Volume 186 Issue 11

Despite advances in treatment, the greatest gains in cancer control are achieved through prevention The translation of basic cancer research on cell growth to the clinic has resulted in a paradigm shift in cancer treatment by providing new therapeutic targets. The initial successes — the monoclonal antibodies trastuzumab and rituximab — have improved the survival of patients with breast cancer and lymphoma, as has the small molecule imatinib mesylate in chronic myeloid leukaemia; all have less toxicity than conventional cytotoxics.1 The challenge is to fund these new high-cost drugs. Although targeted drugs can be limited to the specific patient populations expressing the appropriate target, further funding is then required to screen patients for those targets. New models of cost- and risk-sharing between governments and industry must evolve to pay for these developments. A similar evolution in the diagnosis of cancer will see genomics and proteomics become a more important guide to treatment selection and prognosis than traditional pathology tests.2,3 These research technologies will need to be developed in such a way that they can provide guidance to clinicians as quickly as conventional techniques, and will also require upskilling of current clinicians, pathologists and their trainees. Investment in cancer research pays considerable dividends.4 There is a need for more funding of translational research — it has been an ongoing concern that Australia lacks the infrastructure to take promising new drug discoveries all the way from the laboratory into clinical practice. Newer fields, such as health services research, with its potential to address the pressing issue of inequities in access to treatment and cancer outcomes in rural and remote Australia, and psychosocial research, require new sources of funding. The challenge in Australia is to make research less fragmented and better targeted to questions of international importance, which we have the capability to competitively pursue. Although breakthroughs in cancer treatment generate significant media coverage, the greatest gains in cancer control in Australia are to be made in prevention strategies based on established science. Evidence-based health promotion campaigns have provided strong economic returns, yet governments invest only 1.7% of the overall health care budget in primary prevention.5 More than 21% of cancer deaths in Australia are attributed to tobacco use. Add smoking to excessive sun exposure, inadequate fruit and vegetable intake, alcohol, inactivity and obesity, and more than 34% of cancer deaths in Australia can be attributed to modifiable behaviour.6 Currently, 17.4% of Australians smoke.7 Australia has a smoking prevalence among the world’s lowest, but from a public health perspective it remains unacceptable that almost one in five Australians incurs a significant yet avoidable cancer risk by continuing to smoke. The prohibition of broadcast tobacco advertising in the mid 1970s was the first key policy step in a series of tobacco control reforms that have since been shown to have saved 17 000 Australians from premature death.8 This government initiative required no taxpayer funding, but a cultural shift. Where funds have been invested, the returns have been enormous, with the $176 million spent on antismoking campaigns over the past 30 years delivering $8.6 billion in benefits.9 There remains no more effective cancer control measure than reducing smoking, but there is a risk that the incremental reduction in smoking prevalence achieved over the past 30 years will stall unless the tobacco control effort is sustained. Smoking also contributes significantly to social inequities in health outcomes. For example, a smoking prevalence of 50% among Indigenous Australians10 is believed to be a major cause of the significantly poorer cancer survival rates among Aboriginal and Torres Strait Islander peoples. Targeted approaches are needed to break the cycle of social disadvantage, smoking, and cancer evident in specific population groups. Moreover, studies on tobacco control achievements over recent decades strongly suggest that a more sustained, whole-of-government commitment, built around integrated policy, social marketing, and research, could bring smoking prevalence down in Australia by a further 1% annually. Estimates based on recent trends indicate that reducing smoking prevalence by 5% in 5 years would save more than $1.15 billion in health care costs over the next 30 years.8 Yet some major political parties continue to accept donations from tobacco companies,11 and governments delay legislation to ban smoking in enclosed public spaces, and invest taxpayer funds in tobacco companies on the basis of sound economic management — despite having to spend more taxpayer funds on treating tobacco-related diseases (at least until patients die of them). While public policy has been gradually reducing the tobacco burden, obesity is escalating as a community health crisis. Obesity is linked to colorectal cancer, postmenopausal breast cancer, and kidney, oesophageal, gall bladder and endometrial cancers.12 Obesity control includes encouraging and facilitating physical activity and communicating dietary advice. The tobacco experience suggests that restricting junk-food advertising to children is likely to have an important impact, as supported by early Canadian data.13 This measure is not about restricting choice, as well targeted multimillion-dollar advertising campaigns already create an imbalance in the choices that uninformed and often disadvantaged families see as being available to them. Other lifestyle messages require more subtle public education. Advice from the SunSmart skin cancer prevention program must balance the need to avoid excessive sun exposure with the importance of low-level sunlight for vitamin D production. Similarly, while any alcohol consumption carries some cancer risk, the more you drink, the higher the risk — a factor that should be balanced against the benefits of very low alcohol intake in preventing cardiovascular disease. Cancer screening is another area that is presenting new opportunities and challenges. The benefits of breast cancer screening need to be continually reinforced to ensure high participation rates by eligible women. A new challenge for cervical cancer screening is ensuring continued high participation despite the introduction of the human papillomavirus immunisation program. The new National Bowel Cancer Screening Program requires community and professional education, a patient registry to ensure follow-up, and extra resources and minimum standards to meet increased colonoscopy demand. This will test the shared responsibilities for health care between national and state/territory governments — a potential barrier to efficient health policy implementation. The community must also understand that an ineffective screening test — one that evidence shows lacks the specificity and sensitivity to reduce cancer mortality on a population basis — is worse than no test at all, as the false positives and negatives can lead to poorer health outcomes than would surveillance on a case-by-case basis. The key is ensuring that evidence guides the implementation of government-funded measures aimed at cancer prevention and early detection — at a time when we could prevent well over a third of all cancer deaths in Australia using existing prevention and early detection technology. By investing more taxpayer funds in the high proven returns of cancer prevention and early detection, we could make resources available to better support the significantly increasing numbers of new cancer patients associated with population ageing over the coming years. Savings generated through improved prevention could also fund targeted cancer research to help further reduce the impact of cancer in the future. Increasing the cancer workforce, and improving workforce training and support through a more integrated approach across jurisdictions, is also pivotal to ensuring we can provide optimal multidisciplinary cancer care to meet the challenges of the future.

Ian N Olver MD, PhD, FRACP

High rates of this disease are the face of Indigenous disadvantage While acute rheumatic fever (ARF) has become a rare curiosity in Australia’s non-Indigenous population, its incidence in Indigenous Australians living in remote areas remains among the highest reported in the world. It is unlikely that such a stark contrast between two populations living within the same national borders exists for any other disease or on any other continent. The new evidence-based review and guideline for diagnosis and management of ARF and rheumatic heart disease (RHD) is an important tool for clinicians who care for Indigenous Australians (→ An Australian guideline for rheumatic fever and rheumatic heart disease: an abridged outline).1 But the guideline also prescribes a clear course of action for health policymakers. It makes a compelling case for focusing on the provision of secondary prophylaxis via coordinated, register-based RHD control programs that have guaranteed long-term funding. At the minimum, programs are needed in the Top End of the Northern Territory, Central Australia (including areas of South Australia and Western Australia near the NT border), northern WA, and northern Queensland. Other jurisdictions may also require control programs, but further disease burden data are needed to establish this. It is critically important to ensure that people with ARF and RHD receive good treatment and preventive care. But let’s not lose sight of the main game. Treatment of ARF and RHD, and secondary prevention-based control programs, are bandaid solutions to an underlying tragedy. ARF and RHD are classic diseases of social injustice. The past 50 years have witnessed dramatic declines in the prevalence of ARF and RHD throughout the industrialised world, resulting mainly from improvements in living conditions, socioeconomic conditions, sanitation and medical care, and from reduction in household crowding.2 Unfortunately these improvements are yet to be seen among a number of populations defined by socioeconomic status, ethnicity or geographical location.3 In essence, ARF and RHD are not only diseases exclusively borne by the disadvantaged, but also key indicators of disadvantage itself. In remote Australian Indigenous populations, the effects of disadvantage are so entrenched that it is likely to take several generations, and steadfast political will, before they are overcome. Rates of death from RHD among Aboriginal people in the Top End of the NT exceed those reported in many industrialised countries over a century ago.4 There is little or no evidence of improvement over at least the past three decades.5 As a consequence, Indigenous Australians continue to die before their time from a highly preventable, highly treatable and completely avoidable illness.4 Ongoing disparities in the burden of ARF and RHD reflect a number of failures in the development and delivery of health and health-related services. Failure to provide secondary prophylaxis can be due to missed diagnoses, poor continuity of care, a lack of trust and communication between patients and care providers, high staff turnover, a lack of appropriate health education, and, perhaps most importantly, a lack of political and bureaucratic commitment to solving the problem. Failure in primary prevention of ARF and RHD (ie, in preventing the acquisition of group A streptococcal infections) reflects the failure to provide Indigenous communities with the appropriate type and level of housing and environmental conditions that all Australians should expect. The federal government has targeted a 50% reduction in death due to RHD by 2008.6 While this is an unrealistic expectation, significant achievements are possible within the short to medium term, as has been witnessed with comprehensive approaches to control of ARF and RHD in the French Caribbean7 and with the establishment of register-based ARF/RHD control programs across New Zealand.8 Perhaps the most frustrating thing is that preventing premature death due to RHD is more achievable than solving an ever expanding list of other health and social problems facing Indigenous Australians. To prevent premature death due to RHD, a number of concrete steps must be taken. Firstly, we must commit to alleviating the underlying socioeconomic determinants of ARF and RHD. The most important of these determinants — overcrowded housing — is also the easiest to address, but requires a dramatically greater investment by governments than we are currently seeing. A recent study confirmed the extreme levels of household crowding experienced in many remote communities:9 in two large NT Aboriginal communities, the median number of people per house was 17 and 14, respectively, with a median of 6.9 and 7.5 people per bedroom, respectively. Secondly, we must ensure that each person with a history of ARF or RHD receives appropriate care. This entirely achievable goal would prevent Aboriginal children dying unnecessarily from this disease. Thirdly, we must ensure that political will delivers the deliverable and prevents the preventable. As long as modern Australia continues to accept the large and growing health and social disparities experienced by its Indigenous people, it fails in its duty to protect and provide for the most vulnerable. Will we be brought to account for our failure to deal with these disparities, or will cries for justice be silenced, as has happened with so much of the history of Australia’s first people?

Alex Brown BMed, MPH, FCSANZ · Malcolm I McDonald FRACP · Tom Calma

Objective: To describe the outcome of valve surgery, for rheumatic heart disease (RHD) and non-RHD, in residents of Cape York Peninsula and the Torres Strait Islands referred to the Cairns Base Hospital specialist outreach service.Design and participants: Retrospective review of medical records on all patients residing in the outreach area who had surgery for valvular heart disease between 1 January 1992 and 31 December 2004.Main outcome measures: Operation type and perioperative characteristics; 5- and 10-year survival rates; reoperation rates; complications.Results: Forty-seven patients met the selection criteria; the median age was 40 years (range, 4–76 years); and 39 patients were Indigenous. RHD was the predominant cause of valve dysfunction (30/47 patients). Thirty-seven patients had valve replacements, six had valve repair and four had balloon valvotomy as the initial procedure. There were three bleeding complications, two episodes of operated valve endocarditis, and six embolic complications. There were nine valve-related deaths (six in the first 5 years). At 5 years, all seven patients who had had valve repair or balloon valvotomy were alive. Seven of the 47 patients required reoperation. Survival analysis showed freedom from valve-related deaths to be 83% (95% CI, 66%–92%) at 5 years and 61% (95% CI, 33%–80%) at 10 years. Freedom from reoperation at 5 years was 88% (95% CI, 71%–95%). Among the 30 patients with RHD, freedom from valve-related death was 80% (95% CI, 60%–92%) at 5 years and 52% (95% CI, 21%–75%) at 10 years. In patients with RHD, freedom from reoperation at 5 years was 87% (95% CI, 65%–96%).Conclusion: Valvular heart disease results in substantial morbidity and mortality, despite intervention. Efforts need to focus on prevention of rheumatic fever and closer follow-up.

Anna McLean MB BS · Michael Waters MB BS(Hons) · Emma Spencer MB BS · Clive Hadfield MB BS

Objective: To estimate the incidence and severity of invasive group A streptococcal infection in Victoria, Australia.Design: Prospective active surveillance study.Setting: Public and private laboratories, hospitals and general practitioners throughout Victoria.Patients: People in Victoria diagnosed with group A streptococcal disease notified to the surveillance system between 1 March 2002 and 31 August 2004.Main outcome measure: Confirmed invasive group A streptococcal disease.Results: We identified 333 confirmed cases: an average annualised incidence rate of 2.7 (95% CI, 2.3–3.2) per 100 000 population per year. Rates were highest in people aged 65 years and older and those younger than 5 years. The case-fatality rate was 7.8%. Streptococcal toxic shock syndrome occurred in 48 patients (14.4%), with a case-fatality rate of 23%. Thirty cases of necrotising fasciitis were reported; five (17%) of these patients died. Type 1 (23%) was the most frequently identified emm sequence type in all age groups. All tested isolates were susceptible to penicillin and clindamycin. Two isolates (4%) were resistant to erythromycin.Conclusion: The incidence of invasive group A streptococcal disease in temperate Australia is greater than previously appreciated and warrants greater public health attention, including its designation as a notifiable disease.

Kerry-Ann F O’Grady BScN, GDipPH, MAppEpid · Loraine Kelpie BNurs · Ross M Andrews PhD · Nigel Curtis MB BS, PhD · Terence M Nolan MB BS, PhD · Gowri Selvaraj BSc(Hons) · Jonathan W Passmore BSc, MPH · Frances Oppedisano BAppSc · John A Carnie MB BS, FAFPHM · Jonathan R Carapetis MB BS, PhD

Objective: To study the work satisfaction of general practice staff, the differences between types of staff, and the individual and organisational factors associated with work satisfaction.Design, setting and participants: Cross-sectional multipractice study based on a self-completed job satisfaction survey of 626 practice staff in 96 general practices in Australia between 16 December 2003 and 8 October 2004.Main outcome measures: Job satisfaction scores for all staff and for general practitioners alone; relationship between job satisfaction and the team climate, practice size, particular jobs within practices, demographic characteristics of participants, and geographical location of practices.Results: The response rate was 65%. Job satisfaction was high, with a mean score of 5.66 (95% CI, 5.60–5.72). Multilevel analysis showed that all general practice staff were highly satisfied if they worked in a practice with a good team climate. Practice managers reported the highest satisfaction with their work. Practice size and individual characteristics such as the sex of the participant were unrelated to job satisfaction. GPs tended to have lower satisfaction than other staff in relation to income, recognition for good work and hours of work. Rural GPs were more satisfied.Conclusions: Most general practice staff are satisfied with their work. Facilitating teamwork may be a key strategy for both recruitment and retention of the general practice workforce, especially staff who are not GPs.

Mark F Harris MD, FRACGP · Judy G Proudfoot BEd(Hons), PhD · Upali W Jayasinghe MSc, PhD · Christine H Holton BA(Acc), GDPH · Gawaine P Powell Davies BA, MHP · Cheryl L Amoroso BSc, MPH · Tanya K Bubner GDPH · Justin J Beilby MD, FRACGP

Objective: To assess the impact of iodine fortification of bread on the iodine status of pregnant women, and to determine if studies of iodine levels in school-age children were indicative of women’s gestational iodine status.Design: Urinary iodine surveys of pregnant Tasmanian women before and after bread was fortified with iodine in October 2001.Participants and setting: 285 women attending the Royal Hobart Hospital (RHH) antenatal clinic from 1 October 2000 to 30 September 2001 and 517 women attending the RHH antenatal clinic or primary health care centres in 2003–2006.Main outcome measures: Median urinary iodine concentration (UIC) for comparison against the World Health Organization recommendation of of 150–249 μg/L for pregnant women.Results: Before supplementation, the median UIC of the 285 women attending the RHH antenatal clinic was 76 μg/L. After supplementation, median UICs were 81 μg/L for 288 women attending primary health care centres and 86 μg/L for 229 women attending the RHH antenatal clinic. Differences in mean UIC were not significant for either the antenatal clinic group (P = 0.237) or the primary health care group (P = 0.809) compared with the pre-supplementation group.Conclusions: Iodine deficiency in pregnancy persists despite being corrected in Tasmanian children. Successful iodine supplementation must target reproductive-age and pregnant women and be substantiated by ongoing monitoring during pregnancy and lactation. A robust national program for correcting iodine deficiency is urgently needed. Mandatory universal salt iodisation has international endorsement, and should be considered the preferred strategy for eliminating iodine deficiency in Australia.

John R Burgess BMedSc, MD, FRACP · Judy A Seal MPH, AdvAPD · Georgina M Stilwell MB BS · Peter J Reynolds MB BS, FRACOG · E Roscoe Taylor GradDipEpid, MRNZCGP, FAFPHM · Venkat Parameswaran PhD

Objective: To investigate whether hospital utilisation and health outcomes in Victoria differ between people born in refugee-source countries and those born in Australia.Design and setting: Analysis of a statewide hospital discharge dataset for the 6 financial years from 1 July 1998 to 30 June 2004. Hospital admissions of people born in eight countries for which the majority of entrants to Australia arrived as refugees were included in the analysis.Main outcome measures: Age-standardised rates and rate ratios for: total hospital admissions; emergency admissions; surgical admissions; total days in hospital; discharge at own risk; hospital deaths; admissions due to infectious and parasitic diseases; and admissions due to mental and behavioural disorders.Results: In 2003–04, compared with the Australia-born Victorian population, people born in refugee-source countries had lower rates of surgical admission (rate ratio [RR], 0.85; 95% CI, 0.81–0.88), total days in hospital (RR, 0.74; 95% CI, 0.73–0.75), and admission due to mental and behavioural disorders (RR, 0.70; 95% CI, 0.65–0.76). Over the 6-year period, rates of total days in hospital and rates of admission due to mental and behavioural disorders for people born in refugee-source countries increased towards Australian-born averages, while rates of total admissions, emergency admissions, and admissions due to infectious and parasitic diseases increased above the Australian-born averages.Conclusions: Use of hospital services among people born in refugee-source countries is not higher than that of the Australian-born population and shows a trend towards Australian-born averages. Our findings indicate that the Refugee and Humanitarian Program does not currently place a burden on the Australian hospital system.

Ignacio Correa-Velez MD, PhD · Vijaya Sundararajan MD, MPH · Kaye Brown PhD · Sandra M Gifford MPH, PhD

Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) are diseases of poverty. They occur at world-record rates in Indigenous Australians, yet individual cases are often poorly managed, and most jurisdictions with high rates of these diseases do not have formal control strategies in place. New Australian guidelines formulated in 2005 by the National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand for diagnosis and management of ARF and RHD are a valuable resource for clinicians and policymakers. Key recommendations of the guidelines include: New diagnostic criteria for ARF in high-risk populations, including Indigenous Australians, which include echocardiographic evidence of subclinical valvular disease, and polyarthralgia or aseptic monoarthritis as major manifestations. Clear guidance about treatment of ARF. Non-steroidal anti-inflammatory drugs should be withheld until the diagnosis is confirmed, and corticosteroids may be an option in severe acute carditis. Most cases of chorea do not require medication, but use of carbamazepine or sodium valproate is recommended if medication is needed. Clear guidance about dose, dosing frequency and duration of secondary prophylaxis. Benzathine penicillin G is the preferred medication for this purpose. Establishment of a coordinated control program for all regions of Australia where there are populations with high prevalence of ARF and RHD. Key elements and indicators for evaluation are recommended. Active screening and legislated notification of ARF and RHD, where possible. Development of a structured care plan for all patients with a history of ARF or with established RHD, to be recorded in the patient’s primary health care record.

Jonathan R Carapetis MB BS, PhD, FRACP · Alex Brown BMed, MPH, FCSANZ · Nigel J Wilson MB BS, FRACP · Keith N Edwards MB BS, FRACP, FRCP(Edin)

New Australian government funding for the Better Outcomes in Mental Health Care initiative is a significant step forward for mental health, with general practitioners now able to offer direct referrals to psychologists, social workers, occupational therapists and Aboriginal health workers. Incentives for better teamwork between GPs and other mental health professionals have been introduced, but may have unintended consequences, including an exacerbation of workforce shortages in rural and remote areas. Possible solutions to these shortages include rural scholarships for students in the mental health professions; recruitment and retention of students coordinated by university departments of rural health; better access to continuing professional development; and federally funded rural positions and additional financial incentives for rural mental health practitioners.

James A Dunbar MD, FRCPEdin, FRACGP · Ian B Hickie MD, FRANZCP · John Wakerman MB BS, FFAPHM · Prasuna Reddy PhD, MAPS

Objective: To investigate the relationship between a child’s weight and a broad range of family and maternal factors.Design, setting and participants: Cross-sectional data from a population-based prospective study, collected between January 2004 and December 2005, for 329 children aged 6–13 years (192 healthy weight, 97 overweight and 40 obese) and their mothers (n = 265) recruited from a paediatric hospital endocrinology department and eight randomly selected primary schools in Perth, Western Australia.Main outcome measures: Height, weight and body mass index (BMI) of children and mothers; demographic information; maternal depression, anxiety, stress and self-esteem; general family functioning; parenting style; and negative life events.Results: In a multilevel model, maternal BMI and family structure (single-parent v two-parent families) were the only significant predictors of child BMI z scores.Conclusion: Childhood obesity is not associated with adverse maternal or family characteristics such as maternal depression, negative life events, poor general family functioning or ineffective parenting style. However, having an overweight mother and a single-parent (single-mother) family increases the likelihood of a child being overweight or obese.

Lisa Y Gibson MPsych, PhD · Susan M Byrne MPsych, PhD, DPhil(Oxon) · Elizabeth A Davis MB BS, FRACP · Eve Blair BSc, PhD · Peter Jacoby BA(Hons), MSc · Stephen R Zubrick MSc, MA, PhD

Recent publications on medical professionalism have created an impression of a medical profession under siege in several countries. These publications recommend a new approach to medical professionalism to assist the profession to respond to new challenges. I suggest that the issue is not one of failed professionalism, but a shift in the balance of the ethical responsibilities brought about by major changes in health care systems. This shift has not yet been accepted or responded to by the medical profession. Medical professionalism is not under threat in Australia. Stronger leadership is required to address this altered ethical balance in the responsibilities of doctors.

Kerry J Breen MB BS, MD, FRACP

A young male immigrant from Syria with a vasculitic-appearing leg rash, asymmetrical polyarthritis, microscopic haematuria, and raised inflammatory markers was provisionally diagnosed with Henoch–Schönlein purpura. Skin biopsy showed leukocytoclastic vasculitis. Low-grade fevers persisted despite non-steroidal anti-inflammatory therapy, and Brucella sp. was subsequently grown from both blood and synovial fluid aspirates. Further tests gave positive results for B. abortus, and triple antibiotic therapy produced a rapid clinical response. Cutaneous vasculitis has rarely been described in brucellosis, and this is the first report in the English medical literature of brucellosis mimicking Henoch–Schönlein purpura. Clinical recordA 22-year-old man presented with arthralgia, fevers, weight loss and a leg rash. His medical history was unremarkable, and he was taking no medications. He had emigrated from Syria 2 months before to be with his family in Australia. He had been sexually active before emigration, but did not describe any illness consistent with a sexually transmitted disease. One month before presentation, the patient had left elbow pain and swelling, with subsequent involvement of the left knee, right ankle and foot. One week later, he developed a dry cough and night sweats. The non-pruritic leg rash started 1 week before presentation, ascending gradually to his knees. He had lost 8 kg in weight over the preceding weeks. Blood tests performed 2 weeks before admission showed: C-reactive protein (CRP) level, 18 mg/L (reference range [RR], 0–8 mg/L); erythrocyte sedimentation rate (ESR), 32 mm/h (RR, 1–20 mm/h); and a raised rheumatoid factor of 50 IU/mL (RR, < 40 IU/mL). The patient presented to the emergency department with progressive leg rash and difficulty walking because of knee pain. At initial examination he had a temperature of 38°C, and an erythematous maculopapular rash with a vasculitic appearance on his feet, with discrete lesions on the leg distally and a more confluent appearance around both knees. There was an oligoarthritis involving the left elbow, both knees, right ankle and right metatarsophalangeal joints, as well as axillary lymphadenopathy. Urinalysis showed a large amount of blood, with no dysmorphic cells or casts. The provisional diagnosis was Henoch–Schönlein purpura. Laboratory investigations showed a CRP level of 91 mg/L, an ESR of 78 mm/h, and a γ-glutamyl transferase (GGT) level of 118 U/L (RR, < 61 U/L), with other liver tests, a full blood count and renal function tests giving normal results. A blood and urinary vasculitic screen, including antinuclear antibody and serum complement tests, gave negative results, apart from high levels of anti-dsDNA antibodies (> 100 IU/mL; RR, 0–7 IU/mL). Other tests for an infectious cause including HIV, hepatitis B, hepatitis C, Epstein–Barr virus, cytomegalovirus, syphilis and streptococcal antigens gave negative results. His serum angiotensinogen-converting enzyme level was not raised. A 3 mL aspirate of blood-stained synovial fluid from the right knee was non-inflammatory. Skin biopsy from the leg showed leukocytoclastic vasculitis with IgA immunofluorescence of dermal vessels, consistent with Henoch–Schönlein purpura, and a Gram stain gave negative results. Over the next few days, the oligoarthritis improved with non-steroidal anti-inflammatory therapy, but low-grade fevers continued and a repeat test of his CRP level showed it was still raised (37 mg/L). The haematuria had resolved. Subsequently, microscopy and culture of both blood (aerobic bottle) and synovial fluid samples showed gram-negative rods, which were identified as belonging to the genus Brucella. Antibody testing for Brucella abortus was highly positive (agglutinins, > 1280). Computed tomography scanning of the thorax and abdomen revealed axillary, mesenteric and para-aortic lymphadenopathy, and a radionuclide bone scan showed peripheral arthritis in several sites with no spinal involvement. Transoesophageal echocardiogram showed no evidence of endocarditis. On further questioning, the source of Brucella organisms was thought to be cheese or yoghurt made from unpasteurised milk, consumed before emigrating to Australia. There were no close contacts of the patient who were unwell. Both the hospital’s Infection Control Team and the Sydney South West Public Health Unit (Liverpool Hospital) were notified of the case. The patient was given triple antibiotic therapy of gentamicin, doxycycline and rifampicin, which led to further improvement, and he was discharged after 2 weeks. At discharge, he was fully ambulant, with resolution of joint pain, fevers and rash. He completed a course of gentamicin for 3 weeks and oral antibiotics for 6 weeks. After taking antibiotics for 3 weeks, the CRP level had normalised and the GGT level was still raised at 126 U/L. Repeat tests for anti-dsDNA antibodies at 6 months gave normal results (3 kIU/L). DiscussionBrucella melitensis was first isolated in 1887 by the Australian-born microbiologist, David Bruce, from human spleens of patients suffering from Malta fever or undulant fever. Brucellae are gram-negative, facultative intracellular bacteria, which represent a major global zoonosis.1 Brucellosis is a systemic infection that can involve any organ.2 The different Brucella species are named for their preferred animal hosts. B. melitensis (principally goats and sheep) and to a lesser extent B. abortus (particularly cows) are the two species most closely associated with human infection because of higher virulence compared with other species.3 High-risk foods associated with acquisition of Brucella spp. include unpasteurised dairy products, particularly raw milk, soft cheese, butter and ice cream.3 Brucellosis is rarely transmissible by humans, and the major infectious risk relates to infection from a common food or animal tissue source.2 Brucellosis remains a significant global disease affecting the Middle East, Africa, the Indian subcontinent, Mexico and Central America, as well as parts of Europe including Spain, Greece and Turkey. However, eradication of brucellosis has been effective in certain countries such as Australia, New Zealand and the United Kingdom through stringent agricultural practice.2-4 While animal vaccines are available, there is no human vaccine. As seen in our patient, brucellosis most commonly affects adolescents and young adults. The onset of symptoms is generally 2–4 weeks after inoculation, although with chronic infection a pattern of undulant fever is described.2 Clinical manifestations of brucellosis are protean. Cutaneous lesions in brucellosis are unusual,5 and cutaneous vasculitis has only rarely been reported.6,7 Although dermal IgA deposits have been rarely described in association with Brucella-associated vasculitic rash,6 this is the first case of brucellosis mimicking Henoch–Schönlein purpura. Skin lesions are usually sterile,6,7 but B. melitensis has been cultured from a skin biopsy in a patient with arthritis and papulonodular rash.5 In contrast to skin disease, osteoarticular involvement is common.4 The major osteoarticular manifestations include peripheral arthritis, sacroiliitis and spondylitis. Most frequently involved are the hip, knee and ankle joints. Although a large-joint monoarthritis is the usual presentation of peripheral arthritis, both oligoarthritis and a rheumatoid-like pattern occur.4 In many cases of monoarthritis, Brucella spp. is not cultured from synovial fluid.8 In polyarthritis, the frequency of bacterial isolation from synovial fluid is unclear.9,10 Diagnosis of brucellosis is based on tissue-specific and serological tests. Definitive diagnosis of brucellosis is by isolation of bacteria from body tissue, including blood, bone marrow or synovial fluid. Presumptive diagnosis can be made by specific antibody tests against bacterial lipopolysaccharide or other bacterial antigens. Both high or rising titres of antibodies may aid in the diagnosis.2 Treatment of brucellosis is most effective with combination antibiotic therapy, as monotherapy often results in relapse. Effective antibiotics are those that can penetrate macrophages and work in an acidic environment. Antibiotics generally employed include: gentamicin, doxycycline, rifampicin, co-trimoxazole, quinolones and streptomycin.3 Oral treatment regimens are often based around doxycycline, and the duration of oral therapy is usually 6 weeks. Neurobrucellosis and endocarditis usually require longer treatment periods. Incomplete duration of therapy or an inadequate treatment regimen can result in disease relapse, and chronic infections are usually associated with deep foci of infection.2 This case highlights the diagnostic variability of the presentation of brucellosis and its ability to mimic systemic vasculitic disease, in particular Henoch–Schönlein purpura. This is of particular importance in patients who have recently emigrated from or travelled to high prevalence areas, especially with exposure to unpasteurised animal products.

David Massasso MB BS, BSc, FRACP · Kathryn Gibson BM BCh, FRACP, PhD

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

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

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

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

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

Siaw-Teng Liaw · Douglas I R Boyle

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

Ian D Williams

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

Enrico W Coiera

Victor Wynn, a physician, scholar and philanthropist who was one of the pioneers of the study of metabolism, died in London on 6 October 2006 of heart failure. Born in Melbourne on 12 October 1920, Victor attended Wesley College and the University of Melbourne. After graduating in medicine in 1943, he spent 4 years as a Medical Officer in the Australian Army. He was appointed as a Research Fellow at the Department of Physiology, University of Melbourne, in 1948. In 1950, Victor was awarded a Nuffield Fellowship to conduct research at St Mary’s Hospital, London. He was appointed to the staff of St Mary’s Hospital Medical School in 1953, then became Reader in Human Metabolism in 1960, Director of the Alexander Simpson Laboratory for Medical Research in 1965, and Professor of Human Metabolism in 1969. During this time, he led the establishment of quantitative clinical biochemistry on a large scale and integrated this with clinical research and patient care on an equally large scale. Victor’s interest in the management of surgical patients led to research into the new anabolic steroids. He demonstrated their potent and undesirable effects in relation to sugar and fat metabolism and was among the first to caution against their widespread use. His research also suggested major adverse effects of taking the contraceptive pill. He undertook large, detailed studies of the association between the pill and the risk of heart disease. International prominence followed, with several appearances on the BBC’s David Frost program. The resulting public scare led the Health Secretary to accuse Victor of making “10 000 women pregnant in a single night”. He was also prescient in other areas. In the early 1970s, he was urging cardiologists to pay more attention to blood cholesterol levels; 25 years later, measuring blood lipids would become as critical in evaluating patients with heart disease as measuring electrolytes had been in monitoring surgical patients. Throughout the 1970s and 1980s, Victor increasingly devoted his energies to fundraising, setting up environments in which partnerships between clinical care and high quality laboratory measurement could be pursued more effectively. His department at St Mary’s was the model, combining ward investigation, laboratory facilities, and data acquisition and computing facilities that were, at the time, on an unprecedented scale for medical school research. This concept was extended and enhanced on his retirement, in 1986, with the establishment of the Cavendish Clinic. The Clinic was affiliated with the UK National Heart and Lung Institute, renamed the Wynn Institute and subsequently incorporated into the Faculty of Medicine of Imperial College, London. Victor established two charities, the Heart Disease and Diabetes Research Trust and the Atherosclerosis Research Trust, which contributed over £15 million to research. They provided continuing support to Imperial College, London, and, in 2001, the financial base for a new centre, the Wynn Department of Metabolic Cardiology at the Baker Heart Research Institute, Melbourne. In May 2006, he was made a Fellow of Imperial College, London — the highest honour the College can bestow. Victor had a driving, single-minded personality that was not thwarted by three decades of his own experience of heart disease, from which he began to suffer at the age of 55. He is survived by his wife Marianne, Emeritus Professor of German at the University of London, and daughter Nicola.

John R Rigg

The sudden and untimely death of John Ruhno has deprived many patients of his well regarded expertise in the fields of clinical immunology and allergy. For both patients and colleagues, John’s most significant contribution has been to the management of anaphylaxis in Australia. John was born on 23 July 1952 in Toowoomba, Queensland, and educated at The Southport School. He graduated in medicine from the University of Queensland in 1976. After specialising in paediatrics at Royal Brisbane Hospital, he trained in clinical immunology and allergy at Royal Newcastle Hospital. In 1985, as the Royal Australian College of Physicians’ Bencard Travelling Fellow, he took up the position of Fellow in Immunology and Molecular Virology at McMaster University, Ontario, Canada, documenting basic and clinical research findings on nasal polyposis. Returning to Australia in 1989, John worked in Sydney as a Visiting Medical Officer at The Children’s Hospital, Westmead, and in the Department of Allergy at Royal North Shore Hospital. He also went into private practice in Chatswood and provided a much needed outreach service to the town of Nowra in southern New South Wales. John played a large role in the Australasian Society of Clinical Immunology and Allergy (ASCIA) at a local, national and international level. He was NSW representative from 1995 to 1996 and ASCIA representative to the World Allergy Organization House of Delegates from 1998 to 2005. In addition, John brought valuable expertise to a number of committees including ASCIA’s Computer Committee, Education Committee, and Anaphylaxis Working Party. John was an early and enduring advocate for the ever burgeoning number of patients and their families suffering from anaphylaxis. He was co-founder of the Families of Anaphylactic Children Training and Support Group (FACTS) and Medical Advisor from its inception, then Chair of the Medical Advisory Board of Anaphylaxis Australia, which replaced FACTS. John’s interest in research continued, and in the last 10 years of his life he was involved in collaborative work on several projects investigating the mechanism of egg allergy as a model in allergic disease development. John had a wide range of interests. His knowledge of wine and fine food was prodigious, and his temperature-controlled wine cellar, complete with computerised records of its contents, was the envy of many. He was also a keen sailor and fisherman. Although suffering from cardiomyopathy in the 6 months before his death, John had returned to full-time work. He died on 15 December 2006, at the age of 55. He is survived by his wife Alexandra and daughter Christina.

Janet Rimmer

Re: “Medicines and breastfeeding: information is available on safe use”, by Lisa H Amir, in the 7 May issue of the Journal (Med J Aust 2007; 186: 485). In the editing process, the last two sentences of the letter were altered, including removal of the author’s original emphasis on several words. The sentences should read “Medicines used during pregnancy are given safety ratings and the information is available online.5 Australian clinicians need similar guidance in relation to safe prescribing for breastfeeding women.” The author’s position at La Trobe University was also incorrectly given as “Lactation Consultant” rather than “Health Professional Research Fellow”. Her other positions (not included in the original letter) are General Practitioner at the Women’s Clinic on Richmond Hill, Melbourne, and Medical Officer at Breastfeeding Education and Support Services, Royal Women’s Hospital, Melbourne. The html and pdf versions of this letter have been corrected.

Lisa H Amir

Sequential therapy for Helicobacter pylori Sequential antibiotic therapy against Helicobacter pylori may result in a better eradication rate than standard triple-drug therapy, an Italian randomised controlled trial has shown. A total of 295 patients with proven H. pylori infection underwent endoscopy, biopsy, and bacterial culture of biopsy specimens. One group of patients received a 10-day sequential regimen of pantoprazole, amoxycillin, clarithromycin, and tinidazole. The other group was given standard 10-day therapy of pantoprazole, clarithromycin, and amoxycillin, each given twice daily. After treatment, patients underwent a second diagnostic 13C-urea breath test to detect presence of H. pylori. Sequential therapy resulted in a greater eradication rate and was significantly more effective in the treatment of clarithromycin-resistant strains. Ann Intern Med 2007; 146: 556-563 Salt and the heart Reducing dietary sodium intake can lower the risk of cardiovascular disease overall as well as leading to a significant reduction in blood pressure, according to US researchers. Two large randomised trials involving over 3000 patients were performed, and the incidence of myocardial infarction, stroke, coronary revascularisation, and cardiovascular death were recorded. The Trials of Hypertension Prevention studied adults aged 30–54 years with prehypertension, who were randomly assigned to a sodium reduction intervention group or a control group. The risk of a cardiovascular event was found to be 25% lower in the intervention group in the 10 to 15 years after the trial. The reduced risk persisted after adjustment for confounding factors such as age, race, and sex. The researchers comment that their study, despite being relatively small as a trial of clinical outcomes, has several strengths. These include objective measurement of dietary sodium intake, a heterogenous study population, and the use of a prehypertensive population at risk of negative cardiovascular outcomes. BMJ Online, 20 April 2007 Chocoholic Daily intake of cocoa can cause a significant reduction in blood pressure, according to a meta-analysis of 10 randomised controlled trials. In contrast, consumption of green or black tea is not shown to have a significant lowering effect on systolic and diastolic blood pressure. The review, which included trials performed over a 10-year period, reveals that an intake of between 46 and 100 mg of polyphenol-containing dark chocolate per day results in a pooled decrease of −4.7 mmHg in systolic blood pressure. Polyphenols, present in both cocoa and tea, act by causing arterial vasodilation. The authors of the meta-analysis comment that the reduction in blood pressure on the cocoa-including diet is similar to that achieved using β-blockers or angiotensin-converting enzyme inhibitors. The researchers hypothesise that the difference observed between cocoa and tea in blood-pressure lowering properties is due to the varying types of polyphenols present in chocolate and tea. Arch Intern Med 2007; 167: 626-634 Killing pain softly Morphine still suffers from “bad press”, despite its proven efficacy as a pain-relieving drug in the palliative care setting, according to a commentary by a UK palliative care physician. Dr Nigel Sykes, from St Christopher’s Hospice in London, gives a brief history of morphine use at the end of life and debunks some of the myths surrounding the risk of addiction and respiratory complications. Dr Sykes comments that morphine remains underused due to negative perceptions long held by both the medical community and the public, and that under-prescription of opioids remains a major barrier to effective pain management, particularly in the dying patient. Lancet 2007; 369: 1325-1326 Right brain — right weight Obesity may well prove to be all in the mind, or in the right prefrontal cortex (PFC), if new studies by US scientists continue to shed light on the complex aetiology of weight gain. Researchers from Beth Israel Medical Centre and Harvard Medical School claim that the right PFC is a critical area in the cognitive control of eating. The PFC is a centre in the brain where sensory, limbic and autonomic information converge, making it an essential area in the “top-down” control of behaviour. Using repetitive transcranial magnetic stimulation, which allows non-invasive interference with cortical activity, the neurologists were able to influence their subjects’ decision-making ability. Disrupting the activity of the right dorsolateral PFC induces a disregard for the adverse consequences of choices in the long term. Obese individuals are found to perform more poorly on tasks involving activation of such pathways, leading to the hypothesis that under-functioning of the PFC may result in an inability to project the consequences of poor food choices into the future. The role of the right PFC in mediating self-recognition and promoting physical activity over sedentarism and apathy may also support its role in the development of obesity. JAMA 2007; 297: 1819-1822

Tanya Grassi