Volume 194 Issue 4

The Journal has a new Editor and big plans for the future With this issue, Dr Martin Van Der Weyden retires after 16 years as Editor of the Journal. A tribute to Martin and his many achievements will appear in the next issue. Martin has been a generous and wise teacher, and his columns have set the benchmark in editorial writing. Under his guidance, the Medical Journal of Australia has become the leading publisher of general medical research in Australia. It makes a vital contribution to the debate on local and global medical issues including Indigenous health, patient safety, the honesty and integrity of scientific publishing and peer review, and Australian health policy. The Journal he bequeaths is robust and central to medical communication in this country. As the Journal of the Australian Medical Association, the MJA has a freedom that is unavailable to most other general medical publications in the country: to publish and report free of commercial interests. You can be confident that studies published in the MJA are subject to strict rules requiring disclosure of conflicts of interest, and that they have been expertly peer reviewed. The MJA is uniquely placed to inform and facilitate discussion and education across our profession, and to anchor it within the context of the broader Australian health system. To keep abreast of changes in clinical medicine and professional issues, and to meet the challenge of maintaining the Journal’s relevance for all doctors in the face of these changes, there are plans for the continued evolution of our print publication and an enhanced presence on the web. The MJA will continue to publish major Australian research studies and remain the natural place for publication of data that are important to all Australian clinicians. I want to foster this role for the Journal. My dilemma, however, is that of the editor of any general medical journal: it is difficult to produce an article that meets the needs of both researchers who are interested in the minutiae of their topic and readers who may prefer a brief overview.1 While many Australian studies are appropriately published in specialty and international journals, general medical journals such as the MJA have a crucial role in building and disseminating a strong, usable base of medical knowledge. All doctors have specialised educational requirements and have to be selective in their reading — 75 trials and 11 systematic reviews are published daily2 — thus there is a greater need than ever for relevant interpretation and commentary. I will be inviting the authors of these “specialty” or “international” papers to write editorials for the MJA, which interpret their data. This will feed into an increased emphasis on articles, written by leaders in their field, that synthesise new information for our readership. I want to develop the MJA ’ s natural role as a forum for the presentation of news relevant to doctors and for debate that develops around these issues. Currently, too many medical issues play out in the public media before the profession has a chance to consider or respond. A prime example has been the coverage of prescribing rights for non-doctors.3 Other important issues include the delivery of effective and efficient health care, the planning for, and training of, our medical workforce, and the improvement of Indigenous health outcomes. Our engagement in this process will determine the degree to which we remain an independent and vital profession and will also help to improve health outcomes for the community. One crucial issue is health funding. Currently, Australia spends over 9% of its gross domestic product on health,4 increasing at up to 0.5% per annum.5 The population is ageing and demands on the health system are increasing, necessitating hard choices with respect to the way a limited health budget is spent. As doctors, we need to understand the opportunity costs of ordering a test or admitting an elderly patient to intensive care. In this way, we can participate in decisions involving the allocation of funds within the health budget. The MJA is the appropriate forum for this informed conversation. Discussion about the practice of medicine needs to continue. Good medical practice: a code of conduct for doctors in Australia, adopted by the new Medical Board of Australia, was developed with little discussion within the profession.6 How this code is implemented is yet to be defined, and we should take this opportunity to explore and, perhaps, refine the way we practise. This debate should include doctors’ contributions to the public health care system, the organisation of medical practices, billing practices and time spent with patients, and the complexities of patient education and obtaining informed consent. Our future doctors also need to be included. I plan to engage more with our readers via electronic media. Inevitably our website, planned to be relaunched, will become increasingly important in the life of the Journal. It will embrace new technologies and media, allow for the publication of more research and medical content and facilitate timely discussion around issues. Soon, I hope you will enjoy easy access to the Journal from mobile electronic devices and that you will use this resource to have your say in these conversations. The MJA is your forum. Already, our recently launched email newsletter, MJA InSight, boasts the highest audited email circulation of any medical newsletter in the country.7 My background is as a general practitioner and medical editor, and I will be seeking to both broaden and strengthen the MJA community so that many voices (not just the loudest or best-positioned) are heard. I will be expanding our base of peer reviewers and plan to introduce a rotating position of “Guest Medical Editor”. This person will commission work in his or her field of expertise and refresh and inform our editorial team about advances in his or her area of interest. Already, I have been overwhelmed by the passion and generosity of the MJA community, who, without favour, payment or (much) recognition, contribute to this publication. Peer reviewers are indeed our “unsung heroes”.1 Thank you to all who already contribute to the MJA and to those who will help in the future. I envisage that an enhanced MJA will play an even more important role in the discussion of issues that affect medicine in Australia. With an expanded range of content and new technologies, we have the potential to engage the entire profession. As the new Editor of the MJA, I look forward to guiding its evolution and to working with you.

Annette G Katelaris MB BS, MPH, FRACGP

Is it time to relax or tighten the legislation on human embryo research? Over the past decade, human embryo research has generated both enormous scientific interest and extensive public debate. In response to this, Australia passed two Acts in 2002: the Research Involving Human Embryos Act 2002 (Cwlth) and the Prohibition of Human Cloning Act 2002 (Cwlth). Together, these Acts, and mirror legislation passed by all states and territories, enabled Australian scientists to undertake specific research involving human embryos, provided that they obtained a licence from the Embryo Research Licensing Committee of the National Health and Medical Research Council (NHMRC), reported regularly to this committee, and had their research approved and monitored by the appropriate institutional ethics committee. At the same time, these Acts prohibited a series of practices — including human cloning, creation of animal–human cybrids, maturation of research embryos beyond 14 days, and the buying and selling of human oocytes — and provided substantial penalties for breaches of the provisions. Consistent with the provisions of the Acts, the legislation was reviewed in 2005–2006 by the Lockhart Committee (the Legislation Review Committee chaired by the late John Lockhart). After extensive community consultation, the Committee made 54 recommendations for amending the existing legislation. Following further public and parliamentary debate (which culminated in a conscience vote in both federal chambers), almost all of these recommendations were accepted and implemented, by the amending legislation in 2006 or administrative changes made by the NHMRC and other relevant regulatory bodies. (The current federal legislation is the Research Involving Human Embryos Act and the Prohibition of Human Cloning for Reproduction Act 2002 [Cwlth].) As a consequence, while the major prohibitions present in the 2002 Acts remained, Australian scientists were able to create an embryo by somatic cell nuclear transfer (SCNT) for research purposes and conduct research on human embryos deemed unsuitable for implantation and on eggs in the process of fertilisation up to syngamy. The legislation is again up for review and, as in 2005–2006, the review must consider: developments in assisted reproductive technology and embryonic stem cell (ESC) research, international developments and legislation relating to the use of human embryos in research, the effectiveness of existing legislation (including whether it has acted as a barrier to important research or clinical practice), and community standards. Since 2006, research involving autologous and allogeneic transplantation of adult somatic stem cells has continued to advance (although the best evidence continues to be for treatment of malignant and immunological diseases) and early studies have confirmed that autotransplantation of haematopoietic and mesenchymal stem cells may have regenerative capacity in treating hepatic, pulmonary, cardiac, neurological and arthritic diseases. Over this period, human ESC research has also provided important insights into normal and pathological cellular biology, reproduction and embryogenesis, and the creation of disease models and systems for screening drugs and predicting toxicity.1 Animal studies of ESCs have also shown promising results in the treatment of spinal injury, neurodegenerative and demyelinating disorders and retinal disease, and the first Phase 1 clinical studies involving adults with spinal injury and stroke and children with macular dystrophy have begun.2-4 At the same time, a series of developments in related fields have also created enormous excitement. In 2006 and 2007, teams of scientists in Japan and the United States reported that they were able to derive induced pluripotent stem (iPS) cells by inducing forced expression of specific genes in adult somatic cells.5 These iPS cells, which resemble ESCs in terms of morphology, mitotic activity, telomerase activity and expression of stem cell genes and proteins, appeared to be an important breakthrough as they allowed generation of stem cells without the use of human embryos, did not require the use of donor oocytes, and avoided the problems of immune rejection and graft-versus-host disease because they were autologously generated.6 While proof-of-concept and animal studies of iPS cells in a range of degenerative disorders show great promise, recent research suggests that iPS cells may have a slightly different gene expression profile to human ESCs, have limited differentiation capacity and undergo premature ageing. Also, significant hurdles remain with regard to the efficiency and safety of iPS cells before human trials can begin.7-9 Recent research has also demonstrated that nuclei from “terminally differentiated” adult somatic cells can be induced (“reprogrammed”) to express genes that are typical of ESCs or of other lineages, and differentiated to form other cell types, thereby enabling autotransplantation of normal tissue to areas of disease, or the generation of new organs or tissues using tissue-engineering technologies.10-12 Despite the fact that this research is in its infancy, the promising results of research involving iPS cells and reprogrammed adult somatic stem cells has (predictably) led some to proclaim the demise of ESC research and to call for the repeal of legislative amendments enabling human ESC research and SCNT. This would be a mistake. Although developments in iPS cell research show promise and human ESC research has not yet been translated into medical therapies, this does not provide a reason for prohibiting ESC research. It remains unclear whether human ESCs, reprogrammed adult somatic stem cells and iPS cells will prove to be bioequivalent or to offer alternative or complementary cellular therapies.7 In addition, as the history of medical research demonstrates, the realisation of clinical benefits from basic research can take decades. Furthermore, the stem cells derived from SCNT may also yield benefits other than medical therapies, including cell lines for drug screening and for research into early embryonic development, normal organogenesis and certain disease states. And, perhaps most importantly, the idea that advances in one field of research should mean researchers are prevented, by law, from exploring another related field of research is, in many ways, antithetical to the principles and processes of science in a liberal democratic society. Australia’s existing regulatory framework provides the most effective means for ensuring that research is important, rigorous and ethically sound in its design and conduct. Should research yield important benefits consistent with the needs and goals of the community, it will prosper. Should it prove redundant, useless or totally at odds with the values of the community, it will not. For all these reasons, and because human embryo and stem cell research enjoy high levels of public support, we should not again seek to prohibit research involving human embryos or the derivation of stem cell lines by SCNT. Whether the current legislation needs to be liberalised further to enable research into mitochondrial diseases, the creation of cybrid embryos or the payment of egg donors, is a matter for debate.

Ian H Kerridge MPhil, FRACP, FRCPA · Aric Bendorf BA, MBioethics

Australia should lead in the effort to reduce the huge burden of non-communicable diseases When it comes to global health, the international aid effort is almost entirely focused on the immense burden that communicable diseases inflict on the world’s low- and middle-income nations. But the world is also facing what United Nations (UN) Secretary-General Ban Ki-moon describes as “a public health emergency in slow motion”.1 Across the globe, non-communicable diseases (NCDs) — principally heart disease, cancer, diabetes, kidney disease and chronic lung disorders — are imposing ever greater burdens on individuals, families, health systems and economies. The World Health Organization believes that NCDs now account for some eight million premature deaths (before the age of 60 years) each year in low- and middle-income countries. Altogether, there are an estimated 35 million NCD deaths each year, with around 80% occurring in low- and middle-income countries.2 Deaths from NCDs are projected to increase by 17% worldwide in the coming decade, with the largest increase (27%) occurring in Africa. The highest absolute number of deaths will be in Australia’s local regions: the Western Pacific and South-East Asia.2 And yet, much of this burden is avoidable, with around 80% of heart disease, stroke and type 2 diabetes and over a third of cancers deemed preventable by eliminating shared risk factors, including tobacco use, poor nutrition, physical inactivity and alcohol misuse. Despite the growing burden that NCDs inflict on the developing world, a pittance — just 2.3% — of overall development assistance for health was dedicated to NCDs in 2007.3 This is even more surprising given the impact that NCDs have on productivity. The World Economic Forum, an organisation of private, mostly multinational companies, already considers chronic disease in both developed and developing nations to be a major risk to the global economy.4 While prevention and treatment of NCDs make sound economic sense, calls for help from developing nations have met with little response. The UN said in a report on NCDs last year that “requests for technical support to scale up efforts, through aid and expertise, remain largely unanswered”.5 There is, however, some light at the end of the tunnel. Things are starting to change. After a concerted campaign by international chronic disease organisations and collective action by Commonwealth and Caribbean countries, the UN has agreed to hold a special summit on NCDs, the first health summit since the landmark HIV/AIDS gathering a decade ago. To be held in New York on 19–20 September 2011, the summit will consider what action might be taken to help all countries, but especially those of low and middle incomes, to meet the NCD challenge. It is clear that NCDs must become a key part of the global health and development agenda. This is the goal of the NCD Alliance,6 a coalition convened by the World Heart Federation, Union for International Cancer Control, International Diabetes Federation and the International Union Against Tuberculosis and Lung Disease. While the global campaign is being waged, an Australian group — Australians for Global Action on NCDs — has formed to encourage the Australian Government to help lead global change, by seeking tangible outcomes from the UN summit and playing a strong role beyond it, particularly in the Western Pacific region. Although much remains to be done at home, particularly for Aboriginal and Torres Strait Islander peoples and those from lower socioeconomic backgrounds, Australia should also boost efforts to assist developing nations in our region escalate their NCD-prevention efforts and improve screening, early detection, treatment and palliation. A gathering organised by our group at Parliament House on 2 March 2011 will help sell the message to federal politicians, many of whom are already sympathetic to the cause. Over the coming 7 months, the world will be looking to countries with strong records in prevention and management of chronic disease to help set the agenda for the UN summit on NCDs. While this includes nations across the income spectrum, Australia should be thrusting its hand in the air. We have much to offer. For example, Australia has been a leader in tobacco control. Robust action, including price hikes, comprehensive advertising bans and investment in social marketing, has seen smoking rates plummet in Australia, from 34% of the adult population in 1980 to less than 20% today.7 So, what do we want from the UN summit? Work is underway to define the best possible outcomes, but there is growing international consensus among NCD Alliance members around six primary objectives: Governments must have NCD plans and be accountable for progress. The existing WHO Framework Convention on Tobacco Control should be fully implemented. There must be a global commitment to prevention of NCDs. Globally agreed approaches to treatment and care must be forged. Resources must be available to deliver effective interventions and enhance the capacity of developing nations to meet the NCD challenge. NCDs must be prominently included in the targets that will follow the current Millennium Development Goals. Reducing the burden of NCDs will take dollars. It will take courage. And it will take long-term commitment. But it will pay for itself many times over by helping countless millions of people to lead longer, healthier, happier and more productive lives.

Australians for Global Action on NCDs*

Objective: To assess the utility of glycated haemoglobin (HbA1c) level as an automated screening test for undiagnosed diabetes among hospitalised patients and to estimate the prevalence of undiagnosed diabetes among hospitalised patients.Design, participants and setting: A 3-month prospective study of all adult patients admitted to a tertiary hospital. An HbA1c test was automatically undertaken on admission for all patients with a random plasma glucose (RPG) level ≥ 5.5 mmol/L. Demographic, admission and biochemical data were obtained from hospital databases. A subset of patients was recruited for an oral glucose tolerance test (OGTT) after discharge.Main outcome measures: Prevalence of undiagnosed diabetes (defined as HbA1c ≥ 6.5% in accordance with International Expert Committee and American Diabetes Association recommendations) and utility of automated HbA1c testing.Results: The prevalence of undiagnosed diabetes was 11% (95% CI, 9.8%–12.4%) (262/2360) during the study period. A further 312 patients with known diabetes were admitted. The prevalence of undiagnosed diabetes was highest in the 65–74-years age group. The HbA1c test cost was $152 per new diagnosis of diabetes. Conservatively assuming an annual incidence of undiagnosed diabetes of 0.8%, the ongoing cost of testing hospitalised patients would be $2100 per new diagnosis of diabetes. RPG testing was not sensitive or specific in diagnosing diabetes. Patients were poorly compliant with the post-discharge OGTT (27% completion rate).Conclusions: HbA1c is a simple, inexpensive screening test that can be automated using existing clinical blood samples. Hospital screening for diabetes needs to be coupled with resources for management in the community.

Nyoli A Valentine MB BS · Tariq M Alhawassi BScPharm, MClinPharm · Greg W Roberts BPharm, FSHP, BCPS · Parind P Vora MB BS, MPH · Stephen N Stranks MB BS, FRACP · Matthew P Doogue MB ChB, FRACP

Objective: To evaluate an intern educational project, the More Learning for Interns in Emergency (MoLIE) project, designed to increase intern placements in the emergency department (ED).Design, setting and participants: The study was conducted in the ED of the Royal Brisbane and Women’s Hospital, Queensland, in 2008. As well as the usual direct contact with patients, interns had 8 hours per week of “off the floor” structured learning time supervised by consultants. This allowed for an increased number of interns to complete a term in the ED over a 1-year period. The study was evaluated by an intern exit feedback survey and a senior staff survey.Main outcome measures: Numbers of intern placements in the ED; intern satisfaction with the project; senior medical staff satisfaction with interns’ skills and performance assessments.Results: The number of interns completing a term in the ED increased from 65 in 2007 to 90 in 2008. Overall, the 90 interns surveyed were highly satisfied with their training. Most agreed or strongly agreed that the sessions were relevant and covered the right mix of clinical and professional issues. Most of the 12 senior staff surveyed felt that the participating interns performed slightly or much better than interns in previous years, and that their experience as supervisors and overall patient care were improved.Conclusions: The project successfully combined increased intern numbers with educational outcomes that were well perceived by interns and senior staff, without adversely affecting service delivery or supervision workload in the ED.

Victoria A Brazil MB BS, MBA, FACEM · Jaimi H Greenslade BPsych(Hons), PhD · Anthony F Brown MB ChB, FRCP, FACEM

Objective: To describe the epidemiology of adult patients hospitalised with influenza or pneumonia during a pandemic season in a sentinel network in Australia.Design, participants and setting: Prospective case series of adult hospital admissions to eight acute care general public hospitals (Influenza Complications Alert Network [Flu CAN] sentinel hospitals) in six Australian jurisdictions, 1 July to 4 December 2009.Main outcome measures: Demographic, clinical and outcome measures in patients admitted with laboratory-confirmed pandemic (H1N1) 2009 influenza in the sentinel hospitals compared with data from national notifications and intensive care unit (ICU) surveillance; admissions for influenza and pneumonia over time in each jurisdiction.Results: During 190 hospital-weeks of observation, there were 538 influenza admissions. Of these, 465 patients (86.4%) had the pandemic strain, representing 9.3% of total admissions with pandemic (H1N1) 2009 influenza (n = 4992) recorded nationally in 2009. Of these patients, 250/465 (53.8%) were women, 67/453 (14.8%) were Indigenous, and the median age was 46 years (interquartile range, 29–58 years). Comorbidities were present in 354/464 patients (76.3%), and 40 were pregnant (30.3% of women aged 15–49 years). FluCAN reported that 102 patients (21.9%) were admitted to ICUs, and of patients admitted to hospital, 26 (5.6%) died. FluCAN results were very similar to national notification data and published ICU admissions data. Of those who were followed to 30 days after discharge, 30 (6.5%) were readmitted. Of 1468 patients hospitalised with pneumonia, 718 (48.9%) were tested for influenza and 163 (11.1%) were co-infected with the pandemic strain.Conclusions: Sentinel surveillance systems can provide important and reliable information in a timely fashion and can monitor changes in severity of influenza during a pandemic season.

Paul M Kelly MB BS, PhD, FAFPHM · Tom Kotsimbos MD, FRACP · Anna Reynolds BSc, PhD · Richard Wood-Baker DM, FRACP · Bob Hancox MD, FRACP · Simon G A Brown MB BS, PhD, FACEM · Mark Holmes MB BS, MD, FRACP · Graham Simpson MD, FRCP, FRACP · Simon Bowler MB BS(Hons), FRACP · Grant Waterer PhD, FRACP, FCCP · Louis B Irving MB BS, FRACGP, FRACP · Christine Jenkins MD, FRACP · Phillip J Thompson MD, FRACP · Allen C Cheng FRACP, MPH, PhD

Objective: To quantify women’s uptake of Medicare Benefits Schedule mental health items, compare characteristics of women by mental health service use, and investigate the impact on Medicare costs.Design, setting and participants: Analysis of linked survey data and Medicare records (November 2006 – December 2007) of 14 911 consenting participants of the Australian Longitudinal Study on Women’s Health (ALSWH) across three birth cohorts (1921–1926 [“older cohort”], 1946–1951 [“mid-age cohort”], and 1973–1978 [“younger cohort”]).Main outcome measures: Uptake of mental health items; 36-Item Short Form Health Survey (SF-36) Mental Health Index scores from ALSWH surveys; and patient (out-of-pocket) and benefit (government) costs from Medicare data.Results: A large proportion of women who reported mental health problems made no mental health claims (on the most recent survey, 88%, 90% and 99% of the younger, mid-age and older cohorts, respectively). Socioeconomically disadvantaged women were less likely to use the services. SF-36 Mental Health Index scores among women in the younger and mid-age cohorts were lowest for women who had accessed mental health items or self-reported a recent mental health condition. Mental health items are associated with higher costs to women and government.Conclusion: Although there has been rapid uptake of mental health items, uptake by women with mental health needs is low and there is potential socioeconomic inequity.

Julie E Byles BMed, PhD · Xenia Dolja-Gore BMaths, GradDipMedStats, MPhilMedSci · Deborah J Loxton BPsych(Hons), PhD · Lynne Parkinson BSc(Hons), PhD · Jennifer A Stewart Williams BCom(Econ), MCom(Econ), PhD

Objective: To examine the costs and cost-effectiveness of full implementation of biennial bowel cancer screening for Australian residents aged 50–74 years.Design and setting: Identification of existing economic models from 1993 to 2010 through searches of PubMed and economic analysis databases, and by seeking expert advice; and additional modelling to determine the costs and cost-effectiveness of full implementation of biennial faecal occult blood test screening for the five million adults in Australia aged 50–74 years.Main outcome measures: Estimated number of deaths from bowel cancer prevented, costs, and cost-effectiveness (cost per life-year gained [LYG]) of biennial bowel cancer screening.Results: We identified six relevant economic analyses, all of which found colorectal cancer (CRC) screening to be very cost-effective, with costs per LYG under $55 000 per year in 2010 Australian dollars. Based on our additional modelling, we conservatively estimate that full implementation of biennial screening for people aged 50–74 years would have gross costs of $150 million, reduce CRC mortality by 15%–25%, prevent 300–500 deaths from bowel cancer, and save 3600–6000 life-years annually, for an undiscounted cost per LYG of $25 000–$41 667, compared with no screening, and not taking cost savings as a result of treatment into consideration. The additional expenditure required, after accounting for reductions in CRC incidence, savings in CRC treatment costs, and existing ad-hoc colonoscopy use, is likely to be less than $50 million annually.Conclusions: Full implementation of biennial faecal occult blood test screening in Australia can reduce bowel cancer mortality, and is an efficient use of health resources that would require modest additional government investment.

Michael P Pignone MD, MPH · Kathy L Flitcroft BBSc, MA(Govt), GradCertHlthPolicy · Kirsten Howard MPH, MHlthEc, PhD · Lyndal J Trevena MB BS, MPhilPH, PhD · Glenn P Salkeld MPH, PhD · D James B St John MD, FRACP, AGAF

Computed tomography coronary angiography is the most reliable diagnostic test for coronary atherosclerosis. Stress testing should be reserved for diagnosis of myocardial ischaemia. Revascularisation, either by stenting or bypass grafts, is commonly performed in patients with stable coronary artery disease but is a double-edged sword. In the presence of ischaemia, revascularisation improves outcomes; in its absence, outcomes are worsened. In current practice, the decision of whether to revascularise is mainly made on the basis of the angiographic appearance of the coronary lesion in question. Physiological assessment of coronary lesions by the use of a pressure wire and measurement of fractional flow reserve (FFR) often shows that lesions thought to be sufficiently severe to warrant stenting or bypass do not cause ischaemia. A recent randomised study has shown that using FFR measurements to guide coronary stenting resulted in a lower use of stents, decreased costs and superior outcomes at 2 years, compared with traditional angiographic assessment alone. We believe that changes to the methods of health reimbursement are needed in both the public and private health systems, to facilitate greater use of FFR measurement.

Richard W Harper MB BS, FRACP, FACC · Brian S Ko MB BS, FRACP

The move to national registration of doctors presents both threats and opportunities for the manner in which doctors seek health care and for providing assistance to doctors who may be impaired by illness. The most striking threat is the regressive nature of the provisions for mandatory reporting of ill doctors. The new system should be grasped as an opportunity to achieve national agreement on resourcing adequate services to help distressed doctors and to foster education and research into the health of doctors and medical students. The new system also provides opportunities to explore ways of encouraging doctors to improve their poor record of not attending to their own health, such as denying Medicare rebates for most doctors who self-refer.

Kerry J Breen MB BS, MD, FRACP

Clinical neurology: a primer. Peter Gates. Sydney: Churchill Livingstone, 2010 (450 pp). ISBN 9780729539357. NEUROLOGY is regarded as a difficult specialty but, paradoxically, neurological illnesses are common. Clinicians will come across a large number of patients with neurological symptoms — headaches, strokes, dementia and a variety of pain syndromes, to name a few — in their day-to-day practice, irrespective of their scope of practice. I have been looking for a good clinical neurology textbook to recommend to my students for several years now, and Associate Professor Peter Gates, neurologist at Geelong Hospital and the University of Melbourne, Victoria, has come up with a gem. I read the book from cover to cover and thoroughly enjoyed it. I also gained new skills in teaching neurology. Gates has successfully demystified neurology. Clinical neurology will help cure students and health care practitioners of their “neurophobia” for good, and readers will discover how easy and enjoyable it really is to study and practise neurology. The book starts with an introduction to clinically oriented neuroanatomy that has a novel approach. The author likens the nervous system to a map grid with longitudes (ascending sensory pathways and descending motor pathways) and latitudes (cortical signs, brainstem cranial nerves, nerve roots and peripheral nerves). He uses a number of cases to explain the concepts involved in diagnosis in a way that is easily accessible to the novice. Subsequent chapters take the reader through the neurological examination process and common neurological presentations from a symptom-oriented perspective. Gates then poses the question, “After the history and examination, what next?”, and goes through all possible answers from “no idea what the clinical problem is” to “seeking a second opinion” and “understanding the principles of solving complex clinical problems”. The book is accompanied by a DVD that demonstrates how to perform a neurological examination and includes a series of high-resolution videos on some abnormal neurological signs. Both undergraduate and postgraduate students will find this to be a valuable resource for mastering clinical neurology skills by observing an experienced neurologist in action. The book is aimed at medical students, young doctors and general practitioners; however, clinicians and neurologists should also find it useful.

Tissa Wijeratne

Is Your Child Overweight? What You Need to Know and What You Can Do. Matt Sabin. Melbourne: Wilkinson Publishing, 2010 (96 pp). ISBN 9781921667510. MATT SABIN is an experienced paediatric obesity expert in both clinical and research fields at the Royal Children’s Hospital Melbourne, and this book is written as a “guide for parents that is both comprehensive and at the same time easily understandable”. Sabin’s clinical experience is clearly demonstrated in his approach to obesity management and in the clinical examples he provides, and the reader will appreciate the extent of his knowledge and practical know-how. Perhaps the scientist in him makes it difficult to avoid discussing rarer obesity facts and presenting detailed scientific arguments around clinical situations, which might be better suited to a professional reader. However, this book goes some way towards addressing the dearth of good-quality information on childhood overweight for parents. The focus is children 12 years of age and under, although there is some very good information on adolescent overweight. The question-and-answer format is excellent, as the reader can choose sections of particular interest. The absolute standout sections are: Is “puppy fat” OK? What factors in the environment are contributing to obesity? Are you a bad parent if your child is overweight or obese? How important is breakfast? The repeated reinforcement, in a positive manner, of parents taking charge and making the time to make family changes works well in this format, and follows the evidence base for obesity management in primary schoolchildren and younger. The quality of the writing is exceptional, but I would have preferred avoiding words such as “transpired”, “non-pejorative”, “incorporate” and “parameters”, which could make the book less accessible for parents with limited reading skills. Medication and surgery also needed to be discussed, if only to dismiss these modalities in children. Finally, sibutramine is mentioned, but the drug was recently withdrawn from the market. This book is well priced and should be recommended to parents and also to clinicians, as health professionals are likely to learn a lot from it.

Katharine Steinbeck

In recent years, a phenomenon of “late effects of the Holocaust” has emerged, with impacts on the psychological and physical health of ageing Holocaust survivors. As Holocaust survivors age, they may experience heightened anxiety around normal processes of ageing, worsened post-traumatic stress disorder with cognitive decline, and fear of the medical system. Holocaust survivors are at increased risk of osteoporosis, cardiometabolic disease due to hypothalamic–pituitary–adrenal axis dysfunction, cancer, and sequelae of Nazi medical experiments. From existing medical literature on this topic, practical principles of management are derived to create a framework for sensitive medical management of Holocaust survivors in Australia. The issues discussed are also relevant to the wider geriatric refugee or prisoner-of-war experience.

Elizabeth D Paratz · Benny Katz MB BS, FRACP, FFPMANZCA

We present the first human case of anisakidosis acquired from eating locally caught fish in Australia. A 41-year-old woman experienced gastrointestinal pain, vomiting and diarrhoea of increasing severity over 3 weeks. All symptoms resolved spontaneously after a worm was passed in her faeces. Microscopic examination showed that it was a Contracaecum species larva of the family Anisakidae. Anisakidosis should be considered in patients with gastrointestinal symptoms who have recently eaten seafood. (MJA 2011; 194: 199-200) Clinical recordA 41-year-old Australian woman of Tongan descent presented to the Royal Adelaide Hospital with a 21-day history of intermittent, worsening gastrointestinal pain, vomiting and diarrhoea after eating raw, locally caught South Australian mackerel. She initially experienced vomiting, diarrhoea and right-sided abdominal pain. These symptoms resolved spontaneously after 2 days. Ten days later, she developed nausea, vomiting, right-sided abdominal cramps associated with a sore throat, rhinorrhoea, nasal congestion, cough with production of yellow sputum, myalgia, fevers, chills and sweats. She visited her local medical practitioner 2 days after these symptoms began, and was prescribed metoclopramide, which relieved the main symptoms. However, the symptoms returned 2 days later with increased severity. She was now vomiting up to six times a day and passing up to 10 bowel motions. She then presented to the emergency department and was given metoclopramide, hyoscine and intravenous fluids overnight. Her symptoms persisted and she was admitted to hospital the following day. On admission, the patient was alert, orientated and afebrile, and her blood pressure and heart rate were normal. Cyanosis and jaundice were not present. Her chest was clear, and her liver and spleen were not palpable. Her right lower quadrant was tender to deep palpation and she had a mild pharyngeal erythema. A complete blood examination, including eosinophil count and blood chemistry, was unremarkable. Three faecal samples were submitted to the Institute of Medical and Veterinary Science (IMVS), Infectious Diseases Laboratories, Adelaide; these were negative for macroscopic and microscopic blood, rotavirus, adenovirus, Clostridium difficile toxin and enteric bacterial pathogens, but mucus and inflammatory cells were present. Parasitology investigation was not requested. Three days after admission, the patient passed in a bowel motion a threadlike worm, about 2 cm long, which was still moving. This worm was forwarded to the IMVS for identification. All symptoms resolved on the day the worm was passed and the patient was subsequently discharged with no further follow-up required. The initial presumptive identification of the larva was an intestinal nematode, possibly a species of the Trichostrongylus or Ascaris genera. However, on further detailed microscopic examination, the larva was identified as a species of Contracaecum (Nematoda: Anisakidae) based on the presence of an intestinal caecum and ventricular appendix (Box) and the position of the excretory pore being at the base of the mouthparts. DiscussionAnisakidosis in humans is a well known disease resulting from accidental infestation with larvae of certain genera of anisakids, causing severe gastrointestinal disorders, allergic reaction and even death.1 This is the first reported case of anisakidosis in Australia. The allergic response can occur against live anisakids or food in which worms were killed by cooking or pasteurisation.2 The pathological changes that occur within the gastrointestinal tract during infestation with anisakids are the combined result of the direct action of the larva during tissue invasion and the complex interaction between the host immune system and the substances released by, or contained within, the parasite.2 In our case, the patient’s symptoms lasted about 3 weeks until a larva was passed in a bowel motion. Several cases of transient luminal anisakidosis have been reported in humans where a larva has been passed hours to weeks after consumption of infested seafood.3 In our case, early symptoms, including vomiting, diarrhoea and abdominal pain, could have been due to unsuccessful attempts of the parasite to penetrate the gastrointestinal wall. The medication prescribed before admission to hospital most likely relieved the symptoms for a limited time. We postulate that the larva survived and moved slowly down the gastrointestinal tract, causing additional symptoms. The sore throat, rhinorrhoea, nasal congestion and cough could have been a concurrent respiratory tract infection or a late hypersensitivity response. Other symptoms could have been due to dehydration as a result of vomiting and diarrhoea. Infestation with Contracaecum larvae has been reported less frequently than infestation with Anisakis larvae.4,5 In addition, reports of anisakid larvae in faeces are scarce.3 However, over 90% of cases described worldwide were caused by a single larva.2,3 The symptoms reported are diverse and cannot be related to specific morphotype of the parasite. For example, anisakidosis due to Pseudoterranova larvae is mostly benign in the United States, but can be a severe infestation in Japan.6 It is known that Anisakis type I larvae in Japanese mackerels caught on the eastern coast of Japan are less pathogenic than those caught on the western coast of the country.7 Of the many records of anisakidosis worldwide, only a few reports identified the larva to species level. This is due to the lack of species-specific morphological features in larval stages. Recently, molecular approaches have been developed to identify larvae specifically.8 In our case, it was not possible to identify the larva to a species level due to inappropriate preservation of the specimen. As human infestations occur after eating infested seafood, it is implied that the mackerel eaten by the patient was infested. In Australia, larval and adult stages of various species of anisakids infest a broad variety of fish, including mackerels.8-11 However, our case report represents the first human anisakidosis acquired from eating locally caught fish. Given that the popularity of consuming raw or undercooked fish (eg, sushi) is increasing, it is possible that anisakidosis is underdiagnosed in Australia due to the vague symptoms and limited diagnostic tests. For example, in a clinicopathological study of 92 cases of anisakidosis in Japan, over 60% of cases were diagnosed preoperatively as appendicitis, acute abdomen, gastric tumour or cancer, ileitis, cholecystitis, diverticulitis, tuberculous peritonitis, and cancer of the pancreas.12 An experienced parasitologist can visualise anisakid larvae with the naked eye in infested fish. However, the encysted larvae are rarely observed by the consumer, as the larval colouration and texture makes it difficult to differentiate larvae from the viscera or flesh of the seafood. The occurrence of larval anisakids, with zoonotic potential in Australian fish, raises the question as to the extent of undiagnosed cases of anisakidosis in Australia. We strongly recommend that a presumptive diagnosis of anisakidosis is considered by a treating practitioner in patients with gastrointestinal symptoms and a recent history of eating raw or poorly cooked seafood. Anterior end (A) and posterior end (B) of the Contracaecum larva recovered from the patient’s faeces Scale bars = 0.81 mm (A) and 0.32 mm (B). Diagnostic features include the thick body and annulated cuticle; intestinal caecum about 2.5 times longer than ventricular appendix; gonads not developed short; tail, with a single spine at the tip; body length and width 17.3 mm and 1.11 mm, respectively; nerve ring 0.33 mm from anterior end; oesophagus 2.93 mm long, 17% of body length; ventricular appendix 2.52 mm long, 86% of length of oesophagus; intestinal caecum 0.96 mm long, 33% of oesophageal length and 38% of length of ventricular appendix; anus 0.07 mm from posterior end and 0.4% of body length. Drawing by Shokoofeh Shamsi. This specimen has been deposited in the South Australian Museum, Helminthology collection.

Shokoofeh Shamsi BSc, MSc, PhD · Andrew R Butcher BSc, PhD

Clinical record A 57-year-old woman underwent an uncomplicated vaginal hysterectomy for vaginal prolapse. Three days later, she re-presented with ischaemic chest pain associated with inferior ST-segment elevation. Thrombolysis was not initiated, due to her recent operation. The patient was transferred to a tertiary hospital for an urgent coronary angiogram, which showed normal, smooth coronary arteries and a thrombus in the right posterolateral branch. The patient was conservatively managed. Investigations for a paradoxical embolus were unrevealing: the results of a bilateral lower limb Doppler ultrasound examination were negative, and a transthoracic echocardiogram showed no evidence of a patent foramen ovale. The patient was discharged home. Three days after discharge, she presented to our hospital with an acute, painless loss of vision in the superior medial quadrant of her right eye. An urgent ophthalmological consultation led to a diagnosis of retinal artery thrombosis. A bilateral carotid Doppler ultrasound result was unremarkable. This second thrombotic event within a short time prompted an examination for underlying thrombophilia. A screening test result for antiphospholipid antibodies was strongly positive: anticardiolipin IgG antibody, 143 units (reference range [RR], < 20 units); β2-glycoprotein IgG antibody, 185 units (RR, < 20 units); lupus anticoagulant, 1.5 (RR, < 1.3). Results of tests for factor V Leiden (R506Q) and prothrombin gene (20210) mutations and antithrombin III, protein C and protein S deficiencies were negative. On further questioning, our patient revealed that she had experienced intermittent visual blurriness in the right eye since 1992. She had previously been treated for a lupus-like condition with hydroxychloroquine. She had Raynaud’s phenomenon affecting her fingers, and chronic shoulder and limb pain. Interestingly, the patient also had Dupuytren’s contracture bilaterally in her hands and feet; this may have been part of her connective tissue disorder. While she was being treated, the patient’s visual symptoms resolved. Her hydroxychloroquine treatment had been discontinued several years previously because her test results for serum antinuclear antibody (ANA) became negative. A screen for autoimmune disease at our hospital showed a strongly positive ANA titre of 1/1280 (RR, < 1/160) with a finely speckled homogeneous pattern, consistent with a lupus-like connective tissue disorder. Additional screening test results for autoimmune disease (anti-Ro, anti-La, anti-RNP, anti-Sm, anti-Scl-70, anti-Jo 1, anti-PCNA, antiribosomal P, anti-PM-Scl, and antismooth muscle) were negative. To prevent recurrent thrombotic events, warfarin treatment was commenced, aiming to achieve a target international normalised ratio of 2.5–3.5, and therapeutic enoxaparin was administered during the warfarin titration period. Hydroxychloroquine treatment was also begun, at a dose of 200 mg orally twice a day. We hypothesise that our patient had longstanding untreated connective tissue disease associated with antiphospholipid syndrome (APS). Her previous intermittent visual blurriness may have been caused by microthrombotic events. Her recent hysterectomy was the only major operation our patient had undergone (she had previously had a repair of Dupuytren’s contracture in her right foot). The recent surgery and associated release of inflammatory mediators may have been the trigger that caused endothelial activation in her coronary and retinal arteries, causing myocardial infarction and visual loss, respectively. APS can have multiorgan manifestations, and is commonly associated with a connective tissue disorder such as systemic lupus erythematosus (SLE).1 Unrecognised APS can have life-threatening consequences. It is a rare cause of myocardial infarction and, conversely, myocardial infarction is not an uncommon presentation of APS. In a cohort of 1000 patients with APS, 2.8% first presented with myocardial infarction.2 Recurrent coronary arterial thromboses have also been reported in patients with primary APS.3,4 Myocardial infarction due to APS is often undiagnosed initially, because the association between myocardial infarction and APS is under-recognised. Our case illustrates the importance of screening patients with SLE for APS, and highlights the importance of recognising and treating APS in patients with unusual recurrent thrombotic events. Lessons from practice Myocardial infarction associated with antiphospholipid syndrome is under-recognised. Antiphospholipid syndrome should be suspected in patients with unexplained, recurrent thrombotic events. Patients with systemic lupus erythematosus should be screened for antiphospholipid antibodies at baseline, with repeat screening when new thromboembolic risk factors arise. Low-dose aspirin should be considered in patients with systemic lupus erythematosus who test positive for antiphospholipid antibodies, as primary prevention of thrombosis and pregnancy loss. The European League Against Rheumatism (EULAR) recommends screening patients with SLE at baseline for antiphospholipid (aPL) antibodies, and to repeat screening in previously negative patients when there are new risk factors for thromboembolism, such as pregnancy, surgery, transplantation and use of oestrogen-containing treatments.5 The other indications for screening patients for aPL antibodies are recurrent venous and/or arterial thromboses, especially in patients younger than 50 years, recurrent miscarriages or fetal loss and early or severe pre-eclampsia.1 SLE and a positive test result for aPL antibodies, especially persistent anticardiolipin antibodies and lupus anticoagulant, increase the risk of thrombosis.1 Data on primary prevention in asymptomatic patients are limited. EULAR recommends consideration of low-dose aspirin in patients with SLE for primary prevention of thrombosis and pregnancy loss.6 However, asymptomatic individuals testing positive for aPL antibodies do not appear to benefit from aspirin.7 For patients with SLE or a lupus-like connective tissue disease who test positive for aPL antibodies, we recommend making a case-by-case decision on primary prevention, based on an assessment of each patient’s thromboembolic risk profile.

Bo Xu MB BS(Hons) · John Hounsell FRACP

To the Editor: Before and since 1 July 2010, when the National Registration and Accreditation Scheme for health practitioners commenced, the claim that mandatory reporting laws will deter impaired doctors from seeking help has frequently been made. It was on the basis of this claim that Western Australia legislated to exempt health professionals from reporting impaired practitioners they are treating. At a recent conference of the Royal Australian College of General Practitioners, a representative of a medical indemnity organisation labelled the mandatory reporting laws a disgrace because the health of impaired doctors who are deterred from seeking help for this reason would be put at risk. However, she also indicated that the problem was more one of perception than reality because doctors feared triggering a mandatory report automatically if they sought help from another doctor for a perceived impairment.1 It is a problem of perception because, under the laws, only doctors whose impairment places the public at risk of “substantial” harm are required to be reported.2 If doctors have an unreasonable fear of mandatory reporting, we can infer that many are unaware of the details of the laws, in particular the reporting thresholds. Yet an argument against introducing the laws was that doctors were already under an ethical obligation to report, to the relevant authority, unprofessional conduct, impairment or performance that would put patients at risk.3 For this argument to be valid, doctors would need to be aware of the details of mandatory reporting because the Medical Board of Australia’s code of conduct for doctors states, in its list of ethical obligations, that doctors should be aware of their reporting obligations.4 So this particular argument does not appear to be valid. Because medical professionalism puts the wellbeing of the patient first; because psychological or physical health status may affect professional performance; and because the Board, like the state boards that preceded it, has a primary duty to the safety of the public — any doctor whose impairment poses a substantial risk or, in the absence of that doctor’s insight, any treating doctor who considers that a substantial risk exists should surely feel ethically compelled to report the matter to the Board. No doctor whose impairment does not pose a substantial risk should feel deterred from seeking medical help. The consequences for impaired doctors who are reported under the new legislation are no different from those of reporting a doctor when it was “merely” an ethical requirement — being placed on an impaired practitioners’ register and supported, managed and monitored, while, in most cases, continuing to practise. If impaired doctors and their treating doctors feel deterred by mandatory reporting laws, we are entitled to conclude that there was, and continues to be, significant non-compliance with the ethical obligations that arguments against mandatory reporting depend on.

Malcolm H Parker

To the Editor: A 28-year-old man presented to his general practitioner with a history of epigastric pain and constipation over 1 month. In addition, he had a history of chronic low back pain. Findings on physical examination were unremarkable. Laboratory investigations showed normo-chromic, normocytic anaemia with basophilic stippling (Box 1). His whole-blood lead level was subsequently estimated to be 4.12 μmol/L (level recommended by the National Health and Medical Research Centre for all Australians, < 0.48 μmol/L). The patient was referred for toxicological review. Further questioning revealed he had used three Ayurvedic medicines (Vatyog [Arya Aushadhi Pharmaceutical Works, Indore, India], Sahacharadi [Arya Vaidya Nilayam, Madurai, India] and Gandharvahastadi [Arya Vaidya Nilayam, Madurai, India]) for back pain, dispensed to him 3 months earlier during a trip to India. He ceased taking the medications, and a 19-day course of oral chelation with succimer was administered. His blood lead concentration fell rapidly, with a moderate rebound 6 weeks after the completion of chelation therapy. A negative blood lead result for the patient’s pregnant partner excluded environmental exposure in the patient’s home. Vatyog and Sahacharadi were analysed for heavy metals (Gandharvahastadi was not available for analysis). Sahacharadi was lead-free, but the Vatyog tablet tested contained 448 μg of lead. The patient had potentially ingested 896 μg of lead daily for 3 months. World Health Organization guidelines recommend daily lead intake should not exceed 3.5 μg/kg/day.1 Dietary intake of lead in developed nations has been reported to be about 0.1–0.7 μg/kg/day.1 Ayurvedic medicine originated in India more than 2000 years ago and relies heavily on herbal products.2 Many people take Ayurvedic medicine without any problems. In some traditional remedies, salts of heavy metals are included as active ingredients.3 A study in the United States found that one-fifth of Ayurvedic herbal products manufactured in South India and sold in Boston contained potentially harmful concentrations of lead, mercury or arsenic, or combinations of these.2 In Australia, traditional Indian and Chinese medicines authorised for supply are regulated as complementary medicines and must meet manufacturing and quality standards that ensure the absence of contaminants.3 However, there is no quality control of medications imported for personal use or purchased over the internet. Importantly, this case involved tablets prepared by a registered pharmaceutical manufacturer and presented in sophisticated packaging (Box 2). Reports of lead contamination from traditional Indian and Chinese medicines have been intermittently publicised4,5 and include recent warnings from the New South Wales Health Department concerning Ayurvedic medicines. Patients with lead toxicity commonly present with non-specific clinical features, and lead poisoning might only be suspected when a blood film shows anaemia with basophilic stippling. While enquiring about a patient’s environmental, occupational and social history is important for determining possible sources of lead exposure, clinicians should also ask patients if they have used alternative and complementary medicines and whether these were obtained in Australia or from overseas. 1 Blood film from the patient showing coarse basophilic stippling 2 Packaging from the lead-containing Ayurvedic medicine

Nilika G Wijeratne · James C G Doery · Andis Graudins

To the Editor: I describe two episodes of transient recurrence of psychosis temporally related to ingestion of an “energy drink” in an obese (125 kg) 27-year-old New Zealand Maori man who had been diagnosed with schizophrenia 8 years earlier. The patient had found that risperidone 6 mg/day effectively relieved persecutory ideas and auditory hallucinations. He had stopped using cannabis and alcohol to excess, but continued to drink up to 10 cups of instant coffee throughout the day for a “lift”, apparently without insomnia or other complications. In July 2009, he consumed a 60 mL Demon Shot energy drink and enjoyed an hour-long “buzz”. Repeating the dose did not re-create the desired effect, and instead made him uneasy, irritable and paranoid; for the first time in many months, he had recurrent thoughts, lasting several hours, of people wanting to harm him. One week later, he drank three shots over 15 minutes. He again experienced a buzz and was observed to be emotionally labile — initially laughing and talkative, and later, restless, withdrawn and argumentative. He had a rapid pulse and insomnia. These symptoms subsided over the next day, and when he was back to his usual self after a further 2 days, he described having had paranoid ideas (“gangsters after me ... scared to leave the house”) over several hours after consuming the drinks. His family also associated these symptoms with the drinks, noting a striking similarity to his illness before commencing antipsychotic treatment. He has since avoided energy drinks and continued risperidone monotherapy, remaining stable for 15 months. Demon Shot is a concentrated energy drink, widely available in Australia and New Zealand. The product’s web page describes each “insanely intense” shot as containing 200 mg caffeine, plus taurine, guarana, and B vitamins (http://www.demonenergy.com.au/products/demon-shots). As a regular smoker, the patient does have increased caffeine metabolism, and his response to consuming large amounts of coffee suggests he is not particularly sensitive to caffeine. Nevertheless, he did exceed the maximum recommended dose (two shots per day) on the second occasion, consuming at least 600 mg of caffeine (4.8 mg/kg) virtually as a single dose. The additional presence of guarana extract (48 mg per shot in Australia; unspecified in New Zealand) is probably relevant, as guarana is a further source of caffeine and may have other stimulant properties. Caffeinated drinks are popular among patients being treated for schizophrenia,1 possibly due to partial reversal of the unpleasant effects of dopamine blockade.2 Although case reports3 and a later controlled study4 suggest that high doses of caffeine may exacerbate psychosis, this has only recently been described for energy drinks.5 This case provides naturalistic challenge–dechallenge–rechallenge evidence that some patients with treated schizophrenia may be vulnerable to exacerbation of their illness by such products.

David B Menkes

To the Editor: At budget estimates hearings of the Senate Community Affairs Committee in June 2010, answers were provided to questions on notice asked by Senator Guy Barnett to the Therapeutic Goods Administration (TGA) about the use of mifepristone for medical abortion in Australia since 2006.1 The answers are of interest as they include the number of practitioners who have become authorised prescribers of mifepristone in Australia since the “Harradine Amendment” was overturned in federal parliament in February 2006, as well as details of their practice. Nationally, 81 medical practitioners now have TGA authorised prescriber approval for mifepristone: 33 in New South Wales and 18 in Victoria (several large private clinics have gained approval in these states); 15 in South Australia, six in the Australian Capital Territory, five in Western Australia, and four in Queensland. There are none in Tasmania or the Northern Territory, so women in these two regions have no access to mifepristone abortion. There is very accurate documentation of all adverse effects of mifepristone–misoprostol medical abortion, which must be reported 6-monthly to the TGA. This information is then available to the general public through Senate estimates questioning. To 31 December 2009, 2926 medical abortions using mifepristone and misoprostol were performed in Australia by authorised prescribers. These include early and late procedures. The following adverse events were reported in that period: significant haemorrhage (7; 0.24%); retained products of conception requiring dilatation and curettage (D&C) or dilatation and extraction (84; 2.9%); ongoing pregnancy requiring surgical evacuation (14; 0.48%); and nausea and vomiting (10; 0.34%). These results are all well within the parameters expected from Australian and overseas studies of mifepristone–misoprostol use,2-5especially as a high proportion of the 2926 abortions would have been performed in the second trimester, as reported in a recent WA study.2 Large overseas studies on the use of mifepristone–misoprostol for early medical abortion (to 63 days of pregnancy) show a continuing pregnancy rate of around 1%, the need for D&C in 2%–3% of cases, and heavy vaginal bleeding requiring transfusion among 1 : 500 to 1 : 1000 women.3-5 These complications are more common in second-trimester procedures than in early medical abortions.2-5 Use of mifepristone in Australia is still restricted to authorised prescribers, and it is therefore not accessible to many women who might wish to use it. However, the number of cases performed in Australia is now large enough to conclude that mifepristone is safe and effective for the Australian women able to access it.

Caroline M de Costa

To the Editor: Following the 1918 influenza pandemic, during which an estimated 50 million people died,1 the relationship between influenza and secondary bacterial infections such as Streptococcus pneumoniae (pneumococcus) became recognised as an area of considerable scientific importance. It has been shown that influenza infection results in epithelial damage, up-regulation and exposure of respiratory tract receptors, alterations in the immune response and increased adherence of pneumococcus.2 The most severe form of pneumococcal infection, invasive pneumococcal disease (IPD), has a mortality of 7%–9%.3 It occurs frequently in the Indigenous population of the Northern Territory, with an incidence of 70.5 per 100 000, compared with 7 per 100 000 in Australia overall.3 In population studies, 11%–20% of seasonal increases in IPD have been attributed to influenza.4,5 During the increase in influenza notifications in 2009 in the NT, as a result of pandemic H1N1 (2009) influenza, a concurrent increase in IPD notifications was also recorded. Our study aimed to investigate whether there was a relationship between influenza and subsequent IPD. We calculated the relative risk of IPD in the 4 weeks after laboratory-confirmed influenza compared with the background risk. Cases were defined as patients who were diagnosed with IPD within 4 weeks of laboratory-confirmed influenza being diagnosed. Data concerning cases of influenza and IPD between 2005 and 2009 were extracted from the NT Notifiable Diseases System and merged by date of birth using Stata, version 11 (StataCorp, College Station, Texas, USA), leading to 75 matches. The 75 matched records were checked individually to determine whether they met the case definition, resulting in eight potential cases. Demographic characteristics (name, sex, Indigenous status and address) were then checked to confirm the match. One case was excluded, leaving seven cases eligible for analysis. We identified 2567 cases of influenza and 346 cases of IPD in the study period. The risk of IPD within 4 weeks of influenza was calculated as 7/2567 (2.7 × 10-3). To calculate the background risk of IPD in a 4-week period, we first calculated the annual risk of IPD occurring without previous influenza (339/1 076 470 person-years) and divided this by the number of 4-week periods in a year (13). This gave a background risk of 2.42 × 10-5 and a relative risk of 112.5 (95% CI, 48.9–224.8; χ2 = 758.3; P < 0.001). This analysis is based on population surveillance data, and is therefore limited by the possibility of ascertainment bias due to variations in influenza testing. Nevertheless, our study provides additional evidence that IPD is an important complication of influenza, and reinforces the need for clinicians to promote influenza vaccination in high-risk individuals and to be aware of complications which may occur in the weeks after the initial viral infection. Additionally, achieving high coverage of pneumococcal vaccination in at-risk groups will reduce the impact of influenza.

Laura J Edwards · Peter G Markey · Heather M Cook · James M Trauer · Vicki L Krause

To the Editor: Resistant gram-negative bacteria (especially Escherichia coli) are a major and growing problem worldwide.1 Some strains are resistant to all available antibiotics.2 We report a patient with relapsing multi-resistant E. coli bacteraemia from a prostate infection. Relapses occurred despite treatment with numerous parenteral antibiotics that should have been effective. His infection was cured using azithromycin. A 69-year-old man developed dysuria and fever 2 days after a transrectal prostate biopsy; he had received ciprofloxacin for prophylaxis. He had travelled to Morocco 15 months before this episode and to Vietnam 1 year earlier. Blood and urine cultures grew E. coli that showed sensitivity to ceftriaxone, gentamicin and nitrofurantoin; intermediate sensitivity to ampicillin; and was resistant to ciprofloxacin, cotrimoxazole, tetracycline, doxycycline and cephazolin. He was treated with intravenous ceftriaxone for 2 weeks, followed by oral amoxycillin/clavulanate with a good clinical response. The patient relapsed 1 week after completion of this treatment, with dysuria and fever. E. coli was cultured from his urine, with the same sensitivities as before. He was treated for 4 days with ceftriaxone and 2 weeks with amoxycillin/clavulanate. One week after his second course of therapy, he re-presented with dysuria and fever. Urine and blood cultures grew E. coli with the same sensitivities as the previous cultures. A prostate ultrasound showed no focal abscesses. He received ceftriaxone 2 g and gentamicin 7 mg/kg, yet remained febrile. After 2 days, gentamicin was discontinued and azithromycin 500 mg orally daily was added. He became afebrile within 24 hours and his C-reactive protein level fell. Azithromycin was selected because its minimum inhibitory concentration was 4 μg/mL, and because of its efficacy against multiresistant salmonella.3 The patient was treated for 1 week with ceftriaxone and for 3 weeks with azithromycin. He remained asymptomatic and his C-reactive protein normalised. There were no further relapses. He underwent prostatectomy for confirmed prostate cancer 2 months after discontinuing azithromycin. There was no histological evidence of prostate infection. We believe that while travelling in Morocco or Vietnam, he acquired multiresistant E. coli, which was carried in his bowel and inoculated during transrectal prostate biopsy, a common infective risk of this procedure. We believe the initial treatment failure was due to poor antibiotic penetration of the acidic prostate environment, and azithromycin was responsible for the eventual cure. Case reports and clinical trials have shown successful use of azithromycin in treatment of chronic prostatitis due to Chlamydia trachomatis,4 and that azithromycin is active against E. coli.5 This case report demonstrates successful use of azithromycin for treatment of E. coli prostatitis resistant to ciprofloxacin.

Simon H T Jiang · Peter J Collignon

To the Editor: As a family history of cystic fibrosis (CF) is uncommon among children diagnosed by newborn screening, offering carrier testing in the general population is warranted Cystic fibrosis is the most common severe autosomal recessive genetic condition in children. The carrier frequency in populations of Northern European ancestry is one in 25 and the incidence of CF in Victoria, Australia is 1 in 2874.1 There is no cure for CF, but advances in management have improved life expectancy. A question about a family history of CF is often asked as part of preconception or prenatal care in populations in which CF is more prevalent. However, anecdotally, most parents of a baby with CF do not report a family history and the diagnosis is unexpected. Carrier testing would provide information that may be used by couples to make reproductive decisions, such as prenatal and preimplantation genetic diagnosis of a fetus or embryo, respectively. Australia, the United Kingdom, other European countries, and all states in the United States now offer newborn screening for CF. Apart from records of affected older siblings,1 there are no clinical data for the existence of a family history of CF among children diagnosed with CF through newborn screening. We audited the family pedigrees, collected soon after diagnosis, of all children born in Victoria in 2000–2004 who were diagnosed with CF through newborn screening. From the extended pedigrees of 82 children, we identified five families with a family history of CF. In two pedigrees, the children were first cousins; in another two pedigrees, the children were first cousins once removed; and in one pedigree, the children were second cousins. There were no families in which older siblings had been previously diagnosed with CF, but in two families the diagnosis triggered further examination of older siblings who were subsequently diagnosed. These empirical findings that most babies with CF (77/82; 94%) are born to families with no family history of CF support clinical observations. Although inquiry about a family history of CF is necessary as part of prenatal or preconception care, this is not sufficient. Even when a family history is known, most relatives do not undertake carrier testing. For example, in an audit of cascade carrier testing after a diagnosis of CF through newborn screening, only 11.8% of eligible (non-parent) relatives were tested.2 Not surprisingly, a family history-based approach to offering carrier testing will not provide the vast majority of couples with the opportunity to learn their carrier status and make informed reproductive decisions. Therefore, in addition to newborn screening to diagnose affected babies, CF carrier screening in the general population (of individuals with a risk of one in 25)3 is needed.

Belinda J McClaren · Sylvia A Metcalfe · David J Amor · MaryAnne Aitken · John Massie

To the Editor: Rahman and colleagues suggest that iodine deficiency in Victoria increased between 2001 and 2006, based on the findings of thyroid-stimulating hormone (TSH) levels in neonates at routine newborn screening.1 Indeed, their data as presented suggest a doubling of the percentage of mothers with iodine deficiency to over 9% during that period. This could be correct. Certainly, as they state, there is much evidence to suggest that there is mild iodine deficiency in Australia. However, there are caveats about the data they report which are not mentioned. Data from New South Wales do not show this trend. While they do suggest a degree of mild iodine deficiency, there was no increase in the percentage of neonates with TSH levels > 5 mIU/L of whole blood from 2002 to 2009 (Box), although the average age at sampling falls slightly (from 2.96 to 2.32 days) over this period. The World Health Organization has defined iodine sufficiency as being indicated, inter alia, when more than 3% of newborns aged 3–4 days have a TSH level > 5 mIU/L of whole blood.2 Factors that affect the TSH level in a newborn screening program include the precise age at sampling, and any changes to the method of TSH analysis used. In a Swiss study assessing the efficacy of iodine supplementation, there was a small but significant decrease in the TSH level from Day 3 to Day 4 of age.3 This is unsurprising: following the TSH surge in the first hours after birth, TSH levels decline gradually to a steady level at about Day 7.4 There could well have been a trend to earlier sampling in Victoria, within the bounds of the 2–4 days of age assay that Rahman and colleagues mention, over the period studied, but these crucial data are not given. The dried blood spot TSH assay method is not described either. A change in any aspect of the methodology; for example, if the manufacturer modified the antibody used, may produce a small, clinically insignificant but numerically significant, change in results. If the data presented by Rahman and colleagues for Victoria do not have these biases, then the situation warrants further investigation, but whatever is happening in Victoria seems not to be replicated over the border. Percentage of newborns with thyroid-stimulating hormone (TSH) level > 5 mIU/L of whole blood, detected by routine newborn screening in New South Wales, by year Year Newborns with TSH level > 5 mIU/L 2002 3.80% 2003 3.68% 2004 3.87% 2005 5.02% 2006 4.48% 2007 3.56% 2008 3.92% 2009 4.00%

Bridget M Wilcken · Veronica C Wiley

In reply: The methods used for blood sample collection and analysis remained unchanged during our data collection period. One source of thyroid-stimulating hormone (TSH) calibrators and reagents was used over the study period by a single laboratory covering all of Victoria. Material from the United States Centers for Disease Control and Prevention was used for external quality assurance, ensuring that the results were in agreement with those of other laboratories. The per cent coefficient of variation over the period ranged from 10% to 20%. The table of neonatal TSH values for New South Wales provided by Wilcken and Wiley further demonstrates the value of using TSH levels as a screening tool for population iodine status, even with a decreasing mean age of sample collection. While we dealt with the effect of sample collection time in our published article,1 here we present a table illustrating analysis of the Victorian neonatal TSH values for samples collected at 48, 72 and 96 hours after birth (Box). The percentage of elevated TSH values increased from 2001 to 2006 at each collection time and, although the percentage of elevated TSH values decreased with increasing age, these values were still indicative of iodine deficiency. Iodine status varies between regions. The National Iodine Nutrition Study (NINS) found both South Australia and Queensland iodine sufficient, while the neighbouring states of NSW and Victoria were iodine deficient.2 The results also indicated that iodine status was worse in Victoria than in NSW; therefore, we might expect similar differences in TSH values. We are now in the process of analysing Victorian TSH values for 2007 to 2010. Percentage of newborns with thyroid-stimulating hormone (TSH) level > 5 mIU/L for blood samples collected at 48, 72 and 96 hours after birth, Victoria, 2001–2006 Sample collection time (h) Percentage of neonates with TSH > 5 mIU/L according to birth year 2001 2002 2003 2004 2005 2006 48 5.73% 6.83% 8.47% 10.58% 11.86% 13.53% 72 4.20% 5.15% 6.87% 7.01% 9.13% 9.38% 96 2.49% 3.21% 4.37% 3.78% 5.98% 5.34%

Ashequr Rahman · Gayle S Savige · Nicholas J Deacon · Ivan Francis · Janice E Chesters

To the Editor: O’Leary and Major1 have opened debate on the issues raised by the New South Wales-wide introduction of the Clinical Excellence Commission Between the Flags (BTF) observation charts, which incorporate escalation thresholds for vital signs and other criteria. In the BTF charts, “yellow” zone criteria trigger a clinical review and “red” zone criteria, a rapid response.2 Evidence shows that deterioration can be recognised early, reducing serious consequences.3,4 O’Leary and Major trialled a subset of the draft BTF paediatric calling criteria in the context of triage in an emergency department, applying them retrospectively and comparing the actual triage decision with the one that would have been made using the BTF criteria alone. They also examined patient disposition for patients falling within the yellow and red zones. They concluded that “the physiological parameters ... are not suitable as a triage tool in the paediatric emergency department, do not replace an experienced triage nurse, and are a poor predictor of disposition”.1 We are not surprised by this conclusion. The Australasian Triage Scale is designed to assess a patient’s urgency based on presenting problem and general appearance, possibly combined with physiological observations.5 Trialling a subset of vital signs, on their own, against the triage process, although interesting, is unlikely to demonstrate a strong correlation in decision making for the following reasons. The BTF vital signs observations are designed for use in the context of a “track and trigger system” in a general ward, to monitor trends, not as a substitute for the triage process. Vital sign observations on their own contribute little to triage decisions. Triage decisions are poor predictors of disposition (eg, up to 67% of triage Category 2 patients are discharged home from the emergency department) (Sydney South West Area Health Service emergency department data for July 2010, for Campbelltown, Liverpool and Royal Prince Alfred hospitals). On their own, we would expect vital signs to be poorer predictors of disposition outcome than triage decisions, which have the benefit of information on presenting problem and general appearance. Context for vital sign observations has a major influence on their interpretation. We recommend that more work be done on the value of the BTF vital signs criteria as a complement, not alternative, to triage processes.

Charles H Pain · Clifford F Hughes · Marino Festa · Jodie Ekholm · Matthew O’Meara

To the Editor: Pearce and Haikerwal state that “legislation to introduce health identifiers [was] recently passed by Parliament” and that e-health “can ease the patient journey, improve quality of care and reduce costs”.1 It is critically important to comprehend the purpose of the unique health identifier. Its primary function is to be the “key” to a patient’s clinical data and information. It is not a clinical decision-support tool that will improve care. There are many systems that require multiple identifiers for a given patient. However, the success of these systems is dependent on their ability to provide information management tools.2-5 The authors correctly state that “Australia’s health care system lags behind all other sectors of our economy in the use of computerised systems”. What must be debated is their statement that, although “general practice and community pharmacy are highly computerised, the hospital sector is not”. The debate should move from the uptake numbers for computerisation to the evidence of whether these implementations have improved care — for example, through fewer adverse drug events, decreased resource use, improved quality of care and better patient outcomes. I suspect the evidence is very thin in the Australian context. The authors observe: “Uncoordinated implementation of differing, incompatible systems within and between hospitals compounds a dire lack of national coordination of effort.” This is not a new phenomenon. We actually know what works and, in some advanced systems, what does not work.6 This evidence base should provide the stimulus for pursuing the changes necessary to implement effective health information technologies. These changes are more social, professional and cultural than technical.7 In their final comments on the National E-Health Transition Authority, Pearce and Haikerwal maintain their focus on the technologies. Can we wait 5–10 years for the e-health system to be connected via the National Broadband Network? The necessary information management tools can be implemented now. Care must be a priority. It would help if the focus was on successful implementation and a willingness to listen to those who have some degree of success in this field. A review of the National E-Health Transition Authority’s website list of clinical leaders suggests that there are few clinical informaticians currently involved.

Terry J Hannan

To the Editor: E-health’s great promise is to improve health care delivery efficiency and effectiveness1 by enhancing multidisciplinary care planning and information exchange.2 General practice is now largely computerised.3 However, a chain is no stronger than its weakest link, and Australia’s otherwise slow progress towards linking secondary care into a functioning national e-health system is frustrating.1,4 We join the chorus, raising concerns about the e-health readiness of the paediatric sector. We recently surveyed the e-health readiness of paediatricians via the Australian Paediatric Research Network (APRN), a network of about 370 non-tertiary paediatricians broadly representative of all states and territories.5 Established in 2007, the APRN aims to facilitate multisite research into common chronic childhood illnesses where they are most commonly seen — in paediatric secondary care settings. Core to this goal is testing cross-sectoral care models, which requires shared e-health capabilities. The APRN’s annual web-based Multi-Topic Survey in April–May 2010 (n = 181, 48% response) contained a section on computer use with outpatients and in private rooms (Box). Almost all respondents reported having access to a computer at work. However, the reach of e-health is otherwise disturbingly low, its quality is questionable and, when used, it is mainly for clerical purposes rather than patient care. The 27% of respondents using computerised medical records reported more than 10 different systems, suggesting possible future barriers to information exchange and e-health initiatives. We applaud the rapid progress made in general practice,3 but general practitioners do not work in isolation. Our survey shows that, despite similar computer access, Australian paediatricians (and probably other physicians) are a long way behind. This has major implications for policy, shared care programs and the feasibility of e-research. E-health can only provide national benefits in our new world of chronic disease if all health sectors are involved. On a positive note, the current low rate of computerisation in paediatric patient care means that e-health implementation for secondary care could yet be coordinated and integrated from the outset. This opportunity should be seized while still possible. Resources, government funding, planning, a solution focus and the will to move forward are urgently needed. Australian Paediatric Research Network Multi-Topic Survey 2010: computer and e-health use among paediatricians Variable Proportion Computer access Access to computer at work 97% Access in each patient clinic room 85% Internet access at an acceptable speed 71% Computerised patient booking/billing 67% Clinical e-health use Computerised medical records 27% Writing new/follow-up notes 21% Ordering tests 16% Writing scripts/referrals 13%

Melissa Wake · Sarah A Davies · Harriet Hiscock · Gervase M Chaney

To the Editor: Waxman’s prompt recovery after a stroke was probably a stroke of luck,1 unless perhaps Saint Mary MacKillop was involved. Amid the conflicting evidence on the effect of thrombolysis on recovery in ischaemic stroke, one fact is beyond doubt — thrombolysis gives no greater improvement at 24 hours than placebo.2 It is the various measures of recovery at 3 months, and the risks of adverse outcomes from protocol violations in administering thrombolysis, that are less clear. The European Cooperative Acute Stroke Study III (ECASS III) showed that there is a benefit from administering thrombolysis up to 4.5 hours after stroke onset,3 and the complete Safe Implementation of Thrombolysis in Stroke International Stroke Thrombolysis Register (SITS-ISTR) data showed that this benefit can be reproduced in non-trial hospital practice.4 Simpson and colleagues say that the Australian data support this conclusion, even though outcomes show slightly higher mortality compared with rest-of-world data.5 There are several gaps in that line of reasoning. A modified Rankin score (mRS) of 0–1 (zero or minimal disability) is the standard measure of a good outcome. In ECASS III, an mRS of 0–1 was seen in 52.4% of patients who received thrombolysis compared with 45.1% of patients who received placebo.3 However, the SITS-ISTR data showed an mRS of 0–1 in just 40% of patients treated within 3 hours of stroke onset and 44% of patients treated at 3–4.5 hours.4 This is despite lesser stroke severity (National Institutes of Health Stroke Scale score: 10 in the SITS-ISTR cohort v 11.6 in the ECASS III placebo group), selective patient inclusion, and exclusion of patient data with protocol violations known to give worse outcomes. Achieving a worse result than placebo is hardly evidence for safe and effective use of thrombolysis in normal clinical practice. However, the Australian study presents the data differently, using an mRS of 0–2 and thereby concluding good outcomes in patients with greater disability than is the accepted good outcome measure.5 Rather than providing the actual data and the percentage of patients with good outcomes, a novel measure of odds ratio comparison with rest-of-world data is made. Publishing data in the same format as for the full SITS-ISTR report would allay concerns of what may be unfavourable outcomes compared with clinical trial data. Patients deserve to be told what their likely prognosis will be in hospitals that are less experienced in stroke thrombolysis than The Alfred, where Waxman received world-class stroke care.

Brendon J Smith

In reply: We were delighted to hear of Waxman’s “miraculous” recovery, and admire the world-class standard of stroke care which was delivered at The Alfred.1 The Australian data in the Safe Implementation of Thrombolysis in Stroke (SITS) database up to 2008 included tertiary referral centres and outer metropolitan hospitals, and centres with varying experience of using recombinant tissue plasminogen activator (rt-PA) in clinical practice. There was no difference in outcomes according to experience of the treating centres. We believe that the non-trial clinical data presented in our article are a realistic indication of expected outcomes for all patients receiving thrombolysis for stroke in Australia. The choice of a modified Rankin score (mRS) of 0–2 as an outcome measure in our article was largely dictated by the SITS international analysis. The aim of our study was to compare outcomes in Australia with those in the rest of the world; these were also not significantly different when an mRS of 0–1 was used as an outcome measure (mRS 0–1 at 3 months, 34.6% for Australia v 37.8% for the rest of the world; P = 0.13). The original National Institute of Neurological Disorders and Stroke (NINDS) trial data,2 now more than 15 years old, have been analysed and re-analysed and, arguably, it is time to move on from rehashing the data. However, if one wishes to follow this path, there was in fact a significant difference in improvement at 24 hours between patients in the rt-PA and placebo groups. Smith’s statement that thrombolysis gives no greater improvement at 24 hours than placebo is correct in terms of the proportion of patients with an improvement in National Institutes of Health Stroke Scale (NIHSS) score of 4 or more, but this is a low benchmark and many untreated patients also show a relatively mild improvement at 24 hours. If one considers major neurological improvement (MNI, defined as an improvement in 24-hour NIHSS score of 8 or more), this was seen in a greater proportion of patients in the rt-PA group compared with the placebo group.3 Patients with MNI have a much greater chance of achieving minimal or no disability at 3 months, which is by far the most accepted outcome measure for thrombolytic therapy. This major early recovery is frequently seen in patients who receive rt-PA, and has been termed the “Lazarus effect”. Waxman was fortunate enough to experience this effect — but it occurs far too often with rt-PA in stroke to pass the Catholic Church criteria for a miracle.

Marion A Simpson · Helen M Dewey · Mark W Parsons

To the Editor: We view with concern the listed minimum investigations for chronic suppurative lung disease and bronchiectasis in children and adults recommended in the position statement from the Thoracic Society of Australia and New Zealand and the Australian Lung Foundation, published in the Journal.1 We do not agree with the inclusion of measurement of IgG subclasses in the list. Interpretation of IgG subclasses is fraught with difficulties.2 It is unclear whether the isolated finding of low levels of one or more IgG subclasses is a risk factor for developing severe recurrent bacterial infections. Individuals with complete absence of IgG subclasses due to gene deletions may remain entirely asymptomatic, and the finding of a low or absent response to specific bacterial protein and/or polysaccharide is more closely associated with propensity to infection. In addition, the lack of reproducibility of IgG subclass assays and lack of well standardised age-specific reference ranges hinder interpretation of results. Of major concern is the lack of evidence to provide clear guidance on the efficacy of immunoglobulin replacement therapy in IgG subclass deficiency. In general, the finding of isolated IgG subclass deficiency is not sufficient grounds for commencement of immunoglobulin therapy and is not recommended as an indication for intravenous immunoglobulin therapy in the current Australian guidelines.2 We urge the authors to reconsider the inclusion of IgG subclasses in the list of minimum investigations for chronic suppurative lung disease and bronchiectasis.

David S Gillis · D Sean Riminton

In reply: We thank Gillis and Riminton for their comments highlighting the inclusion of IgG subclasses in the list of suggested investigations when reviewing a patient with chronic suppurative lung disease or bronchiectasis. We agree that a finding of one or more low IgG subclasses in isolation is not an indication for immunoglobulin therapy and that interpretation of serum IgG subclass concentrations is difficult. Indeed, this was debated at length by the position statement authors. However, after considerable discussion, we decided that measurement of IgG subclasses should be included. Although the data are weak, it is an important area of possible aetiology, and there are varying opinions regarding associations with impaired adaptive immunity.1-3 As with some other investigations, an abnormal test result in the context of a child or adult with suppurative lung disease would lead to discussion with an appropriate subspecialist for advice on interpretation and/or further evaluation. Space limitations in the Journal version of our position statement did not permit us to elaborate further.4 In the full document available online,5 we stated that: The benefits of performing IgG subclasses in isolation are particularly controversial as the role of a reduction of a subclass is likely over-diagnosed.[88-91] If IgG subclass is low, assessment of response to vaccinations is advocated.

Anne B Chang

To the Editor: In their paper, Campbell and colleagues list the potential pitfalls of introducing pay-for-performance into Australian primary care.1 They emphasise that, in Australia, the electronic medical records used in general practice would not support the introduction of a scheme such as the Quality and Outcomes Framework (QOF) that is in place in the United Kingdom. In 2009, we demonstrated that it was quite possible to apply a QOF in a large Australian general practice by adapting the in-built search facility of a commonly used medical records program.2 We concluded that the introduction of a QOF in Australia would drive up the quality of our care. The non-clinical standards of a QOF are already similar to those set by the Royal Australian College of General Practitioners for accreditation and could be readily achieved. Campbell and colleagues suggest that the QOF is expensive and without proven benefits.1 This is incorrect. As predicted, the QOF has not only led to a reduction in cardiovascular disease events, but the benefit is greatest in the lowest socioeconomic groups.3 It is now possible to measure the cost effectiveness of a QOF, which is likely to show that it pays for itself by way of reduced morbidity and health service costs.4 Rather than argue for general practitioner remuneration based on pay-for-performance to be less than 20%, one should err on the side of caution, which recognises that 20% has ensured a massive public health gain for the British population. Now that 95% of GPs use computers, at least for prescribing,5 it is plausible that an Australian QOF could be developed, but pay-for-performance may need to include some pay-for-data incentives.

Mark A J Morgan · James Dunbar

In reply: Our article, which related to clinical care, not non-clinical standards, was intended to generate debate, and the points raised by Morgan and Dunbar are important ones. We address the central issue, which relates to the intended purpose of introducing a pay-for-performance scheme, similar to the Quality and Outcomes Framework (QOF) in the United Kingdom, into Australian general practice. Morgan and Dunbar state in their letter, “Now that 95% of GPs use computers for prescribing”; this emphasises that it would not be a level playing field. Even if all indicators only related to prescribing, at least 5% of practices would be disenfranchised. That statement also appears to presume that 95% of practices use compatible and comparable clinical codes. The UK witnessed years of computerisation and clinical code usage across a wide range of clinical issues before the introduction of the QOF. Elliot-Smith and Morgan adapted “the in-built search facility of a commonly used medical records program”, and introducing a QOF-like scheme in Australia would involve this investment in all practices. The percentage of income attributed to pay-for-performance is a political decision, and most people who are involved in the QOF in the UK strongly believe that it is too high. Whatever level is set, it must result in a level playing field for practices.

Stephen M Campbell · Anthony Scott · Rhian M Parker

To the Editor: Although we welcome Boyd and colleagues’ recommendations for changes to infection control guidelines for Australian recipients of human growth hormone (hGH) and human pituitary gonadotrophin (hPG),1 we are concerned about the accuracy of the history provided and do not want it misrepresented. Boyd and colleagues refer to recipients living with anxiety since 1985, when the Australian Human Pituitary Hormone Program (AHPHP) was halted. However, Australian recipients were not aware of the risk until 1991–1992. After the first two recorded deaths from Creutzfeldt–Jakob disease (CJD) of women treated with hPG, their husbands fought for official recognition of the link between their deaths and the AHPHP. In 1992, media attention alerted recipients to the risk and initiated contact from treating doctors. Knowledge that this information had been withheld since 1985 angered recipients. Boyd et al’s article is contradictory in mentioning a possible single, discrete contamination event but also claiming that a higher-risk period is unknown. We challenge this — particularly on behalf of recipients who were informed they had received hormones from a batch identified as likely to have contained the transmissible agent that causes CJD. We dispute the stated lack of availability of detailed treatment information, as the Australian Government Department of Health and Ageing has meticulously obtained and archived patient notes of recipients from their treating doctors, which provide the most accurate source of data. Boyd and colleagues had access to records of the four women whose deaths resulted from AHPHP treatment. The records seem consistent with published data,2,3 confirming that the four women were treated between 1973 and 1978. This surely indicates a high-risk period and gives extra confidence to those treated outside this timeframe. Further, two of the three patients on whom autopsies were performed received treatment from an identical batch of hormones (44); one was treated with this batch only. The third patient received hormones from batches 43 and 45.2 Batch 44 was identified as contaminated, and it was theorised that tainted material was transferred to batch 45 via production equipment. The patient who did not undergo an autopsy received only batch 25, which was produced earlier and indicates another possible contamination event within the 1973–1978 period. Risk estimate percentages do not provide more confidence for recipients than is currently already growing. They do not bring back those who died, take away the guilt of the parents who consented to hGH therapy for their children, or change a history of suicides, broken marriages, anxiety, disgrace and despair. It is important that Boyd and colleagues do not blur the implications of their findings with the continued need for the Australian Government to maintain the Human Pituitary Hormone Trust Account, which was established to provide funding for counselling and support services for recipients, and ongoing support for this group of citizens whose lives changed forever and who continue to battle discrimination and delays when accessing health care. The recommendations inspire hope but provide no immediate relief. The passing of time brings confidence, but the record needs to respect the enormous impact on the lives affected.

Suzanne L Solvyns · David W Ralston

In reply: We thank Solvyns and Ralston for their thoughtful and heartfelt comments and their assistance in ensuring historical accuracy regarding the issues surrounding iatrogenic Creutzfeldt–Jakob disease (CJD) risk and recipients of the Australian Human Pituitary Hormone Program (AHPHP). Whether there is a need for ongoing support of AHPHP recipients for the foreseeable future was not considered in the scope of our report,1 but we unequivocally support provision of optimal health care services for them, which we believe relaxation of infection control measures will assist. The delays and manner in which many AHPHP recipients learned of their risk of CJD is certainly regrettable, but this was not the universal experience of recipients. Some were made aware of the risk by their treating practitioner in 1985,2 with their heightened personal anxiety commencing from that time. As stated in our report, we agree that the close temporal development of CJD in the four Australian human pituitary gonadotrophin recipients appears consistent with a single, significant contamination event,1 such as from tainting of a limited number of treatment batches — an observation broadly in keeping with the existence of a higher-risk treatment window. However, despite assertions to the contrary, data acquired from various sources by the Australian National Creutzfeldt–Jakob Disease Registry for analysis did not permit confident and consistent delineation of a higher-risk treatment group. This is not synonymous with saying that a higher-risk period was unknown to us.

Alison Boyd · Genevieve M J A Klug · Colin L Masters · Steven J Collins

To the Editor: Dinh and colleagues present data on head injuries among cyclists admitted to the emergency department of Sydney’s Royal Prince Alfred Hospital (RPAH) from 1991 to 2010,1 and conclude with their opinion that legislation mandating the wearing of bicycle helmets should be maintained. However, their data provide poor evidence of the efficacy of helmets and of the effectiveness of legislation requiring helmet use. Almost all studies of helmet efficacy are case–control studies, which, to be of high quality, require a well defined and matched control group. In the study by Dinh et al, the control group was made up of patients who had been wearing a helmet. Many possible explanations for injury severity were not considered. For example, were the non-helmeted cyclists drinking alcohol or riding faster? Were they more likely to be risk-takers? Were the helmet wearers also wearing high-visibility vests or using lights at night? Case–control studies of this kind are a weak form of evidence (ranking just above anecdotal evidence and case studies) and cannot answer questions of causality. The two graphs presented by Dinh et al show that head injury rates among cyclists were very low and fairly stable over most of the time period examined. RPAH treats thousands of trauma patients each year. The study reported on 287 cyclists admitted in a 2.5-year period — an average of 115 per year. Of these, only 14 (eight helmeted; six not wearing helmets) incurred major trauma — about six per year. Given that helmet legislation was in place for the entire study period, these data add no evidence for its effectiveness. In public health terms, the risk of injury needs to be weighed against the benefits of increased physical activity, reduced chronic disease and reduced air pollution due to more people cycling. Because of the low absolute rate of cycling injuries, these benefits are nine to 20 times the size of the risk.2,3 Further, it is well documented that levels of cycling in Australia dropped by 30%–40% when helmet legislation was introduced. This had the unfortunate effect of making cycling less safe for the remaining cyclists because of the “safety in numbers” phenomenon.4 The poor uptake5 of the two public bicycle-hire schemes in Australia (in Melbourne and Brisbane) indicates that helmets are a significant barrier to short-trip and spontaneous cycling, with few potential or casual users carrying a bicycle helmet in case they decide to hire a bicycle. Dinh and colleagues obviously believe in the efficacy of the bicycle helmet, but this does not mean that mandating their use is the best public health policy response. When helmet legislation was introduced, we did not have the epidemics of diabetes and obesity that now threaten to bankrupt state health budgets. Strategies to increase levels of physical activity among the whole population are desperately needed, even if there is a small risk involved.

Chris E Rissel · Paul Martin

CorrectionIncorrect mean final scores in figure: In “Conflicts of interest: a review of institutional policy in Australian medical schools” in the 7 February 2011 issue of the Journal (Med J Aust 2011; 194: 121-125), there was a transposition error in Box 6 (page 125). The mean final score for US medical schools should be 58% and the mean final score for Australian medical schools should be 44%. The html and pdf versions of this article were corrected when published online on 7 Feb 2011.

Paul R Mason · Martin H N Tattersall

Stemming the flow The antifibrinolytic drug tranexamic acid (TXA) is best known for preoperative prophylaxis to prevent haemorrhage during and after surgery, and for treating excessive blood loss in women with heavy menstrual periods. It is also likely to be effective in another context — to prevent deaths from bleeding after trauma, according to an updated Cochrane Database review. A systematic review in 2004 of randomised trials in which TXA was given to patients with bleeding following severe injury was inconclusive, but two trials of TXA have been conducted since then. The 2011 review shows that TXA reduces the risk of death from bleeding by 10%-15% compared with patients who receive no treatment with TXA, without causing adverse events. Cochrane Database Syst Rev 2011; (1): CD004896 Progesterone for brains? Progesterone is known to reduce brain tissue oedema and the release of inflammatory mediators that follow brain injury. Should it be a routine treatment after brain injury? Authors of a Cochrane review identified three small randomised controlled trials comparing progesterone with placebo or no treatment. Progesterone showed a modest beneficial effect on mortality and disability; but given the modest number of trial participants, 315 in total, further multicentre randomised controlled trials are required before progesterone should be recommended as a routine treatment for brain injury. Cochrane Database Syst Rev 2011; (1): CD008409 No tip required “Pay for performance” schemes, such as Medicare’s Practice Incentives Program, link a portion of doctors’ payments to measures of health care quality, so as to encourage best practice. But are they efficacious? Serumaga and colleagues reviewed the effect of one such scheme, the Quality and Outcomes Framework, which targeted several chronic diseases including hypertension in primary care in the UK, and evaluated its impact. In a group of 470 725 patients with hypertension, over a 7-year period, a pay-for-performance bonus had no effect on the control of patients’ hypertension, or on clinical outcomes such as myocardial infarction and stroke. It is likely that treatment for hypertension was close to optimal or improving anyway over this period, so the scheme had no effect, the authors say. Other interventions such as educational outreach programs or case management by a team of health professionals may be more worthwhile. At least, pay for performance appears to cause no harm. BMJ 2011; 342: d108 The hard sell The more aggressively drug companies market their product, the less benefit and the more harm those drugs will cause. So say American academics Brody and Light. This “inverse benefit law”, as they term it, is the result of drug companies seeking to extend the market for drugs such as cyclooxygenase-2 inhibitors, statins, and bisphosphonates by exaggerating safety and efficacy claims and by encouraging off-label use. The effect is to increase side effects and costs, and to decrease therapeutic benefits. They say drug trials should be independently designed, funded and conducted; and doctors should view commercial marketing by pharmaceutical companies with scepticism. Am J Public Health 2011. Epub Jan 13 Online rehab Patients who undergo a total knee replacement but who live in rural or remote areas are at a disadvantage; access to high-quality rehabilitation services is not always possible. A solution might be “telerehabilitation” — an internet-based postoperative rehabilitation program conducted in the patient’s own home. Russell and colleagues studied a group of 65 patients who received 6 weeks of either traditional outpatient rehab services or rehab through real-time (live video and audio) interaction with a physical therapist via an internet-based system. The telerehabilitation patients did just as well; indeed, some experienced less stiffness than the traditional rehab patients. The technology is simple and easy to use, and could be the solution to the tyranny of distance, say the researchers. J Bone Joint Surg Am 2011; 93: 113-120

Peter Lavelle

Med J Aust 2011; 194 (4 Suppl).