Letters

To the Editor: In Victoria from 2000 to 2006, infectious syphilis notifications (primary, secondary and early latent infections) increased about 25-fold from 0.2 cases per 100 000 population in 2000 to 4.7 cases per 100 000 population in 2006.1 The number of new diagnoses of HIV has also increased since 2004.1 After observing a few patients presenting with both syphilis and a concurrent new HIV diagnosis, we investigated the association of the two diseases using retrospective laboratory data. As the Victorian Infectious Diseases Reference Laboratory (VIDRL) incorporates the state HIV reference laboratory and also acts as the reference laboratory for syphilis serological testing, it was possible to identify the HIV status and/or time of HIV diagnosis of 85% of patients identified with infectious syphilis, based on syphilis serological findings and polymerase chain reaction testing as previously described.2 Three hundred and forty-seven male patients fulfilled the criteria for infectious syphilis in the period 1 January 2000 to 30 December 2006. This represents 68% of all patients with infectious syphilis notified to the Victorian Department of Human Services over the period. Within the group of 347 patients, there were 310 with a single episode of Treponema pallidum infection, of whom 44.5% were HIV-positive. Thirty-seven patients were reinfected with syphilis, including 21 with their first episode recorded since 2000, and 11 with a serological pattern consistent with old treated syphilis recorded before reinfection during the study period. Of the 37 patients, 33 (of whom 23 were HIV-positive) had a second recorded episode and four (of whom three were HIV-positive) had a third recorded episode within the study period. Overall, 70.3% of patients with multiple episodes of syphilis were infected with HIV. Twenty patients presented with a concurrent diagnosis of infectious syphilis and previously un-diagnosed HIV infection. The trend over time is shown in the Box. Several international studies have highlighted the disproportionate incidence of syphilis in patients infected with HIV in recent years. There is now good evidence that syphilis and HIV act synergistically with regard to both transmission and progression of both diseases.3-5 The above data clearly demonstrate the strong association between HIV infection and infectious syphilis in Victoria, and this trend continued in the first half of 2007. Given the more frequent syphilis reinfections observed in the HIV-infected group, it indicates persons with HIV form a potential reservoir for syphilis infection in this state. We would strongly recommend that any patient presenting with possible syphilis or HIV infection in Victoria or elsewhere in Australia should be tested for both diseases. Episodes of infectious syphilis in Victoria by year of infection and HIV status * Patients with evidence of prior syphilis infection at an unknown time.

David E Leslie · Nasra Higgins · Christopher K Fairley

To the Editor: A 37-year-old male Sudanese refugee presented with lethargy, nausea, abdominal discomfort and bloating. He had chronic hepatitis B and a 2-year history of hazardous levels of alcohol consumption (90 g/day). On examination, there were no features of chronic liver disease. His liver enzyme levels were elevated (alkaline phosphatase, 189 U/L [reference range (RR), 40–110 U/L], γ-glutamyltransferase, 456 U/L [RR, < 50 U/L], alanine aminotransferase, 51 U/L [RR, < 45 U/L], and aspartate aminotransferase, 53 U/L [RR, < 40 U/L]), but synthetic function was preserved and serum bilirubin level was normal. Hepatitis B virus DNA was 1.3 × 103 IU/mL, consistent with a low-level viraemia, while HBeAg and anti-HBeAb were both non-reactive. His platelet count was reduced (115 × 109/L [RR, 140–400 × 109/L]), suggesting portal hypertension. The remainder of his chronic liver disease screen was unremarkable. Endoscopy revealed four grade 1 oesophageal varices, mild portal hypertensive gastritis, and patchy erosive duodenitis. The irregular liver and periportal fibrosis seen on ultrasound (Box 1) raised the possibility of cirrhosis. Subsequently, a biopsy of the liver showed preserved liver architecture, with periportal fibrosis and active schistosomiasis (Box 2). A diagnosis of Schistosoma mansoni infection was made, based on the histological appearance of the ova. S. mansoni is the leading cause of chronic liver disease and portal hypertension in sub-Saharan Africa.1,2 Adult worms reside in mesenteric vessels, but their migrating eggs lodge in hepatic presinusoidal radicals, resulting in inflammation and granuloma formation. The inflammatory reaction eventually leads to occlusion of portal veins and secondary portal hypertension.3 Hepatocellular function usually remains normal.1 Although the “gold standard” for diagnosis of S. mansoni infection is microscopic examination of faeces, this test may be negative (as it was in this case). Serological screening is recommended, but these assays cross-react with other helminthic infections and are unable to distinguish active infections from previous exposure.1 Praziquantel should be offered to previously untreated patients with positive serology results; after a single dose, 70%–100% of patients cease to excrete eggs.1 In patients who have left S. mansoni-endemic areas, an oral dose of 60 mg/kg split in two and given several hours apart should ensure cure.1 Our patient was treated with praziquantel, with ongoing follow-up for hepatitis B and portal hypertension. In retrospect, the patient’s history and the sonographic appearances were consistent with schistosomiasis. This clinical scenario is of increasing relevance, with a growing number of people from Africa now living in Australia. 1 Liver ultrasound Ultrasound shows an irregular liver with marked periportal fibrosis. There is no intra- or extrahepatic biliary tree dilatation. The portal vein flow is antegrade. No focal hepatic lesion is seen. 2 Liver biopsy specimen Preserved round to oval parasites with ova, some with a refractile exoskeleton and small lateral spine, can be seen. The viable forms suggest active infection. The surrounding inflammation contains numerous eosinophils, with fibrous expansion of the portal tracts. The adjacent liver revealed a preserved architecture with a normal METAVIR score of A0F0 (haematoxylin–eosin stain; low-power [A] and high-power [B] magnification).

James Daveson · Graeme Macdonald

To the Editor: Australians are fatter than they have ever been before. The prevalence of overweight and obesity (body mass index ≥ 25.0 kg/m2, or waist circumference > 80 cm for women or > 94 cm for men) in Australian adults is approaching 60% for both sexes and has more than doubled in the past 25 years.1 A prudent public health policy to fight the growing obesity epidemic would undoubtedly be to target strategies that avert this condition in the first place. So we were perplexed by the Australian Medical Association’s recent proposal to the Victorian Government to fund five public hospitals to provide 3000 obesity-related operations (ie, bariatric surgery) over the next 3 years.2 It appears the blueprint for the new millennium is to invest taxpayers’ money in modern technologies in an attempt to arrest overt clinical disease states. To attack the growing burden of obesity by investing in strategies that target secondary and tertiary treatment is an admission that we may win battles on a few fronts, but lose the war. We propose placing greater emphasis on implementing and enforcing primary prevention strategies to fight obesity. Primary defence mechanisms can decrease obesity prevalence by preventing the condition in the first place! Indeed, the health care industry is paradoxical in that its principal goal is to end health problems and human suffering, and by so doing put itself out of business.3 We need to attack the environmental roots of obesity, namely our sedentary lifestyles and caloric excess. Emphasis on secondary and tertiary prevention is too little, too late and will not reverse the growth of obesity — the funds to treat obese individuals are finite, while the number of Australians with the potential to become overweight or obese is not! In a letter to President Roosevelt voicing concerns about the Manhattan Project (the project to develop the atomic bomb during World War II),4 Niels Bohr wrote: A weapon of an unparalleled power is being created which will completely change all future conditions of warfare. Unless some agreement about the control of the use of the new active materials can be obtained in due time, any temporary advantage, however great, may be outweighed by a perpetual menace to human security. Obesity-related disorders impact on daily living. While bariatric surgery may provide a “magic bullet” for a few individuals, the time has come to legislate for minimum health standards, and to provide support for people to effect lifestyle changes to meet these requirements. Otherwise, obesity will remain a permanent threat to Australian society.

John A Hawley · David W Dunstan

Comment: Obesity is a complex public policy issue. There are no easy solutions, and the medical profession needs to work with communities, governments, researchers, teachers, parents, industry and others to help all Australians achieve and maintain a healthy weight. The Australian Medical Association (AMA) Victoria has six priority action areas to promote healthy weight: Ban food advertising to children; Simplify food labels; Promote physical activity every day; Improve clinical tools; Improve treatment options; and Evaluate and educate. Bariatric surgery is one of the treatment options that needs to be further explored. Among many other items, AMA Victoria’s state budget submission for the 2008–09 financial year1 calls for a trial of 3000 bariatric surgical procedures to be performed in public hospitals, as part of a comprehensive approach to weight loss. The evidence before AMA Victoria indicates that bariatric surgery is a safe and cost-effective treatment for a proportion of morbidly obese Victorians.2-5 However, bariatric surgery is an extreme response that should only be explored in extreme circumstances. There are many morbidly obese people who find themselves in these extreme circumstances and may benefit from the surgery if other approaches have failed. Further, bariatric surgery is cost-effective, as the costs are lower than the ongoing costs of treating chronic conditions associated with obesity. Bariatric surgery is not the only policy approach to obesity being pursued by AMA Victoria. We see it as a small part of the solution, although it has been a larger part of recent media attention on the issue. I am pleased that the AMA has been able to highlight obesity as an important public policy issue, and I look forward to working with a range of partners to explore possible solutions.

Douglas G Travis

To the Editor: The article by Haug and colleagues on household food stockpiling is a useful contribution to a neglected aspect of disaster planning.1 However, rather than providing a guide to what foods should be stockpiled, it may be more valuable to encourage families to increase the amount and rotation of the non-perishables they currently purchase. The authors seek to promote a balanced nutritional diet, but encouraging a family to continue their usual purchasing patterns when stockpiling for a pandemic or other disaster is a simpler, more sustainable, and possibly more effective way to promote household food stockpiling. We must assume that the family currently survives, for better or worse, on their current food purchase pattern. While the article states that supermarket stocks will become depleted within 2–4 weeks, it is likely that stocks would become significantly depleted at an individual store level within 2–3 days of the last truck delivery, particularly if panic stockpiling occurs. How long interruptions to the food supply chain last will depend on the nature of the disaster, but the Australian Government Department of Health and Ageing recommends that people have “enough fluids and food on hand to last you and your family a week.”2 It does not provide guidance on how much water is required per day. This is an important issue, as mains water could be unavailable within hours to days of electricity supply outages, because electricity is required to pump water into elevated water reservoirs to maintain water pressure. People may be unaware of their daily fluid requirements and may run out of water and other potable fluids before they run out of food. The US Health and Human Services recommends a 2-week food and water stockpile (“one gallon of water per person per day”), which is roughly equivalent to four litres per person per day.3 A random household survey in the Hunter Region of New South Wales after a storm-related disaster in June 2007 revealed that over 80% of households had enough non-perishable food for 3 days, but less than 40% had enough stored drinking water for 3 days (Hunter New England Health, unpublished data). Community continuity planning should be based on an understanding of baseline household food and water reserves, and household capacity and willingness to stockpile across all social strata. Governments should actively promote household stockpiling and identify strategies to bridge the shortfall in households unable to stockpile.

Craig B Dalton · Michelle A Cretikos · David N Durrheim

In reply: Dalton et al have raised several important points for discussion. They suggest that an adequate food “lifeboat” can be procured by simply encouraging a family to continue their usual purchasing patterns. Unfortunately, accumulating non-perishable items in this way would be a fast route to certain nutritional deficiency. It is the perishable items — fruit and vegetables, bread, meat and dairy products — that supply the bulk of micronutrients in modern food supplies. Within a few short months, an individual relying on usual pantry supplies could be suffering from acute deficiencies of vitamin C, and folate and other B vitamins. Babies conceived during this period would be at risk of neurological defects. We agree that an important issue is the possibility of failure of the mains water. Indeed, many of the foods in our list require water for cooking (rice, pasta etc). Rainwater tanks and the ability to sterilise water by gas heating or chemical means may be lifesavers. We agree that governments should be actively promoting appropriate stockpiling in homes, places of employment and in areas of essential infrastructure.

Jennie C Brand-Miller · Jennifer McArthur · Anna Haug

* It should be noted that the question mark in the title was added at the Editor's discretion. To the Editor: Why are those who market officially sanctioned information about pharmaceutical products not constrained by the advertising standards imposed on those who sell these products? Medicines Australia, which formulates a code of conduct for the pharmaceutical industry, imposes penalties, both financial and withdrawal of offending material, against misleading advertising of pharmaceutical products1,2 Why are similar standards not applied to advertising of information about these products? There are well documented flaws in Australian drug information sources,2,3 such as MIMS (the Monthly Index of Medical Specialties), that are based on product information (PI) authorised by the Therapeutic Goods Administration (TGA). Some PI is decades out of date;2 bottlenecks in updating TGA-approved PI are apparent.4 In this light, advertising of PI-based information in the bimonthly MIMS summaries seems anomalous. The April–May 2008 bimonthly print edition of MIMS claims to present “100% pure knowledge”, and states that “you can count on MIMS being up-to-the-minute”, and that “MIMS is essential knowledge that Australian health professionals can trust”. Previous bimonthly MIMS summaries make similar assertions. Until PI can be brought to an acceptable professional standard — a task that may be slow4 — it would seem appropriate to rein in misleading claims about PI widely used by health workers. Medicines Australia, or the National Prescribing Service, a government-funded body committed to “quality use of medicines”, could lead this initiative.

Jim R Stockigt

In reply: MIMS is held — and has long been held — in high regard in the Australian health care market. The vast majority of MIMS subscribers recognise that the quality information provided by MIMS is essential in their daily encounters with their patients. However, the product information (PI) produced in MIMS publications is only part of the information provided to health care professionals through various MIMS publications. Furthermore, it must be stated clearly that MIMS is not responsible for producing the PI-based drug information. This responsibility remains with the manufacturer, and the PI is subsequently approved by the Therapeutic Goods Administration (TGA). MIMS collates information from various sources, both locally and overseas, and publishes it in an easy-to-use, well structured and familiar format for its customers. MIMS has long been committed to providing such “essential knowledge that Australian health professionals can trust” since the introduction of the first MIMS publication 45 years ago. However, MIMS does acknowledge that there is an issue with some PI not being reviewed more regularly, and is committed to working closely with any appropriate organisation to address deficiencies in the current process. Nevertheless, it would seem inappropriate to say that PI for all drugs is not a quality information source. PI for the vast majority of drugs published in MIMS is as current as possible, given the constraints of publishing, the updating process by pharmaceutical companies and the delays in approvals through the TGA. The study reported and referenced by Stockigt focused on old, generic-based medicines.1 While there is an issue with manufacturers keeping these current, this is clearly a responsibility of the TGA and the manufacturer, not MIMS. PI for newer products is an important quality information source for the prescribers of medicines; if it were not, then the TGA would not permit manufacturers to make PI available in the first place. With respect to Stockigt’s concerns about the accuracy of MIMS advertising, we stand by our assertion that it is MIMS policy to provide the most up-to-date medicines information available, capably delivered by the MIMS professional editorial team.

Elizabeth A Donohoo

To the Editor: Recent media reports1 of events in Aurukun, Palm Island and other Indigenous communities in Queensland may have left the impression that most Indigenous people in the state live short, violent lives in remote, dysfunctional communities. However, census data from the Australian Bureau of Statistics (ABS) contradict one aspect of this impression: in fact, few Indigenous people live in remote communities, with the majority widely spread through the general population (Box). Over the past 10 years, the Indigenous population of Queensland has increased by 33.7% (Box). However, the number of people living in Aboriginal and Torres Strait Islander land council areas was almost stationary, dropping from 17 855 in 1996 to 17 739 in 2006, and the proportion of Indigenous people living in these areas decreased from 18.7% to 13.9% over the 10 years. The other six out of seven Indigenous people lived in the general community (Box). Twenty-four per cent lived in Brisbane city; suburb-by-suburb analysis showed most lived in less affluent areas of Brisbane but, even in these, the percentage of Indigenous people was only 1%–8% in each area. There are no major ghettos. In 2006, 32.4% of Indigenous people lived in south-east Queensland (classified as the “Brisbane Indigenous Region” by the ABS, Box); there is no land council area in this region. On North Stradbroke Island, a group of 366 Indigenous people living in the general community comprised 18% of the local population, but in all other locations the percentage of Indigenous people was well under 10%. Indigenous Australians have also moved to other cities in Queensland. In 1996, 42 571 Indigenous people (44.6% of the state’s Indigenous population) lived in a major city (Brisbane, the Gold Coast, Toowoomba, Rockhampton, Townsville or Cairns). By 2006, 61 672 Indigenous people lived in these cities. This is below the 67.1% for all Queenslanders, but is still nearly half (48.3%) of the Queensland Indigenous population. In the 1996, 2001 and 2006 ABS censuses, an Indigenous person was defined as someone who had ticked one of three boxes on the ABS census form stating that he or she is Aboriginal, Torres Strait Islander or both. All censuses have problems with accuracy of the data submitted and missing returns;2 however, as the results presented here were determined using the same methodology, show linear trends across the datasets, and identify only broad trends, I believe they are robust. Much of the increase in the Indigenous population is probably due to the higher birth rate of Aboriginal and Torres Strait Islander people (26.4/1000 v 12.9/1000 in the overall Queensland population).4 However, “migration” — people reclassifying themselves as Indigenous — may also contribute. These census data show that, as with other Australians, there is a net movement of Aboriginal people from rural to urban areas. Anecdotally, many people move from Indigenous communities and other rural areas to relatives in “town”; some stay for only a short time, but others remain in the city. This move is sometimes to the rural or urban fringe, but more often is into a stable integrated family group. Most Indigenous people in Queensland are widely spread through the general population. ABS census data on Queensland Indigenous people* 1996 2001 2006 Queensland population Total 3 368 850 3 655 139 4 046 880 Indigenous (% of total population) 95 518 (2.8%) 112 772 (3.1%) 127 684 (3.2%) Brisbane population Total 1 468 617 1 605 650 1 782 973 Indigenous (% of total population) 21 462 (1.5%) 26 453 (1.6%) 30 769 (1.7%) Indigenous population (% of Queensland Indigenous population) Brisbane 21 462 (22.5%) 26 453 (23.5%) 30 769 (24.1%) Brisbane Indigenous Region† na 36 323 (32.2%) 41 369 (32.4%) Major Queensland cities‡ 42 571 (44.6%) 52 385 (46.5%) 61 672 (48.3%) ATSI land council areas§ 17 855 (18.7%) 16 567 (14.7%) 17 739 (13.9%) ABS = Australian Bureau of Statistics. na = not available. ATSI = Aboriginal and Torres Strait Islander. * Data are collated from numerous sections of the 1996, 2001 and 2006 ABS censuses.2 † The Australian Indigenous Geographical Classification used by the ABS.3 ‡ Includes Brisbane. § Population for ATSI land council areas is total population.

Alan E Dugdale

To the Editor: As a junior doctor working in Central Australia, who has spent the past year rediscovering my own Aboriginal heritage, I read the recent articles on the Northern Territory intervention- with interest. All authors agree that the current state of health in NT communities is shameful, and that the causes include a wide range of social determinants. However, beyond these similarities there is almost complete discordance between the article by Glasson (of the NT Emergency Response Taskforce) and the other three articles by NT-based doctors (Tait, Boffa et al, and Brown and Brown). Glasson paints a demeaning and misleading picture of NT communities as exhibiting “a complete breakdown of normal mores”. This fits snugly with the “white blindfold” view, described by Tait, that will only further disempower marginalised Aboriginal people and communities. Glasson ignores the vast accumulated knowledge and successes attained by Aboriginal community-controlled health services (ACCHSs) and health workers, relegating their contribution to a half-sentence in his acknowledgements. Boffa and colleagues clearly outline the remarkable successes of ACCHSs and their repeatedly ignored calls for more resources. Glasson leaves no room for real community participation, and justifies the government’s heavy-handed approach as necessary for such a “crisis”. Brown and Brown describe convincingly the absolute necessity of Aboriginal rights and participation in any intervention conducted on their behalf, and the valiant long-term struggles by Aboriginal people to tackle the current situation. In response to the government’s intervention, in June 2007, Mark Wenitong, President of the Australian Indigenous Doctors’ Association, expressed concerns that remain relevant today: “As medical professionals, we question the notion that you can treat poverty, dispossession, marginalisation and despair (the root causes of substance misuse and sexual, physical and emotional abuse) with interventions that further contribute to poverty, dispossession, marginalisation and despair.” Indeed, the Ampe akelyernemane meke mekarle: “little children are sacred” report was very clear about the necessary approach to addressing the issues it raised: “What is required is a determined, coordinated effort to break the cycle and provide the necessary strength, power and appropriate support and services to local communities, so they can lead themselves out of the malaise: in a word, empowerment!” My experience working in NT Government hospitals and ACCHSs has revealed both the enormous challenges facing Abori-ginal people in the NT, and their remarkable resilience and capacity to achieve against all odds. As health professionals and Australian citizens we must recognise these efforts and support interventions that are evidence-based, respectful, and conceived in partnership with Aboriginal communities and their ACCHSs. Without this, the most expensive intervention will only ever amount to a superficial facelift.

Hamish R Graham

In reply: While I acknowledge the arguments many have put forward that the Northern Territory Emergency Response (NTER) has been too rapid and implemented without optimal community consultation — which some perceive to have disempowered Indigenous people — I stress the need to continue and indeed step-up momentum so that communities can regain control of their own futures as soon as possible. The positive impact of the NTER measures in creating better health, social and economic outcomes for Indigenous Australians will only be realised with the total support and focused energy of those “on the ground”, charged with delivering vital primary care and secondary intervention in NT communities. Without the continued engagement of these hardworking individuals who are able to establish the trust required to build bridges into these communities, the initiative is not sustainable. It is into the hands of those who live and work in Aboriginal communities that the NTER Taskforce and government agencies will pass the baton of change — we hope they will run with it.

William J H Glasson

To the Editor: Calcium and vitamin D play a central role in preventing osteoporosis and fractures,1 so a recent study published in the BMJ claiming that calcium supplements increased the risk of heart attacks and strokes in postmenopausal women2 naturally received widespread media attention — so much so that many patients are already stopping calcium treatment. The study, based on a previously published randomised controlled trial of calcium supplementation in 1471 healthy women,3 showed that self- or family-reported heart attack, stroke or sudden death was significantly more common in those taking calcium than in the placebo group (P = 0.008). This conflicted with the findings of a much larger study.4 Further, the difference became non-significant when the analysis was corrected for covariables (P = 0.08), or when the analysis was repeated using data on cardiovascular events obtained from medical records (P = 0.08). Yet, it still gained a place in a leading medical journal. The small excess of cardiovascular events in the women taking calcium could be due to chance and needs to be tested further; one way of doing this is to examine available data for evidence of mortality in patients taking calcium. We have done this. In the 29 randomised trials in a recent meta-analysis of the effect of calcium and vitamin D in fracture risk,1 five trials comprising 12 609 subjects provided crude mortality data.5-9 When these mortality data were pooled using a random effects model, there was no evidence that calcium supplementation increased mortality (Box). We find it hard to believe that calcium can have a significant adverse effect on cardiovascular disease without increasing mortality. Our reservations about this study are further strengthened by the weak theoretical basis of the case against calcium. Metastatic calcification in renal failure, which the authors quote as an analogy,2 is due to the high serum calcium–phosphorus (CaxP) product levels caused by hyperphosphataemia, which may be aggravated by calcium supplementation. In women without this condition, this degree of oversaturation cannot be reached by the 5% rise in plasma calcium10 resulting from the recommended dose of calcium citrate used for supplementation. Moreover, coronary blockage is not due to calcification of atheromatous vessels, which is a dystrophic calcification secondary to tissue damage, but rather to ruptured atheromatous plaques and the thrombi which form upon them. Thus, it is premature to conclude that calcium supplementation should not be given to older women. Effect of calcium supplementation on mortality, data pooled by a random effects model

Benjamin M P Tang · Christopher Nordin

To the Editor: Primary cerebral vasculitis (PCV) is a potentially fatal disease. Early diagnosis and therapy are vital. We describe a case where confounding factors delayed diagnosis. A 42-year-old woman presented with headache, nausea, vomiting, malaise and binocular blindness for 3 days. Two weeks previously, she had presented to the emergency department with headache and vomiting, but investigations, including computed tomography (CT) of the brain and lumbar puncture, gave normal results. She had a history of depression, was a smoker (20 pack-year history), and used cannabis regularly and alcohol occasionally, but denied other recreational drug use. Her mood appeared depressed. Vital signs and findings from a general examination were normal. Eye movements were full, direct and indirect pupillary reflexes were intact, and optic fundi were normal. Results of a CT angiogram were reported as normal by a consultant radiologist. Results of blood tests, including inflammatory markers, and a repeat lumbar puncture, were unremarkable. A toxicology screen was not performed. Depression with conversion disorder was diagnosed, and admission with analgesia was advised. A neurologist’s review on Day 2 did not detect organic disease. The mental health team diagnosed severe depression and prescribed antidepressants. On Day 4, the patient’s condition deteriorated and she become non-communicative with signs of right hemiplegia. An electroencephalogram showed polyrhythmic generalised slow waves consistent with encephalopathy. She was transferred to a tertiary centre where magnetic resonance imaging (MRI) and CT angiography of the brain showed multiple bilateral infarcts (Figure, A) with beaded arteries, the classic appearance of vasculitis. She was given high-dose prednisolone and cyclophosphamide. Investigations were negative for causes of secondary vasculitis. Her condition continued to deteriorate and she died 8 days after admission. Autopsy was refused. Subsequent review of the second CT scan detected irregular cerebral vessels (Figure, B). PCV is an uncommon disorder of the central nervous system, with unknown aetiology and no specific characteristic features, affecting small cerebral arteries but not extracranial vessels. Symptoms and signs vary but include headache, encephalopathy, seizures, personality change, weakness, and altered level of consciousness, as well as superimposed focal cranial neuropathy or hemiplegia. Recognition is difficult, but differentiation from reversible cerebral vasoconstriction syndrome is important.1,2 Brain biopsy is seen as the “gold standard” for diagnosing PCV. CT angiography may show diffuse or localised changes, with vessel beading, aneurysms, and luminal narrowing. MRI may show areas of white and grey matter infarction, or haemorrhage. MRI is more sensitive than CT, but less sensitive than CT angiography. Up to 100% of biopsy-positive cases appear abnormal on MRI. Suspected cases require careful clinical appraisal and either CT angiography or MRI, probably followed by an image-guided brain biopsy.3 Initial reported cases of PCV had a poor prognosis; most patients died within a few weeks.2 Immunosuppressive therapy with glucocorticoids and cyclophosphamide (as used in secondary severe vasculitis) may be beneficial, although there are no clinical trials.4 A future therapeutic alternative may be infliximab, which has been used successfully for one patient with cerebral vasculitis secondary to Behçet’s disease who had known elevated levels of tumour necrosis factor α.5 Despite increasing awareness and advances in angiography, PCV remains an uncommon diagnostic and therapeutic problem which should be considered in cases of severe, non-febrile neurological illness with stroke-like features. A: Magnetic resonance image showing multiple bilateral infarcts. B: Computed tomography angiogram showing irregular cerebral vessels (“beading”, arrows).

Sanjaya S Herath · Dayna B Law · Peter J O Stride · Vernon J Heazlewood · Luke S Gaffney

To the Editor: We report the case of a 71-year-old woman who presented with a 3-week history of lethargy, subacute confusion and drowsiness. She was known to have a seizure disorder for which she had been taking lamotrigine 100 mg and sodium valproate 500 mg twice a day for 2 years. On examination, the woman was disoriented with regard to person and time, and had constructional apraxia and asterixis. The rest of the physical examination was unremarkable. A full blood count, electrolyte levels, coagulation parameters, arterial blood gas measurements and hepatitis serology were normal. Tests for immunological markers of autoimmune liver disease were negative. Liver function tests showed longstanding raised levels of alkaline phosphatase (158 U/L [reference range (RR), 30–110 U/L]) and γ-glutamyl transferase (434 U/L [RR, < 40 U/L]). Serum drug levels were sodium valproate 51.0 mg/L (therapeutic range, 50–100 mg/L) and lamotrigine 9.5 mg/L (therapeutic range, 3–14 mg/L). The venous blood ammonia level was 109 μmol/L (RR, < 50 μmol/L). A liver ultrasound scan was normal. Computed tomography of the brain showed microvascular changes and an old cortical infarct. An electroencephalogram (EEG) showed diffuse slowing, with a predominance of rhythmical theta activity and some delta activity, suggestive of encephalopathy. As hyperammonaemic encephalopathy secondary to sodium valproate therapy (VHE) was considered a possible diagnosis, sodium valproate treatment was discontinued. The patient’s confusion resolved completely and the asterixis disappeared within a week. At the same time, her blood ammonia level fell to 19 μmol/L and her EEG normalised. Eight months after discontinuing sodium valproate treatment, the woman was still asymptomatic. A subsequent percutaneous liver biopsy, to investigate her persistently abnormal liver function, showed features consistent with primary biliary cirrhosis. Sodium valproate is used not only for management of epileptic disorders but also for migraine prophylaxis and treatment of several psychiatric conditions. Although a generally well tolerated drug, it has a few well known side effects, including hyperammonaemia and, rarely, VHE.1-3 The possible pathophysiology of VHE has been described elsewhere.2 Gerstner et al reported on a series of 19 patients with VHE between 1994 and 2003.4 Review of the literature suggests that VHE is under-recognised, leading to considerable delay in the diagnosis of this potentially reversible condition.3,5 In our patient, it is reasonable to presume that sodium valproate precipitated the encephalopathy on a background of evolving unrecognised liver disease. The marked improvement in her clinical manifestations after discontinuation of valproate further supports this presumption. We have drawn attention to this case to highlight that VHE should be considered in patients presenting with confusion. Prompt measurement of the ammonia level and cessation of valproate treatment should be considered if clinically appropriate. Patients with previously unrecognised liver disease may be at particular risk. Acknowledgement: We thank Professor Peter Roberts-Thomson, Director of the Department of Immunology at Flinders Medical Centre, for his expert opinion and advice.

H S Subhash · Robert J Heddle · David W Schultz · John Ring · Campbell H Thompson

To the Editor: The timely article by Healy and colleagues1 should provoke debate within the profession. The authors’ decision to not consider “the relative merits of national versus regional registration boards” should not stifle discussion in the Journal. In particular, Australian doctors and the public should be aware that the medical board system to which we are accustomed is not operational in most countries. In much of the English-speaking world, boards comprise mainly doctors and have considerable independence from government; medical boards in non-English-speaking countries are generally part of the health bureaucracy.2 The fundamental danger of having a Council of Australian Governments-inspired national registration “body” lies in the potential for a switch from the “English” system of self-regulation under common law to the “European” model of bureaucratic rule under administrative law. Public and professional suspicion of self-regulation lay behind the 1987 amendments to the Medical Practitioners Act 1938 (NSW), which removed the power of deregistration from the New South Wales Medical Board, handing it instead to the Medical Tribunal chaired by a District Court Judge. This move avoided both the “Scylla” of public distrust of the profession and the “Charybdis” of criticism, such as have afflicted the boards in Victoria and elsewhere, where boards retained that power. No less important problems with a national board lie in the assessment of local problems and surveillance of doctors whose registration is conditional. This is already difficult in the larger states, such as Queensland, NSW and Western Australia. The continued failure of the centralised Health Insurance Commission to prevent and prosecute the abuse of Medicare by doctors, despite repeated ineffectual changes to the legislation,3 does not encourage optimism that a national medical board could effectively manage impaired doctors or those performing below standard. Having served on Commonwealth working parties on both mutual recognition of medical qualifications and Medicare “overservicing” and “inappropriate practice”, I would opt for an independent, publicly accessible national database containing a “uniform set of items that are allowable under existing privacy legislation”.1 The elements of such a database are already operational in the safe hands of the Australian Medical Council (AMC). It should not be too difficult, and certainly less cumbersome, for state and territory governments and medical boards to agree on that uniform set, on the foundations already laid by the AMC, and to continue the AMC’s ownership of the database.

Peter C Arnold

In reply: Arnold makes some interesting points about the balance of state and professional involvement in medical registration arrangements. Wherever the balance is struck, politicians, bureaucrats and medical professionals all derive their power in some measure from the public whom they serve. Our point is that variations in registration information and public access to multiple registers make it difficult for members of the public to access and use the information, especially given the mobility of the medical workforce between jurisdictions. A public national medical register should be seen as a practical measure to improve public accountability, rather than as a battleground between the profession and the bureaucrats. We did not express a view in our article1 on how national access to medical registration details should be arranged. As Arnold suggests, the Australian Medical Council is one candidate for maintaining a national database. It is well placed to publicly call on the existing state medical registration boards to cooperate speedily to make national access a reality, pending the negotiations underway regarding a national medical board.

Judith M Healy · Paul Dugdale

To the Editor: With the World Health Organization’s annual World No Tobacco Day to be held on 31 May, it is timely to encourage all patients who smoke to reconsider their actions. During my registrar training in the 1970s, I developed a simple and effective method of helping smokers consider some consequences of their tobacco habit. I offer this in the hope that others may find it useful too, as a more meaningful exercise than the concept of “pack-years”.1-3 First, enquire when the patient began to smoke regularly. I call this the “tobacco-arche” (analogous to menarche and coitarche). Next, determine how many years the patient has smoked regularly, remembering to subtract any years he or she may have suspended the habit. Then, have the patient estimate overall daily usage, relying, if possible, on prompting from an accompanying person to determine a realistic rather than idealised figure. Finally, multiply the number of years by the daily usage and by the number of days in a year. A reasonable approximation is to multiply by 400 rather than the more cumbersome 365.25. For example: a 65-year-old person who has smoked 20 cigarettes per day since his or her mid teens (ie, for 50 years) yields 20 × 50 × 400 = 400 000 — approaching half a million cigarettes lifelong. In my three decades of experience as a general physician, I have noted that an accumulated intake of a quarter of a million cigarettes usually results in at least some cough, breathlessness and end-expiratory wheeze on forced expiration, and decreased exercise tolerance; half a million cigarettes generally causes chronic smoker’s bronchitis, with or without some degree of emphysema, and other harmful effects on the body; while three-quarters of a million cigarettes makes cancer a distinct possibility.4 A further inducement for patients to confront the effects of their harmful habit is to calculate the amount of their lifetime tobacco intake in terms of the dollar cost. In the case of cigarettes, 500 000 at 60 cents each yields the impressive figure of $300 000. This usually comes as a sobering revelation to the smoker and their “significant others”. The above method can thus contribute to the desirable effect of reducing or eliminating tobacco consumption, with flow-on benefits to patients’ health, finances, and personal and occupational relationships.

C Ross Philpot

To the Editor: In his article on medical specialist education and training in Australia, Phelan1 raises two major issues: financial and educational. On the financial front, Phelan asks about the advantages and disadvantages of the new funding model for specialist (pre-Fellowship) training. One of the advantages of the model is that it makes the funding process more explicit. We believe that all who benefit from this educational exercise — trainees, supervisors, private hospitals and society — should contribute financially in some way. On the educational front, Phelan is disappointed that we did not provide evidence that university education will enhance the educational experience of trainees. However, undertaking educational studies that meet the standards required of reductionist experiments has proven to be difficult, and we have to make do with a more ecological approach. We have no doubt that our Macquarie University scholars will derive lasting benefit from working in an environment in which learning is one of the primary goals of their existence, rather than an add-on, after-hours, activity. Learning arises not from watching, but from doing. Modern concepts of neurobiology and learning suggest that learning results in structural changes in the brain, and these will be enhanced for the learner by full participation in all processes of care. We shall ensure that learning is maximised by an appropriate balance between scholars’ clinical experience and the educational opportunities that their clinical experience will provide. The Canadian contracting model, which Phelan mentions, is not dissimilar to the arrangement that will flow from the Memorandum of Understanding between Macquarie University and the Royal Australasian College of Surgeons and the Neurosurgical Society of Australasia, in that College trainees will substitute experience at Macquarie University for time spent in public hospitals in the College’s Surgical Education and Training Program. In Australia, we do not share the Canadians’ advantage of having only two postgraduate colleges. Given the current fragmented state of postgraduate medical education in Australia, we believe that it is better to experiment with and to evaluate new models than slavishly to copy what appears to work in a different setting. One of the flavours of the decade is competition, and we believe that competing models should be set up and should be rigorously evaluated from both educational and financial viewpoints. If history shows that the Macquarie lighthouse has illuminated the way to improved health for the Australian people, we shall be well satisfied.

Rufus M Clarke · Michael K Morgan

To the Editor: I recently received written advice from the Australian Safety and Compensation Council (a division of the Department of Employment and Workplace Relations) that the records of the Australian Mesothelioma Surveillance Program (AMSP) have been lost. As some of your readers would be aware, the AMSP, which ran between 1980 and 1985, was one of the most comprehensive medical surveys of mesothelioma undertaken anywhere in the world.1 The records of the program contain full occupational and environmental histories of about 1000 mesothelioma cases reported in the early 1980s. The program has played a significant role in helping to understand the epidemiology of mesothelioma in Australia. The level of detail of data in the AMSP has not been repeated by the Australian Mesothelioma Register, which succeeded the AMSP in 1985. This less detailed reporting scheme is the current basis for mesothelioma reporting to cancer registries in the country. I am a geologist with an interest in medical geology currently studying to obtain a doctorate on naturally occurring asbestos and mesothelioma risk in Australia. I had hoped to use the detailed environmental and occupational data of the AMSP to help determine the possible influence of naturally occurring asbestos on mesothelioma in Australia, in particular in the eastern states and South Australia, but without the records this is no longer possible. Data from the Australian Mesothelioma Register are not sufficiently detailed for this purpose. My intention in writing this letter is not to embarrass staff from the Australian Safety and Compensation Council, who have done their best to find the records and have been supportive of the project, but to create awareness of the loss, in the hope that the publicity may jog someone’s memory and result in the records being located. The potential permanent loss of these records would be a great loss to mesothelioma research in Australia and raises questions about the federal government’s policies surrounding long-term storage and archiving of nationally significant scientific research datasets that may be of benefit to future researchers.

Marc Hendrickx

Comment: The Australian Mesothelioma Surveillance Program (AMSP) operated between 1980 and 1985 and was maintained by the Commonwealth School of Public Health and Tropical Medicine at the University of Sydney. These files were transferred to the National Occupational Health and Safety Commission (NOHSC) on its establishment in 1985. The NOHSC was relocated from Sydney to Canberra in 2001, and AMSP records went into storage at that time. In February 2005, the NOHSC was succeeded by the Australian Safety and Compensation Council. We attempted to locate the records over several months in 2007. This involved manually searching through all files and boxes held by our contracted storage company marked as relating to either the AMSP or the Australian Mesothelioma Register. In addition, we had a staff member of the storage facility manually search the warehouse for these records in case they were in unmarked boxes or filing cabinets. In November 2007, having been unable to locate the records, we informed Mr Hendrickx that we would be unable to assist him with access to the AMSP records for his doctoral studies. It is certainly not our policy to discard records such as these and we were disappointed when they could not be easily located. We regret the potential loss of these important records to the research community and are still attempting to locate them.

Julie Hill

To the Editor: There are two fundamental flaws in the case for reform of youth mental health services outlined recently by McGorry and colleagues.1,2 They argued that 18 years is an unnatural and inappropriate transition point between adolescent and adult services, and that Child and Adolescent Mental Health Services (CAMHSs) are somehow inherently ill equipped to deal with serious mental illness. McGorry has long advocated a “youth model” catering for adolescents and young adults together. I believe this would be a disaster, particularly for adolescents. Adolescents and young adults need very different models of care, because of the differing degrees of responsibility and autonomy they can handle, the legal and moral responsibilities of families, carers, schools and health professionals, and the effectiveness of treatments. McGorry’s well deserved reputation and influence mean there is a real risk his opinions will be accepted as fact, especially as the opposing view is seldom heard. People aged under 18 years (on average) are not expected, or permitted, to take full responsibility for their lives or their mistakes. Legally, they cannot vote, drink or buy cigarettes. They are generally still at school and living in the family home. Those aged under 16 years are not automatically entitled to grant or withhold consent to treatment. Families thus have a central role in the management of illness in adolescents, in a way that is neither possible nor appropriate for adult patients. Adolescent inpatient units need to be highly structured environments where adults would be out of place, with school-like rules, and careful control of group process and peer interactions. Otherwise, there is bullying, sexual exploitation, epidemics of self-harm, and the kind of competitive rebelliousness that leads to riots and fires. In adult units, adolescents are unacceptably vulnerable, not only from exploitative older patients, but from a lack of boundaries to their own behaviour. McGorry made several perplexingly dismissive comments about CAMHSs. Two cannot go unanswered: that CAMHSs “struggle operationally and clinically with . . . mood, psychotic, substance use, and borderline personality disorders”;1 and that “the capacity to skilfully and safely manage highly disturbed behaviour, and the more sophisticated psychopharmacological skills, are often lacking in . . . CAMHSs”.1 The disorders described are, in fact, “bread-and-butter” work for CAMHSs. Further, there is powerful anecdotal evidence that CAMHSs manage them better, not worse, than others. Examination of data held by the Victorian Department of Human Services and the Office of the Chief Psychiatrist on seclusion (sole confinement) rates, consumer satisfaction and suicide rates will bear this out. Child psychiatrists all train as adult psychiatrists first and, in my experience, do not lack psychopharmaceutical sophistication. It is hard to see what adolescents and their families have to gain from being incorporated into young adult services, nor why 30-year-olds should be excluded from specialist early psychosis services. We need greater integration between the current tiers of service, and a more flexible approach to transition between them, not another separate tier of service.

David A Sholl

In reply: Sholl asserts that our case for reform of youth mental health services is based largely on personal opinion. In fact, as detailed in the Journal supplement,1 it is based on hard epidemiological facts, the latest developmental perspectives and a growing evidence base. Consequently, it has been widely supported by young people, families, governments and the community. The youth model ensures that developmental approaches appropriate to all stages of the process of transition from childhood to adulthood continue until the young person is genuinely independent. To design a health system around the transition age of 18 years, based on legal and educational precedents, is outmoded. Many more young people now pursue postsecondary education and are financially and socially dependent on their families well into young adulthood.2 The youth mental health paradigm involves families in a developmentally appropriate way from puberty to the mid-20s, and also recognises the increasing value of peer relationships. The key difference is that young people have increasing choice about the level and pattern of family engagement. Similarly, brain development continues actively up until the mid-20s. We believe Sholl has misunderstood the fundamental issue of youth mental health reform. It is not a binary choice between current child–adolescent and adult service models. A new stream of care is required to respond to these “transition age youth” or “emerging adults”, as they were recently termed.2 This stream borrows many of the features of adolescent psychiatry and extends these to around 25 years of age, complementing them with new evidence-based approaches, which have been difficult to create and nurture within a constrained and under-resourced Child and Adolescent Mental Health Services system. This step is crucial for the “graduates” of state care, who have appalling outcomes when care is withdrawn at 18 years (even though they can vote).3 We have successfully developed and provided such an adolescent–young adult service to a quarter of Melbourne for over a decade. Recently, we extended this to Sydney. The real-world impact of this approach has helped greatly to convince the community, including federal and state government leaders, of its wider value. We want to see genuine reform, restructure and substantial investment in a new stream of care. How well this links, not only with existing child and adult specialist systems, but equally importantly with other key systems — notably education and employment, primary care, housing, justice and drug and alcohol services — will be critical to its success.

Patrick D McGorry · Ian B Hickie · Anthony F Jorm · Rosemary Purcell

To the Editor: Singh and Castle recently commented on the assumptions made in relation to the National Mental Health Policy.1 One such assumption was that the cost of the community care service model could be constrained by limiting services to the “severely” mentally ill. The authors went on to describe the realities associated with making this and other assumptions on current mental health care delivery. Many public wards have become the province of treatment-resistant consumers with limited insight who do not welcome the interventions provided by mental health workers. It may be that this type of inpatient population is influencing medical students’ views of psychiatry and contributing to low numbers in psychiatry training across the country. Students’ perceptions that psychiatry is a difficult and pressured work environment have been reported.2 Public services for consumers who have mental illnesses that do not involve psychosis are under severe pressure in the current paradigm. Despite the availability of effective treatments, anxiety and depressive disorders remain the principal cause of the disability produced by mental disorders, and half the people with such a disorder do not seek help, not realising how well they can become.3 However, the public system appears to be retreating from providing services for such patients. There seems to be a view that all Australians with anxiety and depression can be treated in private practice or by general practitioners. Does targeting low-prevalence disorders for treatment represent an acknowledgement by those in government of the power of mental health stigma? Is there misguided thinking that spending money on patients with psychotic disorders will keep mental illness and violence off the streets? Doctors have an obligation to inform those in power that effective treatments need to be made available to the broadest range of Australians, not just those who are obviously mentally ill. The difficulty of retaining psychiatrists in the public sector has been noted in many countries.4 Health services need to provide variety in the work of clinicians to keep them within the public sector — a diet of chronic psychosis tends not to attract or sustain staff. I believe fostering specialist units dealing with high-prevalence disorders like anxiety and depression, and high-morbidity conditions like eating disorders, would encourage the training of new staff, contribute to research, and strengthen the future of psychiatry. Revitalising public treatment services for high-prevalence psychiatric disorders could provide both symptom relief and a return to productivity for many thousands of Australians, and a more sustaining work environment for mental health clinicians. It is time for our governments to hear the call to provide mental health care for the many, not just the few.

James D Hundertmark

To the Editor: A 20-year-old sub-elite Australian Rules football player presented with pain and tenderness in the lower third of the sternum. He had been involved in a moderate body collision with an opposing player about 3 weeks before presentation, and had continued to train and play despite sternal discomfort. He described no other symptoms. On examination, there was no obvious sternal deformity. There was mild to moderate tenderness over the lower third of the sternum, and minimal sternal discomfort on lateral chest compression. Chest auscultation was clear. Plain chest and sternal x-rays were normal. A technetium-99m HDP bone scan showed increased tracer uptake in the lower sternum, consistent with an undisplaced oblique sternal fracture (Box). Management of the player’s injury and his fitness to train and play were discussed informally with medical and paramedical practitioners. Their opinions ranged from an immediate return to competition to 12 weeks of complete rest. After discussions within the player’s club, he was placed on a training regimen that avoided all upper body clashes and stresses, and he was rested from match play. He was regularly reassessed for symptoms and made an uneventful return to full competition 6 weeks after his initial injury. He remained asymptomatic and competitive for the remainder of the season and at 1-year review. The usual cause of sternal fracture is blunt anterior chest trauma, with about 90% of sternal fractures caused by trauma resulting from the forces associated with motor vehicle accidents.1 Sternal fracture is rarely encountered in Australian Rules football and such a case has not previously been described in the literature. The Australian Football League Injury Report database revealed only four cases of sternal fracture over the period 1992–2006, accounting for a total of 18 missed games (range, 1–11 games) (John Orchard, Conjoint Senior Lecturer, Sports Medicine Program, University of New South Wales, personal communication, May 2007). Patients suspected of suffering a sternal fracture should be investigated with appropriate chest x-rays. If these are inconclusive, it is now suggested the patient should be further investigated with sternal ultrasound, which has recently been demonstrated to be superior to bone scan in identifying sternal fractures,2 and without the associated radiation exposure. Patients with an acute suspected sternal fracture should also undergo electrocardiography. If the electrocardiogram is normal and there is no evidence of intrathoracic injury on radiological investigation, the patient can safely be discharged.3 Chest pain is the predominant persisting symptom after sternal fracture.4 Conservative management with rest, analgesia and/or anti-inflammatories, and, if required, appropriate padding and taping5 should result in full recovery and an uneventful return to competition. Bone delay views from dynamic localised technetium-99m HDP bone scan There is a band of low to moderate tracer uptake running in a slightly oblique line across the lower sternum (arrow), suggesting a sternal fracture.

Robert J Douglas

To the Editor: According to a recent article in the Journal, the pervasive nature of under-age drinking underscores the need to develop prevention strategies to delay the onset of alcohol use and its adverse consequences.1 In the United States, school-based prevention programs have played a prominent role in the alcohol-use prevention scene. Drug Abuse Resistance Education (DARE), the most widely recognised school-based alcohol-use prevention effort, is an elementary school curriculum that focuses on the adverse effects of substances of misuse, and the development of skills to resist peer pressure to use. Despite its nationwide appeal, attempts to empirically evaluate the efficacy of DARE have failed to yield positive results.2 Subsequently, Mothers Against Drunk Driving developed a school-based alcohol-use prevention program called “Protecting You/Protecting Me” (PY/PM). PY/PM centres on instructing children about central nervous system development and the importance of protecting developing brains from substances of misuse. PY/PM appears to be effective in enhancing knowledge of alcohol toxicity and changing attitudes toward binge drinking,3 but its efficacy in decreasing alcohol use remains to be established. Although the efficacy of school-based alcohol-use prevention strategies has been the subject of controversy, such programs have proliferated. School-based multicomponent approaches have also emerged. Project Northland integrated school, neighbourhood, and family components in an effort to decrease alcohol use.4 Project Northland consisted of classroom curricula, extracurricular activities, and parental involvement. Twenty-four school districts were randomly allocated to receive some or all of the prevention package or a control. At the end of 3 years, significantly fewer students in the intervention school districts reported the onset of alcohol use than students in control districts. Efforts to disentangle the impact of its various components show differential effects. While the classroom curricula proved moderately effective, the strongest effects in decreasing drinking were seen for those who participated in the extracurricular activities and parent program components.4 The robust benefits noted from the parent program in Project Northland parallel effects of some other studies suggesting the utility of family-based approaches to alcohol-use prevention. In one study, the Iowa Strengthening Families Program significantly delayed the initiation of alcohol use.4 This program, which is geared towards optimising parenting skills, showed persistence of positive effects on alcohol outcomes 4 years after the intervention.4 These data suggest that parenting and family skills training may play a part in school-based alcohol-use prevention packages. Further evaluation of these programs in other countries is necessary, and may help to reduce the widespread adverse effects of early alcohol use among children.

Vania Modesto-Lowe · Nancy M Petry · Melissa McCartney