Letters

To the Editor: The prophylactic use of inferior vena cava filters (IVCFs) in trauma patients for whom anticoagulation is contraindicated has markedly increased over the past few years. Their need for caval filtration is usually only transient, and once the risk of venous thromboembolism is deemed to be minimal, it would seem appropriate that IVCFs be retrieved. However, a large number of IVCFs remain in situ, due to either failure of retrieval or lack of follow-up. We observed a case that touches on both of these two major problems associated with IVCF retrieval. A 34-year-old man received a prophylactic IVCF after he had sustained severe pelvic fractures, several undisplaced spinal fractures and a splenic laceration in a motorbike accident. He was deemed to be at high risk of venous thromboembolism, and immediate prophylactic anticoagulation was contraindicated because of his pelvic and splenic injuries. The scheduled IVCF retrieval, 8 weeks after insertion, failed due to technical difficulties. A large clot between the struts of the IVCF (Figure) meant further withdrawal attempts were deemed too dangerous. The patient was informed that he had two options: if the filter remained in situ, he would possibly need lifelong oral anticoagulation; or the IVCF could be surgically removed. Soon after this, the patient was discharged with instructions to continue oral anticoagulation. About 5 months later, at a follow-up consultation with the orthopaedic surgeon about his injuries, the patient expressed his concern about the IVCF and especially about the anticoagulation. He was taking it for no other indication than the IVCF. The radiologist who had inserted the IVCF was contacted, and subsequently removed it without any complications. In the case described here, an initial retrieval attempt was thwarted by filter tilt and a large clot burden. After discharge, the patient was lost to follow-up with respect to the IVCF. Fortunately, this was addressed by one of the specialists involved in management of the patient’s other problems. Without this intervention, the patient may have ended up with the filter permanently in situ, with its attendant risks, and an unwarranted lifetime of anticoagulation. When filters have a significant clot burden, anticoagulation can help dissolve this to the point at which retrieval can be effected safely.1 This case highlights the need for appropriate follow-up after IVCF insertion. Various studies have outlined different follow-up strategies, some using a protocol drawn up in a multidisciplinary team setting,2 others designating a key person (usually the clinician who inserted the filter) to undertake this task.3,4 Both strategies have been shown to reduce the number of patients lost to follow-up. The clot, occluding nearly the whole lumen of the inferior vena cava (IVC), is seen as a radiolucent area between the IVC filter struts as the contrast agent passes by.

Dominik Baschera · Jonathan K Sebunya · René Zellweger

To the Editor: We welcome the thoughtful analysis from Elkin and Studdert on international students missing out on internship places.1 Given the impending shortage of available internships in Australia, this is of considerable interest to the over 500 international students who graduate each year. Sydney Medical School (University of Sydney) should be commended for explicitly discouraging international students’ expectations of internship.2 Sadly, this is an isolated example. We agree with the authors that universities have an ethical obligation to ensure this information is adequately conveyed to current and prospective international students. Education policymakers and medical school administrators should be forthcoming with vital information on the future of training for international students in Australia. The Australian Medical Students’ Association is currently developing a comprehensive information booklet, which we will distribute to prospective international students. Among other details, this will clearly outline the issue. However, the issues raised by Elkin and Studdert are not confined to international students. The authors observe that the recent health ministers’ communiqué only guaranteed internship to students in Commonwealth-supported places.3 This not only excludes international students, but also local fee-paying students at private universities and those in state-funded places. The authors argue that international students have no legitimate expectation that they will be provided with an intern place on graduation, given the “clear” statements from the federal government. However, there has been no similar guidance for local private university or state-funded students. Do these students have a legitimate expectation of internship? One could argue that state-funded students do, given the funding bodies are the same ones that will also provide their internships. While Australian permanent residents and citizens currently have first or second priority for internships, depending on their state of study and the state to which they are applying, it seems that in the future these students may miss out in favour of Commonwealth-supported students covered by the health ministers’ guarantee. Elkin and Studdert concluded that Australian courts would be unlikely to find that international students hold a legitimate expectation of internship. It is less certain whether this conclusion might apply to state-funded students or Australian permanent residents and citizens at private universities. At a minimum, these applicants too deserve “full and frank information” about their internship prospects.

Christopher X J Wong · Samuel J Whitehouse · Thomas D Crowhurst · Ross L Roberts-Thomson

To the Editor: Blecher correctly asserts that alarm is not the appropriate reaction to the potential dangers of computed tomography (CT) scans.1 Such alarm risks discouraging patients from having the CT scans they need. Appropriate CT scans are good; inappropriate ones are bad. Blecher is also correct in stating that the linear, no-threshold (no dose is entirely safe however small) model of radiation risk is theoretical.2 However, the advice of all international regulatory radiation protection authorities is to assume that the model is correct. To do so is prudent, even if overly conservative. And while these authorities hold this position, it would be professionally irresponsible to ignore it. Notwithstanding the Health Physics Society statement that the risk of ionising radiation below 100 mSv is negligible,3 the risk is thought to be cumulative. Furthermore, a single CT scan of the chest, abdomen and pelvis may expose a patient to 30 mSv or more, and the risk in children and young adults is considered to be 2–3 times greater than the average.4 The atomic bomb data are based on radiation dose levels as low as 5 mSv,5 with the cohort exposed to doses between 5 and 20 mSv showing an 85% chance that the risk is worse than we think and a 15% chance that it is better than we think. Although not statistically significant at the 95% confidence level, these figures indicate that great care is needed. The dimensions of the risks of low-dose radiation are contentious, but are we willing to ignore the danger of accepting Blecher’s argument? It is a Pascal’s wager. Providing we do not spook patients from having necessary scans (and this requires better communication with patients), our possibly over-cautious approach should result in more appropriate use of diagnostic imaging. The benefits go beyond those of limiting unnecessary radiation. Blecher finds it ironic that concerns about the dangers of CT are rising as radiation doses are falling. Doses may be falling, although that depends on where the baseline is drawn. When multidetector CT scanning was introduced, doses rose,6 but if, since then, doses have been falling, there is nothing ironic about this. Doses are falling because of the concern. Whether a patient undergoes an imaging procedure should be subject to the process of justification mandated in the Australian Radiation Protection and Nuclear Safety Agency code of practice.7 If the potential benefit outweighs the risk, the procedure is justified and the examination should proceed, but optimised to ensure that the lowest possible dose of radiation is used to provide diagnostic images — the ALARA principle (As Low As Reasonably Achievable). In summary: If a CT scan is clinically justified, then it should be performed and we should certainly avoid alarming our patients. If a scan is not justified, it should not be performed. We should adhere to the ALARA principle. Whenever appropriate, a non-ionising alternative to CT scans should be considered, particularly for children and young patients.

Richard M Mendelson · Richard A Fox · Nicholas H de Klerk

To the Editor: Seizures can be precipitated by treatment with praziquantel in patients with underlying neurocysticercosis, but this is rare and has not previously been described in Australia. We describe the case of a patient who developed seizures after antischistosomal therapy. An asymptomatic 23-year-old Burmese man underwent migrant health screening by his local doctor a month after arriving in Australia. His schistosomal serological results were positive (titre, 1:32) and he received three doses of 600 mg praziquantel. Three days later, he experienced several generalised tonic–clonic seizures in short succession, each lasting a few minutes. A magnetic resonance imaging (MRI) scan revealed three ring-enhancing lesions less than 1 cm in diameter, suggestive of neurocysticercosis. He was treated with phenytoin and also received dexamethasone for 1 month. A repeat MRI scan 6 months later showed significant reduction in the size of the lesions, to less than 3 mm. Phenytoin therapy was ceased after 3 months, with no seizures at last review (6 months). In view of the temporal association between the treatment and the seizures in this previously asymptomatic patient, we believe the seizures were precipitated by the praziquantel therapy. Cysticercosis, which is endemic across the developing world, is caused by the helminth Taenia solium. Clinical disease, including neurocysticercosis, is often asymptomatic. Symptomatic neurocysticercosis often presents as seizures, especially as the cysts degenerate, and is the commonest cause of acquired, late-onset epilepsy in the developing world.1 The benefit of treatment remains controversial, especially when there are only a few cysts.1-3 Praziquantel and albendazole therapy accelerate cyst degeneration, and subsequent inflammation may precipitate seizures, which are sometimes pre-emptively managed with corticosteroids.1 There is conflicting evidence on the benefit of treatment for long-term seizure frequency.2,3 Although screening for some parasitic infections in refugees in Australia is recommended,4 this does not include cysticercosis. Serological tests for T. solium cannot differentiate between active and past infections, have limited sensitivity, are not widely available in Australia, and cannot differentiate between neurocysticercosis and cysticercal disease elsewhere.5 The only reliable method for diagnosis is neuroimaging, which is impractical for mass screening. Nevertheless, we advocate a high degree of suspicion for neurocysticercosis in migrants from Taenia-endemic areas. Geographical origin alone is insensitive for identifying an at-risk population. A history of seizures, or the presence of subcutaneous nodules, should prompt investigation with serological testing and subsequent neuroimaging before consideration of treatment. In such symptomatic patients, this will allow the need for anthelmintic therapy to be assessed, along with consideration of adjunctive corticosteroid therapy.

Saliya S Hewagama · Jonathan D Darby · Harsha Sheorey · John R Daffy

To the Editor: “Student medical journals” are a very broad church, encompassing everything from pseudo-magazines to rigorously peer-reviewed publications. In April this year, a national journal of the latter variety was launched here in Australia: the Australian Medical Student Journal (AMSJ).1 The AMSJ accepts research, review and opinion articles from students of medicine or health sciences at Australian universities. The journal’s volunteer staff comprises only medical students, and peer-review is by academics associated with Australian medical schools, or clinicians at Australian teaching hospitals. The inaugural issue could hardly have been more national in its focus, with students from 14 Australian medical schools, covering every state, being represented among the authors. The issue was recently distributed free of charge to thousands of medical students around Australia in both print and electronic formats. After the success of the inaugural issue, we plan to begin biannual production from 2011, continuing in both formats. The AMSJ operates as a not-for-profit student organisation, and printing and other costs are provided for by sponsors, including the Australian Medical Association, Australian General Practice Training, and the Royal Australasian College of Physicians. While it is unique in a number of facets, the AMSJ is not the first publication of its kind. The Australian Medical Students’ Association magazine Panacea began life in 1968 as a journal, albeit not peer-reviewed.2 Several individual Australian medical schools have had their own academic publications for varying periods, such as the Sydney University Medical Journal, which was first published around 1905.3 More recently, our counterparts across the Tasman were well ahead of us, with the New Zealand Medical Student Journal releasing its first issue in 2004.4 Further afield, some of the better known student journals are the McGill Journal of Medicine (MJM) in Canada and the Student BMJ in the United Kingdom. Most student journals fall roughly into one of two categories: those whose focus is primarily instruction and entertainment, with shorter educational or blog-style articles (often written by non-students) having appeal to time-constrained students (eg, Student BMJ); and those that publish academically rigorous student work, perhaps at the expense of reader interest (eg, MJM). The AMSJ has a number of aims (Box), although central to our mission is to transcend this artificial tension and attract student-authored articles that are both thoroughly interesting and academically substantial. The rationale is that anything short of a proper peer-reviewed journal is patronising towards students, but, on the other hand, articles that are not appropriately pitched cause disenchantment. Medical students have played key roles in the history of medicine: notable discoveries made or shared in by medical students include heparin, insulin, the sinoatrial node, the pancreatobiliary sphincter, ether anaesthesia, islets of Langerhans, and spermatozoa.6 We hope that the AMSJ can continue to promote and foster this tradition of student achievement. Aims of the Australian Medical Student Journal5 To provide a medium for Australian medical students to publish their work and share ideas with their peers. To provide a suitable forum for students to make the transition between assignment writing and producing publishable academic work. To inform students about medical topics and issues not typically addressed in core curricula. To facilitate discussion of current issues relevant to medical students. To allow Australian medical schools to showcase the research aspects of their programs. To provide a further incentive for students to produce high-quality work in their studies. To foster the next generation of Australian medical researchers and physician–scientists. To provide an avenue for students interested in a career in medical editing or publishing to pursue this interest as a student staff member.

Matt D Schiller

To the Editor: In February 2009, a 68-year-old man presented to the Royal Victorian Eye and Ear Hospital within hours of developing an itchy, red left eye. The patient, who was otherwise healthy, lived in suburban Melbourne, usually with his pet dogs, but the last of his dogs had recently died. The patient was unsure if all his dogs had been dewormed regularly because he spends about 6 months a year in Europe. General inspection of the eye suggested subconjunctival haemorrhage. However, slit-lamp examination showed a mobile, tightly coiled structure within the subconjunctival blood. It grew increasingly agitated with higher slit-lamp light intensity (Box, A). Assessment of the patient’s visual acuity and the anterior and posterior chambers of the eyes was unremarkable. Blood tests revealed a positive filarial serology and eosinophilia. The patient was transferred to the operating theatre and, under topical anaesthesia, a 5 mm conjunctival incision was made and the mobile structure removed (Box, B and C). The patient was discharged with a prescription for prednisolone acetate 1% and chloramphenicol 0.5% eye drops (one drop four times a day). He made a full recovery. The extracted specimen was reviewed by one of us (D M S). The 150 mm worm was identified as a young adult female filarioid nematode, Dirofilaria immitis (commonly named dog heartworm) after comparisons with laboratory specimens of D. immitis and Pelecitus roemeri. Infection with either P. roemeri (kangaroo and wallaby knee worm) or Loa loa (loiasis) was excluded. Our specimen did not have lateral alae and the distance from anus to tail was shorter than would be expected for the kangaroo worm. In addition, the patient had never been to Africa where loiasis is endemic to several countries. Subconjunctival dog heartworm is rare, but its incidence is increasing in parts of the world.1,2 Dogs are the natural hosts and transmission to humans occurs through mosquito bites of the skin (into which the third-stage infective larva may escape). For an unknown reason, the worm sometimes takes an abnormal migratory route and ends up in the eye of the host. Ophthalmic cases have been reported in dogs.3,4 Careful measures to exterminate mosquitoes and deworm dogs and cats are important in limiting its transmission. Surgical extraction is the definitive treatment and further treatment with systemic anthelmintics is unnecessary.5 Humans are non-natural hosts for this parasite and, therefore, its life cycle cannot be completed within the human body. When a larva does evade the human immune system, as in the case of our patient, the chances of another larva being present elsewhere in an immunocompetent person seems remote. Furthermore, unless the larva becomes clinically apparent, it would be impossible to find. Subconjunctival Dirofilaria immitis infection in a 68-year-old man A: A whitish mobile structure coiled in the haemorrhagic subconjuctival space B: The female Dirofilaria species measuring about 150 mm C: Day 1 after removal of worm and necrotic temporal conjunctiva, exposing bare sclera

Elaine W Chong · Harsha Sheorey · Cheng Hean Lo · David M Spratt · Enrique Graue-Hernández

To the Editor: The medical view, which is repeatedly stated in the literature,1-3 is that up to 100% of those who complete suicide are suffering from a mental disorder. This leaves many doctors feeling they can be held responsible for all those who suicide, including those for whom there is no evidence of mental disorder. A recent High Court of Australia judgment, Stuart v Kirkland-Veenstra,4 illustrates that the medical and legal views of the relationship between suicide and mental disorder are different. In this case, a wife alleged that police officers had failed to provide a duty of care towards her husband, who had been found by the officers in a car with a hose leading from the exhaust pipe into a rear window, but with the driver’s window down and the car engine cold. The officers talked to the husband, who claimed marital problems but that he had changed his mind about suicide and was planning to go home and discuss matters with his wife. The officers felt the husband was rational, cooperative and responsible, with no evidence of alcohol or drug misuse; they offered him assistance (which he declined) and allowed him to leave. Later that day, the husband completed the suicide. He had not told the officers that he was expecting to be served with papers relating to fraud charges that afternoon. The Stuart v Kirkland-Veenstra judgment,4 in favour of the police officers, includes the following statements: Suicide and attempted suicide are seen as reflective of psychological or psychiatric issues which may or may not involve ‘mental illness’ according to established diagnostic conventions . . . Given the complexity and variety of factors which may lead to suicidal behavior, it would be a bold legislative step indeed to sweep it all under the rubric of mental illness, however widely defined. Word limits prevent me from giving more detail about the case, but interested readers will find this accessible judgment valuable. Clinicians dealing with “difficult” (but not mentally disordered) people in difficult circumstances often feel themselves to be in a perilous legal position, able to be held responsible for the actions of all those who choose to end their lives. The Stuart v Kirkland-Veenstra judgment clarifies the legal perspective, that suicide does not necessarily indicate the presence of a mental disorder, and that where mental disorder does not exist, human services personnel will not necessarily be held responsible for the actions of others.

Saxby Pridmore

To the Editor: The current political debate on health reform has made no mention of the 300 000 people who were identified by the National Health and Hospitals Reform Commission as facing “stark health inequalities”.1 We refer to people with intellectual disability, who face a life expectancy 5–20 years shorter than people in the general population, substantial unmet health needs and significant barriers to getting these needs met. A recent review of health inequalities in England states: To reduce the steepness of the social gradient in health, actions must be universal, but with a scale and intensity that is proportionate to the level of disadvantage. We call this proportionate universalism.2 In its health reform initiatives, the federal government has quite rightly included specific funding for the health of Indigenous people and residents of aged care facilities, and for rural health and mental health. Many of these measures are just a start, but they are direct acknowledgement of specific disadvantage. However, the government has taken no such action on the health of people with intellectual disability. In fact, recent changes to Medicare (in May 2010)3 include a step backwards for people with intellectual disability. The merging of intellectual disability health assessment items into four new time-based items means that data are no longer kept on the uptake of intellectual disability assessments. This was the one piece of information on the health of people with intellectual disability that the government collected. Many of the government’s health reforms will have wide community benefit. However, we are long used to people with intellectual disability missing out on the benefits of generic programs. To give one example, funding hospitals on the basis of the “efficient price” of services may create a disincentive to treat people with intellectual disabilities, who need much more time than other patients. To avoid this disincentive, the government needs to create a price-loading for people with intellectual disability, which in turn will require the government to redress the absence of data on hospitalisations of people with intellectual disability. With each plank of its reform, the government at least needs to ask: “What adjustments are needed to make this work for people with intellectual disability?” We are happy to provide the answers.

Nicholas G Lennox · James C Simpson

To the Editor: The recent review by Hayes and colleagues1 does not sufficiently emphasise practical approaches to managing the later stages of Parkinson disease (PD). Nazem and colleagues2 reported active suicidal or death ideation in 30% of patients with PD of mild-to-moderate severity, and an overall rate of major depression of 27.6%. They found that psychiatric symptoms and disorders, especially major depression, rather than PD-related variables, predicted suicidal or death ideation. Only half of the depressed patients were being treated with an antidepressant. Screening for psychiatric disorders should occur on assessment. Skilled counselling is required, and carers need to be well supported, particularly if the patient has intermittent suicidal ideation and a strong wish for the end of life. Clozapine is the only antipsychotic shown to be effective for treating psychosis in patients with PD.3 If the psychosis is schizophrenia-like, with persistent bizarre delusions and florid hallucinations causing agitation, clozapine can be prescribed in Australia by a registered psychiatrist and the patient can be registered with the clozapine monitoring service. If the patient is started on a very low dose (6.25 mg daily) that is only very gradually increased, side effects can be minimised. Successful use of clozapine enables remission of the psychosis and optimal treatment of motor symptoms. Mild hallucinations may be tolerated without specific treatment while the patient retains insight. In an open-label study of patients with mild hallucinations comparing no treatment with quetiapine therapy (or clozapine therapy in a minority of cases),4 the rate of progression to hallucinations without insight, or delusional psychosis, was significantly slowed. Hely and colleagues5 have argued that pathological processes in addition to Lewy body disease may have a role in the appearance of dementia, as age is a better correlate than PD duration. If it is clear that the dementia is a PD dementia, or dementia with Lewy bodies, a cholinesterase inhibitor such as rivastigmine could be prescribed. As rivastigmine is not subsidised on the Pharmaceutical Benefits Scheme in Australia for this indication, a private prescription could be provided in the first instance, and if there was a likelihood of significant Alzheimer disease associated with PD, an authority prescription would be justified. Hely and colleagues pointed out that, in the later disease stages of PD (at 20 years), less than 50% of patients still see their neurologist. However, the quality of life for PD patients in nursing-home care could still be significantly improved by specialist review by members of a multidisciplinary team on an inpatient, outpatient or outreach basis.

David S Tofler

To the Editor: Although Clarke and Fitzgerald’s claim that prices for generic medicines in Australia are high compared with prices in other countries1 is valid, their claim that the Pharmaceutical Benefits Scheme expenditure on statins could be reduced by up to $9.31 billion, by increasing the proportion of generic prescriptions to 100% and paying equivalent prices to those in England, is problematic. For the proportion of generic prescriptions to be increased to 100%, the available generic statins would need to be directly substitutable for currently available statins, including those whose patents have not yet expired (eg, atorvastatin and rosuvastatin). Nicholls and colleagues present the results of a meta-analysis of various doses of atorvastatin, rosuvastatin and simvastatin.2 The findings of the Pharmaceutical Benefits Advisory Committee (PBAC) on the comparative effectiveness of the various statins can be summarised as follows:3 Simvastatin is the benchmark statin; the maximum recommended dose is 80 mg/day. Pravastatin is equivalent to simvastatin on a milligram-for-milligram basis: pravastatin 10 mg is equivalent to simvastatin 10 mg. The maximum recommended dose of pravastatin is 80 mg/day. Atorvastatin 1 mg is equivalent to simvastatin 2 mg: atorvastatin 10 mg is equivalent to simvastatin 20 mg. The maximum recommended dose of atorvastatin is 80 mg/day. It is notable that a simvastatin dose equivalent to atorvastatin 80 mg (ie, simvastatin 160 mg) is beyond the maximum recommended dose of simvastatin. Rosuvastatin 1 mg is equivalent to atorvastatin 3 mg, which would be equivalent to simvastatin 6 mg (ie, rosuvastatin 10 mg is equivalent to atorvastatin 30 mg, which would be equivalent to simvastatin 60 mg). The maximum recommended dose of rosuvastatin is 40 mg/day. It is notable that a simvastatin dose equivalent to rosuvastatin 40 mg (ie, simvastatin 240 mg) is beyond the maximum recommended dose of simvastatin. By applying the therapeutic relativities accepted by the PBAC to the results reported by Nicholls and colleagues, the dose–response curves for rosuvastatin, atorvastatin and simvastatin, all expressed in simvastatin mg equivalents, can be generated as shown in the Box. As seen in the graph, simvastatin (available as a generic) may not be substitutable for atorvastatin or rosuvastatin in patients who need a reduction in low-density lipoprotein cholesterol level of > 45 mg/dL (> 1.15 mmol/L). Although having patients switch to generic prescriptions would reduce expenditure on statins, the possibility that such a switch might be associated with inferior outcomes needs to be considered. Dose–response curves for rosuvastatin, atorvastatin and simvastatin LDL-C = low-density lipoprotein cholesterol.

Liliana Bulfone

In reply: Our recent study1 estimates pharmaceutical expenditure from 2009 to 2019 for various levels of use of off-patent statins, ranging from 25% (close to the current proportion) to 100%. We also show that England has much higher use of generic statins and consequently much lower pharmaceutical expenditure. However, our study does not advocate a particular level of generic use and so it is unclear why Bulfone has chosen to focus on only one of the cases (100% use of generics) presented in our study. We agree with Bulfone’s view that it is important to consider whether the greater use of generic statins has an impact on health outcomes in addition to examining the implications for pharmaceutical expenditure. This is one of the points we have already made: “The key question is whether the health benefits resulting from using statins under patent or combination therapies justify the substantially higher subsidies from the [Pharmaceutical Benefits Scheme].”1 The appropriate framework to use to consider this question would be to examine incremental cost-effectiveness of those statins still under patent (atorvastatin and rosuvastatin) compared with off-patent alternatives (simvastatin and pravastatin). Such an evaluation would be timely, as Australia faces billions of dollars of extra pharmaceutical expenditure over the next decade if we continue to prescribe patented statin formulations at current levels.

Philip M Clarke · Edmund M FitzGerald

To the Editor: We read with interest the article by Cleland and colleagues describing an urban–rural comparison of weight status among women living in socioeconomically disadvantaged neighbourhoods.1 After adjusting for socio-demographic factors, the authors reported no difference in prevalence of obesity, determined using women’s self-reported height and weight, between urban and rural areas. We would like to provide further evidence for the suggestion that obesity might be attributable to sociodemographic composition of areas. We have previously examined the association between area-based socioeconomic status (SES) and different measures of obesity in a randomly selected, population-based female cohort (aged 20–93 years, 77% participation)2 and in a similarly recruited male cohort (aged 20–96 years, 67% participation)3 within the Barwon Statistical Division in Victoria. An inverse association between SES and obesity was observed for both sexes,2,3 and was evident across three different SES indices developed by the Australian Bureau of Statistics (ABS).4 Within our female cohort, we investigated body mass index (BMI) in urban versus rural areas across the SES continuum, for 192 participants aged 20–45 years. We used standard geographical classification5 of 2006 ABS Census data to define participants’ residences as urban or rural (incorporating rural and semi-rural areas). Participants were further grouped according to the 2006 ABS Index of Relative Socio-economic Disadvantage, based on Barwon Statistical Division cutpoints. In our multivariable regression analysis, SES was categorised into the lower 30% (most disadvantaged), mid 40%, and upper 30% (least disadvantaged). Approval for this analysis was obtained from the Barwon Health Human Research Ethics Committee. No differences in unadjusted BMI were observed between participants residing in urban and rural areas (Box). These results were sustained after adjusting for age (data not shown). No interactions were identified between SES and urban or rural residence. No differences in BMI between urban and rural residence were observed for any SES group. These data suggest the lack of difference in BMI between urban and rural residents may be consistent across the SES spectrum. SES was associated with BMI (P = 0.001), while urban–rural residence was not (P = 0.5). Given these data, we suggest that SES is a stronger driving force for BMI than urban or rural residence. In our population, participants in the most disadvantaged group were more likely to be resident in urban areas. This is indicative of Geelong, the main urban centre of the Barwon Statistical Division, being one of the largest public housing areas in Victoria; urban areas provide more low-cost housing options than do rural areas. In contrast, residence in rural areas may be influenced by factors such as the “sea change” movement or prestigious real-estate options, such as the scenic coastal areas located away from the urban centre of Geelong. Mean body mass index (95% CI) of 192 women aged 20–45 years in the Barwon Statistical Division, Victoria, by area of residence Socioeconomic status* Urban† Rural† P‡ Lower 30% (most disadvantaged) 29.5 (26.8–32.1) 37.4§ 0.3 Mid 40% 27.8 (26.1–29.4) 25.3 (21.8–28.9) 0.2 Upper 30% (least disadvantaged) 25.5 (21.2–29.7) 25.5 (24.1–26.9) 1.0 Total population 27.3 (26.3–28.4) 26.1 (23.4–28.7) 0.43 * Defined by the Australian Bureau of Statistics (ABS) Index of Relative Socio-economic Disadvantage of the Socio-economic Indexes for Areas using 2006 Census data, and cutpoints of Barwon Statistical Division for 2006. † Defined by the 2006 ABS Australian Standard Geographical Classification Urban Centres/Localities. ‡ For pairwise difference. § There was only one participant in this category.

Sharon L Brennan · Margaret J Henry · Geoffrey C Nicholson · Julie A Pasco

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

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

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

Nicholas S Glozier · Matthew Large

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

David M Studdert · Harold Luntz · Genevieve Grant

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

Alex Collie · Niki Ellis

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

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

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

Jessica D Pearse

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

Jon L Wardle

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

Edzard Ernst

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

Bebe Loff · Brad R Crammond

To the Editor: Infections caused by multiresistant gram-negative organisms are difficult to treat. Carbapenems are often used as a last resort but even these are under threat with the emergence of acquired metallo-b-lactamases worldwide, including Australia,1,2 India, China and Europe. We report the first case of a Providencia rettgeri producing the blaNDM-1 (New Delhi metallo-b-lactamase) type of metallo-b-lactamase in Australia. A man from Canberra, aged in his mid 50s, had elective plastic surgery in India in September 2009. This was complicated by a hypoxic brain injury, after which the patient spent 4 weeks in an intensive care unit. He was subsequently transferred to Canberra for ongoing hospital care. A urinary catheter specimen collected on admission in November 2009 showed a heavy growth of multidrug-resistant P. rettgeri and Pseudomonas aeruginosa. The P. rettgeri was resistant to all b-lactam antibiotics, including meropenem, as well as to all aminoglycosides, ciprofloxacin, tigecycline and colistin. The P. aeruginosa was resistant to all antipseudomonal antibiotics except for colistin (tigecycline was not tested as it has low or no antipseudomonal action). The patient was not given antibiotic therapy but the indwelling urinary catheter was changed and contact precautions were put in place. Both organisms were sent for molecular testing, which showed that the P. rettgeri had 100% homology with blaNDM-1.3 The patient cleared the organisms after 2 months, and since then has received ongoing inpatient care in the rehabilitation unit. The first NDM-1 type of metallo-β-lactamase was found in Klebsiella pneumoniae isolated from a Swedish patient who had recent medical contact in India.3 Data from the United Kingdom’s Antibiotic Resistance Monitoring and Reference Laboratory suggest that isolates with the NDM-1 enzyme have recently been repeatedly imported to the UK from the Indian subcontinent. There may now be circulation of these resistant isolates in the UK because some infected patients have no identifiable overseas links. Hospitals have been urged to be vigilant for multiresistant gram-negative bacteria in patients with recent hospital contact in the Indian subcontinent as well as the Eastern Mediterranean.4 Identification of an Enterobacteriaceae organism carrying blaNDM-1 is very concerning. No antibiotic may be available to treat patients who develop serious infection with such organisms, and there is the added concern regarding cross-infection in health care facilities. The plasmid carrying blaNDM-1 also contains genes that confer resistance to several other antibiotics.3 It appears likely that, in the near future, the NDM-1 enzyme will become a very successful metallo-b-lactamase globally. Patients infected with multiresistant gram-negative bacteria have entered the “post-antibiotic era”.

Geethanie A T P Fernando · Peter J Collignon · Jan M Bell

To the Editor: The arrival of national registration of health professionals on 1 July 2010, and consequential amendments to state and territory legislation, overcomes registration and recognition complexities currently facing Australian medical practitioners who wish to practise in multiple jurisdictions. However, national registration stops short of removing current inconsistencies among state and territory laws in various areas of medicine — including those that regulate prescription of Schedule 8 (S8) medicines. Despite recognition of S8 restrictions in every part of the country, medical practitioners potentially need to have a working knowledge of up to eight separate sets of controlled substances laws when prescribing S8 medicines. Imagine a general practitioner providing a morphine prescription with repeats to a couple caravanning around Australia for 3 months. That prescription may need to comply with the laws of each jurisdiction as to what details need to be included on the prescription form. Getting it wrong could result in significant delay and inconvenience for the holidaymakers if the pharmacist refused to dispense the prescription because it didn’t comply with local laws. For example, in South Australia a prescription for a drug of dependence must not be dispensed by a pharmacist if the patient’s date of birth is not included on the prescription form1 — yet there is no similar requirement in New South Wales, Tasmania, Victoria or the Australian Capital Territory.2-5 Conceivably, through unawareness or habit, a prescriber in one of the latter jurisdictions might omit a patient’s date of birth from a relevant prescription form, leading to problems for the patient when travelling in other states. Granted, such a situation could be corrected with a few phone calls or faxes, but in a busy practice, who has time to be repeating tasks? National regulation of health practice (achievable through referral of powers or harmonising state and territory laws) — in this case, the prescription of S8 medicines — would logically complement national registration and help maximise anticipated benefits after 1 July 2010.

Colin M Brown

To the Editor: We report the case of a 19-year-old female veterinary student who presented with a 2-week history of a rapidly growing mass on the lateral side of the deltoid area of her left arm. On examination, the mass was soft, freely movable, slightly warm and non-tender. There was no regional lymphadenopathy. The patient was afebrile, with no signs of systemic illness. Ultrasound showed a 3.2 × 2.3 × 1 cm, low-echogenic, lobulated lesion in the subcutaneous fat, with surrounding increased echogenicity suggestive of inflammation. Magnetic resonance imaging showed a poorly defined lesion throughout the deep and superficial fascia, with infiltration into the underlying deltoid muscle (Box 1). A provisional diagnosis of sarcoma was made, but an ultrasound-guided core biopsy sample showed non-necrotising epithelioid granulomas (Box 2). Two weeks after presentation, the patient noticed a smaller raised lump, about 1 cm in diameter, on the volar aspect of her left forearm. Four months before presentation, following negative results of both Q fever serological testing and a Q fever skin test administered on the volar aspect of her left forearm (at the site of the smaller lump), the patient had received a Q-VAX (CSL, Melbourne, Vic) vaccination in the left deltoid (at the site corresponding to the larger mass). Three months after this, and about 3 weeks before the deltoid mass first appeared, the patient received a Fluvax (CSL, Melbourne, Vic) influenza vaccination at the same left-deltoid site as the Q fever vaccination. This raises the possibility that the influenza vaccination may have been associated with the subsequent Q fever granuloma reaction. Q fever, a disease caused by the zoonotic rickettsial organism Coxiella burnetii, is an occupational hazard for many Australians in animal-related professions. The disease is characterised by an acute, self-limiting febrile illness, with pneumonia and hepatitis being infrequent complications. In 2001, an Australian national Q fever vaccination program was initiated, which led to a 50% decline in the incidence of Q fever.1 Side effects are normally rare and minor; during 2001–2004, only 86 adverse reactions were reported from about 49 000 vaccinations.2 Development of non-necrotising granulomas following Q fever vaccination is uncommon, with only six cases previously described.3-5 To explore the possibility of a causal association between influenza vaccination, Q fever vaccination, and development of a granuloma, we traced four of these six patients with Q fever granuloma by contacting the authors of the previous reports. One patient had been vaccinated against influenza 2 months before the time of Q fever vaccination, and another had influenza vaccination afterwards (as in our case). Of the five cases (including our case) for which clinical history was available, three had a temporal association between influenza vaccination and Q fever vaccination, followed by the development of the non-necrotising granuloma. The indurated lesion at the separate Q fever skin-test site on the volar forearm, found in two other patients5 as well as ours, supports the notion of a systemic immune reaction rather than simply a local reaction at the vaccination site. The Naranjo score in this case was 7, indicating a “probable” adverse drug reaction. Although the granuloma was self-limited in all known cases, this case shows that there is significant risk of misdiagnosis on clinical grounds. It seems prudent to be aware of the possible association between these two vaccinations. Magnetic resonance images of lesion Axial (top) and coronal T1-weighted fat-saturated post-contrast (bottom) images demonstrate a poorly defined enhancing lesion (red arrows) in the subcutaneous fat, which superficially infiltrates and extends in a plaque-like manner in relation to the underlying deltoid muscle (white arrows). 2 Ultrasound-guided core biopsy sample of lesion The core biopsy of fibroadipose tissue shows numerous well formed non-necrotising epithelioid granulomas (arrows). The granulomas are composed of epithelioid histiocytes and a few multinucleated giant cells, surrounded by numerous lymphocytes (a mixture of B and T cells, with a greater proportion of T cells). (Original magnification × 100; haematoxylin–eosin stain.)

Deborah Burnett · Leslie Burnett

To the Editor: When I looked at the cover of the 5 April issue of the MJA, I feared finding another article focused on discrediting the prostate-specific antigen (PSA) test. Instead, I congratulate the authors, and the Journal, for presenting one of the rare balanced articles on this topic.1 Denham and colleagues called for an end to taking sides in the debate over PSA testing, and focused instead on helpful guidance. The problem is not whether PSA helps us find prostate cancer, but that we lack clinical tools for deciding which patients would benefit from aggressive treatment. However, the authors point out that there are two important tools that can help with this decision: low free to total PSA ratios, and rapid PSA doubling time (< 3 years).1 The PSA test is now one of the most sensitive, precise and highly standardised immunoassays in the clinical laboratory. The difficulty does not lie with the measurement but with its application. The Royal College of Pathologists of Australasia, together with the Urological Society of Australia and New Zealand, recently produced a monograph that discussed the appropriate use of the PSA test.2 It emphasised using age-related cut-offs for PSA levels, the free to total PSA ratio, and the calculation of PSA doubling time as modern tools to achieve optimal benefit from the test. The Australian Medicare Benefits Schedule (MBS) was changed in May 2009 (following a suggestion from the Urological Society of Australia and New Zealand) to improve utilisation of free to total PSA ratios. The Box indicates the per capita request rates of PSA testing (MBS item number 66655) and free to total PSA ratios (MBS item number 66659) from May 2009 to February 2010. Consistent with Denham et al’s observation that there are regional differences in the attitudes to prostate cancer,1 there is a twofold variation in PSA requesting and a sevenfold difference in free to total PSA ratio requesting across the Australian states. Furthermore, the relationship between the two tests is, if anything, inverse, suggesting that increased use of PSA testing is less commonly followed up by modern tools such as free to total PSA ratio. As a chemical pathologist, the appropriate clinical use of the PSA test has been a career-long concern of mine.3 Even though the discoverer of PSA has labelled the test a public health disaster,4 recent “case–controlled” studies using PSA in an outdated approach (without free to total PSA ratios or doubling times) have shown a marginal benefit for screening.5,6 The indiscriminate use of PSA testing can be helpful to some but disastrous for others. Modern PSA tools may significantly improve management beyond these marginal effects. As always, the value of medical investigations lies in how intelligently we use them. Average per capita request rates of PSA testing* and free to total PSA ratio,† May 2009 – February 2010 PSA = prostate-specific antigen. ACT = Australian Capital Territory. NSW = New South Wales. NT = Northern Territory. Qld = Queensland. SA = South Australia. Tas = Tasmania. Vic = Victoria. WA = Western Australia. * Medicare Benefits Schedule (MBS) item number 66655. † MBS item number 66659.

Kenneth A Sikaris