Cancer

Objective: To describe trends in prostate-specific antigen (PSA) testing, prostate cancer incidence and mortality in New South Wales.Design and setting: Descriptive analysis using routinely collected data of observed trends in PSA testing from 1989 to 2006, and prostate cancer cases and deaths from 1972 to 2005 in NSW.Main outcome measures: Age-standardised and age-specific rates and joinpoint regression to identify changes in trends; projected trends observed before the introduction of PSA testing to quantify its impact on incidence and mortality rates.Results: The number of PSA tests per year more than doubled between 1994 and 2006. Age-standardised incidence of prostate cancer peaked in 1994, fell by 10.0% per year to 1998 and then increased by 4.9% per year from 2001 to 2005. An estimated 19 602 (43%) more men than expected from preceding trends were diagnosed with prostate cancer between 1989 and 2005 after PSA testing was introduced. The incidence of recorded advanced prostate cancer at diagnosis fell from 13.0 per 100 000 men in 1987–1991 to 7.0 per 100 000 men in 2002–2005. The age-standardised mortality from prostate cancer increased by 3.6% per year between 1984 and 1990 and then fell by 2.0% per year to 2005.Conclusions: There was a sustained increase in prostate cancer incidence in NSW after PSA testing was introduced. While falls in the incidence of advanced disease at diagnosis and mortality from prostate cancer after 1993 are consistent with a benefit from PSA testing, other explanations cannot be excluded.

David P Smith BA, MPH · Rajah Supramaniam MSc, MPH(Hons) · Villis R Marshall MD, FRACS · Bruce K Armstrong MB BS, DPhil, FRACP

Obesity control in Australia is imperative, and has much to learn from tobacco-control strategies The increasing incidence of obesity in Australia is set to impose a major additional cancer burden at a time when population ageing alone is projected to cause unprecedented growth in cancer incidence. While obesity is frequently associated with type 2 diabetes, hypertension, lipid abnormalities and death from heart disease and stroke, there is growing evidence for its role in causing cancer. A systematic review and meta-analysis, which included the Million Women Study, investigated the link between body mass index (BMI; calculated by dividing weight in kilograms by height in metres squared) and types of cancer.1,2 In men, a 5 kg/m2 increase in BMI was strongly associated with adenocarcinoma of the oesophagus, and thyroid, colon and renal cancers, and in women with adenocarcinoma of the oesophagus, and endometrial, gallbladder and renal cancers. There were weaker associations for melanoma and rectal cancer in men, and postmenopausal breast, thyroid and colon cancer in women. Leukaemia, myeloma and Hodgkin disease were associated in both sexes. One postulated mechanism for the link between obesity and cancer is that chronic hyperinsulinaemia results in raised levels of free IGF-I (insulin-like growth factor), with higher mean concentrations in men compared with women. This alters the environment of cells to favour cancers developing.3 In adipocytes, androgens are converted to oestradiol, and chronic hyperinsulinaemia also reduces sex-hormone-binding globulin, leaving more oestrogen to impact on oestrogen-sensitive tissues. Further, adiponectin, a protein hormone secreted by adipocytes, is an insulin-sensitising agent that is anti-angiogenic and anti-inflammatory, inversely correlated with BMI, found in higher concentrations in men than in women and, in some studies, its level is inversely associated with cancer risk.4 Obesity is linked to 11% of colon cancers and 9% of post-menopausal breast cancers5 — both increasingly common tumour types in Australia as a result of population ageing. With high percentages of endometrial cancer (39%), oesophageal adenocarcinoma (37%), kidney cancer (25%) and gallbladder cancer (24%) attributed to obesity and overweight, these rarer cancers may become more common as Australia’s obese population ages.5 The risk of an obesity-related increase in cancer burden in this country is amplified, with the link between BMI and cancer compounded by a 50% increase in the number of obese or overweight Australians over the past 15 years. An estimated 7.4 million Australians are obese or overweight, including a quarter of children aged between 5 and 16 years.6 Multiple strategies are needed to control obesity. Decreasing the consumption of energy-dense, nutrient-poor foods and encouraging consumption of healthy foods and increased physical activity are clearly the keys. What is not so obvious is what works. The high risk of childhood obesity continuing into adulthood and the lag time before the development of cancer make children a critical target for obesity-control programs. A range of interventions have been introduced, such as regulating school canteens, eliminating soft drink sales in schools, physical activity programs and education, but there is no coherent national strategy. The debate on whether such a national strategy should include restricting junk-food advertising is likely to continue for a number of compelling reasons. Australian children are exposed to more food advertising than children in the United States, United Kingdom, New Zealand and 11 western European nations,7 much of it potentially misleading in its use of healthy imagery to promote products high in sugar, fats and salt.8 Governments in Sweden, Norway and Quebec have restricted junk-food advertising to children, with some encouraging results.9 Great Britain adopted a similar policy in 2007, so more data on the efficacy of this strategy will emerge. In the absence of empirical Australian data, modelling by the Victorian Government shows that restrictions on junk-food advertising would be the most cost-effective intervention for reducing adolescent obesity.8 The South Australian Government has announced a phase-out of junk-food advertising during children’s television viewing hours, using its sovereign authority to act independently of federal broadcasting laws. Other jurisdictions may follow, and this presents an opportunity for the federal government to show national leadership towards a uniform approach. Product labelling that informs consumers in making healthier choices is also pivotal to food marketing reform, while government assistance to make healthier foods more affordable and accessible, particularly to disadvantaged groups, should also be considered. A whole-of-government response to fostering healthier communities, including initiatives to support increased physical activity, must also be built into a national obesity strategy. Consideration of the options for reducing obesity draws historical comparisons with the experience of tobacco control in the early 1970s. While minimising the use of tobacco (which has no safe consumption level) differs in many ways from reducing junk-food consumption (which is low risk if consumed in moderation), there are compelling parallels. The disease burdens related to both tobacco and obesity are disproportionately prevalent among disadvantaged population groups. Tackling both smoking and obesity requires a combination of research, policy, social marketing and program-based interventions. And, of particular interest to the debate on food advertising, there are commercial interests with a clear stake in maximising junk-food consumption, just as there are in maximising tobacco consumption. Moreover, public health advocates cite “de-normalisation” as a key to Australia’s historical success in reducing tobacco consumption. It could be argued that excessive junk-food consumption is effectively “normalised” at an early age by the sheer volume of advertising pitched at children. An important lesson from tobacco control is that an array of modest government interventions to influence healthy behaviour will fall well short of their potential if they must compete with big-budget advertising from industry encouraging unhealthy choices; smoking rates in Australia dropped markedly when broadcast advertising of tobacco was phased out in the mid 1970s.10 With an increasing incidence of cancer, now is the time for a range of tough decisions that will modify dietary behaviour and put public health before corporate interests.

Ian N Olver MD, PhD, FRACP · Paul B Grogan

To the Editor: We read with interest the article by Rosenfeld and Duggan,1 who speculate on the possible psychological downsides of colorectal cancer (CRC) screening with faecal occult blood testing, and possible barriers preventing women accessing screening. We are concerned that the article has multiple limitations, and would like to report prospective data on CRC screening in Australia. While not mentioning three studies showing no long-term psychological harm from CRC screening,2 the authors have chosen to quote anecdotes from breast cancer screening, and a study of diagnostic testing for hepatitis C in a high-risk population, which is not a population screening test. Further, in the quoted study by Mant et al,3 an example they give of anxiety after a screening test, they neglected to mention that 98% of participants with false positive results felt the test worthwhile, and almost 40% were more likely to take part in other screening. The quoted reduction of 16% in CRC mortality is from one trial only, and potentially misleading as, overall, the studies have shown a 15%–33% reduction in mortality.2 Benefit also goes well beyond reduced mortality, as the 20% reduction in incidence2 with early detection averts some of the physical and financial costs of surgery, radiation therapy and chemotherapy. Further, there are the definite negative impacts of dealing with the consequences of surgical management of a more advanced-stage symptomatic cancer (such as colostomy bags), compared with a screen-detected cancer managed by simple polypectomy. The additional negative effects of diagnosis of a potentially terminal illness are also relevant. Data on participation in CRC screening are available from two sources. The National Bowel Cancer Screening Program evaluations to date have shown that significantly more women participate in the screening offer than men.4 Data from a multicentre Australian prospective CRC database5 reveal 56 of 619 cases in women (9.0%) and 65 of 759 cases in men (8.6%) were detected by screening. Australia has been slow to adopt CRC screening despite the almost 5000 deaths annually, and the major potential benefits. Unlike Rosenfeld and Duggan, we argue that studies specific to CRC screening show no clear negative impact, and that the negative impacts of not screening are undisputed. Also, the available data indicate that women are participating in CRC screening to a greater extent than men.

Suzanne Kosmider · Kathryn M Field · Finlay A Macrae · Peter Gibbs

Objectives: To test the hypothesis that television news coverage of different cancers reflects their incidence and burden, and to examine the journalistic approaches used in reporting cancer.Design and setting: Content analysis of all news, current affairs and infotainment reports on cancer broadcast on five free-to-air television channels in Sydney, New South Wales, 2 May 2005 – 6 January 2008.Main outcome measures: Number of items on specific cancers, relationship with burden of that cancer (disability-adjusted life-years [DALYs]), and category of “story lead” used for the item.Results: Cancer was the fifth most reported health issue, with 1319 items; 25 different cancers received news coverage. The most reported cancers were breast cancer (42.5% of all items on specific cancers), melanoma (11.9%) and cervical cancer (11.6%). Some cancers were significantly over-reported in relation to their DALYs (eg, cervical cancer was over-reported by a factor of 10.2 compared with the number of reports predicted on the basis of DALYs) while others were under-reported, including colorectal, lung and pancreatic cancers. The most common story leads used in cancer reports were treatment (32% of items) and celebrities with cancer (21%), particularly breast cancer.Conclusions: The current predominance of reports on breast and cervical cancer and on young women with cancer may be distorting public and political perceptions of the burden of cancer. The success of advocates in raising the news profile of breast cancer may hold lessons for agencies wishing to improve the newsworthiness of other cancers.

Ross MacKenzie MA · Simon Chapman PhD · Natalie Johnson MIPH · Kevin McGeechan MBiostat · Simon Holding BA

General practice is still somewhat adrift in the complex world of cancer services General practice has not traditionally had a central role in cancer care. Typically, general practitioners have had the task of identifying and referring patients to specialists in a timely manner, but have stayed on the periphery of cancer care until patients reach the palliative stage. But the climate is changing — driven partly by the growing burden of cancer and the need to expand and diversify the workforce. The prevalence of cancer has increased substantially in Western countries,1,2 largely due to the ageing of the population: in Australia, by the age of 75 years, the risk of cancer is 1 in 3 in men and 1 in 4 in women.1 There is now an explicit recognition that GPs should be involved in all stages of the cancer journey, from first presentation to palliative care, and that service reforms must incorporate more significant roles for primary care.3 This has found its way into policy and practice in the United Kingdom and Australia, where service guidance emphasises integration of services and urges all those involved in delivering cancer services to better connect the various stages of the cancer journey and to provide care that is accessible and convenient — all predicated upon significant primary care input.4,5 Management of cancer is complex. It requires specialised skills and knowledge, access to sophisticated diagnostic and treatment facilities, and often long-term management of symptoms and recurrences. Despite this complexity, when cancer patients are asked about how their care could be improved, their requests are often simple: they want to know who is in charge of their overall care, they want ready access to care that is convenient and non-threatening, and they want reassurance that they will have access to specialised services if needed.6 A diagnosis of cancer has a profound psychosocial impact, and those who care for cancer patients need to address a range of complex and often rapidly changing needs. Ideally, cancer care should be provided by teams, supported by a network of services. The concepts of multidisciplinary teams and managed clinical cancer networks have been widely advocated,7 but the place of primary care within these teams has remained poorly defined and highly variable.8 This variability is demonstrated by urban–rural differences: in Australia, rural GPs tend to play a more active role in treating cancer patients than their urban counterparts. General practice is still somewhat adrift in the complex world of cancer services. In this issue of the Journal, Jiwa and colleagues describe the many challenges faced by general practice in providing cancer care that is truly integrated with other parts of the health care sector.9 They emphasise that integrated care is required at all stages of the cancer journey. Just as cancer screening should link public health and clinical perspectives, post-diagnosis treatment needs a range of health care providers, including GPs, to be part of the team effort. Effective communication between specialist and primary care services is an essential component of this integration. There is growing emphasis on the concept of survivorship in cancer patients — rightly so, as cancer has taken on the characteristics of other chronic illnesses such as diabetes and coronary heart disease. Increasing numbers of patients have very prolonged periods of survival after cancer diagnosis, and die with their illness rather than of it. Survivorship is a very positive concept, and general practice, with its capacity for multidimensional care, is well placed to play a leading role in improving services for people living with cancer, providing follow-up that addresses patient priorities, and developing more personalised care for cancer survivors.10 This typically involves “survivorship care plans”, which include a range of tools for health care providers and users. It features heavily in the UK’s Cancer Reform Strategy.5 A challenge for primary care is to recognise its unrealised potential for promoting survivorship and to develop new models of care that allow it to do so.11 Primary care must be able to respond to rapidly changing health care needs of cancer patients in an appropriate and flexible manner. If we are to develop and test new models with enhanced roles for primary care, we need to better define and understand current patterns of care. Do GPs and primary care teams provide the kinds of services that cancer patients need? How well do they detect and manage recurrence of disease and toxicity from treatments? Do they provide the kinds of psychosocial support cancer patients need, and do they help or hinder truly integrated care? How well do they address issues of patient choice, and how good are they at providing education and support? The experiences and needs of cancer patients and their carers vary tremendously. We have perhaps been slow, in general practice, to respond to the needs expressed by our cancer patients. But if we take time to listen to our patients, from the time of diagnosis to death and bereavement, many ideas emerge about how the services we provide could be improved. Cancer patients have a range of illness and social trajectories, their patterns of wellbeing fluctuate, and they often perceive a lack of integration in the services they receive.12 GPs also need to maximise their contribution to primary prevention of cancer, especially in relation to smoking cessation and lifestyle risk factor management — despite the challenges of time constraints, practice systems and patients’ reluctance to change.13-15 To meet the challenges of the future and to adapt to changing health service environments, general practice must be prepared to evolve.16 A better understanding of the role of primary care in cancer management is vital if we are to improve outcomes and quality of life in our cancer patients.3,17 We need to know how primary care can contribute to new models of care. At present, there is little evidence on which to base service design and innovation. We need to develop new, genuinely integrated models of care that address important priorities for cancer patients, such as the availability of care close to home, timely management of symptoms, early detection of recurrences, and comprehensive psychosocial support. Until we have done so, GPs will remain at the periphery of cancer management, and there will be ongoing confusion over how we can make our most effective contribution.

David P Weller FRACGP, FAFPHM, PhD · Mark F Harris FRACGP, MD

One in three men and one in four women in Australia will be diagnosed with cancer in the first 75 years of life. The majority will survive the cancer and ultimately die from unrelated causes. Many cancer patients and their families will experience some physical, social, economic and psychological sequelae, regardless of the prognosis. A recurring theme is that patients are disadvantaged by the lack of coordination of care and their needs are not being adequately met. We argue that greater integration of care through a multidisciplinary team of professionals, peer support groups and primary health practitioners functioning within a care hub could offer better practical and psychosocial supportive care for patients and their families.

Moyez Jiwa MD, MRCGP, FRACGP · Christobel M Saunders FRCS, FRACS · Sandra C Thompson FAFPHM, PhD · Lorna K Rosenwax BAppSc(OT), MSc, PhD · Scott Sargant BPharm, MPS · Eric L Khong MB BS, PGradDipPrimHlthCare, FRACGP · Georgia K B Halkett BMedRad(Hons), FIR, PhD · Gloria Sutherland BAppSc, PGradDipHlthEd · Hooi C Ee MB BS, FRACP, PhD · Tanya L Packer BSc(OT), MSc, PhD · Gareth Merriman BAppSc(Psych) MPsych, PhD · Hayley R Arnet BHSc(Pod), PGradDipHlthInform

Cervical cancer screening needs to take into account a partially vaccinated population and new technologies A national, well funded and organised program of screening using the conventional Pap smear has significantly reduced the incidence of and mortality from cervical cancer in Australia.1 While the program has been in place, there has been a great increase in knowledge of the pathogenesis of cervical cancer, with certain oncogenic subtypes of human papillomavirus (HPV) shown to be a necessary cause for development of this disease.2 In addition, a national program of vaccination against two of the 15 oncogenic viruses began in April 2007, and tests to detect HPV are now available. Furthermore, research showing that new technologies for screening cervical samples are superior to conventional cytology has also been published.3,4 How is the cervical screening program responding to the presence of a partially vaccinated population and these newly available tests? When the Pharmaceutical Benefits Advisory Committee assessed the value of funding HPV vaccination, it noted that the current cumulative lifetime risk of cervical cancer in Australia’s screened population is 0.78% — a substantial reduction from the estimated 2.4% risk in an unscreened population, reflecting the success of the screening program. With continued screening, this risk was predicted to further decrease to 0.38% following vaccination of 12-year-old girls, 0.43% for 14-year-old girls and 0.59% for 26-year-old women.5 The Committee further commented that there would be cost savings if vaccination were to completely replace cervical screening, but the cervical cancer lifetime risk would increase to 1.173%.5 The recommendation therefore is that screening must continue after vaccination. The screening interval and screening test for vaccinated women should be different to those for unvaccinated women and should be determined by population-based research over the next 5–10 years, as the vaccinated cohort reaches maturity. A national HPV vaccination register is being established, which will be critical for determining the appropriate screening regimen. HPV testing is already recommended and funded as a “test of cure” for follow-up of high-grade cervical disease after treatment. The Digene HPV test is used in Australia and detects any one of 13 high-risk HPV subtypes but does not identify the specific subtypes. Although some individual HPV subtyping assays are available, these are expensive and not widely used, and no serological tests for HPV are available in routine practice. Use of the HPV test is therefore limited but, given its importance, should its use be expanded for screening and management of cervical disease? There has been much discussion overseas about replacing cervical cytology tests with HPV testing for primary screening.6 Currently, there is no justification for this as HPV testing is highly sensitive but not specific. It has a limited role in women under the age of 30 years, as large studies have shown that about 25% of women in this age group test positive for the oncogenic viruses.7 The great majority of these women clear the virus naturally, usually via a cell-mediated immune response or, less often, through an antibody response. Such infected women may not show any sign of disease. It is when the virus persists that women are at greater risk of both high-grade cervical intraepithelial disease and invasive cancer. HPV testing is also not recommended before vaccination8 in women who request it but are already sexually active as the decision to proceed with vaccination will not be altered by the results of the test. HPV testing may have a greater role in the management of indeterminate abnormalities detected by cervical cytology tests. Data from large United States studies are fairly compelling in assigning a true risk of significant disease based on cervical cytology and HPV testing. The latter is more accurate than colposcopy in determining the significance of low-grade squamous intraepithelial lesions detected by cervical cytology. So-called “reflex” HPV testing in women with these findings is recommended in the US.9 Another major question for cervical cancer screening in the short term is whether image-guided liquid-based cytology samples should be used as the preferred screening test. The use of liquid-based cytology in this country has long been controversial.10 However, there is now good evidence that one of the techniques — the ThinPrep Imaging System (Hologic, Marlborough, Mass, USA) — is superior to conventional cytology.4 This technique decreases the number of unsatisfactory samples and detects more true abnormalities. There are also substantial laboratory efficiencies when using this technology, which could potentially overcome the chronic shortage of trained scientists. The increased sensitivity might allow the screening interval to be lengthened. This technique also provides a sample for HPV and other microbiological testing, and is ideal for a vaccinated population in which the number of screen-detected abnormalities will decrease. Although Australia has an enviable record in the control of cervical cancer, new knowledge and associated technologies should be incorporated into screening and management of cervical disease, as they offer real benefits. Both HPV testing and ThinPrep imaging are more expensive than conventional cytology, but they could be cost-effective if used appropriately in conjunction with a comprehensive review of the cervical screening program.

Annabelle Farnsworth FRCPA, FIAC, DipCytopath(RCPA)

Objective: To determine if the recent rapid fall in use of hormone replacement therapy (HRT) in Australia has been followed by a reduction in breast cancer incidence among women aged 50 years or older, but not among younger women.Design and setting: Analysis of trends in annual prescribing of HRT, using Pharmaceutical Benefits Scheme data, and in annual age-standardised breast cancer incidence rates in Australian women for the period 1996–2003.Results: In Australia, prescribing of HRT increased from 1996 to 2001, but dropped by 40% from 2001 to 2003. Age-standardised breast cancer incidence rates in women aged ≥ 50 years also increased to 2001 but declined thereafter. The incidence rates in this age group were lower by 6.7% (95% CI, 3.9%–9.3%; P < 0.001) in 2003 compared with 2001, equivalent to 600 (95% CI, 350–830) fewer breast cancers (out of about 9000 incident breast cancers annually for women this age). There was no significant change in breast cancer incidence for women aged < 50 years.Conclusions: While other factors may have contributed to a recent reduction in breast cancer incidence among Australian women aged ≥ 50 years, the available evidence suggests that much of the decrease is due to the recent fall in use of HRT. This is consistent with other evidence that the HRT-associated increase in risk of breast cancer is reversible after ceasing use of HRT.

Karen Canfell DPhil · Emily Banks MB BS(Hons), PhD, FAFPHM · Aye M Moa MPH · Valerie Beral FRS

Low socioeconomic status and assumptions about Indigenous people may be jeopardising their access to care In this issue of the Journal, the case–control study by Coory et al1 shows that Indigenous people in Queensland are less likely than non-Indigenous people to receive adequate management for lung cancer, even after controlling for geographic location and socioeconomic factors (→ Survival of Indigenous and non-Indigenous Queenslanders after a diagnosis of lung cancer: a matched cohort study). Other studies and reports have also shown that Indigenous people have a lower cancer survival rate and are much less likely to be offered diagnostic and therapeutic procedures,2-6 but the study by Coory et al is the first to show a clear treatment bias for cancer. Why are Aboriginal people less likely than other Australians to receive treatment for lung cancer? Drawing on my experience in Aboriginal health over the past 20 years, I think there are some likely explanations for this finding, most of which Coory et al have considered. Late diagnosis is a key factor leading to poorer treatment outcomes and lower survival rates for Indigenous people.1,5 As Indigenous people do not have the same level of access to primary medical care as non-Indigenous people, early detection of cancer by general practitioners is less likely. In spite of significant additional Australian Government funding provided through the Office for Aboriginal and Torres Strait Islander Health (OATSIH) (an additional $500 million recurrent since 1995), the gap in access to primary medical care resources appears to be still widening, primarily due to worsening access to the Medicare Benefits Schedule and the Pharmaceutical Benefits Scheme, which is not compensated for by the OATSIH funding.2,7 The “Close the Gap” campaign recently announced by the federal government is indeed timely.8 Achieving better participation rates in cancer screening programs has also been recognised as an important issue, and systemic changes are needed.2 In the Northern Territory, breast cancer rates are increasing significantly among Aboriginal women, with a 223% increase reported between 1991 and 2001.3 However, for many Aboriginal women, access to mammography services remains poor. For example, the mammography screening service visits Alice Springs three to four times a year for 3 weeks at a time, but often with only a few weeks’ notice. Women who are more organised and literate can read the advertisements in the newspapers and make their own appointments at short notice, but many Aboriginal women do not do this. Health services can try to contact them to let them know, but this is not always effective. It would be possible to redesign the system to give much better access for Indigenous women, and this needs to occur. For example, the service could again be provided from the more culturally secure local Aboriginal women’s health service, Congress Alukura, on a regular planned basis. This would better utilise transport services, Aboriginal liaison officers and the Patient Assisted Travel Scheme (PATS) to improve attendance for Aboriginal women. Coory et al consider the possibility that access to specialist care could be one of the issues involved. Schemes such as PATS9 allow rural and remote residents to have access to specialists in major centres, but I think it is very likely that Indigenous people from rural and remote areas do not receive the same access to care through such schemes as other rural and remote residents. In addition, the gap fees charged by private specialists in all localities present a more significant economic barrier to many Indigenous people, who are therefore much more reliant on the public hospital outpatient system, with its substantial delays. In Alice Springs, for example, men with raised prostate-specific antigen levels have been waiting 6–12 months or longer to see a urologist and have a prostate biopsy in order to be given a definitive diagnosis and treatment for prostate cancer. If patients can afford to pay about $300 to have the procedure done privately, they are sent by PATS to see a urologist in Adelaide, thus avoiding a long waiting period. However, public patients do not have this option. Although steps are now being taken to reduce the barriers that have led to these unfortunate delays, this is occurring as the result of a complaint from the Central Australian Aboriginal Congress in December 2007, rather than in response to an analysis of routine data, which could have revealed the problem much earlier. It is very unlikely that this type of problem is unique to Alice Springs. What we do not know is whether there is a differential waiting time for Indigenous men compared with non-Indigenous men, or whether the system equally disadvantages all men who do not have private health insurance. Is there a systemic bias against Indigenous men that needs to be better understood and addressed? The results from the study by Coory et al add to other evidence suggesting that barriers to care for Indigenous people need to be systematically explored throughout the Australian health system. Whether it is cancer treatment, access to renal transplantation,10 access to prostate biopsies for suspected cancer, or a range of other key endpoints, it seems that the system is not working well for Indigenous people. A final question that was not considered by Coory et al is whether cancer specialists themselves make different decisions about the appropriateness of certain treatment options for Aboriginal people based on their own assumptions about the socioeconomic and cultural circumstances of Indigenous people. I learned this lesson many years ago when two of my Aboriginal patients with rheumatic heart disease and atrial fibrillation died suddenly and unexpectedly in their early forties, from intracardiac clots. These women had been seeing the visiting cardiologist every 6 months and seeing me as often as needed in between. The use of warfarin in such patients was not yet standard practice at the time, but the cardiologist had already been routinely prescribing warfarin for non-Aboriginal people in these situations for about 12 months. He had never suggested warfarin treatment for these women because he assumed that they would not be able to take it safely and that they would have nowhere to store the drug, thus putting children at risk because of the possibility of them accessing and accidentally taking warfarin tablets. This was the late 1980s, and as a GP who was unaware of recent evidence confirming the benefits of warfarin in such patients, I was assuming I would be getting the best practice advice from the visiting cardiologist. It was not until after the women had died that I spoke to him and discovered the assumptions he had made in deciding against warfarin treatment. These types of assumptions may also be being made by specialists about other routine treatments. In the NT, this situation has been improved over recent years through a range of initiatives, including the strengthening of links between key specialists and Aboriginal health services. Many specialists, including cardiologists, now routinely provide services through Aboriginal health services. However, this still needs to occur more widely and to include a broader range of specialists. Given the evidence now available on the differential survival rates for Indigenous people with cancer, it is imperative that better data be routinely collected on the comparative rates of access to specialists and key diagnostic and therapeutic procedures in secondary and tertiary hospitals. State and territory governments could be induced, as part of the Australian Health Care Agreements, to collect more rigorous data in this area. The Australian Health Care Agreements are agreements reached between the Australian Government and the state and territory governments on the health system. They provide a mechanism through which the Australian Government can influence the states and territories, through financial levers, to improve key health system outputs such as equity of access to specialist services and procedures. Key data to be collected would include the comparative times on waiting lists for specialist appointments in public hospitals; the rate of access to key diagnostic procedures; the frequency of giving radiotherapy and chemotherapy for specific cancers (where these treatments are known to be effective); and the rate of surgery performed on patients with cancers amenable to treatment. These types of indicators have been suggested by Aboriginal health services for more than a decade. It is too often assumed that Indigenous people do not wish to travel long distances to access care and be away from their families, or that they have different priorities in life and do not value treatment for illnesses that are likely to be terminal. While poorer compliance or higher refusal rates for treatment may be pertinent factors in some cases, it is important not to assume these types of explanations when there are obvious systemic barriers to accessing care in the current health system. Once these barriers have been addressed, any remaining barriers, if they actually exist, can be explored and dealt with separately.

John D Boffa MB BS, MPH

Handbook of advanced cancer care. Raphael Catane, Nathan Cherny, Marianne Kloke, et al, editors. Oxford: Taylor & Francis, 2006 (ix + 278 pp). ISBN 978 0 415 37530 6. As it discusses issues that lie at the interface of oncology and palliative care in this country, the Handbook of advanced cancer care is more useful than its title might suggest. It will be valuable not only to specialists but also to nurses, general practitioners and doctors in training. The book was commissioned by the European Society for Medical Oncology and describes many situations that would be familiar to Australian cancer specialists. The treatments too are familiar and readily available. Overall, the text is pleasingly comprehensive for a small book, up to date and practical. The authors begin by making the important point that even in advanced cancer, specific anticancer treatments (chemotherapy, radiotherapy) can be the best way of improving quality of life, and in some far advanced cases can even still be curative: think, for example, of disseminated germ cell tumours. In addition to the expected topics (such as pain, constipation, and hypercalcaemia), there are useful entries concerning fungating wounds, hiccups, sweating and pressure sores. Modern drugs such as buprenorphine are included. For this older oncologist, it was comforting to read that ‘‘[o]lder patients in overall good health are able to tolerate chemotherapy as well as their younger counterparts...”. This is a statement that might not have been made a few years ago. There are useful chapters about communication for the health professional, the place of psycho-oncology, and how to handle bereavement. In the latter chapter, I particularly endorse the advice that medical practitioners should routinely indicate to the relatives that they are available for a visit after the patient’s death to discuss “leftover” questions. There is limited repetition — Tables 1.1 and 7.1 are identical and Tables 1.2 and 7.2 virtually so. Although the idea of providing algorithms is useful for clinical practice, the deep colours chosen for the various boxes make it difficult to read the text within. There is a description of massive terminal haemoptysis but not of catastrophic terminal haematemesis. Perhaps the most serious shortcoming, though, is that the chapter on pain glosses over the need to make a diagnosis of its cause before considering symptomatic treatment options. In summary, this is a useful, concise handbook which would soon be well thumbed if made available on the oncology and palliative care wards. In days gone by, it would have fit neatly into the pocket of a white coat, but who wears those any more?

Raymond M Lowenthal

Objective: To explore the involvement of members of the Royal Australasian College of Surgeons (RACS) Section of Breast Surgery in Australia and New Zealand in multidisciplinary care (MDC) teams.Design and setting: Questionnaire sent to all full members of the RACS Section of Breast Surgery in December 2006.Participants: 239 of 262 active full members of the RACS Section of Breast Surgery (response rate, 91.2%).Main outcome measures: Surgeons’ use of, and the composition and functioning of, MDC teams in public and private practice, and in metropolitan, regional and rural settings.Results: 85% of responding surgeons reported participating in at least one fully established MDC team. Public-sector teams were operationally more consistent and functional than private teams, and rural teams were less well developed than those in metropolitan and regional centres. The six core disciplines recommended by the National Breast Cancer Centre appear to be well represented in most teams. Patients and their general practitioners were not considered to be part of the treatment team by surgeons.Conclusions: MDC is supported by most breast surgeons, but there are deficits in rural areas, and in the private sector relative to the public sector.

Claire J Marsh BHSc(Hons) · Margaret Boult BSc(Hons), GDIM · Jim X Wang PhD · Guy J Maddern PhD, FRACS · David M Roder PhD · James Kollias MB BS, FRACS

Concerns about medicolegal implications of a multidisciplinary approach to cancer care may act as a barrier to the implementation of best practice approaches. While multidisciplinary meetings carry a low level of medicolegal risk, improved documentation and transparency in approach will assist in limiting liability for individual health professionals and health services. The medicolegal implications of a multidisciplinary approach are not affected by whether a health professional bills the patient for attendance at multidisciplinary meetings.

Alison C Evans BSc, PhD · Helen M Zorbas MB BS, FASBP · Megan A Keaney MB BS, MHA · Mark A Sidhom BEc, LLB, MB BS · Holly E Goodwin BAppSc, GradCertPH · Janice C Peterson BHSc, GradCertHSc

The psychological downsides, equity of access for women, and patients’ understanding of the limitations of screening need consideration Australian states are currently rolling out colorectal cancer screening as part of the National Bowel Cancer Screening Program. Its success depends on the “physical or psychological harm to those concerned be[ing] less than the chance of benefit”.1 The benefits are clear. Randomised controlled trials show a 16% reduction in colorectal cancer mortality with faecal occult blood testing and colonoscopy of people with a positive faecal occult blood test (FOBT) result.2 In contrast, less attention has been paid to the psychological impact of colorectal cancer screening. Its effective management may also improve screening outcomes. Breast cancer screening studies show that a screening invitation may cause severe anxiety and, in some cases, non-attendance; people who do not attend for one form of screening are more likely not to attend for other screening.3 Screening studies also show that participants can experience severe anxiety irrespective of results.4,5 An audit of suicides found two occurred between notification of recall after mammography and reattending; one suicide note was written on the recall letter, the other mentioned fear of hospitalisation.4 Neither woman had cancer. These findings emphasise the importance of education, rapid outpatient review and, if required, prompt access to colonoscopy to avoid delay in managing a positive FOBT result.5 FOBT-based screening studies report distress among both those with negative and positive results, and breast and colorectal cancer screening studies show that anxieties may continue even after a subsequent negative result.4-6 Among those who screen negative, distress may be sustained, indicating that this is a risk of screening healthy adults. A general-practice-based coronary heart disease screening study found that participants with no detected abnormality had significantly more psychological distress at 3 months than their unscreened counterparts. If not done carefully, screening may distress individuals who have clinically inconsequential disease.7 Women screened for hepatitis C and found to be positive after inadvertently receiving infected anti-D immunoglobulin reported high levels of psychological distress and poorer quality of life compared with their counterparts 22 years later, despite no progression of their disease.8 These studies emphasise the importance of assessing the appropriateness and benefits of screening. For colorectal cancer screening, with direct-to-patient kit provision, the group most vulnerable are patients unlikely to benefit because of other life-threatening comorbidities. Clinicians, particularly general practitioners, have a pivotal role in counselling these patients. The implications for patients of direct-to-patient kits should become clearer as screening progresses and its analysis should improve management further. A relatively unexplored potential contributor to morbidity is lack of choice of colonoscopist.3,9,10 A United States survey of women’s attitudes to colorectal cancer screening found that almost half reported a preference for a female endoscopist. Eighty per cent of these patients were willing to wait more than 30 days for one, and 14% would pay more for one. Seventy-five per cent of women gave embarrassment as the reason for their preference.10 If this is applicable to Australia, strategies are needed to ensure that women (particularly those who are uninsured, who have fewer options) have equity of access. Currently, fewer than 10% of Australian gastroenterologists are female, and the proportion of female gastrointestinal surgeons is even lower. It will be important for the success of colorectal cancer screening to know whether this workforce shortage has a substantial impact on female participation in the program. Informed participation is the ideal. Challenges include ensuring that patients understand the limits of screening for detecting colorectal cancer; in particular, that an FOBT sensitivity of 92% misses eight per cent of cancers.2 Information supplied in the National Bowel Cancer Screening Program kits emphasises the need for patients to seek medical advice irrespective of a screening result to have any symptoms they may have assessed in their own right. It is clearly important that participants are encouraged to develop realistic expectations about screening’s capacity to prevent cancer. An important unintended outcome of screening can be the “certificate of health effect”, a sense of immunity developing as a result of a negative test. Interpreting screening as a panacea against disease can strengthen unhealthy routines and the idea that regular screening rather than healthy lifestyle maintains health. Screened individuals still need to be encouraged to continue to limit red meat and fat intake, stop smoking and increase their physical activity, not only to reduce their subsequent colorectal cancer risk, but also to improve their general health status. As people value benefits and harms differently, more information is needed, not only on the physical and economic impact of colorectal cancer screening, but also on its psychological impact and on strategies to reduce this impact. Triggers to screening such as the perceived ease of use of the FOBT kit, and social acceptability and mechanisms for encouragement, need to be further assessed, as highlighted in the National Bowel Cancer Screening Pilot Program evaluation. As fewer than 10% of Australian gastroenterologists are female, strategies to ensure equity of access for all Australians, both men and women, may need to be emphasised. Now is an appropriate time to undertake further prospective studies into the impact of colorectal cancer screening on the population groups involved to ensure that its benefits continue to outweigh its risks, and that we maximise its benefits and minimise its risks.

Emma L Rosenfeld MB BS · Anne E Duggan BMed, FRACP, PhD

Objective: To describe the incidence and risk of suicide in cancer patients in Western Australia from 1981 to 2002.Design, setting and patients: Retrospective cohort study of patients diagnosed with cancer in WA from 1981 to 2002, using data from the WA Linked Database.Main outcome measure: Age-standardised mortality ratios (SMRs).Results: A total of 121 533 patients were diagnosed with cancer, corresponding to a total of 543 696 person-years at risk. There were 129 suicides in this group (108 in men). The SMR for suicide in cancer patients was 1.61 (95% CI, 1.36–1.92). An initial period of peak risk was seen in the first 3 months after cancer diagnosis (SMR, 5.75; 95% CI, 3.89–8.51), mainly in patients with a poor prognosis. A second peak period of risk was found to occur 12–14 months after diagnosis (SMR, 2.33; 95% CI, 1.11–4.89) in those with a good or moderate prognosis.Conclusion: The rate of suicide in cancer patients in WA is low and represents an excess of two to three suicides per year, or 0.3% of all cancer deaths, comparable to studies in other Western countries. The risk is highest in the first 3 months after diagnosis, and a second period of increased risk 12–14 months after diagnosis may occur in response to cancer recurrence or treatment failure.

Nigel R C Dormer MB BS, MRCGP, DRCOG · Kieran A McCaul MPH · Linda J Kristjanson RN, BN, PhD

The patient from hell: how I worked with my doctors to get the best of modern medicine and how you can too. Stephen H Schneider, with Janica Lane. Cambridge, Mass: Da Capo Press, 2006 (xix + 300 pp). ISBN 978 0 7382 1078 0. When Doug, the father of a patient of mine, handed me this book, I should not have been so worried. I am a paediatrician and practitioner of evidence-based medicine; reading this has triggered me to reflect on my own thought processes and practice. The book is written by world-renowned climate expert, Professor Stephen Schneider. He was diagnosed with a rare lymphoma in 2002 and chronicles his course, making astute observations on the processes surrounding his tests and treatments. He questions everything, suggesting changes to just about anyone who will listen. Schneider and his wife, both intelligent academics, gather information but also take responsibility for his disease and make health care professionals part of their team, rather than the other way around. When the data are absent, they challenge doctors to make decisions using decision analysis and Bayesian thinking tools (prompting me to re-examine notes from a course I took on decision analysis and to read more about Bayes’ theorem). There is much we can learn about the health care conveyor belt by taking the patient’s perspective. Paediatricians know that children with good advocates generally get the best out of health professionals, and other patients would probably benefit from good advocacy too. Schneider overstates it by calling himself a “patient from hell” — he is simply doing what he can to get the best out of the health care team. Every patient should attempt to do so, but not many could use Schneider’s approach. I wonder what the health consumer may feel reading it — perhaps intimidated if they can’t be as dogmatic and thorough as he is. Hence, this book is perhaps more valuable for health professionals than patients. I still don’t know what Doug was trying to say by lending me this book, but I’m glad he did. I commend this book to every doctor.

Rob Roseby

A diagnosis of meningioma presents challenges but more so when you discover that mifepristone, which could halt the growth of the tumour, is unapproved in Australia Medical practitioners often face the difficult challenge of delivering unpleasant news to patients. When my doctor used the words “brain tumour”, like most people who have to deal with that diagnosis, I found it difficult to comprehend anything else for a few moments. However, the word “benign” did bring me some comfort. I had had no pain and just a little hearing loss in my right ear so was stunned by the finding. Over the next few months, I saw specialists for opinions on treatment options for meningioma. It was important for me to gain a better understanding of what I had to deal with and my treatment options and their associated risks. I didn’t let family or friends know for some time and needed more information to be equipped to deal with those who might react emotionally, particularly my elderly mother who was convinced my hearing loss was probably caused by ear wax. It soon became apparent to me that, owing to the tumour’s location at the skull base, adjacent to the brainstem (Box), and its involvement with three facial nerves and the carotid artery, removal or treatment was not going to be without considerable risk. While doing some research on the subject, I came across references indicating that a high percentage of meningiomas contained progesterone receptors, and there was mention of a drug that could halt the growth of the tumour. The drug was RU486 (mifepristone), the most effective progesterone antagonist available. In overseas clinical studies, it had been successful in some meningioma patients.1-3 In my view, a trial of the drug was a better option than the 50% risk of irreparable damage to my vision through surgery. The uncertainty of the long-term prognosis after stereotactic radiotherapy was also unappealing. After doing more research on the drug itself, I found that it had extensive medical uses, such as treatment of meningioma, some breast and ovarian cancers, endometriosis and fibroid tumours and, in higher doses, its action as a glucocorticoid antagonist in Cushing’s syndrome.4 Research on the drug’s myriad medical uses had been plagued by controversy. Why? Well, apparently because progesterone is the hormone necessary to sustain a pregnancy, and not interfering with it is considered to be sacrosanct by the powerful antiabortion lobby groups. As a result, research into and clinical trials on the drug’s other uses have been hampered and delayed. I contacted the Feminist Majority Foundation and the Association of Reproductive Health Professionals in the United States and had several email conversations with their representative. The insights provided were invaluable, and we maintained regular contact for some time. I will always be grateful for the information and support she provided at that time. When I looked into the drug’s availability in Australia, I came across a story on the website of the Australian Broadcasting Corporation titled “No room at the inn for RU486”, posted only a few months earlier in November 2004. It included dialogue with representatives of the Minister for Health and Ageing. In closing, the message to those who were interested in the drug being made available in Australia was “don’t hold your breath”.5 I had a tumour growing in a confined space that threatened to compromise the functioning of vital nerves and life itself. I understand there is about a 1 : 50 000 chance of a diagnosis of meningioma and 20% of these are at the skull base, therefore a 1 : 250 000 chance of diagnosis of a skull-base meningioma. What are the chances of having a diagnosis of meningioma while working in the Department of Health and Ageing, as I was at the time? There was no point in raising the issue internally. I was acutely aware of the precarious position I was in, but, nonetheless, I had to do something about this issue. After giving the matter some thought, I contacted Senator Lyn Allison, the leader of the Australian Democrats, who made some enquiries in Parliament via Questions on Notice to the Minister for Health. I was later provided with a copy of the response. The government knew the drug could be used for a range of serious medical conditions and advised it could be obtained through the Special Access Scheme of the Therapeutic Goods Administration (TGA). I thought it peculiar that the government knew this, but did not make that information public to ensure patients and doctors were also informed. I contacted my general practitioner with the details, and she lodged an application with the TGA. On 7 September 2005, Senator Allison gave a speech in Parliament titled “Matters of public importance — mifepristone”.6 The campaign to amend the legal status of the drug was subsequently launched. Thankfully, Senator Allison had the courage to take on this enormous challenge and the breadth of vision to do so in the interests of public health. The day after Senator Allison’s speech in Parliament, the TGA issued a permit to my GP to import the drug to treat my tumour. I was elated and spent the next month and a half trying to track down overseas suppliers, with the help of a local pharmacist. When I obtained those contact details, I then saw my GP again so we could get the importation under way. At that point she advised me that she had decided not to proceed, because of medical indemnity insurance issues. I offered to get a lawyer to draw up a personal indemnity. She refused the offer. My GP gave me a copy of the letter which accompanied the permit. It was signed by a “delegate of the Secretary” and dated 8 September 2005. It stated “All parties involved need to recognise the practice may carry medico-legal risk, and there may be implications regarding indemnity”. Why did the TGA wait until they issued a permit before providing that advice? Clearly, no consideration was given to the impact on the patient who had the rug pulled out from under her feet in an instant. I contacted Senator Allison to inform her of this problem and she raised it at the public hearings in the Senate in December. Senator Allison asked the following question of the Secretary of the Department of Health and Ageing and the head of the TGA: “Could you outline the issues to do with medical indemnity, which I gather are a problem in some of these cases?”. They both replied, “not that we are aware of”. When asked whether the Department had done any studies of the drug, the Secretary advised that they had not. She also advised that the Department was responsible for administering the legislation and believed it did so with “due diligence”.7 She claimed there were no barriers for anyone wanting to do research here into the drug’s non-abortifacient uses, but the experiences of some have been to the contrary.8 Unknown to most people is the fact that the supplier succumbed to pressures via threats of boycotts by the powerful antiabortion lobby groups some years ago and decided that “. . . the company would not sanction exports unless ranking government officials in the country urged them to do so . . . there must be an actual wish for the licensing of mifepristone in a particular country . . . the letter indicated such a wish could come in the form of a written request from a representative, competent body such as the government or health authorities”.9 Lobbying during the campaign to change the legislation to allow the TGA to regulate RU486 was intense, and to help raise awareness of the drug’s use as a treatment for meningioma, I participated in some broadcasts, with the help of the Australian Broadcasting Corporation.10 My contact in the US kindly did a submission for the Senate Inquiry,11 and I later found one from Professor Healy,12 who wrote the first clinical review of the drug in 1985.13 Because of the hard work of many, the parliamentary conscience vote to repeal ministerial responsibility for approval of RU486 in early 2006 was won by a resounding majority. The vote was an important milestone, but there is still a long way to go before the drug will be readily available. The amendment changed the legal status of the drug and allowed a drug company to lodge an application with the TGA for approval of mifepristone for use as an abortifacient. Easier access to the drug will facilitate research and clinical trials into the drug’s uses in Australia, depending on the necessary funding approvals by government. Access to the drug for individual patients and for non-abortifacient uses is, at this stage, only available via the TGA’s Special Access Scheme. It was over a year after I found out about mifepristone, and nine months after the TGA issued its first permit, before I was finally able to start my treatment, with the assistance of an oncologist who heard of my predicament. He was willing to import the drug and required only my written agreement to be treated with an unapproved drug. I have now been taking mifepristone for just over a year at 200 mg per day and can say from personal experience that it has very little in the way of side effects, and I am happy to continue with my treatment. It will be another year or so before any meaningful responses can be measured via magnetic resonance imaging. A few months ago, I was contacted by another patient with meningioma (diagnosed several years earlier and treated by monitoring of the progress of the tumour). She would have liked to have had a trial of mifepristone, but like most people, thought it was unavailable here. Unfortunately, her vision had deteriorated since her initial diagnosis. I provided her with information, and as a result, she has recently commenced treatment on the drug as well. Why don’t GPs refer patients to oncologists when they refer them to specialists for opinions, especially when standard treatment options carry such substantial risks? If the Australian Government is serious about “better health outcomes for all Australians”, including those who would benefit from the drug’s non-abortifacient uses, some thought should be given to the people who could be helped by this drug. Interestingly, in addition to the medical uses mentioned earlier, recent developments in overseas research indicate that mifepristone has potential use in some gastric cancers as well,14,15 and it also has viability for use as a helper-dependent adenovirus vector in gene therapy for cancer treatments.16 The more research I did, the more fascinated by this drug I became. The anti-glucocorticoid effects are dose-dependent, but on the basis of animal trials it has been shown to be neuroprotective17 and can minimise the adverse effects of ischaemic stroke.18 Mifepristone can prevent retrograde amnesia induced by electroconvulsive therapy19 and is currently being trialled for that purpose (ClinicalTrials.gov identifier NCT00285818). In animal studies the drug has been shown to help ameliorate the symptoms of diabetes.20 The drug’s potential use in overcoming the adverse effects of elevated cortisol due to a dysfunctional hypothalamic–pituitary–adrenal axis means it is a potential treatment for Alzheimer’s disease, in which higher cortisol levels are associated with a higher level of impairment.21 The US Food and Drug Administration has just approved mifepristone for the purposes of reversing the side effects of corticosteroids and for use in patients with Cushing’s disease.22,23 If only a drug sponsor in Australia would consider sponsoring the drug for the TGA’s Orphan Drug Program. This would see it subsidised via a special appropriation until such time as it is made available on the Pharmaceutical Benefits Scheme, which may take up to 10 years for some non-abortifacient uses pending further clinical trials. It saddens me to think that those on low incomes or age or disability pensions would not be able to afford the drug via the TGA’s Special Access Scheme, even if other treatment options are not suitable. Although the Senate amendment was an important campaign to be part of, and I feel honoured to have contributed, given my personal circumstances, it was a challenge I really could have done without. The next is to be able to continue to pay the cost of this currently unsubsidised drug. Coronal magnetic resonance images showing a meningioma (arrows) compressing and displacing the brainstem.

Mary Lander

In April 2004, Melbourne’s Peter MacCallum Cancer Centre, Australia’s only stand-alone dedicated cancer hospital, became the first Australian site to offer digital mammography (DM). In the first year of DM operation, 1208 mammograms were performed on 1157 women; 17 new cases of invasive carcinoma and six new cases of ductal carcinoma-in-situ (DCIS) were detected; and 30 hook-wire needle localisations were conducted in 29 patients. We developed a unit policy to manage indeterminate microcalcifications newly demonstrated on DM that were not previously detected by conventional screen-film mammography (CM): those believed to have malignant morphology were recommended for biopsy, and those without were recommended for 6-month DM follow-up to confirm microcalcification stability. DM detected 56 new stand-alone microcalcifications (18 suspicious and 38 indeterminate). Tissue diagnosis of 12 suspicious microcalcifications yielded four cases of DCIS and one of atypical ductal hyperplasia. Of the indeterminate microcalcifications, 35 have demonstrated stability at DM follow-up to date, over a mean period of 23.6 months. From our experience, we believe DM’s superior demonstration ability uncovered microcalcifications previously undetected by CM, rather than microcalcification progression. We suggest that routine review with DM, rather than biopsy, is appropriate management when new indeterminate microcalcifications without malignant characteristics are identified by DM.

Emma Pun MMed, FRANZCR · W F Eddie Lau BPharm, FRANZCR · Robin Cassumbhoy FRANZCR · Anthony J Taranto FRANZCR · Alexander G Pitman BMedSci, FRANZCR

Clinical recordA 35-year-old British man was admitted with a 2-week history of abdominal discomfort, fatigue and intermittent high fevers associated with drenching night sweats. He reported having returned to Australia 2 months before presentation from a 12-year around-the-world trip, having travelled extensively for 6 months through South-East Asia and northern Australia. Before that, he had been to Argentina, the Maldives, Egypt, India and Cambodia, where he had worked as a professional kitesurfing instructor. His past medical history was unremarkable and he was not on regular medication. His social history revealed intravenous heroin addiction in his early 20s. He had consumed more than 80 g of alcohol daily for a number of years, with occasional binges, until recently, when drinking alcohol provoked nausea and vomiting. The patient appeared unwell with a tympanic temperature of 40°C. He was fair-skinned and of muscular build. Physical examination showed conjunctival jaundice but no evidence of needle tracks, rashes, finger clubbing, lymphadenopathy or suspicious cutaneous lesions. Tender hepatomegaly was noted, but no ascites or splenomegaly. Findings of cardiac, respiratory and neurological examinations were normal. Abnormal laboratory findings on admission were: albumin concentration, 29 g/L (reference range [RR], 33–47 g/L); alkaline phosphatase titre, 164 U/L (RR, 30–115 U/L); γ-glutamyl transferase titre, 207 U/L (RR, 0–45 U/L); alanine aminotransferase titre, 76 U/L (RR, 0–40 U/L); aspartate aminotransferase titre, 279 U/L (RR, 0–40 U/L); lactate dehydrogenase titre, 4268 U/L (RR, 100–225 U/L); white cell count, 13.4 × 109/L (RR, 4.0–11.0 × 109/L); absolute neutrophil count, 9.7 × 109/L (RR, 1.5–6.0 × 109/L). There was no evidence of thrombocytopenia, renal dysfunction or coagulopathy. Findings on abdominal ultrasonography the day before admission were reported to be normal. Despite there being few clinical features to suggest a source of sepsis apart from the hepatomegaly, because of his travel history and previous history of injecting drug use, a wide variety of infectious diseases, including subacute bacterial endocarditis, typhoid, malaria, and viral hepatitis, were all initially considered in the differential diagnosis. Multiple sets of blood cultures, urine and stool samples were sent for microscopy, culture and sensitivity. Three sets of thick and thin films for malaria as well as a test for Plasmodium falciparum antigen were negative. In view of the clinical hepatomegaly, a computed tomography (CT) scan of the abdomen was performed, which was reported as strongly suggestive of microabscesses (Box). The presumptive diagnosis at this stage was a tropical pyogenic liver abscess, although military tuberculosis and candidiasis were also considered. Intravenous therapy with flucloxacillin, ceftriaxone, ciprofloxacin and metronidazole was initiated. The ceftriaxone was subsequently changed to meropenem, and the ciprofloxacin ceased 5 days after there had been no growth on any cultures. Serological tests for a wide variety of pathogens and diseases were also performed, including: HIV 1 and 2; hepatitis viruses A, B and C; cytomegalovirus; Epstein–Barr virus; Q fever; brucellosis; cryptococcosis; Entamoeba histolytica; Ross River virus; Dengue virus; flavivirus; leptospirosis; schistosomiasis; cysticercosis; and melioidosis. Results for all of these eventually returned negative. Despite the antibiotics and fluids given intravenously, the patient’s condition deteriorated over the course of 6 days and he developed hepatic encephalopathy, ascites, pleural effusions and peripheral oedema. He also continued to spike high temperatures daily, but repeated blood cultures were sterile. A CT scan performed a week after the initial CT scan suggested enlargement of the liver lesions. Although hepatic abscesses were still considered most likely, given the markedly elevated lactate dehydrogenase titre and lack of clinical improvement with broad-spectrum antibiotic therapy, alternative diagnoses, in particular malignancy, were also considered. We therefore performed a core biopsy of the liver under ultrasound guidance. There was no evidence of pus, and the lesional tissue showing strong monoclonal antibody staining against Melan-A and HMB-45 confirmed liver infiltration by a poorly differentiated malignant melanoma. Repeat physical examination included dilated pupil fundoscopy, which showed a brown, dome-shaped subretinal lesion just below the left optic disc, most suggestive of a primary choroidal melanoma. The patient said that he never used sunglasses while kitesurfing. DiscussionExposure of the unprotected eye to sunlight or sunlamps is an important risk factor for the development of intraocular melanoma.1 The incidence of ocular melanoma in dark-eyed individuals is lower, probably because they are less sensitive to solar radiation, or less is transmitted to the choroids.2 Uveal melanoma (affecting the iris, ciliary body, and choroids) is the most common primary intraocular malignancy in the Western world, affecting six to eight adults per million each year. Although fewer than 2% of patients show evidence of metastatic spread at presentation, over 40% will eventually die from widespread disease.3 Most intraocular melanomas are initially asymptomatic. Tumour enlargement may then cause distortion of the pupil (iris melanoma), blurred vision (ciliary body melanoma), or decreased visual acuity caused by either central growth close to the macula or secondary retinal detachment (choroidal melanoma). Because the uveal tract is a vascular structure without lymphatic channels, tumour spread occurs primarily by either local extension or by haematogenous dissemination. The first site of systemic metastases is the liver, although spread to other organs such as lung, bone, and subcutaneous sites have been described.3 Metastasis of melanoma to the liver, although rare, can produce a dramatic initial presentation with fulminant hepatitis, shock, and multisystem organ failure.4 An elevated lactate dehydrogenase titre is one of the most predictive factors for metastatic spread and decreased survival in patients with malignant melanoma, with a sensitivity of 79% and specificity of 92% in detecting disease progression to stage IV melanoma.5 Extraocular extension and metastatic spread are associated with an extremely poor prognosis, and response rates with contemporary single-agent chemotherapy are generally below 10%. A recently published study investigated the use of chemotherapy with intra-arterial hepatic fotemustine.6 Median survival rates were among the longest reported, with an overall response rate of 36%, a median overall survival of 15 months, and a 2-year survival rate of 29%. Our patient was scheduled for three cycles of intravenous fotemustine therapy, but developed significant tumour lysis syndrome with intractable hyperkalaemia. He died shortly after the second cycle, only 28 days after being admitted to hospital. The final diagnosis was hepatic failure secondary to metastatic melanoma from an intraocular primary melanoma. An autopsy was not performed. Coronal reconstruction computed tomography image of the abdomen showing hepatomegaly with numerous low-density lesions scattered throughout both lobes of the liver

Stefan Buchholz MD, MRCP(UK) · George Rudan MB BS, FRACP

A 64-year-old man was referred for assessment of a symmetric violaceous rash of the dorsal aspect of the fingers (Figure, A), trunk, olecranon processes and malleoli. An oedematous, blue-purple discolouration of the eyelids was also apparent. The patient complained of severe weakness of the proximal muscles and dysphagia. T2-weighted magnetic resonance imaging showed muscular inflammation and a pulmonary mass (Figure, B) that was histologically identified as squamous cell carcinoma and staged as T3 N0 M0. The dermatomyositis, confirmed by elevation of serum muscle enzymes and electromyography, improved clinically with oral prednisone plus hydroxychloroquine, and did not recur after surgical excision of the tumour. A: Symmetrical violaceous rash with papules on the dorsal aspect of the interphalangeal and metacarpophalangeal joints. Cuticle telangiectasias can also be seen. B: T2-weighted magnetic resonance image showing marked swelling and diffuse dyshomogeneity of skeletal muscles (thick arrows), a 4 cm peripheral mass in the upper lobe of the right lung (thin arrow) and bilateral pleural effusion (arrowheads).

Daniele Torchia · Emiliano Antiga · Letizia Ricupero · Marzia Caproni · Paolo Fabbri

Provision of incorrect information or incorrect data interpretation does not serve anyone well In this issue of the Journal, MacKenzie and colleagues present data to show that, over an 18-month period, media reports about prostate cancer were dominated by statements emphasising Australian men’s risk of prostate cancer, encouraging screening for early detection, and providing reassurance about side effects for treatments that emphasise emerging technologies (→ "The news is [not] all good": misrepresentations and inaccuracies in Australian news media reports on prostate cancer screening).1 In particular, they draw attention to rhetoric that unequivocally supports screening, which would seem to be irresponsible, given the lack of definitive data to show that population-based screening will reduce mortality. Although this is a fair comment to make, the enthusiasm with which the media has responded to the call to promote screening should not take anyone by surprise. Prostate cancer is the most common internal male malignancy in Australia and the second most common cause of cancer deaths in men.2 In 2003, there were 13 526 new cases of prostate cancer and 2837 deaths. By contrast, in that same year, 11 788 women were diagnosed with breast cancer and 2710 died of this disease. Although the biology of these cancers may differ, from the lay public point of view it is a “line ball” call. Little wonder then that, in the face of seeming inaction by government, consumer advocacy groups and some clinicians find a willing media to enter into a discourse that promotes action. In the context of a disease with a high community and individual burden, uncertainty about effective management plans and with no clearly articulated national public health strategy in place, advocacy such as this may be inevitable. A particular characteristic of this debate has been the polarisation of views for and against screening to the point where, at times, constructive debate has been constrained. However, it is important to differentiate between prostate-specific antigen (PSA) screening, with indiscriminate testing of all men (between prescribed ages), and testing after informed consent, as recommended by peak Australian cancer control and health agencies.3-6 Apart from the fact that PSA is not a test for prostate cancer and has no threshold level providing a high sensitivity and specificity, but rather has a continuum of prostate cancer risk at all values,7 a raised PSA level often commits men to the invasive procedure of transrectal ultrasound (TRUS) guided biopsies. Most men presenting for TRUS biopsies have serum PSA levels of 4–10 ng/mL and do not have prostate cancer detected with extended numbers of biopsy cores. If the diagnostic process were non-invasive and treatments with curative intent were not associated with significant unwanted effects, few would quibble about whether it is appropriate to be tested. Although estimates vary, there is no doubt that many men having treatment with curative intent are unlikely to benefit in terms of survival.8-10 Problematically though, such men are at risk of physical and psychosocial adverse effects from treatment that will affect both them and their partners.11,12 As a consequence, there is increasing support for stratifying patients, with an active surveillance protocol advocated for men identified as having low-risk prostate cancer.13 One expert advocates an intense monitoring protocol to identify the minority of low-risk patients (about 30%) with unappreciated aggressive disease for whom definitive therapy should be considered.13 However, this strategy can be undertaken only after biopsy diagnosis. There is no doubt that timely intervention does save lives. However, at the outset, men need to be fully informed of the possible adverse effects of potentially curative treatments and then consider whether, in the event of an abnormal PSA result and subsequent prostate cancer diagnosis, they would wish to proceed to treatment. Only then should they have a PSA test. Nomograms indicating cardiovascular life expectancy accurately may have a role in the future to allow a more tailored approach to overall management, including whether to proceed with prostate cancer testing. MacKenzie et al call for health authorities to commission and promote decision aids to assist men in making an informed decision about PSA testing for the early detection of cancer.1 Such decision aids already exist in a wide range of formats and have been shown to improve men’s understanding and knowledge about prostate cancer and to reduce decision-related conflict, although they have little effect on actual testing behaviour.14 The current need is not to develop more decision aids, but to translate shared and informed decision making about prostate cancer testing into primary care, the place where the decision to test is enacted.15 Barriers to translation include time constraints in busy general practices, general practitioner concerns about medicolegal risks, and GPs’ own knowledge and attitudes to prostate cancer testing. To address these barriers, a consortium, led by The Cancer Council Queensland and including The Cancer Council Australia, Australian Prostate Cancer Collaboration, Urological Society of Australia and New Zealand, and the National Cancer Control Initiative, developed an educational program and decision-aid showcard to support shared decision making about the early detection of prostate cancer in primary care.15 With funding from Andrology Australia, these materials are now available online, and uptake from general practice has been steady, with positive review by users.6 Importantly, the Prostate Cancer Foundation of Australia, as the leading prostate cancer consumer group in Australia, has been included in this initiative. This has been an important step in moving towards a constructive dialogue about this contentious issue. Whatever strategies emerge in terms of diagnosis and treatment in the future, provision of incorrect information, incorrect data interpretation or adverse consequences of the editing process itself do not serve anyone well, least of all patients and their relatives. Moreover, the task of supporting informed patient decision making is made more difficult when having to address misconceptions that may be derived from such reports. Articles such as that by MacKenzie et al highlight the need for media spokespeople to ensure that public discussion of prostate cancer is directed towards a realistic representation of the current status and limitations in relation to PSA testing and prostate cancer management in this country.

Suzanne K Steginga PhD · Robert (aka Frank) A Gardiner MD, FRCS, FRACS

Objective: To describe tumour characteristics and clinical management of melanomas newly diagnosed in 1996 and in 2000 — before and after publication of the clinical practice Guidelines for the management of cutaneous melanoma by the Australian Cancer Network (1997), and their endorsement by the National Health and Medical Research Council (NHMRC) and republication (1999).Design and setting: Survey of clinicians involved in the management of patients with melanoma sampled from the Victorian Cancer Registry. The Registry is notified of all cases of cancer diagnosed by pathology laboratories and hospitals in both the public and private health sectors in the state of Victoria.Patients: People with a cutaneous melanoma newly diagnosed in 1996 and 2000. All invasive melanomas > 1.50 mm in thickness were included, and for each year random samples were selected of 100 each of invasive melanomas 0.76–1.50 mm in thickness, invasive melanomas ≤ 0.75 mm, and in-situ melanomas, plus 50 melanomas of unknown thickness.Main outcome measures: Biopsy method, adequacy of pathology reporting, adequacy of definitive excision (compared with margins recommended by the Guidelines), and follow-up procedures.Results: The use of partial biopsies increased between 1996 and 2000. Recommended margins of definitive excision were used in only 33.6% of cases. Margins were smaller than recommended for 36% of in-situ melanomas, risking recurrence of primary melanoma. Documented follow-up examinations for subsequent primary skin malignancy were uncommon (6%).Conclusions: Many aspects of the management of primary cutaneous melanoma appear not to meet the recommendations of the published Guidelines. Further studies to explore the reasons for failure to meet the Guideline recommendations are needed.

John W Kelly MD, FACD · Michael A Henderson MD, FRACS · Vicky J Thursfield BSc, GradDip(Applied Stats) · John Slavin FRCPA · Jill Ainslie FRANZCR · Graham G Giles PhD

To the Editor: A recent MJA Supplement discusses prognostic and end-of-life communication for health professionals on the basis of a systematic literature review and an expert advisory panel.1 It is usually the case that malignant disease is diagnosed after biopsy, and this is usually undertaken by a surgeon. In a consecutive series of 100 patients presenting with a lesion in a bone with no past history of malignancy, the lesion was the presenting feature of systemic malignancy in 44 of those patients.2 Hence, it is usually the surgeon’s role to advise the patient (and caregivers) that the patient has a terminal disease and, in some cases, the prognosis can only be measured in weeks. It will be obvious that this can be a significant shock to all, particularly when there was no prior indication that malignancy was a possibility. I note that not one of the 35 experts was a surgeon. I also note that surgery as palliation is given virtually no role other than a brief mention in Box 11, despite the well documented role of surgery.3 It has been my experience that the most common question asked by patients with the diagnosis of a terminal malignancy is about the role of surgery; the question “Why can’t you just cut it out?” is a universal feature. This has not been addressed. It is my sincere hope that further expert advisory panels addressing this area become truly multidisciplinary and include perhaps the most relevant discipline — surgery.

Mark T Clayer

In reply: We agree that the content area of these guidelines is very relevant for surgeons, as for all health professionals involved in the care of adult patients with advanced life-limiting illnesses and their caregivers. Surgical representation on our expert panel would have been very useful. We agree that surgery has an important role in terms of palliative treatment options that may be available for certain clinical circumstances. The issue of how to respond to the question “Why can’t you just cut it out?” is an important one. We believe that the principles outlined in these guidelines would be relevant when responding to this question, but would welcome specific suggestions from Clayer and other surgeons about how they respond to such patients. We would hope to include these suggestions along with other input from surgeons in any future update of these guidelines.

Josephine M Clayton · Karen M Hancock · Phyllis N Butow · Martin H N Tattersall · David C Currow

A 61-year-old woman diagnosed with multifocal, poorly differentiated epithelial mesothelioma in September 2002 went into sustained spontaneous remission within months. She was completely disease-free within 6 months, and remained so 5 years later. This case demonstrates that this tumour may, very rarely, regress spontaneously, with no recurrence for many years. A greater knowledge of the underlying immune mechanisms would aid future management of this and other tumours. Clinical recordIn early September 2002, a 61-year-old woman was referred to our centre from the emergency room of a local private hospital. She had presented with a 2-day history of intermittent, sudden onset, severe right-sided lateral pleuritic chest pain lasting a few minutes. In the private hospital emergency room, chest radiography and computed tomography (CT) had shown pleural masses, which were subsequently found to be poorly differentiated epithelial mesothelioma. The patient reported that, over the previous week, she had felt weak and lethargic, but was otherwise well. She had no previous serious illnesses, but had recently started taking iron supplements for anaemia and occasionally took non-steroidal anti-inflammatory agents for osteoarthritis. She was a non-drinker, and had ceased smoking 5 months previously. (She started smoking at the age of 16 years and had been smoking 40 cigarettes a day.) She was a widow with three adult children, and had emigrated from the United Kingdom in 1969. Her husband died at the age of 39 years of a myocardial infarction. Her father died of carcinoma of the oesophagus, and her mother of “old age”. Her four siblings and three adult children were all well. Although she had no history of asbestos exposure from any of her husband’s occupations, she could have been exposed to asbestos during two periods of her life. From the age of 15–22 years in the UK, she worked as a machinist in a factory where asbestos lagging was used for the steam pipes of steam presses and central heating. Then, in 1984, her son worked for a year for a company making asbestos gaskets, and throughout this period she washed his work overalls. On examination, she looked well and was not in pain. She weighed 74 kg and was of normal build, but had slight conjunctival pallor. An electrocardiogram showed sinus rhythm; her blood pressure was 140/60 mmHg, and her jugular venous pressure was not elevated. There was no cyanosis or clubbing. Examination of the chest, cardiovascular system, breast, abdomen and peripheries showed no abnormalities. InvestigationsA chest radiograph taken before referral showed a pleural density measuring 10 cm × 2 cm overlying the posterior aspect of the right lower lobe, with no pleural plaques or other stigmata of asbestos exposure. A CT pulmonary angiogram performed the same day to exclude pulmonary embolism showed three pleural masses in the right side of the chest — the first corresponding to the opacity visible on the chest radiograph in the right costovertebral gutter at the level of the tracheal bifurcation, the second having a diameter of 6 cm and located in the right cardiophrenic angle (not of fatty attenuation), and the third in the right posteromedial costophrenic recess, just above the diaphragm (Box 1A and Box 1B). The lungs, mediastinum and upper abdomen (including the pancreas and para-aortic nodes) were normal. Laboratory tests showed her haemoglobin level was 104 g/L (reference range [RR], 115–160 g/L), with a normochromic normocytic anaemia; she had thrombocytosis (555 × 109/L [RR, 150–450 × 109/L]) and leukocytosis (11.2 × 109/L [RR, 4.0–11.0 × 109/L]), with mild neutrophilia (8.2 × 109/L [RR, 2.0–7.5 × 109/L]). Her erythrocyte sedimentation rate was markedly elevated at 110 mm/h (RR, 1–30 mm/h), as was her serum C-reactive protein level (294 mg/L [RR, 0–6 mg/L]). She had mildly elevated concentrations of liver enzymes (alanine aminotransferase, 98 U/L [RR, 0–45 U/L]; aspartate aminotransferase, 70 U/L [RR, 0–41 U/L]; and lactate dehydrogenase, 268 U/L [RR, 80–250 U/L]), with normal serum bilirubin and alkaline phosphatase levels. Her serum iron level was low (2 μmol/L [RR, 10–33 μmol/L]). A core biopsy (20 mm × 1 mm) of one of the right pleural masses showed morphological and immunohistochemical features of a poorly differentiated epithelial mesothelioma. A pathology report by an experienced pathologist with a special interest in pulmonary and pleural pathology read: There is a proliferation of poorly cohesive large cells many of which had vesicular nuclei, prominent nucleoli and abundant eosinophilic cytoplasm. Occasional binucleate and multinucleate forms are present and there is a small amount of associated collagenous stroma with a mild chronic inflammatory cell infiltrate [Box 2A]. There is no evidence of mucin production, and immunoperoxidase stains for a variety of keratins are strongly positive, along with positive staining for calretinin [Box 2B] and cytokeratin 5/6, both markers of mesothelial differentiation [Box 2C]. Stains for LCA and S100 protein are negative. The pathology results were later reviewed by another pathologist with considerable experience of mesothelioma, who drew the same conclusion. ManagementThe patient was told the diagnosis and referred to an oncologist with a special interest in mesothelioma in another tertiary hospital where clinical trials of drugs for the treatment of mesothelioma were in progress. She was offered chemotherapy and entry in a thalidomide trial, but, by the time she was entered, the tumour was already showing signs of spontaneous regression. The patient opted for no treatment, as she felt well. By 30 December 2002, a repeat CT scan of the chest showed a decrease in the size of the large, right-sided pleural mass in the costovertebral gutter from 17 mm × 9 mm (CT chest scan, 29 November 2002) to 12 mm × 6 mm. The second pleural mass was now so small it was difficult to see. The third mass was not visible, and there were two small intrapulmonary nodules — one in the right middle lobe and the other in the left lower lobe. By March 2003, the first and second pleural masses were even smaller (Box 1C) and, by June 2003, they had disappeared (Box 1D). A CT chest scan in June 2004 was normal except for the two tiny intrapulmonary nodules that had not changed in size and were probably granulomas. The patient was last reviewed in June 2007 and was in good health, with no evidence of tumour, and was scheduled for next review in 6 months. DiscussionThere have been a few reports of spontaneous regression of malignant mesothelioma, but prolonged, disease-free periods are rare. Our report appears to be the first to describe a patient in Australia with a poorly differentiated, multifocal epithelial mesothelioma that regressed spontaneously, with the disease remaining in remission for 5 years. There has been one case report of a patient with malignant mesothelioma of the pleura that regressed spontaneously, but after 6 years there was a single recurrence, which was resected surgically, and the patient was followed up for a total of 12 years.1 This raises the question in such cases of the duration of follow-up. In the latter case, a prominent host response to tumour was seen in both the primary tumour and the recurrence. In another case, a patient had a spontaneous remission of a malignant peritoneal mesothelioma, and had high spiking fevers when the tumour recurred.2 A report from Western Australia described a woman whose tumour regressed spontaneously but who eventually died 20 months later.3 It was noted that the tumour tissue was infiltrated with mononuclear cells, and as the tumour recurred some malignant mesothelioma antigens disappeared. Several aspects of our case should be noted. Histopathology The histopathological findings for our patient’s tumour were re-examined by another pathologist. Not all three lesions were biopsied, as it was felt highly probable that the pathological findings for all three would be identical. Author’s experience I have considerable experience in the management of mesothelioma and benign asbestos-related conditions and currently see about 600 patients with this condition a year. I also act as an expert witness for the courts. Mesothelioma is a relatively common condition in Australia at present and, as a result, our thoracic physicians, oncologists and pathologists have considerable experience in this area. Course of the disease The patient had markedly elevated inflammatory markers and is likely to have had the tumour for several months before diagnosis. It is suspected that her natural killer cells and cell-mediated immunity accounted for the regression of the tumour. Evidence of the beginning of spontaneous regression was unusually rapid, occurring within months of diagnosis. Exposure Our patient’s exposure to asbestos seems to have been relatively mild and incidental, as often occurs with women who develop mesothelioma. Self-treatment The patient did not use any unusual therapies, such as alternative medicines, diets and faith healing, after the diagnosis. This case highlights the possibility that spontaneous regression of mesothelioma may occur occasionally. Spontaneous tumour regression therefore should be seen as part of the spectrum of the natural history of mesothelioma and other tumours. A detailed study of the immunity of such individuals “after the event” is unlikely to reveal any particular abnormality but, in hindsight, it would have been interesting to have performed detailed immunological studies during the initial regression period. The role of mesothelin-related serum proteins needs further evaluation. The understanding of this process is likely to be pivotal in the improved treatment of this usually lethal condition. 1 Computed tomography (CT) scans of the chest at referral (September 2002) and 6 and 9 months later A, B: CT pulmonary angiogram at referral (September 2002) showing (A) the pleural-based mass in the right costovertebral gutter at the level of the tracheal bifurcation (arrow) and (B) the two lower pleural-based masses — one in the right cardiophrenic angle and the other in the right posteromedial costophrenic recess (arrows). C: CT scan (March 2003) showing that the pleural-based mass in the right costovertebral gutter had all but disappeared (arrow). D: CT scan (June 2003) which appeared normal apart from a small stable nodule in the left lower lobe which was probably a granuloma (arrow). 2 Histological examination of a core biopsy specimen from one of the pleural masses (Box 1) A: Histological section of the core biopsy of the pleural mass in Box 1A showing sheet-like proliferation of pleomorphic epithelioid cells with abundant eosinophilic cytoplasm, representing a poorly differentiated epithelioid malignant mesothelioma. B: Core biopsy showing a positive result on immunoperoxidase staining for calretinin. C: Core biopsy showing a positive result on immunoperoxidase staining for cytokeratin 5/6.

Roger K A Allen FRACP, FCCP, PhD

Objective: To evaluate the outcomes 10 years after a flexible sigmoidoscopy colorectal cancer (CRC) screening program in asymptomatic average-risk individuals.Design, setting and patients: In 1995, a program of flexible sigmoidoscopy-based screening of asymptomatic average-risk individuals aged 55–64 years was established at Fremantle Hospital, Western Australia. Insertion depths, pathological findings and subject-rated pain scores have been prospectively recorded. A follow-up flexible sigmoidoscopy examination was offered to attendees 5 years after the initial screening. Post-screening malignancies were determined by linkage with the Western Australian Cancer Registry in September 2006.Main outcome measures: Yield of neoplasia at initial and follow-up sigmoidoscopy, and the incidence of CRC detected after screening.Results: Between 1995 and 2005, 3402 people underwent an initial flexible sigmoidoscopy screening examination (mean age, 60 years; women, 41%) and 1025 had a 5-year recall examination. Mean insertion depth was greater in men than women (60 cm v 52 cm, P < 0.001). The insertion depth in women was more likely to be < 40 cm (17% v 6%, P < 0.001). Mean pain score was 2.9 for men and 4.0 for women (P < 0.001). Fourteen per cent of initial screenings detected at least one adenoma. Over a mean follow-up time of 8 years, invasive CRC was detected by flexible sigmoidoscopy screening in 0.4% of participants; 0.7% of those with a normal result of screening later developed CRC, with 75% of these found proximal to the splenic flexure.Conclusions: Flexible sigmoidoscopy is a viable screening method, with well defined utility and limitations, for CRC screening of asymptomatic people with average risk.

Charlie H Viiala MB BS, FRACP · John K Olynyk MB BS, FRACP, MD