colleagues were concerned that we used univariate differences to identify control variables. We adopted this process to replicate the statistical methodology used by Gabbe et al,1 in an attempt to replicate their findings. In conclusion, our study illustrates the complexity of compensation research and the importance of carefully defining populations — a point that has not yet been adequately addressed. Indeed, a recent review of the literature argues that most compensation research is methodologically limited.2 We agree that there are limitations to our methodology, as there are in previous studies, and recognise that conducting this kind of research is inherently difficult. We welcome the establishment of the Institute for Safety, Compensation and Recovery Research, noted by Collie and Ellis, and its support of this challenging and complex research.

Meaghan L O’Donnell · Mark C Creamer · Richard A Bryant · Alexander C McFarlane · Derrick Silove

To the Editor: I would like to clarify some of the statements made about the National Coroners Information System (NCIS) in the article by De Leo and colleagues.1 The article cites a study conducted by the NCIS concerning the presence of intentional self-harm determinations in coronial findings. Unfortunately, De Leo and colleagues did not note that this study was an internal and informal review of a small random sample of findings conducted by the NCIS that examined disparities between codes assigned on the NCIS and coronial findings. On the basis of this limited study, I would not endorse the statement (which was attributed to me) that “nationally, 29% of coroners omit reference to intent”. Further, it is important to note that NCIS staff do not assign intent codes on entries in the NCIS, and that this coding is performed by clerks in each of the coroners’ offices. The statement in the article that “the NCIS judged 111 (39%) as involving intentional self-harm” is therefore misleading, and should instead have indicated that the coding on the NCIS showed 111 deaths (39%) as involving intentional self-harm. I acknowledge that De Leo and colleagues did not intend to mislead readers as to the work of the NCIS.

Jessica D Pearse

To the Editor: I applaud the Medical Journal of Australia’s recent attempt to increase the evidence base of complementary medicine.1 However, it is disappointing that the Journal’s idea of doing so seems to be to import the same dogmatic and misinformed debate currently occurring in the United Kingdom. Ernst makes little secret of his antihomeopathic agenda and engages in some “cherry picking” of his own, neglecting, for example, to mention the substantial methodological criticisms of some of the references he chooses to use to support his points.2 Further, expert testimony at the British House of Commons Science and Technology Committee’s evidence check on homeopathy identified 24 condition-based systematic reviews and meta-analyses on homeopathy, of which nine were positive, five were negative and 10 were inconclusive.3 As a system of medicine, this compares more closely with the evidence base for conventional medicine than many would care to admit.4 It has also long been observed that the complex and individuated nature of complementary therapies — and many conventional therapies, for that matter (including many surgical and psychological interventions) — makes clinically relevant evaluation with a placebo-controlled trial difficult.5 Cochrane reviews may certainly be “the best” at reviewing the trials, but this means little if those trials were not an appropriate evaluation tool in the first place. Rarely do these trials reflect the real-world settings in which patients, medicines and practitioners exist. The challenge is not simply to be better than placebo, but to produce the largest clinical effect possible in a real-world setting. In his article,1 Ernst himself seems to acknowledge the potential broader real-world benefits that patients receive from homeopathic treatment, as confirmed by observational data,6 yet seems inclined to focus only on reductionist approaches to evaluation that are well known to be ill suited to homeopathic research, or focuses on the implausible nature of the medicine itself. We need to take a different approach and work out why it is that patients who choose to use homeopathy get better (as they quite often do). To do this, we need not just more basic and clinical research, but more health services and public health research on homeopathy — reviewing the reviews adds little if there is simply not enough to review in the first place. Throwing out the baby with the bathwater helps no-one, least of all the patient. And the patient, not ideology, is what it should be all about.

Jon L Wardle

In reply: Wardle’s letter raises several points that deserve comment. Wardle calls me dogmatic, misinformed and antihomeopathic. Such ad hominem attacks hardly promote a rational debate. When I started my job of scrutinising homeopathy 17 years ago, I was pro-homeopathy1 — I once worked in a German homeopathic hospital — and became more sceptical as the evidence base for homeopathy became more clearly negative.2 This, it seems to me, is the opposite of dogmatic. Wardle cites the report by the House of Commons3 in the United Kingdom and claims that it “identified 24 condition-based systematic reviews and meta-analyses on homeopathy, of which nine were positive . . .”. In truth, it was a submission from homeopaths to the House of Commons that made this statement. The report itself found no positive evidence for homeopathy and even criticised how the homeopaths tried to mislead the inquiry.3 Wardle also thinks that clinical trials are “ill suited” to evaluate homeopathy because homeopathy is “complex and individuated” and clinical trials “rarely . . . reflect the real world”. The notion here is that, if the scientific method does not support our belief, it must be the former rather than the latter which is at fault. Adopting this attitude would take us right back into the Dark Ages. After discussing these issues for 17 years, I have the impression that most homeopaths are in favour of rigorous, reductionist science — insofar as it generates the results they want. Whenever this is not the case, they point to observational studies that are wide open to bias and confounding, and therefore show us precious little. Finally, Wardle seems to imply that homeopathy works because patients like it and that this is what truly helps patients. The truth is that medicine has made huge advances only since we buried this attitude. It is time now that proponents of homeopathy do the same — not to conform with a dogma, but because patients would live longer and healthier lives.

Edzard Ernst

To the Editor: At the risk of appearing self-serving, we refer to our recently published article in which we recommended that there should be “greater uniformity in [food] packaging design, colour and descriptions”.1 In light of the Australian Government’s recent mandate on plain packaging for tobacco products,2 we can see no reason why this should not be extended to processed foods possessing no redeeming nutritional qualities. This would include soft drinks, potato chips, a great many of the so-called foods offered as replacements for fruit in children’s school lunches, biscuits and sweets. We challenge the Prime Minister and Minister for Health to do this, or explain why they won’t.

Bebe Loff · Brad R Crammond

A 38-year-old woman presented with sudden onset of haematemesis and melaena. She had no abdominal pain or jaundice, and she had not taken drugs before the bleed. On examination, she had cutaneous features of neurofibromatosis (Figure, A). Upper gastrointestinal endoscopy showed a smooth polypoidal mass, with central umbilication, in the body of stomach (Figure, B). A contrast-enhanced computed tomography scan of the abdomen showed an exophytic mass confined to the stomach. Following another haematemesis, the patient underwent an emergency sleeve resection of the mass. Histopathological examination of the removed tissue revealed spindle-shaped neoplastic cells with elongated nuclei arranged in fascicles (Figure, C), and immunostaining (Figure, D) was positive for CD117 (c-KIT), confirming gastrointestinal stromal tumour (GIST). The prevalence of GIST in neurofibromatosis type 1 (NF1) varies between 4% and 25%.1 The clinical presentation of GIST associated with NF1 is similar to sporadic GIST but differs in being multiple; large, often involving the small intestine; and having a favourable prognosis.1 Several cutaneous syndromes are associated with gastrointestinal haemorrhage as a prominent feature. Prompt recognition of these disorders is required as early intervention can be life saving.

Pazhanivel Mohan · Mohan Kaduganoor Ramakrishnan · Jayanthi Venkataraman

Functional histology. 2nd ed. Jeffrey B Kerr. Sydney: Mosby Elsevier, 2010 (viii + 512 pp). ISBN 9780729538374. Histology can be a dry subject. In medical curricula, it has suffered variably from overexposure to underexposure, to the point where graduates may feel perfectly comfortable identifying normal tissues under the light microscope, or squirm uncomfortably when confronted with the same at a multidisciplinary meeting. Finding a balance between pure information and visual references can be difficult and, to paraphrase Elvis, the reader is likely to plead, “a little less longwinded text, a few more pictures please”. The second edition of Functional histology, by Jeffrey Kerr, strikes a good balance. The book has numerous clear, vivid light micrographs, excellent electron micrographs, and superb drawings and diagrams aimed at describing and explaining the organisation and function of body tissues. Traditionally laid out in systems, the text tells an interesting story for each organ, taking the reader through the structure, microscopic appearance, physiology, and function of each tissue, before delineating common abnormal conditions and clinical features. Kerr, an Associate Professor of Anatomy and Developmental Biology at Monash University in Melbourne, says he prepared Functional histology for “those with an interest in biological science as applied to the health professions and for the research community”. The book more than accomplishes this goal, being suitable for a range of users from medical students and pathology registrars through to researchers in the biological sciences. It is distinguished from other works in the discipline by the use of concise, plain language. The useful, friendly “tips”, scattered throughout the text, further engage the reader. The addition of topical references to molecular biology keep the content current and this, together with the text’s accessible style, will maintain the interest of those returning to histology for the purposes of research or postgraduate study.

Tanya Grassi

Clinical examination. A systematic guide to physical diagnosis. 6th ed. Nicholas J Talley, Simon O’Connor. Sydney: Churchill Livingstone, 2010 (xviii + 478 pp). ISBN 9780729539050. “Talley and O’Connor” just keeps getting better. Written by Australian clinicians Nicholas Talley, currently Professor of Medicine and Epidemiology at Mayo Clinic in the United States, and Canberra-based cardiologist Simon O’Connor, the book was already an accessible and thorough guide to physical examination. Each successive edition brings extra features. This sixth edition has tables of differential diagnoses for abnormal signs, more anatomical illustrations, and new sections on “examination anatomy”. There is useful advice on the examination of patients with a variety of important or common problems, and coverage of examination of the eyes, ears, nose and throat has been expanded. Many of the photographs of pathological signs and of physical examinations are clear and memorable. The art of physical examination is evolving into a quantifiable science, and this edition adds information about interobserver reliability to the very important positive and negative likelihood ratios for key physical signs. The accompanying DVD contains sequences illustrating a systematic approach to physical examination, hints on objective structured clinical examinations with suggestions for a more focused approach to a wide range of clinical problems, and libraries of images and electrocardiograms. The libraries would be useful for revision and self-testing as the accompanying text can be turned on or off. A website allows the full text to be searched online. Inevitably, I have some criticisms. The paragraph on taking a history of illicit drug use is overly short and omits important issues. And if the patient was lying on a low bed, as in the DVD, I would prefer to palpate the abdomen from a sitting or kneeling position — or raise the bed! The escalating assessment of suicide risk should include questions about acts, not just feelings, thoughts and plans. But these are mostly minor points. The book remains excellent value for money, is a sound guide for students, trainees and more experienced clinicians working beyond their speciality, and is highly readable with a leavening of sly humour.

Timothy P Usherwood

MMR, Wakefield and The Lancet: what can we learn? Julie Leask, Robert Booy and Peter B McIntyre MJA 2010; 193 (3): 192 Missing text: In “MMR, Wakefield and The Lancet: what can we learn?” in the 5 July 2010 issue of the Journal (Med J Aust 2010; 193: 5-7), a line of text was omitted in the third-last paragraph (page 6). The text, from the beginning of the paragraph, should be “Second, public communication about vaccine risk, particularly regarding responses to adverse events following vaccination in new vaccine programs, needs to be planned, and should involve multiple stakeholders, as new issues can arise with little warning. This occurred as recently as 23 April 2010, when Australia’s Chief Medical Officer advised a temporary suspension of the 2010 trivalent seasonal influenza vaccine to children 5 years of age and under.15”

Julie Leask · Robert Booy · Peter B McIntyre

On being lactose intolerant Most people with presumed lactose intolerance or lactose malabsorption can tolerate a cup of milk — according to the US authors of a systematic review. Shaukat and colleagues identified 36 unique randomised studies of individuals with lactose intolerance or malabsorption. They found that 12 to 15 g of lactose — approximately one cup of milk — is well tolerated by most adults. Symptoms occurred with increasing doses, with substantial symptoms reported in most studies testing the effects of 50 g of lactose. The researchers found there was insufficient evidence to determine the effectiveness of various treatments for lactose intolerance, including lactose-reduced milk, yoghurt, probiotics, the antibiotic rifaximin, and colonic adaptation. Ann Intern Med 2010; 152: 797-803 Suicide and the luminous veil In 2002-2003, the “luminous veil” — a 5 m high barrier — was constructed at Bloor Street Viaduct in Toronto to prevent suicides. Prior to the barrier being put in place, Canadian researchers Sinyor and Levitt said that the viaduct had the dubious distinction of being the second most popular bridge for suicide studied in the world, after San Francisco’s Golden Gate Bridge. Four years later, although the barrier had prevented any further suicides from this bridge, it had no effect on rates of suicide by jumping in the region.1 In a linked editorial, Gunnell and Miller said jumping was a relatively rare method of suicide and more promising targets for reducing the incidence of suicide may be methods that are more commonly used, highly lethal and readily accessible — such as toxic pesticides in developing countries and firearms in the United States.2 1. BMJ 2010; 341: c28842. BMJ 2010; 341: c3054 No smoking in public housing? In Australia, from 2012 all tobacco products will be sold in standardised plain packs. Chapman and Freeman have said that this vanguard decision by the Australian Government could bring down the curtain on a century of the tobacco industry packaging carcinogenic, addictive products in attractive, beguiling boxes.1 Now, US authors have called for the US government to put a blanket ban on smoking in all public housing.2 Winickoff and colleagues reported that only 4% of Public Housing Authorities in the US have voluntarily opted to ban smoking in their public housing units. Federal regulation or contractual mechanisms would ensure that non-smoking policies were implemented in all public housing. In their view, an individual’s right to smoke would be over-ridden by a greater need to protect the vulnerable people who live in public housing from the harms of exposure to tobacco smoke. 1. BMJ 2010; 340: c2436 2. N Engl J Med 2010; 362: 2319-2325 Trialling physician assistants The Feldsher — an assistant to the doctor — was used by the Russian army during the 17th century. Since that time, the fortunes of this health professional have waxed and waned. Today, the United States may be the only country using physician assistants (PAs) but there are more than 50 000 of them in current practice. Ho and colleagues reviewed the evidence for the use of PAs in health care delivery, finding that PAs have been shown to provide safe and high-quality care in surgical units, working best under the supervision of a consultant. With the widespread shortage of health care professionals, several countries are trialling PAs, including Canada, England, Scotland, the Netherlands, South Africa and Taiwan. Australia has joined this group with two PAs, both US-trained, involved in a pilot trial in a South Australian hospital. So far, these PAs have been generally well accepted by staff and patients. ANZ J Surg 2010; 80: 430-437 Top surgeons Harrier fighter pilots outperform both medical and non-medical undergraduate students in executing simulated laparoscopic surgical training tasks. Tsim and colleagues put 25 medical students, nine non-medical students and eight Harrier fighter pilots through their paces, asking them to complete four simulated tasks, including a bile duct cannulation and an appendicectomy. The Harrier pilots not only made fewer errors than the students, they were also quicker than the medical students in completing the appendicectomy task. The researchers said more laparoscopic simulation training could be offered to doctors. They also made the point that pilots are selected by aptitude for the role, including strong hand-eye coordination and spatial awareness. Perhaps surgical trainees might be similarly selected — as such candidates would likely require less time to reach competency. Ann R Coll Surg Engl (Suppl) 2010; 92: 58-61

Ann T Gregory