Volume 194 Issue 6

An estimated four out of five Australians with coeliac disease are undiagnosed — we need greater awareness and increased testing According to criteria published in 1990, which remain the most widely accepted, the diagnosis of coeliac disease is based on typical histological features of the small intestine of an individual on a gluten-containing diet: villous atrophy, crypt hyperplasia and intra-epithelial lymphocytosis.1 Serological tests for coeliac disease, such as for endomysial IgA or transglutaminase IgA, are predictive, but alone are not sufficient for diagnosis. The diagnosis of coeliac disease is confirmed by clinical, serological or histological improvement on a gluten-free diet.1 To become a member of a state coeliac society in Australia, a person requires a doctor’s letter indicating a medical need for a gluten-free diet. As a result, over 80% of members have biopsy confirmation of coeliac disease; this is also the case in the United Kingdom. Over the past 10 years, there has been a steady compound annual growth of a little less than 10% in new memberships for coeliac societies in the UK and Australia (Norma McGough, Head of Diet and Health, Coeliac UK; Graham Price, President, Coeliac Society of New South Wales; and Jane Davies, Executive Officer, Coeliac Society of Victoria, personal communication). Both countries have now developed active education programs for doctors in family medicine. It appears that these programs have been successful in increasing serological testing and reducing the “backlog” of symptomatic patients with coeliac disease who were previously unrecognised.2 Today, coeliac disease is very much a diagnosis made in adulthood; children under the age of 10 years make up only 11% of new members joining coeliac societies in the UK and Australia, while the median age of new members is 40 years. However, best estimates, based on there being about 1% prevalence of coeliac disease in Western populations, suggest that no more than one in five Australians with coeliac disease are now diagnosed.3,4 Finland, where about 0.5% of the total population have now been formally diagnosed with coeliac disease,5 is accepted as having the most coeliac-aware health system. Australia still has a long way to go to achieve the level of awareness present in Finland, where gluten-free Big Macs have been available for more than 20 years and restaurant menus routinely indicate whether food is gluten free. Although awareness of coeliac disease has generally been low in the United States, a recent report by Mayo Clinic suggested that in Olmsted County, the home of Mayo Clinic, as many as 0.35% of the local community have been formally diagnosed with coeliac disease, suggesting a 35% ascertainment rate.6 It was also reported that no additional mortality was observed in the residual group of individuals with unrecognised coeliac disease in Olmsted County, suggesting that aware physicians and prompt, appropriate diagnosis of symptomatic coeliac disease are effective in minimising serious complications.7 Conversely, very low clinical awareness of coeliac disease, observed by researchers of historical cohorts in Germany and the US, is associated with substantially increased mortality, usually caused by malignancies and infection.8,9 Experience in Finland also supports the principle that high levels of clinical awareness and diagnosis minimise morbidity and mortality among individuals with unrecognised coeliac disease.10 Three reports, including one published in July 2010, suggest that, because of the rise in the disease’s prevalence, progress in clearing the backlog of undiagnosed coeliac disease may be slower than we thought.5,8,9 In Finland, the prevalence of coeliac disease doubled from 1% to 2% between 1979 and 2000, while diagnosed coeliac disease increased from 0.03% to 0.52% of the population.5 In the US, Mayo Clinic researchers showed that the seroprevalence of coeliac disease rose almost five times, from 0.2% to 1%, between 1950 and 2000.8 Now researchers have shown that, in a cohort of mostly adult volunteers in Maryland, US, who were enrolled in 1974 and followed up in 1989, the seroprevalence of coeliac disease more than doubled from 0.2% to 0.5% in 15 years.10 Those who showed seroconversion between 1974 and 1989 were all adults, indicating that coeliac disease does not necessarily begin in childhood. Data from Finland also show that the prevalence of coeliac disease in older people is double that in children.11-13 Although confirmation of coeliac disease by biopsy is ideal, these new epidemiological insights are reshaping our understanding of coeliac disease and should better inform clinical practice. No longer can we assume that a single serological test for coeliac disease is adequate to exclude coeliac disease for life. The only test that seems capable of excluding coeliac disease for life is HLA-DQ genetic testing.14,15 Absence of genes encoding the susceptibility antigens HLA-DQ2 or HLA-DQ8 effectively excludes coeliac disease; however, over a third of European populations possess these genes, while only 1% to 2% of the population has coeliac disease.16 Increased testing for coeliac disease using transglutaminase IgA and the new generation “deamidated gliadin peptide” IgA and IgG, and more systematic collection of small bowel biopsy samples by endoscopists, will steadily define those patients with coeliac disease who have a clear medical need for a strict gluten-free diet.17,18 The popularity of the “fad” gluten-free diet might be peaking,19 but the medical need for gluten-free diets continues to rise.

Robert P Anderson MB ChB, PhD, FRACP

How one man’s vision to fund health research grew to become the country’s largest non-government funder of research into mental illness This year marks the 30th anniversary of the founding of Australian Rotary Health (ARH), a uniquely Australian organisation operating under the auspices of Rotary International (a worldwide organisation of humanitarian service clubs) that allows Rotary clubs to support health research. From small beginnings, ARH has evolved to become a key non-government funder of research relevant to preventing and treating mental illness. ARH had its birth in 1981, when Ian Scott, a bank manager from Mornington in Victoria, heard a radio interview about the tragedy of sudden infant death syndrome (SIDS) and the lack of funding available for research into the problem. He resolved to do something about it. As a member of Rotary, Ian approached his club with an ambitious proposal to set up a research foundation, with a principal of $2 million to provide funds for health research, and the initial grants to be allocated to research into SIDS.1 Scott’s aims were achieved within a few years. By 1983, the Australian Rotary Health Research Fund had been established, and in 1985 the first grants were given for research into SIDS. By 1987, the initial goal of raising $2 million had been reached through appeals to Rotary clubs and Rotarians to donate some of their fundraising money to ARH. The organisation had spectacular success with its initial grant funding, when a study investigating the incidence of SIDS in Tasmania identified prone sleeping position of infants as a key risk factor.2 Within 5 years of this finding, promotion to parents of the importance of infant sleeping position led to a dramatic decline in the incidence of SIDS.3 Subsequently, ARH gradually grew and supported research in a range of other areas including environmental health problems of the aged, adolescent health, family health, Ross River virus, and first aid and emergency care. A major change in direction occurred in 2000, when it was decided that ARH would fund mental illness research. This decision was in response to the Global Burden of Disease Study, which found that mental illness was a major source of disease burden and the biggest source of disability globally,4 and findings from the 1997 National Survey of Mental Health and Wellbeing, which showed that around one in five adults in Australia were affected with mental disorders in a 12-month period.5 The move into mental illness research was strongly supported by senior policymakers in the then Commonwealth Department of Health and Aged Care.1 Support for mental illness research has continued for over a decade, and ARH is now the largest non-government funder of research in this area. During this time, ARH has also offered PhD scholarships and postdoctoral fellowships, and supported research symposia. Support from ARH has complemented research funding provided by the National Health and Medical Research Council (NHMRC) by focusing on more applied projects, particularly intervention research, that offer more immediate benefits to the community. ARH has also supported work in its earliest stages, when research questions and ideas are still evolving and data are needed to guide planning for larger-scale proposals. It has been a major source of support for emerging areas such as prevention of mental illness in children and adolescents, and innovative approaches to treatment such as e-therapy. A strong partnership has developed between ARH and the Australian Government Department of Health and Ageing, which has encouraged ARH to broaden its focus beyond supporting research. This reflected the recognition by policymakers that Rotary clubs had the potential to play an important role in destigmatising mental illness, because their membership encompasses influential members of local communities who could lead the way for greater understanding and acceptance of people affected by mental illness. To facilitate this work, the Department funded ARH to run community forums on mental illness across Australia. This involved Rotary clubs organising meetings in their local community where mental health professionals, people with mental health problems and carers presented information and personal experiences, and local mental health services promoted what they had to offer. More recently, the Department has engaged ARH to increase community understanding of mental illness by supporting Rotary clubs to deliver Mental Health First Aid courses in their local communities.6 Despite the significant support that ARH provides to Australian health research, the demand for funding continues to greatly exceed the available funds. In 2010, ARH was only able to fund 10% of applications it received for mental illness research projects. To overcome this problem, ARH is broadening its base of support beyond Rotary clubs, which have to date been the major sources of donations. In 2011, ARH will launch a national appeal to the Australian public for funding to support mental illness research. Over 30 years, ARH has grown from one man’s vision to fund health research to become an organisation that plays a key role in supporting research relevant to mental illness, funding research training, and advocating for the needs of those with mental disorders. This reflects the recognition by ARH of the benefits of involving Rotary clubs as agents for health promotion and stigma reduction, rather than simply as a source of research funds. No other country has involved Rotary clubs in this way, but we believe it is a model that deserves to be emulated.

Anthony F Jorm PhD, DSc, FASSA · Michael G Sawyer MB BS, PhD, FRANZCP · Joy Gillett OAM

A national interdisciplinary body is urgently needed to manage the looming antimicrobial resistance crisis The introduction of antibiotics was one of the most important developments in modern medicine. Their availability has facilitated increasingly complex care and, not surprisingly, microbial resistance to antibiotics has been identified as one of the greatest threats to human health. A return to the “pre-antibiotic era” would render many routine infections untreatable and would seriously affect current practice in surgery, intensive care, organ transplantation, neonatology and cancer services through major increases in morbidity and mortality. The time to act is now — before we lose these “miracle” drugs for good. Preserving the “miracle” of antibioticsIn response to a looming crisis in antimicrobial resistance, the Australasian Society for Infectious Diseases and the Australian Society for Antimicrobials convened the Antimicrobial Resistance Summit in Sydney on 7–8 February 2011. The meeting brought together an interdisciplinary group of experts from the medical, veterinary, agricultural, infection control and public health sectors to establish priorities and a joint plan for action, focusing on the key elements shown in Box 1. The threat of antibiotic overuseThe keynote address at the Summit was given by Professor Otto Cars (Professor of Infectious Diseases, Uppsala University, Sweden, and Chair of STRAMA, the Swedish strategic program against antibiotic resistance). STRAMA, a government-funded body, has supervised a multidisciplinary effort to improve surveillance and infection prevention and promote rational antimicrobial usage. This has been very successful in reducing usage in Sweden. Professor Cars highlighted that the key factor contributing to the alarming resistance trend in bacteria is the indiscriminate use of antibiotics. This is occurring in a number of settings including hospitals, general practice and veterinary medicine. Agricultural practices involving the use of antibiotics for prophylaxis and growth promotion rather than treatment also contribute to this problem. Repeated studies have demonstrated that a significant proportion of antibiotic use is unnecessary and that antibiotic use varies markedly between countries despite similar clinical outcomes.1 For many bacterial pathogens, resistance to last-line antibiotics, such as carbapenems, fluoroquinolones, glycopeptides and third-generation cephalosporins, is now commonly found in Australian hospitals and, to an increasing extent, in the community. Examples include methicillin-resistant Staphylococcus aureus, multiresistant Streptococcus pneumoniae, vancomycin-resistant enterococci and multiresistant Escherichia coli.2 This growing ineffectiveness of once-reliable drugs has seen health care professionals increasingly turning to alternatives that are more toxic, more expensive and less likely to be orally available, putting increased pressure on a strained hospital system. In addition, compared with susceptible bacteria, antibiotic-resistant strains are associated with increased patient morbidity and mortality and increased costs of health care.1 A dwindling pipelineWhile the issue of antimicrobial resistance is not new, it has long been assumed that this problem would be overcome by the ongoing development of new compounds. However, there has been an alarming decline in antibiotic development over time, highlighting that this strategy cannot be relied upon.1 The Antimicrobial Resistance Summit plan for actionSurveillanceMeasuring the extent of antimicrobial resistance in community- and health care-associated infections is crucial to defining the issue and measuring outcomes of any interventions designed to address it. While passive surveillance by electronic collation of routine susceptibility results can provide the broadest view of phenotypic changes, targeted surveillance by prospective studies of specific pathogens of interest provides details of newly emerging resistance mechanisms and strains. At present, the extent of antimicrobial resistance in Australia remains poorly defined. The current systems of data collection and collation vary between states and territories and there is limited coordination at a national level. In addition to measuring antimicrobial resistance, it is important to understand antibiotic usage. Currently, the National Antimicrobial Utilisation Surveillance Program represents the only nationwide systematic surveillance of antibiotic usage, but it is based on voluntary data submitted from major hospitals, representing about 50% of Australian tertiary referral beds3 (Box 2). Education and stewardshipEducation of the public as well as medical, veterinary and public health sectors is a crucial component in achieving judicious prescribing and dispensing of antibiotics. However, research has demonstrated that education campaigns and guidelines are ineffective unless they are combined with sustained interventions such as audit and feedback methods and/or a system where proactive steps are taken to assist prescribing and interventions are made to address poor performance.4 Antimicrobial stewardship acts at an organisational level and defines collective strategies to optimise antimicrobial prescribing through sustainable changes in practice. Further initiatives are required in the community, where the majority of human antibiotics are prescribed (Box 3). Infection prevention and control strategiesGeneric measures such as hand hygiene, avoidance of patient contamination during invasive procedures, environmental cleaning and disinfection, vaccination, and antibiotic stewardship are crucial in infection prevention and control. Surveillance is critical for determining the health care infection burden, identifying the people who are most at risk, and demonstrating the effectiveness of infection prevention or control interventions. To be effective, nationally coordinated surveillance is essential. Screening and effective isolation of patients carrying multiresistant organisms also has an important role1 (Box 4). Future research agendaWhile basic science research on microbiology is currently adequately funded by the National Health and Medical Research Council (NHMRC) and the Australian Research Council, a number of essential aspects required to combat antibiotic resistance do not find a ready place in existing project grant structures (Box 5). RegulationImplementing effective regulatory controls represents an important aspect of reducing indiscriminate use of antibiotics and keeping levels of antimicrobial resistance low in both human and animal settings (Box 6). An urgent call to actionThe threat of multiresistant bacteria is a critical public health issue that requires a coordinated, multifaceted response. To achieve this level of cooperation, we propose the creation of a national antimicrobial resistance management body comprising a wide range of stakeholders, including health care professionals, veterinarians, agriculturalists, pharmaceutical manufacturers, government, media representatives, consumers and other interested parties. The role of this body would include: implementing a comprehensive national resistance monitoring and audit system coordinating education and stewardship programs implementing infection prevention and control guidelines expanding funding to support research into all aspects of antibiotic resistance reviewing and upgrading the current regulatory system applying to antibiotics. This strategy is recommended by the World Health Organization1 and has been adopted by many other countries. The scourge of antimicrobial resistance has increased inexorably over the years. We believe that the window for overcoming antimicrobial resistance is still open, but we must act decisively now — Australia cannot bury its head in the sand any longer and hope that the problem will just go away. 1 An agenda for addressing antimicrobial resistance 2 Surveillance: key recommendations Antimicrobial resistance surveillance A comprehensive national surveillance system encompassing both passive and targeted components should be developed to monitor how much resistance is present, in which bacteria and where. This should include medical (hospital and community) and veterinary areas, as well as agriculture (including imported food). Priority should be given to staphylococci and Escherichia coli, which have the greatest impact on human health (emerging resistance in E. coli and other Gram-negative bacteria poses a major new threat). Methods used in resistance testing should be standardised wherever possible to enable comparison and pooling of data. In particular, minimum inhibitory concentration breakpoints need to be standardised. Antibiotic usage surveillance A comprehensive national monitoring and audit system covering all areas of antibiotic usage should be established. This should include comprehensive surveillance of hospital usage (eg, by expanding the National Antimicrobial Utilisation Surveillance Program), representative sampling of community prescribing, and collating distribution data from agricultural antibiotic suppliers. Data on the appropriateness of usage should also be evaluated (using point-prevalence surveys comparing diagnosis with prescription). Voluntary identification of hospitals in surveillance programs is recommended to encourage benchmarking and transparency. 3 Education and stewardship: key recommendations Educational initiatives need to define antimicrobial resistance as an urgent public health issue. The skills of social marketers and behavioural change experts should be used to drive a national campaign targeting both the public and prescribers. The National Prescribing Service (NPS) antibiotic educational campaign should also be reinstituted. A uniform national medical curriculum should be implemented that acknowledges overuse of antibiotics and embraces better stewardship, building on the NPS National Prescribing Curriculum. Stewardship, based on national antibiotic guidelines and local epidemiology, must be mandated in all hospitals within a quality framework based on audit and feedback. Effective stewardship requires a team-based approach including infection prevention units, microbiologists, pharmacists and clinicians. It must be strongly supported by senior hospital management and underpinned by effective use of information technology. Stewardship should also be extended beyond health care institutions to community care, long-term care facilities and non-medical antibiotic use. A well resourced national body should be created to provide effective national coordination of educational activities and antibiotic stewardship. Recognising that antibiotic resistance does not respect international borders, Australia has an obligation to contribute to international programs to control antibiotic use and resistance. 4 Infection prevention and control strategies: key recommendations Improved training on strategies for infection prevention and control should be provided to health care workers. All major hospitals should have the epidemiological capacity to identify and investigate outbreaks of multiresistant organisms, and to monitor and respond to changing patterns of pathogens causing health care-associated infections. National evidence-based standards for multiresistant organism control in aged care facilities should be developed, implemented and robustly enforced and monitored. A national coordinating centre for the control of antimicrobial resistance is needed, with the authority and capacity to collect and analyse data on multiresistant organisms from all jurisdictions. This will facilitate timely, consistent and effective control of multiresistant organisms. 5 Future research agenda: key recommendation A new National Health and Medical Research Council funding call (similar to that for pandemic [H1N1] 2009 influenza) is needed for research on antimicrobial resistance and usage in Australia and its near neighbours. The key areas of focus should be: epidemiology (in both human and animal settings) effective interventions for the public sectors, focusing on education and behavioural change effective interventions for the health care sector. 6 Regulation: key recommendations Resistance risk assessments should be part of the regulatory process for bringing new antibiotics to market for both humans and animals. The Pharmaceutical Benefits Advisory Committee should consider resistance in the criteria for inclusion or restriction of antibiotics in the Pharmaceutical Benefits Scheme. Strategies should be implemented to fast-track important new antimicrobials through the regulatory approval system. Strategies should be implemented to enable the registration of non-commercial “orphan” drugs that have the potential to improve patient outcomes and reduce disease burden. Adopting an antibiotic importance rating system as regulatory policy should be considered.

Thomas Gottlieb MB BS, FRACP, FRCPA · Graeme R Nimmo MD, FRCPA, FASM

Rosemary Stanton believes that the Heart Foundation Tick program misguides consumers YES The National Heart Foundation of Australia plays a valuable role in bringing heart disease to public attention. However, shortcomings of their Heart Foundation Tick program1 demand caution. Media releases proclaim that the Tick has been “awarded to” or “earned by” particular foods. These must meet the Heart Foundation’s nutritional criteria, but companies then pay to use the Tick. For food companies, whose purpose is to make a profit, the Tick is a marketing exercise. By tweaking products (where necessary) and paying for the Tick, companies gain credibility by linking their brand to the positive emotions attached to the Heart Foundation. The extra cost is passed on to the shopper. Effects on food pricesThe cost of food is a particular concern for people on low incomes, who have a higher incidence of diet-related health problems.2 Processed foods that bear the Tick almost invariably have a higher price, while cheaper products in many food categories may have a nutritional profile at least as good as those with the Tick — sometimes better. Rolled oats with the Tick are 4.5 times the price of house-brand oats. How can this be justified? A similarly expensive Tick approved product dilutes rolled oats with 20% wheat starch, adding inulin for extra fibre. Why? Tick criteriaThe Heart Foundation’s criteria for “earning” the Tick are a cause for concern, especially the variation in its criteria for different product types. To earn the Tick, tomato sauce must have no added salt, but a similar restriction does not apply to salad dressings. Some salad dressings with the Tick contain more than 600 mg sodium per 100 mL. A much healthier option is homemade dressing, such as olive oil with lemon juice or vinegar — quick and easy to make, with virtually no sodium. In food categories such as pies, frozen pizza, fast foods, sweet biscuits, rolled fruit confectionery and frozen meals, products with the Tick may represent a slight improvement on similar products, but these food types do not deserve any stamp of credibility. The appropriate message for an overweight population is to avoid such products. Fresh fruit is a better option than a sweet biscuit or sticky fruit bar bearing the Tick. Salt and fatMany diet-related health problems stem from intake of salt, saturated fat and added sugar. The Heart Foundation has been strong in condemning saturated fats, and their lifestyle modifications for hypertension support choosing foods that are processed without salt. However, while the Heart Foundation quotes the number of tonnes of salt and saturated fat that have been saved by reformulating products to meet Tick criteria,3 this has little meaning when the proportion of total salt and fat consumption that these amounts represent is not provided. In any case, avoiding consumption of these reformulated products would save even more salt and saturated fat, and reduce energy intake. The Heart Foundation Tick program’s leniency for added salt is also perplexing. One mayonnaise with the Tick has more sodium than the same company’s regular brand (735 mg per 100 g v 550 mg per 100 g). Some ready-made soups with the Tick have 1280 mg sodium per serve. To put that into perspective, the adequate daily intake for sodium is 460–920 mg, and 2300 mg per day is the upper limit.4 Almost 80% of sodium that is consumed comes from processed foods. The obvious solution is to substitute processed foods with fresh foods. SugarThe Heart Foundation’s Tick criteria exclude sugar, claiming that added sugar does not differ from sugars in fruit or milk. However, fruit and milk contain a range of essential nutrients with their intrinsic sugars, whereas added sugar does not, and dietary guidelines for Australia and most other countries recommend limiting added sugar. Of 44 cereals awarded the Tick in 2011, many contain about 30% sugar. Dried fruit contributes some of this sugar, but some cereals that bear the Tick have “straight” added sugar only. At any level of energy intake, nutrient density falls as the proportion of added sugar in the diet increases.5 A recent analysis showed that intake of essential nutrients decreases significantly with each 5% increase in added sugars above 5%–10% of total energy intake,6 and the World Health Organization recommends that no more than 10% of energy should be from added sugars.7 The Tick criteria for cereals stipulate more than 50% wholegrain content. Lower levels of sugar would encourage even more of the beneficial wholegrain ingredients. Breakfast cereals with 97%–100% wholegrain content, and little or no added sugar, are popular and have no need to buy the Tick for credibility. The Heart Foundation should use these as a benchmark. ConclusionA recent editorial in the Canadian Medical Association Journal notes that partnerships between the food industry and health organisations can risk jeopardising public health goals, leading to health organisations becoming “inadvertent pitchmen for the food industry”. The authors conclude that “corporate dollars always introduce perceived or real biases that may taint or distort evidence-based lifestyle recommendations and health messages”.8 This is a particular problem when fast foods are awarded the Tick. The healthier option lures extra customers, but the bottom line is an increase in sales of regular burgers and fries. Most Australians need to eat less of almost everything except fruit and vegetables, and the new dietary guidelines for Americans have taken such recommendations on board.9 It is not a message that pleases the processed or fast food industries, but that is their problem — it is not the role of health organisations such as the Heart Foundation to keep these companies profitable. Doctors should, therefore, exercise caution when recommending products that bear the Heart Foundation Tick. The important message for Australians is that we need to change our attitude to food — from quantity to quality, and from highly processed foods to home-cooked fresh produce. The Tick is simply a distraction.

Rosemary A Stanton PhD(Hon), BSc, APD

James Tatoulis, Lyn Roberts and Anne-Marie Mackintosh argue that the Tick highlights healthier choices NO The vision of the National Heart Foundation of Australia is for Australians to have the best cardiovascular health in the world. The Heart Foundation Tick program is a cost-effective,1 population-based approach to improving the health of Australians by challenging food manufacturers and food outlets to improve the nutrition of their products.2 Doctors can be confident that the Tick signposts healthier food choices3 that have been independently tested to meet criteria for health maintenance and chronic disease prevention. The Heart Foundation recommends that products with the Tick be used in the context of a healthy eating pattern; for example, eating Tick approved fish products at least twice a week. Patients with specific dietary needs related to an illness should, as with any condition, seek tailored advice from health professionals. The Tick has proven to be popular with and trusted by Australians,4 as it provides one clear, easily identifiable symbol that highlights healthier choices without needing to read and interpret nutrition information panels and ingredient lists when shopping in supermarkets or eating out. Licensing and costsThe Tick logo is a certification trade mark, which means that the logo is registered to certify that products displaying it have met specified standards of quality and accuracy. The Heart Foundation must be able to demonstrate that these standards are met, and it is responsible for ensuring that the logo is used in accordance with the Tick criteria and regulations that govern its application. The Tick criteria are lodged with the Australian Competition and Consumer Commission. If food manufacturers fail to operate within the rules, their licence to use the Tick logo can be terminated. Manufacturers submit independent analyses, from a laboratory accredited by the National Association of Testing Authorities (NATA), to prove compliance with the Tick criteria. This process is mandatory for all food products that carry the Tick except fresh produce. Licensees sign a legal agreement to abide by the Heart Foundation’s requirements, which include compliance with Food Standards Australia New Zealand codes (Food Standards Code and Code of Practice on Nutrient Claims in Food Labels and in Advertisements), random auditing, nutrient testing, and pre-approval of labels and promotions before going to market. As the Tick is not funded by governments or by public donations, a license fee is incurred for the right to use the Tick logo. The fees are used to pay for developing nutrition criteria, laboratory analysis, and independent random auditing by SAI Global (an independent auditor), which sends auditors to “mystery shop” at food outlets. The fees for Tick approved products that are sold in supermarkets are based on a sliding scale of sales volume per annum. For food outlets, fees are based on the number of outlets and degree of auditing required. The frequency of audits is determined by SAI Global. Supermarket foods are randomly audited throughout the year, with every category audited at least once every 12 months, and all Tick approved products are analysed by the NATA-accredited company DTS Food Laboratories to ensure ongoing compliance with the applicable Tick nutrient standards. The Heart Foundation Tick program is governed by the Food Information Program Oversight Committee — a group of external honorary volunteers who report to the Heart Foundation National Board. In addition, the Criteria Working Group is responsible for developing the Tick criteria; it comprises experts in food science and technology, public health and nutrition science. No members of the Oversight Committee or Criteria Working Group have any conflicts of interest related to the food industry. Tick criteriaThe category-specific nutrient criteria5 are developed using a combination of scientific evidence, Heart Foundation position statements, key government policies, and food technology and food law considerations. The nutritional profile of foods sold in supermarkets is collected independently by Synovate Aztec (an agency that collects supermarket grocery scan data) so criteria can be set in relation to current food-purchasing trends. The criteria are made incrementally tougher. For example, the criteria for sodium levels in bread were reduced significantly for Tick approval, dropping from 450 mg per 100 g to 430 mg per 100 g in 2005, and again to 400 mg per 100 g in 2006. Tick criteria have recently been used by the federal government’s Food and Health Dialogue to help set voluntary whole-of-category targets for the food industry to meet within an agreed time frame. The Tick criteria are based on scientific evidence on chronic disease prevention,6 and include nutrients and food components deemed by the World Health Organization to be important for maintaining good health, such as fruits, vegetables, and high-fibre and wholegrain ingredients.7 They also specify sodium, saturated fat and trans fat levels, as well as energy limits and portion sizes. Although out of step with popular opinion, added sugar is not a criterion. This is because existing levels of evidence indicate that there is no direct causal relationship between added sugar and coronary heart disease,8 diabetes9 or obesity10 (with the possible exception of sugar-sweetened beverages). The sugar in Tick products may be from added sugars and/or naturally occurring sugars. The body does not differentiate their similar effects,11 and laboratory testing cannot accurately distinguish between them. Sugars — like other carbohydrates, fats, proteins and alcohol — contribute to the energy in foods; therefore, the Tick criteria limit these by setting energy limits. There is strong evidence for limiting energy intake to prevent chronic disease.12 ConclusionThe Heart Foundation Tick program has resulted in increased awareness of healthier eating and a significant reduction in saturated fats, trans fats and salt in many foods. It is also transforming the practices of food companies to benefit Australians.

James Tatoulis MS, MD, FCSANZ · Lyn M Roberts PhD · Anne-Marie Mackintosh BApplSc, PostGradDip(Diet), PostGradCert(PubRel)

Objective: To study variation in mortality associated with time and day of admission to the intensive care unit (ICU).Design: Retrospective cohort analysis using the Australian and New Zealand Intensive Care Society Adult Patient Database.Setting and participants: 245 057 admissions to 41 Australian ICUs from January 2000 to December 2008.Main outcome measures: Observed mortality and standardised mortality ratio (SMR) based on Acute Physiology and Chronic Health Evaluation III, 10th iteration (APACHE III-j) scores. Subgroup analysis was performed on the basis of elective surgical or emergency admission to ICU.Results: 48% of patients were admitted after hours (18:00–05:59) and 20% of patients were admitted on weekends (Saturday and Sunday). Patients admitted after hours had a 17% hospital mortality rate compared with 14% of patients admitted in hours (P < 0.001); and SMRs of 0.92 (95% CI, 0.91–0.93) and 0.83 (95% CI, 0.83–0.84), respectively. Weekend admissions had a 20% hospital mortality rate compared with 14% on weekdays (P < 0.001), with SMRs of 0.95 (95% CI, 0.94–0.97) and 0.92 (95% CI, 0.92–0.93), respectively. Variation in outcome with time of admission to ICU was accounted for predominantly by elective surgical patients.Conclusions: Patients admitted to ICUs in Australia after hours and on weekends have a higher observed and risk-adjusted mortality than patients admitted at other times. Further research is required to determine the causes and relationship to resource availability and staffing.

Deepak Bhonagiri MB BS, MD, FCICM · David V Pilcher MRCP, FRACP, FCICM · Michael J Bailey PhD, MSc, BSc(Hons)

Objective: To update our previous analysis of trends for prostate-specific antigen (PSA) testing, prostate cancer incidence, radical prostatectomy and prostate cancer mortality to assess whether men in rural and regional areas of Australia now have more equitable access to prostate cancer services, and improved outcomes.Design, setting and participants: Descriptive study using population-based data for Australian men aged 50–79 years from 1982 to the 2008–09 financial year (depending on data availability for each outcome measure).Main outcome measures: Age-standardised rates per 100 000 men and 5-year survival rates.Results: Overall, rates of PSA screening and radical prostatectomy increased, accompanied by reductions in mortality and improvements in survival throughout Australia. Incidence rates were similar for men in urban and rural areas. However, in the last year of data collection, for men in rural areas compared with urban areas, rates of PSA screening (21 267/100 000 v 24 606/100 000; P < 0.01) and radical prostatectomy (182.2/100 000 v 239.2/100 000; P < 0.01) remained lower, mortality remained higher (56.9/100 000 v 45.8/100 000; P < 0.01), and survival outcomes continued to be poorer (5-year relative survival, 87.7% v 91.4%; P < 0.01).Conclusions: With some limitations, these ecological data demonstrate that the use of diagnostic and treatment services among men living in rural areas of Australia remains lower than among their urban counterparts, their survival and mortality outcomes are poorer, and these differentials are continuing. There is an urgent need to explore further the reasons for these differences and to implement changes so these inequalities can be reduced.

Peter D Baade PhD · Danny R Youlden BSc · Michael D Coory PhD · Robert A Gardiner MD · Suzanne K Chambers PhD

Objectives: To examine the experience of fear, the fear response, and factors affecting fear in adolescents undergoing school-based human papillomavirus (HPV) vaccination.Design, participants and setting: A purposive sampling strategy and qualitative methods, including observation and face-to-face interviews. Focus groups comprised adolescent girls who were involved in HPV vaccination in 2007 at schools in Sydney, New South Wales. Individual interviews were conducted with parents, teachers and vaccination nurses.Results: Data from observing vaccination days at three schools and from interviewing 130 adolescents in 20 focus groups, 38 parents, 10 teachers and seven nurses were included in the analysis. All participants discussed the issue of fear and distress experienced by adolescent girls in relation to HPV vaccination. Observations corroborated the focus group and interview data. Our results indicated that fear was promoted by witnessing the fear reactions of peers; perceived judgement by peers; lack of information or misinformation; and being vaccinated later in the day. Fear was moderated by procedural factors, the support of peers, appropriate knowledge, and nurses’ distraction techniques or approach. Fear also affected acceptance of HPV vaccination.Conclusions: Fear of HPV vaccination was a near universal experience among adolescents in the school setting and was often associated with significant distress that had an adverse impact on the vaccination process. School vaccination could be improved by proactively managing fear and distress.

Diana M Bernard MPH · Spring C Cooper Robbins PhD · Kirsten J McCaffery PhD · Caroline M Scott MHlthSc(Nurs) · S Rachel Skinner PhD, FRACP

Androgen deprivation therapy (ADT) in men with prostate cancer increases the risk of osteoporotic fractures, type 2 diabetes and, possibly, cardiovascular events. There is considerable uncertainty about the risk–benefit ratio of ADT in non-palliative treatment; the benefits of ADT in treating non-metastatic prostate cancer need to be carefully weighed against the risks of ADT-induced adverse events. Baseline assessment of bone health at the initiation of ADT should include measurement of bone mineral density (BMD) by dual energy x-ray absorptiometry and, in men with osteopaenia, a thoracolumbar spine x-ray. General measures to prevent bone loss, including regular physical activity, as well as ensuring calcium and vitamin D sufficiency, should be instituted routinely. All men with a previous minimal trauma fracture should receive pharmacological therapy unless contraindicated; for those who have not sustained a minimal trauma fracture, treatment is advised if the BMD T score is ≤ − 2.0, or if the 10-year risk of a major osteoporotic fracture exceeds 20%. Men with prostate cancer who are receiving ADT should be closely monitored for weight gain and diabetes; intensive lifestyle intervention is recommended to prevent ADT-induced weight gain and insulin resistance. Management of the metabolic sequelae of ADT includes optimal reduction of cardiovascular risk factors, with particular attention to weight, blood pressure, lipid profile, smoking cessation, and glycaemic control.

Mathis Grossmann MD, PhD, FRACP · Emma J Hamilton MB BS · Christopher Gilfillan MB BS, PhD, FRACP · Damien Bolton MB BS, FRACS · Daryl Lim Joon MB BS, FRANZCR · Jeffrey D Zajac MB BS, PhD, FRACP

Issues relating to voluntary euthanasia that are currently being debated by Australian society are distinctly different from those encountered by battlefield doctors. Doctors in war undertake to treat those affected by conflict; their participation in euthanasia challenges the profession’s definition of “duty of care”. Euthanasia must be distinguished from “triage” and medical withdrawal of care (which are decided within a medical facility where, although resources may be limited, comfort care can be provided in the face of treatment futility). Battlefield euthanasia is a decision made, often immediately after hostile action, in the face of apparently overwhelming injuries; there is often limited availability of pain relief, support systems or palliation that would be available in a civilian environment. The battlefield situation is further complicated by issues of personal danger, the immediacy of decision making and difficulties with distinguishing civilians from combatants. Regardless of the circumstances on a battlefield, doctors, whether they are civilians or members of a defence force, are subject to the laws of armed conflict, the special provisions of the Geneva Conventions and the ethical codes of the medical profession.

Susan J Neuhaus CSC, PhD, FRACS

Clinical research is an area of increasing activity for hospitals, universities and research institutions, which requires formal governance and oversight to manage risks. Monitoring research practice should be a part of research governance activities. However, formal audits have proved time consuming for researchers and auditors. To increase attention to good research practice and screen for poor practice, the Department of Epidemiology and Preventive Medicine at Monash University and the Alfred Research and Ethics Unit in Melbourne have developed a brief self-audit tool for researchers. We evaluated the self-audit using a questionnaire for researchers. The results were positive, with most respondents believing that it promoted good research practice.

Bradley R Crammond BA LLB, LLM · Anna V Parker BA(Hons), MA, MBioeth · Megan Brooks BAppSci, GradCert(ClinRes), PhD · Marina Skiba BEd(Sec)Sci · John J McNeil PhD, FRACP, FAFPHM

Renal tubular acidosis is an underreported complication of ibuprofen misuse, and can result in life-threatening hypokalaemia. We describe four patients who presented with profound hypokalaemia and muscle weakness associated with excessive ibuprofen ingestion. Ibuprofen cessation and supportive management resulted in complete biochemical resolution within a few days. These cases remind practitioners about potential complications of unmonitored use of over-the-counter analgesics, including those with potential for misuse due to their codeine content. (MJA 2011; 194: 313-316) Clinical recordsPatient 1A 32-year-old woman presented to the emergency department with a 2-day history of evolving paralysis associated with profound hypokalaemia (potassium, 1 mmol/L; reference range [RR], 3–5 mmol/L). She also had epigastric pain without diarrhoea or vomiting and a past medical history of depression, iron deficiency anaemia, chronic constipation, migraines, cigarette smoking and previous intravenous drug use. Family history was unremarkable. Her only medications were citalopram 20 mg daily and a combination of ibuprofen (200 mg) and codeine phosphate (12.8 mg) for migraines. She denied taking laxatives, diuretics, alcohol or illicit drugs. On examination, the patient weighed 38 kg (body mass index, 14 kg/m2), her blood pressure was 90/55 mmHg, and other vital signs were normal. There was generalised flaccid weakness (graded 3/5) with normal sensation. She also had epigastric tenderness. Results of initial laboratory investigations (Box 1) were consistent with distal renal tubular acidosis (dRTA). An electrocardiogram (ECG) demonstrated features of hypokalaemia, including widespread ST-segment depression and U waves. Endoscopy revealed oesophageal erosions and a benign gastric ulcer. An abdominal computed tomography scan demonstrated enlarged, oedematous kidneys without nephrocalcinosis. The patient’s husband revealed she had been consuming the combination ibuprofen–codeine over a prolonged period — at least 25 tablets (5.0 g of ibuprofen) per week and up to 20 tablets in 1 day. Ibuprofen toxicity explained both the gastrointestinal symptoms and the biochemical manifestations of dRTA. No alternate explanation for dRTA was found. The ibuprofen–codeine combination was ceased, and intravenous potassium chloride (KCl) was administered (610 mmol at 5–10 mmol/h over 5 days), with concurrent oral replacement of 64 mmol potassium/day. No signs of opioid withdrawal were detected. Within 5 days, her serum potassium level stabilised at 4 mmol/L and bicarbonate levels normalised without bicarbonate supplementation. She was discharged 3 weeks later on a regimen of 16 mmol of potassium daily; her serum potassium level at discharge was 5 mmol/L. Patient 2A 37-year-old man presented with 3 days of progressive muscle weakness. He had been taking ibuprofen–codeine for several years, with a daily dose of 24 tablets (4.8 g ibuprofen). He was a smoker and denied taking any other medications. There was no history of diarrhoea or vomiting, and family history was unremarkable. He had proximal muscle weakness (graded 3/5) with hyporeflexia and muscle tenderness, but sensation was preserved. Initial investigation revealed a very low serum potassium level (2 mmol/L) and biochemical features consistent with dRTA (Box 1). The ibuprofen–codeine was ceased, and intravenous KCl was administered for 4 days (10–30 mmol/h) with 112 mmol of oral potassium/day. The weakness resolved after 2 days. Oral sodium bicarbonate supplementation (2520 mg/day for 9 days) contributed to normalisation of serum bicarbonate levels. Symptoms of overt opioid withdrawal developed on Day 3 and buprenorphine treatment was commenced. He was discharged on Day 9 after cessation of potassium and bicarbonate supplements, with a serum potassium level of 4 mmol/L. Patient 3A 45-year-old woman, with a remote history of intravenous drug use, presented after 7 days of lethargy and anorexia. She had multiple dental caries, and for several months had ingested 9.6–14.4 g/day of ibuprofen (about 50 tablets per day). She took no other medications and had an unremarkable family history and physical examination. Initial investigations revealed hypokalaemia (potassium, 2 mmol/L) with acute kidney injury, renal potassium wasting and biochemistry consistent with dRTA (Box 1). Gastroscopic investigation of microcytic anaemia found gastric antral ulceration with a peptic oesophageal stricture. No cause for RTA other than ibuprofen overdose was found. Ibuprofen was ceased, and intravenous sodium bicarbonate and KCl (220 mmol over 3 days at a maximum rate of 10 mmol/h) were administered. Concurrent oral potassium replacement occurred at 60 mmol/day. On discharge, 5 days later, renal function was normal and the serum potassium level was 3 mmol/L. Patient 4A 40-year-old man presented with a 2-day history of profound generalised weakness associated with hypokalaemia (potassium, 1 mmol/L). He had consumed 1.4–2.0 g/day of ibuprofen for 3 months for degenerative back pain. There was no history of diarrhoea or vomiting, he took no other medications and had no significant family history, and he was a smoker. The patient had normal vital signs apart from bradycardia (50 beats/min), with generalised flaccid weakness (graded 1–2/5) with preserved reflexes and sensation. An ECG demonstrated sinus bradycardia with prolonged QTc interval and U waves. Initial biochemistry results (Box 1) were consistent with RTA. Although the urine pH of 6.5 was higher than expected for the low serum bicarbonate level (11 mmol/L), proximal RTA (pRTA) was diagnosed in view of the negative urine anion gap and findings suggesting proximal tubular dysfunction. These included hypouricaemia (0.18 mmol/L; RR, 0.20–0.42 mmol/L), hypophosphataemia (0.40 mmol/L; RR, 0.8–1.5 mmol/L) and mild proteinuria. As there were no features suggesting alternative causes for pRTA, ibuprofen was considered the most likely causative factor, and was discontinued. Intravenous potassium (1010 mmol over 3 days at a maximum rate of 20 mmol/h), bicarbonate (total dose, 500 mmol) and phosphate (total dose, 50 mmol) were administered under electrocardiographic monitoring. The patient’s muscle strength improved within 24 hours and he was discharged 4 days later with a serum potassium level of 3 mmol/L. Potassium supplementation was ceased on discharge. DiscussionIbuprofen, a non-steroidal anti-inflammatory drug (NSAID), is widely used and readily available over the counter (OTC). Excessive ingestion of ibuprofen, in combination with codeine or alone, can result in ibuprofen toxicity, including RTA. In Australia, the maximum quantity of ibuprofen–codeine available OTC has recently been reduced from 72 to 28 tablets due to problems related to codeine misuse. We have described four patients with profound hypokalaemia due to ibuprofen-induced RTA. This is an underreported complication, which may present with hypokalaemic paralysis. Three of the patients were admitted to the same tertiary care hospital within 3 months of each other. The remaining patient was admitted to a peripheral hospital the previous year. In each case, the differential diagnosis of hypokalaemia initially included transcellular potassium shift, renal potassium wasting and gastrointestinal losses. Medication histories were uniformly negative for drugs known to cause intracellular potassium movement. Thyroid function was normal and there was no family history of hypokalaemic periodic paralysis. Urinary potassium wasting was documented in all cases by excessive urine potassium excretion (> 20 mmol/day or spot urine potassium > 20 mmol/L) in the presence of hypokalaemia.1 This was not explained by diuretic use or magnesium deficiency. The hyperchloraemic metabolic acidosis and non-acidified urine pH were in keeping with RTA. Gastrointestinal potassium and bicarbonate loss was unlikely in the absence of diarrhoea or laxative use. In two cases, gastric ulceration provided corroborative evidence for ibuprofen toxicity. Investigations found no alternative aetiology for RTA (Box 2). Ibuprofen cessation and supportive therapy allowed complete biochemical resolution within days. Unfortunately, no follow-up information could be obtained to ascertain whether the RTA was recurrent, or whether a previously unrecognised aetiology for RTA had become apparent. Characteristics of RTA are summarised in Box 3. Renal acidification is impaired, resulting in a hyperchloraemic metabolic acidosis.2 Hypokalaemia due to kaluresis is a feature of both proximal and distal RTA. Multiple factors contribute to hypokalaemia. Metabolic acidosis impairs proximal sodium reabsorption, leading to increased distal sodium delivery, secondary hyperaldosteronism and increased potassium secretion.3 In distal RTA, impaired hydrogen ion excretion promotes potassium loss in exchange for sodium to maintain electroneutrality. Reduced H–K-ATPase pump activity results in reduced distal potassium reabsorption.4 Four previously published case reports5-8 have described similar clinical presentations occurring with ibuprofen use of 4.8 to 28 g per day. However, one of our patients (Patient 4) developed RTA at a dose below the maximum recommended. No other NSAID has yet been implicated with this complication. The mechanism by which ibuprofen induces RTA is unknown. Other nephrotoxic effects of NSAIDs, including acute and chronic kidney injury, interstitial nephritis and nephrotic syndrome, result from impaired synthesis of cytoprotective prostaglandins, a consequence of cyclo-oxygenase-1 (COX-1) inhibition. It is hypothesised that the pathogenesis of ibuprofen-induced RTA may involve carbonic anhydrase (CA) inhibition. CA catalyses the interconversion between carbon dioxide and bicarbonate and is crucial to renal acid–base regulation. It is present in renal proximal tubules and collecting ducts as well as a variety of other tissues, including bone, brain and gut.9 Congenital CA deficiency is characterised by proximal and distal RTA, osteopetrosis and cerebral calcification.10 High titres of an auto-antibody directed against CA II have been noted in some patients with dRTA associated with Sjögren syndrome.11 Induction of these auto-antibodies has resulted in the development of RTA in a mouse model of Sjögren syndrome.12 Other NSAIDs including aspirin13 and flurbiprofen14 have been shown to have CA-inhibitory activity in vitro. More recently, celecoxib and valdecoxib, which are COX-2 selective NSAIDs, have been demonstrated to be potent inhibitors of CA due to binding of their sulfonamide moiety to its zinc (Zn2+) ion.15 Although ibuprofen lacks a sulfonamide moiety, it can inhibit human and bovine erythrocyte CA II.14 CA inhibition would be consistent with our observations of both proximal and distal RTA. In conclusion, profound hypokalaemia due to RTA is a potentially fatal complication of ibuprofen use. Although it usually occurs with excessive doses, it can occur at doses below the maximum recommended. The pathogenesis is unknown but may involve CA inhibition. Opioid addiction with deliberate misuse of ibuprofen–codeine analgesics is common.16 Therefore, ibuprofen toxicity should be considered in the differential diagnosis of patients presenting with severe hypokalaemia or hypokalaemic paralysis. 1 Baseline laboratory investigations and other characteristics of four patients with ibuprofen-induced renal tubular acidosis Reference range Patient 1 Patient 2 Patient 3 Patient 4 Sex, age in years Female, 32 Male, 37 Female, 45 Male, 40 Ibuprofen dose* 0.6–4.0 g/day 4.8 g/day 9.6–14.4 g/day 1.4–2.0 g/day Other medications Citalopram 20 mg/day; no complementary medicines, laxatives, diuretics or illicit drugs No prescription medicines, laxatives, diuretics or illicit drugs No other prescribed or over-the-counter medicines No other prescribed, over-the-counter or complementary medicines, diuretics or laxatives Serum pH 7.32–7.43 7.26 7.28 7.16 (venous) 7.27 Pco2, mmHg 37–50 21 32 22 27 HCO3-, mmol/L 22–32 10 14 8 11 Anion gap 7–17 10 8 16 15 Na+, mmol/L 134–146 141 140 134 141 Cl-, mmol/L 98–108 122 120 112 116 Urea, mmol/L 3.8 3.9 5.4 18.0 6.0 Creatinine, μmol/L 60–110 106 83 222 83 K+, mmol/L at presentation 3–5 1 2 2 1 K+, mmol/L on discharge 3–5 5 4 3 3 Urine pH 6.5 6.9 6.5 6.5 Na+, mmol/L 63 49 35 42 K+, mmol/L 25 25 22 25 Cl-, mmol/L 85 69 32 78 Anion gap 3 5 25 − 11 Pco2 = partial pressure of carbon dioxide. HCO3- = bicarbonate ion. Na+ = sodium ion. Cl- = chloride ion. K+ = potassium ion. * Maximum recommended: 3.2 g/day. 2 Causes of renal tubular acidosis (RTA)1 Causes of proximal RTA Primary Secondary With Fanconi syndrome (eg, multiple myeloma, light chain disease) Drugs and toxins (acetazolamide, outdated tetracycline, aminoglycosides, sodium valproate, 6-mercaptopurine, streptozotocin, iphosphamide, lead, cadmium, mercury) Associated with other clinical entities (vitamin D deficiency, hyperparathyroidism, chronic hypocapnia, cyanotic congenital heart disease, medullary cystic kidney disease, Alport syndrome, corticoresistant nephrotic syndrome, renal transplantation, amyloidosis, recurrent nephrolithiasis) Causes of distal RTA Primary Secondary Autoimmune diseases (eg, systemic lupus erythematosus, Sjögren syndrome, chronic active hepatitis, primary biliary cirrhosis, thyroiditis, fibrosing alveolitis, rheumatoid arthritis) Drugs and toxins (amphotericin B, lithium, toluene, amiloride, trimethoprim, pentamidine, vanadium) Calcium disorders (eg, primary hyperparathyroidism, vitamin D intoxication, idiopathic hypercalciuria with nephrocalcinosis) Dysproteinemic syndromes (hypergammaglobulinemia, amyloidosis, cryoglobulinemia) Renal diseases (eg, renal transplant rejection, medullary sponge kidney, obstructive and reflux nephropathy) Liver disease (hepatic cirrhosis) Genetic diseases (eg, osteopetrosis, sickle cell disease, Ehlers–Danlos syndrome) 3 Characteristics of renal tubular acidosis (RTA)1 Distal RTA (type 1) Proximal RTA (type 2) RTA type 4 Primary defect Impaired distal H+ excretion Impaired proximal HCO3 2 reabsorption Decreased aldosterone secretion or effect Plasma potassium Usually reduced (hyperkalaemic forms exist) Reduced Increased Urine pH > 5.5 Variable: usually > 5.5 if plasma HCO3- > 16mmol/L; < 5.5 if plasma HCO3- < 16 mmol/L < 5.5 Urine anion gap Positive Negative Positive Nephrocalcinosis Common Rare Rare Other tubular defects Rare Common (generalised proximal tubular dysfunction) Rare H+ = hydrogen ion. HCO3 - = bicarbonate ion.

Jennifer L Ng MB BS(Hons) · David J R Morgan MB BS, DCH, DRANZCOG · Nelson K M Loh MB BS, BMedSci, FRACP · Seng K Gan MB BS(Hons), FRACP, PhD · Patrick L Coleman MB, MRCPI, FRACP · Gregory S Y Ong MB BS · David Prentice MB BS, FRACP

Gwen Fleming was born in Taree, New South Wales, on 9 June 1916, the third of John and Caroline Lusby’s six children. She graduated in medicine from the University of Sydney in 1939, just in time to answer the call to military service. Appointed to the rank of Captain, Gwen worked at Yaralla Military Hospital at Concord (“They called me ‘Sir’, during the war”). In 1945, she became the first woman major in the Royal Australian Army Medical Corps and was subsequently appointed Officer Commanding Medical Company. In 1945, Gwen was one of the first women admitted as a Member of the Royal Australasian College of Physicians and, in 1973, she was admitted as a Fellow. She married the brilliant young surgeon Justin Fleming, a Flight Lieutenant in the Royal Australian Air Force, in 1946. Justin was awarded an Oxford Nuffield Medical Fellowship to the University of Oxford, and they took up residence at the Radcliffe Infirmary. In 1950, they returned to Sydney to raise what became a family of six children. The children flourished in an environment where a love of cricket, theatre, art, music and literature was encouraged. Gwen and Justin wanted happiness for their children, not duty from them. The family motto was animo toto laborate (“no half jobs”). After Justin’s death in 1974, Gwen became the family breadwinner. She joined Dr Brian McEwen in his Macquarie Street practice and took a teaching position at St Vincent’s Hospital in Sydney, a demanding regime that she continued until she was 77 years of age. Her patients and students were struck by her calm, clear approach which elucidated both the detail and the big picture. Gwen was innately altruistic and held a firm Christian belief that God travelled through human action. Among the gifts that she brought to medicine were clarity of judgement, patience of manner and accuracy of diagnosis. To her, gaining the trust of the patient was part of the healing. In her last weeks, Gwen suffered from severe angina and a subsequent heart attack, and passed away on 18 January 2011. She is survived by her sister, Sr Elizabeth Lusby OP, and children Margaret, Paul, Justin, Judith and Peter — another son, James, died in 1999.

Justin Fleming

Clinical record Two overseas backpackers presented to the emergency department of a tertiary referral hospital with epididymo-orchitis. Patient 1 was a 23-year-old unvaccinated Frenchman who presented in February 2009 with a 7-day history of unilateral, then bilateral, painful scrotal swelling. He had arrived in Australia a month before the onset of symptoms. He was treated with ceftriaxone and azithromycin for presumed sexually acquired epididymo-orchitis and was discharged “home” (to a youth hostel). He returned 10 days later with worsening scrotal pain, requiring admission for analgesia. Mumps serology revealed an elevated IgM but undetectable IgG titre. Test results for Chlamydia trachomatis and Neisseria gonorrhoeae polymerase chain reaction (PCR) on first-pass urine were negative. On reflection, the patient recalled mild parotid pain a week before his scrotal symptoms. He recovered after 2 days of inpatient treatment with non-steroidal anti-inflammatory drugs, paracetamol and bed rest. Patient 2 was a 25-year-old English traveller who presented to the same hospital in February 2009 with fever for 3 days, then unilateral scrotal swelling and moderately severe headache. He had arrived in Australia from England, via Thailand, a week earlier. He had been vaccinated against measles and rubella, but not mumps. On the sixth day of his illness, he required admission for pain management and inability to mobilise. Investigative ultrasounds showed features of epididymo-orchitis. An elevated mumps IgM titre was detected, and IgG was undetectable. Concurrently, a urinary PCR test for C. trachomatis was positive. He received oral doxycycline (for C. trachomatis), opiate analgesia and bed rest, and recovered after 4 days in hospital. Patient 3 was a 25-year-old unvaccinated French woman who presented to the same hospital in March 2009 with 2 days of fever, marked parotid swelling and dry mouth. She was a travelling companion of, and shared accommodation with, Patient 1. A saliva sample tested positive for mumps PCR. She was hospitalised for 3 days for pain management and cross-infection prevention. She was given non-opiate analgesia and oral rehydration. Droplet isolation precautions, such as isolation in a single room and use of facemasks, gloves and gowns by those attending her, were instigated. In this article, we use a series of cases to highlight the diagnostic challenges, risk factors and public health implications of mumps orchitis. Although mumps orchitis is well described in the literature, some general practitioners and hospital clinicians may be relatively inexperienced in its diagnosis and treatment because of the low prevalence of mumps in Australia. Mumps classically presents with a prodrome of fever, malaise and myalgia, and is followed by parotitis, which is usually bilateral.1 However, 10% to 20% of symptomatic cases of mumps have no parotid symptoms.2 The incubation period is 2 to 3 weeks, and the prodromal symptoms and parotitis usually persist for 7 days. People with mumps are infectious from 5 days before to 5 days after the onset of parotitis.3 Individuals without parotid symptoms are also infectious. Orchitis is the most common complication of mumps in post-pubertal males, occurring either unilaterally or bilaterally after 10 days of illness in up to 40% of this demographic with mumps.4 Less common complications include meningitis (in up to 10% of patients), encephalitis, pancreatitis, arthritis and oophoritis.2 Consequences of mumps orchitis include testicular atrophy (up to 50%), oligospermia or asthenospermia (up to 13%), and, rarely, sterility.2 There is conflicting evidence for the use of subcutaneous interferon alpha-2b in preventing testicular atrophy in mumps orchitis, and the drug is not given routinely.2 Two doses of the combined measles–mumps–rubella (MMR) vaccine confer detectable IgG antibodies in 95% of people.5 However, complete childhood vaccination is no guarantee of enduring immunity, as demonstrated by recent outbreaks in the United States and the Czech Republic where 84% to 90% of patients developing mumps had previously received two documented mumps vaccinations.6,7 Australian residents born between 1978 and 1982 are more susceptible to mumps, as they escaped natural mumps infection; were not targeted in the 1998 Measles Control Campaign, which involved MMR vaccination of primary school-aged children; and might have missed a second dose of MMR despite secondary school catch-up campaigns.8,9 Similarly, an under-vaccinated cohort (around 60% of eligible children) exists in the United Kingdom following anxiety created by a well publicised 1998 paper associating MMR vaccine with autism, which was later rebutted by several studies, reviews and conclusions reached by the World Health Organization’s Global Advisory Committee on Vaccine Safety.10 The three travellers described here missed childhood mumps vaccinations and opportunities for pre-travel vaccination. Herd immunity offers protection to unvaccinated individuals when more than 90% of the population is immune to mumps.10,11 Yet when susceptible people travel outside communities with high vaccination coverage, they lose the protection of herd immunity. Patient 2 probably acquired mumps in Thailand, and his case illustrates the infection risks for under-vaccinated adults travelling to mumps-endemic countries. In the absence of systemic symptoms, there are few clinical features that distinguish mumps from bacterial epididymo-orchitis. Sexually transmitted pathogens, including Chlamydia trachomatis and Neisseria gonorrhoeae, and other bacteria infecting the urinary tract, such as Escherichia coli, are common causes of epididymo-orchitis, and may be associated with urethral symptoms, or microscopic pyuria. The distinction between testicular swelling alone and epididymal involvement as a guide to bacterial causes is not helpful in practice because it is hard to assess clinically. Moreover, a recent review suggests that mumps itself can cause epididymitis in up to 85% of cases preceding a mumps orchitis.12 Other viral causes of orchitis include rubella, coxsackievirus, human parvovirus and echovirus. Lessons from practice Mumps transmission still occurs in Australia because of incomplete vaccination, either in Australia or overseas, or waning immunity over time. Mumps should be considered as a differential cause of epididymo-orchitis in an unvaccinated individual. For patients with epididymo-orchitis where no common urinary tract or sexually transmitted pathogen is isolated, mumps serological testing should be performed. There is no specific post-exposure treatment for contacts of a patient with mumps, but opportunistic vaccination of contacts could provide immunity against future exposure. Given ongoing mumps transmission in endemic regions, measles–mumps–rubella vaccination should be offered to Australians travelling abroad. Our report of Patient 2 highlights diagnostic uncertainty even with laboratory testing: results showed the presence of both C. trachomatis (positive urinary polymerase chain reaction [PCR]) and the mumps virus (positive IgM serology). Mumps IgM can be undetectable in vaccinated individuals (estimated 24%–51% sensitivity) but, when detected, it is highly specific (82%–96%).13,14 Clinical features of the patient’s condition, including orchitis and mild meningitis, were consistent with mumps, so concurrent infections were felt to be plausible. A convalescent serum sample showing a rising mumps IgG titre would have confirmed the mumps diagnosis, but testing was not possible because the patient resumed his travels. In severe cases requiring hospitalisation, or where there is diagnostic uncertainty and risk of transmission, serological investigations (or PCR assay before the emergence of detectable mumps IgM antibodies around the fifth day of the illness) are warranted to establish the diagnosis. Mumps is highly infectious and spread by droplets. Infected travellers pose a particular risk of transmitting mumps because use of shared accommodation and public transport places them in close proximity to others. Notification of mumps is required in Australia, and can help public health authorities identify outbreaks and manage infectious patients. Voluntary isolation outside hospital of young adults is encouraged by public health authorities; however, there are no routine practices for enforcing isolation for mumps (Dr Rosemary Lester, Deputy Chief Health Officer, Victoria, personal communication). As home isolation during the infectious period is impractical for travellers living in communal accommodation, hospital admission could be justified to protect the health of both the individual and the public. Moreover, there is no proven prophylaxis for contacts. Neither use of normal human immunoglobulin nor MMR vaccination has been shown to prevent acquisition after exposure to mumps.15 However, for contacts who have not had two documented MMR vaccinations, opportunistic offers of vaccination might, if taken up, confer immunity against future mumps exposure. In the demographic of young men, particularly when travelling, GPs and emergency physicians need to be aware of mumps as an alternative cause of epididymo-orchitis. As the case of Patient 1 shows, mumps transmission in Australia is ongoing. Clinicians treating epididymo-orchitis should ask the patient about parotitis symptoms. Where a typical bacterial pathogen is not found, mumps serological testing is recommended. If mumps is recognised, there is an opportunity to interrupt direct transmission by isolating patients, especially travellers living in close contact with potentially non-immune people. Finally, these case reports should remind clinicians to offer pre-travel MMR vaccination to young susceptible adults.

Joseph S Doyle MB BS, BA(Hons), MSc · Emma K Paige MB BS · Denis W Spelman MPH, FRACP, FRCPA

Newborn screening (NBS) programs are a well established and cost-effective method for early identification of genetic disorders. However, a raft of legal questions surrounds the collection, storage, ownership and secondary use of NBS cards. The absence of clear legal rules governing NBS programs in Australia means that there are few straightforward answers to these questions. A series of controversial incidents have exposed this uncertainty in Australia, and remarkably similar controversies have occurred in the United States and European Union. We review the situation, using Victoria as a case study. We also make the case for a dedicated regulatory regime for NBS programs, arguing that the lack of such a regime threatens public trust and the robust operation of NBS programs in Australia. New rules would likely introduce stricter requirements for informed consent at the point of blood collection than has been the norm to date. However, the scope for use of cards in research could expand rather than contract, and it may be possible to reduce the risk that vast card archives will need to be destroyed in response to future public outcries.

Diana M Bowman BSc, LLB, PhD · David M Studdert LLB, ScD, MPH

Terminal decline. A surgeon’s diagnosis of the Australian health-care system. Dr Mohamed Khadra. Sydney: Random House, 2010 (xiii + 263 pp, $34.95). ISBN 9781864711370. THE AUTHOR of this work is a respected surgeon, educator and author, who has done more than most in giving back to the community in which he now lives, as well as to other, more distant, communities. It is therefore disappointing that his latest book is a passionate but superficial tour through the recent history of the Australian health care system. It lacks the rigour required for such analysis. Many of the key political and medical figures involved in the introduction of universal health insurance were interviewed. Not surprisingly, they provide a retrospective justification for their stance of some decades ago. The method of diagnosis is lacking, in that there was no attempt to revisit contemporary texts and media of the time under evaluation. There is much extrapolation from powerful anecdote, leading to gross generalisations and oversimplification of the issues under discussion. There is an almost paranoid obsession with the meddling bureaucracy who obeyed the command to go forth and multiply. The obsession is justified to some extent but does not provide the entire explanation for the system’s woes. Reference to “an anti-doctor nurse turned journalist” bobs up out of nowhere. A glass half empty approach is adopted, from the title through to the denouement. There is repetitive pining for the days, viewed through rose-tinted spectacles, when the medical profession ruled the system and uninsured patients allegedly received wonderful care from charitable consultants. However, once the negativism has passed, which, unfortunately, is not until near the end of the book, the author makes some reasonable recommendations for cure. The publication is more suited to a series of media articles. If one is looking for serious investigative journalism, then the book does not, at least in the opinion of this reviewer, represent value for money.

Allan D Spigelman

To the Editor: The recent article by Lewis and colleagues highlights the important role of long-acting reversible contraceptives (LARCs) in reducing unintended pregnancy in Australian teenagers.1 LARCs are defined as contraceptives that are administered less than monthly and include hormonal implants and injections, and intrauterine devices (IUDs).2 The critical importance of improving access to LARC methods has been recognised in the United Kingdom by the National Institute of Health and Clinical Excellence, which produced guidelines for implementing this policy in 2005.2 The United States has recently followed this lead. In 2009, expanding access to intrauterine devices and other LARCs, particularly for younger women, was declared a national public health priority by the US Institute of Medicine.3 Our particular interest is to expand Australian women’s access to intrauterine contraception, including the copper devices and the levonorgestrel-releasing device (LNG-IUD). IUDs provide highly effective long-term contraception, and the LNG-IUD offers additional benefits for women with heavy menstrual bleeding.2 Although IUDs are the most widely used reversible contraceptives in the world, they are underused in Australia; the most recent available data suggest use by about 1.2% of women using contrceptives,4 compared with 17% in France and 21% in Sweden.5 The reasons for the low uptake of IUDs are undoubtedly complex, but appear to include lack of information, and misinformation in relation to infection risk and their unsuitability for younger women. There is now good evidence that modern devices present minimal risk of infection and no increased risk of subsequent infertility. There is increasing experience of their use in younger women, and nulliparity is not considered a contraindication.6 To investigate barriers to acquiring an IUD, we surveyed 334 of the 366 women who attended for IUD insertion over 3 months in 2009 at family planning clinics in New South Wales and Queensland. Excluding the 16 women (5%) for whom there were missing data, 16% of respondents (51 of 318) had not found it easy to obtain IUD-related information and almost a fifth (58; 18%) had been told it was not a suitable method for them by either a health professional or a friend or family member (or both), despite these women meeting appropriate medical eligibility criteria at the family planning clinic. Although family planning organisations are currently engaged nationally in developing and delivering IUD-insertion training for general practitioners, we suggest that increasing appropriate use of IUDs in line with other countries will only be achieved if the misperceptions of the risks relating to modern IUDs among consumers and health professionals are addressed. This is crucial to reducing the burden of unintended pregnancy, particularly in young women.

Deborah Bateson · Caroline Harvey · Julia Williams · Kirsten I Black

To the Editor: Hereditary haemorrhagic telangiectasia (HHT) or Osler–Weber–Rendu syndrome manifests as vascular dysplasia involving the nose, skin, lung, brain and gastrointestinal tract. It is an inherited disorder manifesting as unbalanced angiogenesis.1 Bevacizumab is a recombinant, humanised monoclonal antibody that binds to and neutralises vascular endothelial growth factor (VEGF), preventing its association with endothelial receptors. VEGF binding initiates angiogenesis (endothelial proliferation and the formation of new blood vessels). VEGF and transforming growth factor β play a role in the pathogenesis of HHT, with affected patients having increased levels of these factors.2 Anecdotal reports have demonstrated the effectiveness of bevacizumab in patients with HHT. To date, good responses have been documented in patients presenting with epistaxis, haemoptysis, anaemia,3 pancreatic arteriovenous malformations4 and hepatic vascular abnormalities.5 We were referred a 71-year-old man who related a 45-year history of recurrent nose bleeds, pulmonary and gastrointestinal haemorrhage and significant facial and oral telangiectasias. He had a history of multiple hospital admissions for haemoptysis and malaena necessitating blood and iron transfusions. The patient averaged three blood transfusions and four iron infusions a year, and his haemoglobin level ranged from 90 to 120 g/L. The patient also received argon laser treatment for his gastric and duodenal telangiectasias, and was taking bovine colostrum for nosebleeds with minimal effect. Shaving resulted in regular bleeding as a result of his facial telangiectasias. Because of his significant morbidity, the patient was referred for a trial of bevacizumab therapy and underwent six cycles at 5 mg/kg by means of fortnightly intravenous infusion from March to May 2010. This treatment has resulted in an effective and tangible response. Since completing the treatment, the patient has been followed up monthly, and he reports only two nosebleeds compared with daily bouts before therapy. Further, the telangiectasias on his face and in his mouth have reduced considerably, and he has had only one gastrointestinal bleed, which occurred after heavy lifting. His haemoglobin level 2 weeks after treatment was 163 g/L and has remained stable since that time. A follow-up gastroscopy in November 2010 showed that his multiple vascular lesions had reduced to just one angiodysplastic lesion in his gastric body (Box). The only adverse effect he experienced from the bevacizumab was poor sleep with associated tiredness, but the patient was able to tolerate this in light of the amelioration of the symptoms of his HHT. Other reported side effects of bevacizumab such as hypertension, proteinuria and thrombosis did not manifest in this patient. With growing anecdotal evidence of the effectiveness of bevacizumab in treating symptomatic HHT, an argument for using bevacizumab as an adjunctive or even first-line treatment for HHT is becoming stronger. Gastroscopic images of the patient’s stomach before and after treatment with bevacizumab

Ross P Cruikshank · Boris W Chern

To the Editor: Nash and colleagues have produced another report on medicolegal matters and Australian doctors.1 This report, and one that preceded it in 2009,2 are derived from responses to a questionnaire from nearly 3000 doctors. The survey showed that 65% of respondents had been involved in “medicolegal matters”. From a mass of data, the authors conclude that medicolegal concerns impact on doctors’ practice of medicine. As potential benefits of medicolegal matters, they list improved communication of risk to patients, disclosure of diagnostic uncertainty, and better methods to track test results and non-attenders. Negative impacts included increased referral to specialists, ordering more tests, and seeing fewer patients. The authors recommend targeted training in patient safety and medicolegal aspects of practice to help doctors to be “better informed”. However, as 65% of the group had been involved in medicolegal matters, it seems unlikely they need to be better informed about them. In the title and throughout the article, there is much emphasis on the word “perceived”. With this heavy emphasis on perception, it might be thought that the key finding was that fear of a medicolegal matter was greater than the reality. In fact, the reverse was found. Of those who had experienced medicolegal matters, 46% had considered retiring early, 39% considered giving up medicine and 38% considered reducing hours of work. The respective figures for those who had not experienced medicolegal matters were 29%, 22% and 21%. The difference was highly significant. An inescapable conclusion is that medicolegal matters result in large numbers of demoralised doctors. The reality is worse than the perception. Unfortunately, the obvious question — What was the outcome of the medicolegal matter? — was not included in the survey. Given the numbers involved, it seems likely that for many doctors, although the outcome was favourable, the process had a profoundly negative effect on their work. Forty-one per cent now regard every patient as a potential litigant. A logical response to these data might have been to ask: (1) Could there be a problem with the way medicolegal matters are conducted? and (2) Is the demoralisation of a large percentage of the medical workforce good for society? Neither question was asked here. This is perhaps not surprising as, in their previous article, the authors questioned, without embarrassment and on the basis of a questionnaire, whether “psychiatric morbidity in doctors is a cause or effect of the medicolegal process”.2 This study is “one of the largest [of its kind] in the world”. Sadly, the authors’ negativity towards doctors and their unquestioning allegiance to current medicolegal practice have greatly diminished its value.

Padraic J Grattan-Smith

In reply: I agree with Grattan-Smith that current medicolegal processes have profoundly negative effects on doctors. I do not agree that my coauthors and I have “negativity” towards doctors and an allegiance to current medicolegal practice. Our aim was to investigate the impact of medicolegal matters on Australian doctors — their emotional response and their practice changes.1,2 We have shown that doctors who have a current medicolegal matter have higher levels of psychiatric morbidity,2 and that most doctors believe they change how they practise due to medicolegal concerns — more so in the case of doctors who have experienced a medicolegal matter.1 Justice Ipp and colleagues,3 when reviewing the law of negligence for the Commonwealth of Australia in 2002 with the objective of limiting liability and damages arising from personal injury or death, made note of the lack of empirical evidence in the submissions they received. We have now provided some empirical evidence of medicolegal matters from the doctors’ perspective. If such a review were conducted now, I would suggest the current medicolegal systems are not good for patients, for doctors, or for the health system in general. The evidence from our studies1,2 now allows a more informed conversation on this issue to take place.

Louise M Nash

To the Editor: The supplement of the Journal published on 16 August 2010 — “Bipolar disorder: new understandings, emerging treatments”1 — illustrates a number of features of the current implementation of the Journal’s supplement policy that are problematic. While it is clearly stated that the supplement “was supported by an unconditional grant from AstraZeneca Neuroscience”, the amount of sponsorship, to whom it was paid, and how it was used were not disclosed. Such information is particularly pertinent as evidence suggests that the pharmaceutical industry has financial motivation to see a widening of the diagnostic boundaries of bipolar disorder and a rebadging of atypical antipsychotics as “mood stabilisers”.2 The provenance of the articles is not revealed — it is not clear whether the articles were solicited, part of a symposium, or from some other source. Bipolar disorder is a controversial area in psychiatry,3 yet despite much useful information in the articles in the supplement, discussion of this controversy is a minor feature and no significant critical appraisal is offered. To give a more balanced view to readers, it would have been desirable to have included articles that highlight the controversy regarding bipolar II and bipolar spectrum diagnoses and discuss the ways in which personality disorders arising from developmental trauma and attachment problems can present with mood and behavioural disturbances that can be confused with bipolar disorder.

Jon N Jureidini · Peter I Parry · Catherine M Houen · Malcolm W Battersby

In reply: Jureidini and colleagues raise legitimate issues pertinent to our Medical Journal of Australia supplement on bipolar disorders, and we are pleased to respond. First, the extent of sponsorship from AstraZeneca was for publication only. One of us (D J C) discussed the idea of the supplement with the Editor of the Journal, and AstraZeneca expressed interest in supporting the project. Neither the Journal editors nor any of the supplement authors were involved in the sponsorship negotiations between AstraZeneca and the publisher of the Journal, and neither received any financial or other assistance or reimbursement from AstraZeneca. Second, as Coordinating Editors of the supplement, we determined the content of the supplement without any input from AstraZeneca, and we directly solicited articles from leading experts of our choice in appropriate fields. All articles were subject to the usual review process accorded all publications in the Journal. Regarding the general issue of the boundaries of the bipolar concept, we are very much aware of the ongoing debate. This is a pervasive issue for a discipline devoid of biological markers that can be used to define a plane of cleavage. Indeed, we highlighted this in the second paragraph of our editorial1 as an “immediate area of controversy”. We also solicited the article by Tiller and Schweitzer specifically to address the diagnostic problems in the area of mood instability; in that article, there is specific mention of both the bipolar spectrum and mood instability in the so-called personality disorders.2 With respect, Jureidini and colleagues fall into a common trap by considering that the use of some atypical antipsychotics in bipolar disorder is a rebadging exercise. This is silliness. One could equally argue that sodium valproate, carbamazepine and lamotrigine are not legitimate mood stabilisers but, rather, rebadged anticonvulsants. Tricyclic antidepressants started life as antihistamines. What matters to us as clinicians and researchers is that people with bipolar disorder are offered the best possible care, irrespective of labels. We are also very much aware of the undeniable burden associated with mood instability and hope that the supplement we helped produce will assist general practitioners, in particular, to deliver better care to patients so afflicted.

David J Castle · Michael Berk · Barbara M Hocking

To the Editor: I found Van Der Weyden’s editorial “Whither medicine? The expansion of non-doctor practice”1 to be an unduly negative view of the emerging new clinical roles, such as nurse practitioners, in our health system. To imply, for example, that the access to prescribing rights for nurse practitioners is a significant challenge (rather than a help) to doctors is contrary to the experience of many such implementations of these roles. I have a clear view of the role of doctors. They should: be in charge and lead the decision-making process of multidisciplinary teams; be responsible for the cognitive and integrative aspects of clinical care, including the initial assessment and planning of management for undifferentiated patient presentations in all care settings; and provide high-level complex care, including procedural and diagnostic services that require their level of expertise. Doctors should not continue to provide clinical services that are not a good use of their considerable training and experience. These services, that could be provided by nurse practitioners, include routine monitoring and prescribing (under protocol and medical leadership) of maintenance treatments (such as haemodialysis treatment or routine diabetes review), and simple repetitive diagnostic or therapeutic procedures. In my experience, many doctors are bored with these intellectually limited aspects of their practice and find the quality of their clinical life substantially enhanced when given the opportunity to work in partnership with nurse practitioners. Again, in my experience, some tertiary-educated nurses are also bored with their limited clinical roles (still dominated by personal care) and can offer much more to the clinical team by focusing on the higher end of their skill base. There are clear differences between doctors and nurses in terms of selection process, education and training. However, this does not preclude both professional groups from looking at their scope of practice and focusing on the tasks that best use their expertise, rather than retaining roles based on custom and practice that are no longer relevant. If doctors embrace and lead the role redesign program, they can ensure that sensible delegations of their clinical tasks to other health practitioners can occur with benefit to all. Resistance and disengagement of doctors will not stop role redesign, as we clearly cannot sustain a health workforce in the future with a staffing model that has not changed materially for 100 years. Resistance and disengagement are more likely to lead to dysfunctional new roles being produced, without the necessary strong relationship with the medical profession required for the best patient care.

Brendan F Murphy

To the Editor: In his recent editorial,1 Van Der Weyden laments the “displacement” of doctors in modern health care by nurse practitioners and physician assistants, and bemoans the fact that discussion and debate about these matters is largely confined to medical tabloids such as Australian Doctor. In this context, the editorial cites unsubstantiated and inflammatory comments from Australian Doctor correspondents claiming that nurse practitioners place patients at risk.2,3 Remarks that nurse practitioners are “a disaster unfolding” and “people will die”3 are not only inflammatory but also inaccurate. Medical and nursing insiders have made these claims with self-appointed legitimacy and without evidence. They demonstrate a surprising level of ignorance about the role of nurse practitioners and the evidence base that supports their practice, particularly in emergency care.4 In an era where the drum of quality and safety in health care and evidence-based practice beats the loudest, where is the evidence to support such claims? Perhaps the lack of evidence is the reason why such claims implying that nurse practitioners present a risk to patients are housed in medical tabloids, where they escape the rigorous scrutiny of peer review that would otherwise expose this deficit. Van Der Weyden bewails that nurse practitioners are the only health professionals “whose skills and talents are extolled”.1 We doubt whether such trivialities are at the forefront of the minds of emergency nurse practitioners, who comprise a large proportion of nurse practitioners in Australia. As part of the broader health care team, their focus — and the focus of their physician, nurse and allied health colleagues — would be on the immediate and ongoing needs of their patients. Van Der Weyden asserts that an assumption of the equivalence of nurses and physicians underpins the political and industrial agenda for “doctor displacement” in general practice in Australia. Such an assertion is entirely moot. High-quality and safe health care cannot be realised by a monopoly of nurses, or physicians, or any other health profession. Nurses and physicians are only two of the many threads in the tapestry of high-quality, safe and evidence-based health care. Their success lies in symbiotic mutualism, not commensalism, amensalism, or parasitism. And, just like in tapestry, pulling any one thread from the fabric renders the picture incomplete.5 Unless there is substantial evidence to the contrary, bringing the safety of nurse practitioners into question is senseless, particularly given the well deserved support they have from their peers in the wider health community and their patients, both in Australia and overseas.

Ramon Z Shaban · Julie M Finucane · Dianne J Crellin

In reply: I welcome the comments of Murphy and of Shaban and colleagues on my recent editorial,1 which explored, as Shaban et al say, the “displacement of doctors in modern health care by nurse practitioners and physician assistants”. The main focus of the editorial was on the current philosophical relativism muddying the definition of what a doctor is and the academic qualifications underpinning all professional training. It calls for equally rigorous criteria to be applied to non-doctor practitioners and their scope for independent practice. Undoubtedly, the potential utility of non-doctor practice is dependent on bilateral mutualism, with a clearly defined scope of practice. However, the push for independent practice remains problematic. Whether there is a genuine commitment for bilateral mutualism to occur, beyond the usual rhetoric, is of concern — witness the recent difficult negotiations on defining the framework for cooperative practice, and the reticent views of doctors on the suitability of nurse practitioners and their scope for independent practice, as reported in Australian Doctor.2-4 The fundamental question, which must be addressed, is whether the granting of Pharmaceutical Benefits Schedule and Medicare Benefits Schedule privileges to non-doctors is simply a political strategy to create a two-tiered health system under the illusion of cost containment.

Martin B Van Der Weyden

Nitro for bones? Cheap and widely available, nitroglycerin is known to stimulate bone formation and inhibit bone resorption. Might it have a role to play in the treatment of bone loss? Jamal and colleagues from the University of Toronto and other centres did a double-blind, placebo-controlled trial of 243 postmenopausal women with lumbar spine T scores of between 0 and - 2.0.1 The women were randomised to receive either nitroglycerin ointment (15 mg/d) or placebo applied every night at bedtime, over a 2-year period. After 2 years, those who used nitroglycerin had a modest but significant improvement in bone density in the lumbar spine, femoral neck, and total hip compared with placebo. Hence, nitroglycerin might be useful in preventing fractures, say the authors. A larger study of the effects of nitroglycerin in preventing fractures is needed, writes Dr Sundeep Khosla from Mayo Clinic in an accompanying editorial.2 1. JAMA 2011; 305: 800-807 2. JAMA 2011; 305: 826-827 Stress and infertility Many infertile women believe that emotional distress such as tension or worry may be the cause of either their failure to become pregnant naturally, or their lack of success with fertility treatment. They’re wrong, at least on the last count, say Boivin, from the Cardiff Fertility Studies Research Group in the UK, and colleagues. The researchers conducted a meta-analysis of links between stress and the success of the fertility treatment, reviewing 14 studies of 3 583 infertile women who were undergoing a cycle of fertility treatment. The women were assessed prior to their treatment for anxiety and stress; the researchers then compared those women who achieved success in infertility treatment with those who didn’t. Emotional distress was not associated with either success or failure; thus emotional distress won’t jeopardise a woman’s chances of falling pregnant, the authors concluded. BMJ 2011; 342: d223 Fractured bisphosphonates Oral bisphosphonates are a mainstay of treatment for osteoporosis; but have also been associated with “atypical” fractures of the subtrochanteric or shaft regions of the femur. The nature of the risk has been unclear in the past; small observational studies have shown conflicting results, say Laura Park-Wyllie from St Michael’s Hospital, Toronto, and colleagues. They conducted a large, population-based, case-control study of 205 466 women aged 68 years or older who took bisphosphonate therapy, comparing those who developed a fracture with those of the same age who did not. The risk of atypical fractures was about 2.7 times greater in those women who had taken bisphosphonates for more than 5 years. But there was no increased risk when the drugs were used for less than 5 years. Moreover, the absolute risk of atypical fractures is low, and bisphosphonates reduce the risk of standard osteoporotic fractures (of the femoral head and intertrochanteric region) by about 25 % say the researchers, which more than offsets the risk of atypical fractures. They say women with osteoporosis should not stop taking bisphosphonates because of the small risk of atypical fractures. JAMA 2011; 305: 783-789 Deafness dementia link Hearing loss appears to be a risk factor for dementia. And the greater the degree of hearing loss, the greater the risk. So say Lin and colleagues from Johns Hopkins School of Medicine and affiliated institutions. They studied 639 individuals aged 36 to 90 years, of whom 125 had hearing loss of varying severity (as measured by audiometry) at the start of the study, but none of whom had dementia. Over a median follow-up period of 11.9 years, 58 people were diagnosed with dementia. The researchers found that the risk of dementia from any cause increased with the severity of the hearing loss; for every 10 decibels of hearing loss, the risk increased by 27%. But further studies are needed to determine if hearing loss is a marker for dementia, or a causative factor in itself. If it is the latter, treatment — for example, with digital hearing aids and cochlear implants — might reduce the risk of dementia, say the researchers. Arch Neurol 2011; 68: 214-220 Back surgery wins out Is surgery effective for discogenic low back pain? Past trials comparing surgical with non-surgical treatments give conflicting results, say Ohtori and colleagues from the Graduate School of Medicine at Chiba University, Japan. In a small randomised trial, they compared the effectiveness of various treatments in 41 patients with discogenic low back pain. A control group of 20 received minimal exercise-based treatment; 15 received anterior interbody fusion (ABF); and, six received posterolateral fusion (PLF) with pedicle screws. Before surgery, there was no difference between the groups in pain and disability scores; but 2 years after surgery, both ABF and PLF groups had less pain and disability than those in the minimal treatment group. Provided it is correctly diagnosed to start with, discogenic low back pain responds to surgical treatment, the researchers concluded. Spine 2011; 36: 347-354

Peter Lavelle