Issues
Volume 169 Issue 1
Editorials Cancer control in Australia Alan S Coates (MJA 1998; 169: 8-9)Prostate-specific antigen testing for prostate cancer: the case for informed consent Margaret McCredie, Brian Cox (MJA 1998; 169: 9-10)Management of localised prostate cancer: state of the art Mark Frydenberg, Gillian Duchesne, Phillip D Stricker (MJA 1998; 169: 11-12)Delays in referral for palliative radiotherapy Michael B Barton, Paul A Glare (MJA 1998; 169: 12-13)Colorectal cancer screening in average-risk, asymptomatic Australians Judith A Collett, John K Olynyk (MJA 1998; 169: 14-15) Research Prostate cancer in Western Australia: trends in incidence and mortality from 1985 to 1996 Timothy J Threlfall, Dallas R English, Ian L Rouse (MJA 1998; 169: 21-24) Abstract - Article Healthcare Do general practitioners use prostate-specific antigen as a screening test for early prostate cancer? Jeanette E Ward, Leena Gupta, Nicholas J Taylor (MJA 1998; 169: 29-31)Symptom duration and delay in referral for palliative radiotherapy in cancer patients: a pilot study Andrew Wirth, Jennifer G Smith, David L Ball, Hedy Mameghan, June Corry, David L M Bernshaw, Roslyn M Drummond (MJA 1998; 169: 32-36) Medicine and the Community Colorectal cancer: a survey of community beliefs and behaviours in Victoria Robert J S Thomas, Valerie A Clarke (MJA 1998; 169: 37-40) Personal View What price, compassion? Mohamed H Khadra (MJA 1998; 169: 42-43) Clinical Practice Management of metastatic prostate cancer Mark A Rosenthal (MJA 1998; 169: 46-50)
Editorials
Prostate-specific antigen testing for prostate cancer: the case for informed consent
Prostate-specific antigen testing for prostate cancer: the case for informed consent Informed consent should be obtained before testing asymptomatic men MJA 1998; 169: 9-10 The prostate-specific antigen (PSA) test is only the first step in screening asymptomatic men for prostate cancer. Its lack of specificity usually necessitates transrectal ultrasound-guided multiple biopsies for confirmation of the diagnosis. These procedures will discover a large number of cancers, many of which, viewed from one perspective, will be potentially curable by surgery1 or radiotherapy. However, epidemiological evidence suggests that most cancers localised to the prostate will not cause clinically significant disease for at least 10 years.2 PSA-based screening presents unique difficulties because at present there is no means to distinguish those cancers which will impair health to a degree that justifies the risk of iatrogenic morbidity of investigation (biopsy-related sepsis) and curative treatment (incontinence, impotence, and radiation damage to adjacent organs). This issue of the Journal includes four pertinent articles: the incidence of prostate cancer and the prevalence of PSA testing are described and compared in Western Australia3 (Threlfall et al) and New South Wales4 (Smith & Armstrong); reasons for PSA tests being ordered by general practitioners (GPs) in central Sydney are reported5 (Ward et al); and the prevalence of PSA testing among South Australian men is given, together with findings concerning men's understanding of the immediate consequences of having a PSA test6 (Pinnock et al). PSA tests were the sixth most frequent pathology item ordered by GPs in the June quarter of 1996,5 but their use has fallen since the peak in 1995.3,4 This may indicate that GPs are adopting a more discerning approach, in line with guidelines that recommend against the use of PSA tests to screen for prostate cancer.7 However, in the period 1992-1996, it is clear that GPs and asymptomatic men adopted the test enthusiastically. Medicare data show that one in every four Australian men (27%) aged at least 50 years had a PSA test in 1995 or 19964 and, in a random survey of households in South Australia carried out in 1996, 28% of men aged 50 years or older without prostate cancer reported having a PSA test in the preceding 12 months.6 A high proportion of PSA tests were ordered by GPs for screening ("routine for age") or in response to patient request.5,6 Men over 70 years old have been tested as frequently as younger men4,6 -- but the older the man when prostate cancer is detected, the less likely it is that a benefit from early intervention is possible.8 In South Australia, there was an association between PSA testing and visiting a doctor for urinary symptoms.6 PSA testing is not recommended for men presenting with uncomplicated lower urinary tract symptoms (because such symptoms are unlikely to be indicative of localised prostate cancer),6,9 but it is understandable that GPs may order the test because the question of prostate disease has been raised during the consultation. It is evident that PSA tests have been carried out without the consequences of an abnormal test result being adequately explained.6 GPs need a clear-cut structured framework within which the paucity of good scientific evidence and the potential harms and benefits can be discussed with patients. Most GPs will have had difficulty reconciling the negative evidence relating to the cost-benefit of PSA testing with their natural inclination to detect and treat cancer at an early stage. However, in asymptomatic people the balance of harm versus benefit must demonstrably be more clearly in favour of benefit than in usual clinical practice. In the United States, where enthusiasm for both case-finding by PSA testing and treatment by radical prostatectomy occurred some years earlier than in Australia, there appears to have been a small fall in mortality from prostate cancer in the period 1990-1995.10 Interpretation of this fall is far from clear, but it may be attributable to the dramatic increase in use of radical prostatectomy11 or other therapeutic advances in the 1980s. Conclusive evidence of reduced mortality from prostate cancer as a result of PSA screening must await the completion of randomised controlled trials. From an intention-to-treat analysis of men aged 50-79 years with clinically localised prostate cancer in the population-based US Surveillance, Epidemiology, and End Results (SEER) Program, no advantage in 10-year disease-specific survival was found for either radical prostatectomy or radiotherapy compared with conservative management for men with tumours with a Gleason score of 2-4 (well differentiated).12 For men with tumours with a Gleason score of 5-7 (moderately differentiated) there was an advantage for radical prostatectomy but not for radiotherapy -- this may reflect the fact that patients selected for surgery excluded those whose general health, and therefore prognosis, was already bad when prostate cancer was diagnosed. The 10-year disease-specific survival was better for men with tumours with a Gleason score of 8-10 (poorly differentiated) treated by either radical prostatectomy or radiotherapy compared with conservative management. Because of the way screening for breast and cervical cancers has been promoted, the general public will perceive that finding a cancer earlier is beneficial because treatment is more likely to be effective. However, using the PSA test for detecting prostate cancer in asymptomatic men is not analogous to mammography for early detection of breast cancer in asymptomatic women. Apart from the unproven benefit, there is a need for universally applied guidelines for the management of men with an abnormal test result, comparable with those built into the mammographic screening program. Such guidelines would include counselling and provision for a multidisciplinary approach when a decision is being made about the best course of management. At present, the cascade of events following an abnormal PSA test result proceeds without the man always making an informed choice before the test. Indeed, when men are given prior information about the PSA test and its characteristics, the consequences of having a raised PSA level, follow-up diagnostic procedures, treatment options and side effects, they are less likely to decide to have the test.13 GPs have a professional responsibility to give appropriate advice based on current evidence and, where there is uncertainty, this should be conveyed. Obtaining informed consent is accepted in the context of an invasive procedure. Given the medical uncertainties, the invasive nature of the confirmatory and therapeutic procedures that will be required if the test is positive, and the possibility of doing more harm than good, informed consent should be obtained from asymptomatic men before ordering a PSA test. Margaret McCredie Professorial Research Fellow, Department of Preventive and Social Medicine University of Otago, Dunedin, New Zealand, and Cancer Epidemiology Research Unit, NSW Cancer Council, Woolloomooloo, NSW Brian Cox Senior Research Fellow, Department of Preventive and Social Medicine University of Otago, Dunedin, New Zealand Kaye KW. Prostate cancer: enthusiasm for screening. Med J Aust 1995; 162: 540-541. Johansson J-E, Adami H-O, Andersson S-O, et al. High 10-year survival rate in patients with early, untreated prostatic cancer. JAMA 1992; 267: 2192-2196. Threlfall TJ, English DR, Rouse IL. Prostate cancer in Western Australia: trends in incidence and mortality from 1985 to 1996. Med J Aust 1998; 169: 21-24. Smith DP, Armstrong BK. Prostate-specific antigen testing in Australia and association with prostate cancer incidence in New South Wales. Med J Aust 1998; 169: 17-20. Ward JE, Gupta L, Taylor NJ. Do general practitioners use prostate-specific antigen as a screening test for early prostate cancer? Med J Aust 1998; 169: 29-31. Pinnock CB, Weller DP, Marshall VR. Self-reported prevalence of prostate-specific antigen testing in South Australia: a community study. Med J Aust 1998; 169: 25-28. Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. Fleming C, Wasson JH, Albertsen PC, et al. A decision analysis of alternative treatment strategies for clinically localized prostate cancer. Prostate Patient Outcomes Research Team. JAMA 1993; 269: 2650-2658. National Health and Medical Research Council. Clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: AGPS, 1996. Mettlin CJ, Murphy GP. Why is the prostate cancer death rate declining in the United States? Cancer 1998; 82: 249-251. Lu-Yao GL, Greenberg ER. Changes in prostate cancer incidence and treatment in USA. Lancet 1994; 343: 251-254. Lu-Yao GL, Yao S-L. Population-based study of long-term survival in patients with clinically localised prostate cancer. Lancet 1997; 349: 906-910. Flood AB, Wennberg JE, Nease RF, et al. The importance of patient preference in the decision to screen for prostate cancer. Prostate Patient Outcomes Research Team. J Gen Intern Med 1996; 11: 342-349. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>
Margaret McCredie · Brian Cox
Management of localised prostate cancer: state of the art
Management of localised prostate cancer: state of the art The decision to treat should be based on the age of the patient and the grade of the cancer MJA 1998; 169: 11-12 We know that the incidence of prostate cancer increases with age and that many men "die with, but not from, prostate cancer".1 This has made the medical community concerned that, because of the high prevalence of comorbid illnesses among elderly men, many cancers detected by screening based on prostate-specific antigen (PSA) testing will be clinically insignificant, and that most patients would be overtreated. Unfortunately, we are also faced with the reality that approximately 2500 men succumb to prostate cancer annually, and many, particularly younger men, in fact "die of the disease and not with it".2 Most patients with localised prostate cancer will be given three management options: watchful waiting, radiotherapy, or radical surgery. Watchful waiting is defined as no initial treatment, with regular patient surveillance (which involves frequent consultations, digital rectal examinations and PSA testing) and commencement of androgen ablative therapy when clinical progression occurs. The success of watchful waiting depends on the predicted biological aggression of the cancer (related to the histological grade), as well as on the age and the associated comorbid illnesses of any individual patient. A pooled analysis of 828 patients treated conservatively in six non-randomised studies concluded that histologic grade was an important determinant of outcome. The 10-year cause-specific survival of patients with well or moderately differentiated cancers was 87%, compared with only 36% for those with poorly differentiated disease (who were at high risk of cancer progression and death).3 The cancer had metastasised by 10 years in 19% of men with well differentiated disease and 42% of men with moderately differentiated disease, despite the satisfactory cause-specific survival. Although watchful waiting may be an appropriate treatment choice for men with life expectancy of less than 10 years with well or moderately differentiated cancers, the outcome at 15 years may be less favourable. In another series, among men who survived more than 10 years from their initial diagnosis, prostate cancer was the direct or contributing cause of death in 63%.4 A report from the Connecticut Tumour Registry has shown that in men diagnosed with moderately differentiated cancer there is a modest, but not insignificant, risk of death from prostate cancer (28%) at 15 years with conservative treatment, and a potential loss of 4-5 years of life.5 Both mortality and potential years of life lost were even higher in men diagnosed with poorly differentiated disease. Contemporary radiotherapy offers an alternative to radical surgery for men who prefer not to undergo surgery or who have comorbidities which increase the risks of surgery. It also offers a chance of local tumour control to men with locally advanced cancer deemed unsuitable for curative surgery. There has been debate over the contribution of radiotherapy because surgery achieves higher rates of clinical and biochemical freedom of disease in the long term (although there have been no valid prospective, randomised controlled trials which directly compare these two treatments). However, the apparent advantage of surgery could be a reflection of the use of radiotherapy in patients with more advanced disease than those for whom radical prostatectomy would be contemplated. Success with radiotherapy has been shown to be dependent on both the stage and grade of the cancer. Fifteen-year cause-specific survival rates varied from 84% for low-stage to 52% for high-stage clinically localised cancers, and from 85% for well differentiated to 32% for poorly differentiated cancers.6 Traditional external beam radiotherapy involves a treatment course lasting up to seven or eight weeks. Acute proctitis and cystitis occurs in most patients, and there is a 2%-3% risk of long term rectal morbidity (diarrhoea, rectal bleeding) and a 30%-60% risk of permanent impotence. There are increasingly convincing data to support the hypothesis that local control and disease-free survival rates in patients with apparently localised disease improve with increasing radiation dose.7 Current research strategies are therefore aimed at increasing radiation dose without increasing surrounding normal tissue damage. This may be achieved by three-dimensional conformal therapy or brachytherapy, either alone or in combination with external beam radiotherapy. Another approach is to use androgen ablation to shrink the tumour, and then to deliver radiotherapy to maximise tumour cell kill.8 All these techniques have shown encouraging preliminary results, but follow-up has been relatively short. Improvements in surgical techniques, together with an increased understanding of the anatomy of the prostate, have made radical prostatectomy a popular treatment option for localised prostate cancer since the mid 1980s. A Mayo Clinic review of 3170 men treated by radical prostatectomy for clinically localised disease included 93% of men with clinically palpable disease and 25% with poorly differentiated disease. Cause-specific survival among those with palpable disease at 10 and 15 years was 90% and 82%, respectively, and 82% and 71%, respectively, among those with poorly differentiated cancers.9 The morbidity of radical surgery in an Australian setting has been discussed recently in the Journal.10 Independently administered questionnaires indicated that incontinence requiring daily pads occurred in approximately 10% of men who underwent surgery. Most of those affected required a maximum of one pad per day and the degree of inconvenience was generally low. The nerve-sparing technique may give reasonable postoperative potency rates in selected younger patients,11 but impotence occurs in most older men, and this is the issue that most affects quality of life.10 Nonetheless, men in most series indicated that they would choose to have surgery again,10 suggesting that the patients' desire to be cured of the disease outweighed the disadvantageous side effects. In a comparison of watchful waiting, radiotherapy and surgery, Surveillance, Epidemiology and End Results (SEER) data from the United States have shown that men with well differentiated cancer treated by watchful waiting have 10-year cause-specific survival rates comparable to those treated actively, while in those with moderately or poorly differentiated cancers treatment provides a survival benefit (Table).12 The gap between these groups is likely to widen further at 15 years as more men treated by watchful waiting live long enough to succumb to the disease. In most watchful waiting series, the mean age of the patients is over 70 years, and therefore few patients (5.9%-8.9%) actually survived 15 years.5,13 A recent study comparing 10-year data with 15-year data for men treated conservatively has shown a 15% reduction in cause-specific survival over the additional five years in men with well or moderately differentiated cancer,14 indicating a cumulative increase in prostate cancer mortality even in this cohort with lower grades of cancer. The hypothesis that death rates are declining as a result of increased diagnosis of localised disease treated at an earlier stage is supported by recent National Cancer Institute data showing that prostate cancer mortality in younger white men had declined by 11.7% this decade.15 It is to be hoped that randomised controlled trials currently under way will provide evidence that this is the case. A preliminary report suggests that this may be so.16 However, until the substantive results of these trials are known, men must be thoroughly counselled about the benefits and risks of early detection and treatment of prostate cancer. Aggressive, early therapy should be recommended for patients who are more likely to benefit from treatment -- those with greater than 10-year life expectancy, especially if diagnosed with a higher histological grade of cancer -- while patients less likely to benefit should be spared the morbidity of treatment. Mark Frydenberg Clinical Associate Professor, Department of Surgery, Monash University Head of Urology, Monash Medical Centre, Melbourne, VIC Gillian Duchesne Associate Professor, Department of Urology and Radiation Oncology Peter MacCallum Cancer Institute, Melbourne, VIC Phillip D Stricker Attending Urologist, Department of Urology, St Vincent's Hospital, Sydney, NSW Canstat -- Cancer in Victoria. Melbourne: Anti-Cancer Council of Victoria, 1994. Albertsen PC, Murphy-Setzko MA, Hanley JA, et al. Long term survival following conservative management of localised prostate cancer: fifteen year follow up among men aged 55-75 [abstract]. J Urol 1998; 159: 251. (Abstract No. A963.) Chodak GW, Thisted RA, Gerber GS, et al. Results of conservative treatment of clinically localised prostate cancer. N Engl J Med 1994; 30: 242-248. Aus G, Hugosson J, Norlen L. Long term survival and mortality in prostate cancer treated with non-curative intent. J Urol 1995; 154: 466-469. Albertsen PC, Fryback DG, Storer BE, et al. Long term survival among men with conservatively treated localised prostate cancer. JAMA 1995; 274: 626-631. Bagshaw MA, Cox RS, Hancock SL. Control of prostate cancer with radiotherapy: long term results. J Urol 1994; 152: 1781-1785. Hanks GE, Martz KL, Diamond JJ. The effect of dose on local control of prostate cancer. Int J Radiat Oncol Biol Phys 1988; 15: 1299-1305. Zagars GK, Johnson DE, Von Eschenbach AC, Hussey DH. Adjuvant estrogen following radiation therapy for stage C adenocarcinoma of the prostate: long term results of a prospective randomized study. Int J Radiat Oncol Biol Phys 1988; 14: 1085-1091. Zincke H, Oesterling JE, Blute ML, et al. Long term results after radical prostatectomy for clinically localised prostate cancer. J Urol 1994; 151: 1583-1586. Heathcote PS, Mactaggart PN, Boston RJ, et al. Health related quality of life in Australian men remaining disease free after radical prostatectomy. Med J Aust 1998; 168: 483-486. Quinlan DM, Epstein JI, Carter BS, Walsh PC. Sexual function following radical prostatectomy: influence of preservation of neurovascular bundles. J Urol 1991; 145: 998-1002. Lu-Yao GL, Yao SL. Population based study of long term survival in patients with clinically localised prostate cancer. Lancet 1997; 349: 906-910. Johanssen J-E, Holmberg L, Johansson S, et al. Fifteen year survival in prostate cancer: a prospective population based study in Sweden. JAMA 1997; 277: 467-471. Adolfsson J, Steineck G, Hedlund P-O. Deferred treatment of low grade prostate cancer: actual 10 year and projected 15 year follow up of the Karolinska series [abstract]. J Urol 1998; 159: 252. (Abstract No. A965.) Mettlin CJ, Murphy GP. Why is the prostate cancer death rate declining in the United States? Cancer 1998; 82: 249-251. Charatan FB. Prostate cancer screening reduces death. BMJ 1998; 316: 1626. Reprints: Clinical Associate Professor M Frydenberg, Suite 21, Cabrini Medical Centre, Isabella Street, Malvern, VIC 3144. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>
Mark Frydenberg · Gillian Duchesne · Phillip D Stricker
Research
Prostate-specific antigen testing in Australia and association with prostate cancer incidence in New South Wales
Prostate-specific antigen testing in Australia and association with prostate cancer incidence in New South Wales David P Smith and Bruce K Armstrong MJA 1998; 169: 17-20 For editorial comment, see McCredie & Cox Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objective: To describe patterns and trends in prostate-specific antigen (PSA) testing in Australia and assess its role in the increasing incidence of prostate cancer. Design: Descriptive analysis of (i) Medicare records of PSA testing in Australia, and (ii) prostate cancer recorded incidence in New South Wales. Data: (i) Medicare data for all males who received a Medicare-reimbursed PSA test between August 1989 and December 1996. (ii) NSW Central Cancer Registry data for all males in NSW with prostate cancer diagnosed between 1988 and 1995. Main outcome measures: (i) Number of PSA tests, age-standardised rates of PSA tests by State and Territory, and proportions of males who had a PSA test. (ii) Recorded incidence of prostate cancer in NSW. Results: (i) More than 2.2 million PSA tests were done on more than 1.1 million Australians between 1989 and 1996. The annual number of males tested increased fivefold in this period and peaked in 1995. Twenty-seven per cent of Australian men aged 50 years or over had at least one PSA test in 1995 or 1996; 33% of men aged 60-69 years had a test in this period. (ii) In NSW the number of PSA tests per quarter was highly correlated with the number of new cases of prostate cancer (R2 = 0.92). Conclusions: Although no organised program for prostate cancer screening exists, and despite repeated advice against it, opportunistic screening has been occurring at high rates. There was a high correlation between PSA testing and prostate cancer incidence between 1990 and 1995 in NSW. Introduction Prostate cancer is the most common cancer in Australians after non-melanocytic skin cancers, and accounts for about a third of all newly diagnosed internal cancers in males.1,2 It is the second most common cause of cancer death among Australian males.3 During the late 1980s and early 1990s, recorded prostate cancer incidences increased substantially in Australia, while mortality from prostate cancer remained stable.1,2,4-6 Much of the increase in incidence has been attributed to detection of latent cancers by increased use of the prostate-specific antigen (PSA) test, transurethral resection of the prostate, prostatic biopsy and radical prostatectomy.7There are considerable arguments for8,9 and against10,11 screening for prostate cancer. In 1996 the Australian Health Technology Advisory Committee reviewed the evidence and recommended against screening. However, the committee recognised that de facto screening occurs in the community and stated a need to monitor and review the evidence when important developments occur.12 Data collected by the Health Insurance Commission provide the best available means to monitor trends and patterns in PSA testing. We analysed these data to determine the association between PSA testing and reported incidence of prostate cancer in Australia and in New South Wales. Methods Data PSA tests: The Commonwealth Department of Health and Family Services Medicare Estimates and Statistics Unit provided de-identified data, extracted from the national dataset of all services rendered on a fee-for-service basis for which a Medicare benefit has been paid. The data included all tests itemised under the Medicare Benefits Schedule codes that included PSA tests. PSA tests first appeared in the Schedule in August 1989, but were included with 20 "other" biochemical tests until November 1993. Since then they have been itemised together with prostatic acid phosphatase (PAP) tests. PSA tests could not be differentiated from PAP tests with the available information. To estimate the proportion of non-PSA tests in the dataset, we investigated the patterns of use of the other tests, using data provided by the Commonwealth Department of Health and Family Services. We calculated retrospective projections using exponential regression on the number of tests by age group and annual quarter to give an adjusted number of PSA and PAP tests for the period between August 1989 and November 1993. This study included data for all males who had at least one PSA or PAP test between 1989 and 1996 reimbursed by Medicare. The data included a unique identification number for each person, age, date of service, postcode, and fee charged for the service. The identification number allowed individuals to be linked over time to quantify those who had multiple tests, but was not linkable to any other identifying data. Prostate cancer: Data on prostate cancer incidence in NSW were obtained from the NSW Central Cancer Registry, a population-based register which began collecting data in 1972. Notification of malignant neoplasms has been a statutory requirement for all NSW public and private hospitals, radiation oncology departments and nursing homes since 1972, and for all pathology and outpatient departments since 1985.1 Population: The Australian Bureau of Statistics provided the estimated resident populations of Australia by five-year age group and State or Territory for the years 1989 to 1996.13 Analysis We calculated the rate of testing and the number of males tested by age group, State or Territory, and year from August 1989 to December 1996. We calculated the number of males having multiple tests from January 1995 to December 1996 and the proportion of males tested in each age group in this period. We used a two-year period for these calculations to reduce errors introduced by men moving up age groups. We compared the number of tests carried out in NSW by quarter with the number of prostate cancers diagnosed between 1990 and 1995 (the most recent year for which prostate cancer data were available). All rates, standardised to the total male and female Australian 1991 population, are expressed per 100 000 males. We used SAS software for statistical analysis.14 Results PSA testing in Australia From August 1989 to December 1996 more than 2.2 million PSA or PAP tests were reimbursed by Medicare in Australia. About 1.1 million males were tested during this period. Eighty-eight per cent of the tests were for men aged 50 years or over, with the largest proportion (34%) for men aged 60-69 years (Table 1). Age-standardised rates for males having one or more PSA/PAP tests per year increased fivefold between 1990 and 1996, and the greatest increases occurred between 1993 and 1995. There was substantial variation in the rates of testing by State and Territory (Figure 1). Except in the Australian Capital Territory, the rates peaked in 1995, when the highest rates were in Western Australia (8668 tests per 100 000) and the Australian Capital Territory (8284 tests per 100 000) and the lowest in the Northern Territory (3270 per 100 000). From January 1995 to December 1996, 709 523 Australian males had at least one PSA/PAP test reimbursed by Medicare. Most of those tested (73%) had one test, 17% had two tests, 5% had three tests and 5% had four or more tests. Older men were more likely to have had multiple tests (Table 2). In this period, 27% of Australian men aged 50 years and over had one or more PSA/PAP tests reimbursed by Medicare. This figure peaked at 33% in men aged 60-69 years (Table 3). In 1996 the Medicare schedule fee for a single PSA/PAP test was $19.90 or, where two or more tests were undertaken at the same consultation, $36.65. The overall amount reimbursed by Medicare for PSA/PAP tests in 1996 was $10 675 880 (mean per test, $20.73; mode, $19.90; range, $11.00 to $36.65), not including the fee that may have been charged for the accompanying consultation. PSA/PAP tests and prostate cancer in NSW Between 1990 and 1995, more than 625 000 PSA/PAP tests were carried out in NSW, and 20 120 prostate cancers were diagnosed. The number of tests was highly correlated with the number of prostate cancers diagnosed (R2 = 0.92) (Figure 2). The ratio of number of tests performed to number of new cases of prostate cancer diagnosed increased from about 19 in 1990 to 45 in 1995. In 1995, in NSW, 150 479 males had one or more PSA/PAP tests. Figure 3 shows the age-specific rates of testing and reported incidence of prostate cancer. The number of PSA/PAP tests per prostate cancer detected in 1995 varied between age groups from a high of 579 in men aged 40-49 years to fewer than 24 in men aged 70 years or over. Discussion More than 2.2 million PSA tests were carried out in Australia from 1989 to 1996. More than 1.1 million males were tested in this period, and the annual number of males tested peaked in 1995. Data from this study support the hypothesis that the rising incidence of prostate cancer is associated with increased PSA testing. In NSW, the number of PSA tests was highly correlated with the number of new cases of prostate cancer. The PSA test is a blood test used in diagnosis and monitoring of prostate disease. First used in Australia in the late 1980s to monitor clinically identified disease, it has since been used in the diagnosis of relevant symptoms and as a screening test for asymptomatic men. It was not possible to identify from Medicare data the reasons why the tests were ordered. However, recent research found that 67 of 118 PSA tests (57%) were ordered for screening.15 Although we adjusted for other tests included under the same Medicare Benefits Schedule item from 1989 to 1993, we could not adjust for PAP tests, which are used to monitor the clinical progress of prostate cancer. However, in a continuous six-month period the ratio of PAP tests to PSA tests processed by a large, representative private pathology laboratory in NSW (covering city, suburban and regional centres) was less than 2% (Dr G Caldwell, Pathologist, Douglass Hanly Moir Pathology, personal communication). Data from a large public pathology laboratory in South Australia indicate that the proportion of PAP tests to the total PSA and PAP tests fell from 50% in 1991 to 6% in 1996 (Dr H A Morris, Manager, Endocrine Unit, Institute of Medical and Veterinary Science, personal communication). At their peak in 1995, the rates of PSA/PAP testing in Australian males ranged from 3270 per 100 000 in the Northern Territory to 8668 per 100 000 in Western Australia. These are probably underestimates because Medicare data do not include services provided free to public patients in public hospitals, to Veterans' Affairs patients and to men offered screening under the research activities of centres such as the Perth-based Urological Research Centre. In the one-year period April 1993 to March 1994, 39 626 PSA tests were done on 30 739 veterans.16 Data from the Department of Veterans' Affairs show about 50 000 tests were done each year in Australia between 1994 and 1996, which would have contributed a further 10% to the number of Medicare-reimbursed PSA tests. In South Australia 72 000 PSA tests that would not appear in Medicare statistics were undertaken between 1990 and 1996 by a public laboratory (Dr H A Morris, personal communication). These and the tests done on veterans would have accounted for an approximate under-enumeration of 33% annually in South Australia. Nationally, considering all these extra sources of PSA tests, we estimate that Medicare data underenumerate PSA tests by 14%. In a recent study of self-reported rates of prostate cancer screening in the Central Sydney Area Health Service, about one in five men aged 50 years or over reported being screened in the previous 12 months.17 This agrees quite closely with our results, which show that during the two years 1995 to 1996 about one in four Australian men aged 50 years or over had a PSA test, and in 1995 one in six (17%) had a test. More prostate cancers would result in more PSA tests used for monitoring. However, the overall effect of this on PSA test-ordering is thought to be small. More than 70% of males tested in 1995 and 1996 had only one test, suggesting that most tests were for screening rather than monitoring disease activity. A further possible indication that most tests were undertaken for screening rather than for monitoring or diagnosis is the increase in the ratio of tests to newly diagnosed prostate cancers in New South Wales. This ratio continued to increase in 1995, when the reported incidence of prostate cancer had begun to fall. Increasing recorded incidences of prostate cancer have been reported from the United States,18-22 France23 and elsewhere in Australia.1,2,4-6 Incidence figures began rising earlier in the United States than in Australia, and appeared to peak in 1992 and 1993.20 South Australian and Western Australian age-standardised recorded incidences peaked in 1994 and fell by 22% and 13%, respectively, between 1995 and 1996.2,4,5 The rate of PSA testing peaked in 1995 in both States and fell 10% and 16%, respectively, in 1996. These data and the high correlation between PSA tests and newly diagnosed prostate cancers in NSW support the hypothesis that the rising incidence figures for prostate cancer in the early 1990s were a direct result of screening.7 Based on these trends and correlations, it is likely that the recorded incidence for prostate cancer in most Australian States and Territories will continue to fall after 1995. Given that screening for prostate cancer has never been recommended in Australia, the rates of de facto screening in men aged over 50 years, and especially those aged between 60 and 69 years, are quite remarkable. These findings have important implications for public health policy and for patient and practitioner education aimed at reducing prostate cancer screening. Acknowledgements We would like to thank Mr Ross Saunders, Director of the Medicare Statistics Section of the Department of Health and Family Services, for supplying the data. References Coates M, Armstrong B. Cancer in New South Wales. Incidence and mortality 1994. Sydney: NSW Cancer Council, 1997. South Australian Cancer Registry. Epidemiology of cancer in South Australia. Incidence, mortality and survival 1977 to 1996, incidence and mortality 1996 analysed by type and geographical location. Twenty years of data. Adelaide: South Australian Health Commission, 1997. Australian Bureau of Statistics. Causes of death, Australia, 1995. Canberra: AGPS, 1996. (Catalogue No. 3303.0.) Threlfall T, Whitford M, Thompson J. Cancer incidence and mortality in Western Australia 1992 to 1994. A report of the Western Australian Cancer Registry. Perth: Health Department of Western Australia, 1996. Threlfall T, Thompson J. Cancer incidence and mortality in Western Australia, 1995. A report of the Western Australian Cancer Registry. Perth: Health Department of Western Australia, 1997. Shugg D, Dwyer T, Blizzard L. Cancer in Tasmania. Incidence and mortality 1994. Hobart: Menzies Centre for Population Health Research, 1997. McCredie M, Coates M, Churches T, Rogers J. Rising incidence of prostate cancer in Australia: a result of 'screening'? J Epidemiol Biostatistics 1996; 1: 99-105. Lange PH. Is screening for prostate cancer the current gold standard? -- "Yes". Eur J Cancer 1997; 33: 354-356. Kaye KW. Prostate cancer: enthusiasm for screening. Med J Aust 1995; 162: 540-541. Kramer BS, Gohagan JK, Prorok PC. Is screening for prostate cancer the current gold standard? -- "No". Eur J Cancer 1997; 33: 348-353. Hirst GHL, Ward JE, Del Mar CB. Screening for prostate cancer: the case against. Med J Aust 1996; 164: 285-288. Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. Australian Bureau of Statistics. Estimated resident population by sex and age: States and Territories of Australia 1996. Canberra: Australian Bureau of Statistics, 1997. (Catalogue no. 3201.0.) SAS [computer program]. Version 6.12. Cary, North Carolina: SAS Institute, 1996. Ward JE, Gupta L, Taylor NJ. Do general practitioners use prostate-specific antigen as a screening test for early prostate cancer? Med J Aust 1998: 169; 29-31. Parkes AJ, Killer GT. Prostate-specific antigen -- is it already being used as a screening test? [letter]. Med J Aust 1994; 161: 722-723. Ward JE, Hughes A-M, Hirst GHL, Winchester L. Men's estimates of prostate cancer risk and self-reported rates of screening. Med J Aust 1997; 167: 250-253. Stephenson RA, Smart CR, Mineau GP, et al. The fall in incidence of prostate carcinoma. On the down side of a prostate specific antigen induced peak in incidence -- data from the Utah Cancer Registry. Cancer 1996; 77: 1342-1348. Jacobsen SJ, Katusic SK, Bergstralh EJ, et al. Incidence of prostate cancer diagnosis in the eras before and after serum prostate-specific antigen testing. JAMA 1995; 274: 1445-1449. Merrill RM, Potosky AL, Feuer EJ. Changing trends in U. S. prostate cancer incidence rates. J Natl Cancer Inst 1996; 88: 1683-1685. Gann PH. Interpreting recent trends in prostate cancer incidence and mortality. Epidemiology 1997; 8: 117-120. Lu-Yao GL, Greenberg R. Changes in prostate cancer incidence and treatment in USA. Lancet 1994; 343: 251-254. Menegoz F, Colonna M, Exbrayat C, et al. A recent increase in the incidence of prostatic carcinoma in a French population: role of ultrasonography and prostatic specific antigen. Eur J Cancer 1995; 31A: 55-58. (Received 28 Nov 1997, accepted 24 Apr 1998) Authors' details Cancer Control Information Centre, New South Wales Cancer Council, Sydney, NSW. David P Smith, BA, MPH, Research Coordinator, Cancer Epidemiology Research Unit; Bruce K Armstrong, DPhil, FRACP, Director. Reprints will not be available from the authors. Correspondence: Mr D P Smith, Cancer Epidemiology Research Unit, NSW Cancer Council, PO Box 572, Woolloomooloo, NSW 2011. E-mail: dsmithATnswcc.org.au Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>
David P Smith · Bruce K Armstrong
Prostate cancer in Western Australia: trends in incidence and mortality from 1985 to 1996
Prostate cancer in Western Australia: trends in incidence and mortality from 1985 to 1996 Timothy J Threlfall, Dallas R English and Ian L Rouse MJA 1998; 169: 21-24 For editorial comment, see McCredie & Cox Abstract - Introduction - Methods - Results - Discussion - References - Addendum - Authors' details - - ©MJA1998 Abstract Objective: To measure trends in recorded incidence and mortality rates of prostate cancer in Western Australia from 1985 to 1996 and to relate these to prostate-specific antigen (PSA) testing for prostate cancer. Design: Descriptive study based on data from the Western Australian Cancer Registry, the Australian Bureau of Statistics and the Health Insurance Commission. Data: All newly diagnosed cases of prostate cancer and all deaths from prostate cancer in Western Australia from 1985 to 1996. Main outcome measures: Recorded incidences and mortality rates for prostate cancer. Results: After increasing steadily from 42 per 100 000 person-years in 1985 to 61 in 1992, the recorded incidence more than doubled to 134 per 100 000 person-years in 1994, then fell sharply to 87 in 1996. Among men aged 50 years or more, those aged 50-54 years had the largest annual increases: 14% (95% confidence interval [CI], 10%-19%) from 1985 to 1992 and 108% (95% CI, 84%-134%) from 1992 to 1994. They also had the smallest annual decline between 1994 and 1996 (8%; 95% CI, 1% increase to 16% decrease). The mortality rate showed no sudden increases or decreases. In men aged 60 years or older, the mortality rate increased annually by 2.9% (95% CI, 2%-4%) from 1985 to 1996. The number of Medicare reimbursements for PSA tests increased until May 1995, then fell. There was a significant correlation between the monthly number of PSA tests and new cases of prostate cancer (P < 0.01). Conclusions: Following a period of steady increase, the recorded incidence of prostate cancer increased dramatically in 1992 because of screening by PSA testing. From 1994, these incidence figures declined almost as sharply, partly because of reductions in testing. The mortality rate has not shown any systematic deviation from its long-term trend. Introduction In the early 1990s the recorded incidence of prostate cancer increased dramatically in Australia,1,2 several years after a similar increase in the United States.3-7 Testing for the disease among asymptomatic men by measuring plasma prostate-specific antigen (PSA) is believed to be responsible for the increases.1,3,4,7We report here on trends in incidence figures and in the mortality rate for prostate cancer in Western Australia from 1985 to 1996, and their relationship to PSA testing. Methods Data sources We obtained data on prostate cancer cases and deaths from the Western Australian Cancer Registry, and population estimates from the Australian Bureau of Statistics (ABS).8 We standardised rates to the World Standard Population and calculated the risk of men developing prostate cancer before the age of 75 years.9 Because mortality rates based on coding of cause of death by the ABS were not available for 1996, we used 1996 rates from the Registry, which began coding causes of death in 1990; from 1990 until 1995, the two mortality rates were almost identical. Data relating to the number of PSA tests reimbursed by Medicare in Western Australia were obtained from the Health Insurance Commission in July 1997. Socioeconomic status To investigate any effect of socioeconomic status (SES) on recorded incidence we used an index, derived from the 1991 census, in which each census collection district (about 50 households) is assigned a score.10 For Perth patients, addresses at the time of diagnosis were mapped to collection districts for the 1991 census using MapInfo.11 Geographical coordinate data were provided by the Western Australian Valuer General's office and the Department of Land Administration. The SES index was divided into quarters of its distribution. Because population data were available at the collection district level for census years only (ie, 1986 and 1991), we could not calculate SES-specific incidence. To determine whether any changes in numbers of cases by SES might be the result of different changes in population size in areas of different SES, we compared numbers of cases of prostate cancer and lung cancer. Trends in age-specific rates We used Poisson regression in EGRET12 to model age-specific recorded incidences and mortality rates. Analyses of incidence were restricted to men aged 50 years or older and analyses of mortality rate to men aged 60 years or older because there were few events in younger age groups. We analysed recorded incidence for each of the periods January 1985 to December 1992, January 1992 to December 1994 and January 1994 to December 1996. (Because the periods overlap, the results were not independent.) A single analysis of mortality rate was conducted. Likelihood ratio tests were used to obtain P values. We fitted age group as a categorical (ie, factored) variable and year of diagnosis as a continuous variable. The coefficient for year was exponentiated to give an annual percentage increase in the rate (eg, a coefficient of 0.35 when exponentiated is 1.42, equivalent to an annual increase of 42%). Age was added first, followed by the year of diagnosis, and then the interaction between the two. The interaction was fitted with age as a categorical variable and as a continuous variable, and the difference between these models was tested. Fitting the interaction with age as a categorical variable tests whether the secular trend was the same for all age groups; fitting it with age as a continuous variable tests whether there was a greater increase in younger men than in older men (or vice versa). In the analyses of incidence, P values for comparison of the two types of interaction were 0.17 for 1985-1992, 0.32 for 1992-1994 and 0.70 for 1994-1996. As there were no significant differences, the results reported for recorded incidence are from models in which the interaction involved age as a continuous variable. In all analyses, the final models provided good fits to the data -- the smallest P value for goodness-of-fit (for incidence in the period 1992-1994) was 0.09. Prostate-specific antigen testing Medicare began identifying PSA tests, together with prostatic acid phosphatase (PAP) tests, as a separate item during November 1993. Fewer than 1% of these tests would be PAP tests (Dr Glen Edwards, Chemical Pathologist, Western Diagnostic Pathology, personal communication). We plotted the number of tests reimbursed by Medicare each month from December 1993 to December 1996. To investigate the trends in the numbers of tests, we fitted a curve through the data. Results Incidence From 1985 until 1992, the age-adjusted recorded incidence increased steadily from 42 to 61 per 100 000 person-years (Figure 1). In the next two years it more than doubled to 134 per 100 000 person-years, but then fell almost as sharply to 87 in 1996. The risk of prostate cancer before age 75 years was one in 23 in 1985, one in six in 1994 and one in nine in 1996. Age: In men aged over 50 years, the recorded incidence of prostate cancer increased annually by 5% (95% confidence interval [CI], 3%-6%) between 1985 and 1992 (trend, P < 0.001). The largest relative increases in recorded incidence between 1985 and 1992 occurred in the youngest men (Table 1; interaction between year and age, P < 0.001). The largest relative increases between 1992 and 1994 were also seen in the younger age groups (interaction between year and age, P < 0.001), and from 1994 to 1996 the decline was greatest in the oldest men (interaction between year and age, P < 0.001). As a result of the different relative changes in different age groups, the differences in age-specific rates in 1996 were smaller than in earlier years. In 1985, the recorded incidence for men in the oldest age groups was close to 1000 times higher than for men aged 50-54 years, but by 1996 the relative difference was about 100-fold. We also examined the absolute changes in recorded incidence between 1992 and 1996 (Table 2). Between 1992 and 1994, the largest absolute increases were in men aged 65-79 years. Between 1994 and 1996, the largest absolute decreases were in men aged 70 years or older, so that between 1992 and 1996 the overall increases were greatest in men aged 60-69 years. The overall changes in men aged 55-59 years and 70-74 years were similar. The mean age at diagnosis was 73 years in 1985, 74 years from 1986 until 1990, 73 years in 1991 and 1992, 72 years in 1993, 70 years in 1994 and 69 years thereafter. Place of residence: We examined age-standardised recorded incidence for prostate cancer separately for the Perth metropolitan region and the rest of Western Australia. Before 1992, the two rates were similar in all years. During the sudden rise and fall, these incidences were, respectively, 1992: 65 per 100 000 person-years (Perth), 51 per 100 000 person-years (non-metropolitan areas); 1993: 141 per 100 000 person-years, 107 per 100 000 person-years; 1994: 141 per 100 000 person-years, 110 per 100 000 person-years; 1996: 87 per 100 000 person-years, 84 per 100 000 person-years. Socioeconomic status: We mapped 94% of lung cancer and prostate cancer cases in the Perth metropolitan area to a 1991 census collection district, with no apparent trend over time in the proportion mapped. Before 1993, the numbers of prostate cancer cases in the four SES groups were similar (Figure 2). However, the increase in cases in 1993 and 1994 was greatest in areas of highest SES, and the largest declines in numbers of cases from 1994 to 1996 were also in these areas. Over the same period, there was no consistent change in the distribution of lung cancer cases by SES (Figure 2). Mortality rate The age-adjusted mortality rate from 1985 to 1996 showed no sudden increases or decreases (Figure 1). In men aged 60 years or older, the estimated annual increase from 1985 to 1996 was 2.9% (95% CI, 2%-4%; trend, P < 0.001). Adding quadratic (P = 0.78) or cubic (P = 0.92) terms for year did not improve the fit of the Poisson model. Furthermore, models using year as a continuous or a categorical variable fitted equally well (P = 0.14), indicating that year-to-year variations in the trend of the age-adjusted rates could be a result of chance alone. The increase differed across age groups (interaction between age as a categorical variable and year of death, P = 0.03), but the trends by age were inconsistent (Table 1; interaction between age as a continuous variable and year of death, P = 0.96). Prostate-specific antigen testing On average, there were 5337 tests reimbursed each month in Western Australia. The numbers of tests initially increased before falling, although there was substantial monthly variation (Figure 3). A cubic curve fitted the data well (R2 = 0.46) and provided a better fit than a quadratic curve (P < 0.001) or a linear model (P < 0.001). The fitted maximum monthly number of tests occurred in May 1995. Spearman's rank correlation between the monthly number of PSA tests and new cases of prostate cancer was 0.48 (P < 0.01). Discussion After increasing steadily during the 1980s, the age-adjusted recorded incidence of prostate cancer more than doubled between 1992 and 1994. By 1996, it had fallen to a level about 40% higher than that in 1992. In contrast, the mortality rate increased by about 3% per year, with no sudden increases or decreases. The youngest age groups showed the largest relative increases in recorded incidence up to 1994, and the oldest age groups showed the greatest decrease after 1994, causing a substantial compression of the range of age-specific recorded incidence in Western Australia. When the rates rose steeply in 1992, the absolute increases were greatest in men aged 65-79 years. However, men aged 70 years or older had the greatest absolute falls from 1994, so that, between 1992 and 1996, the largest absolute increases were in men aged 60-69 years. The increase appeared first in Perth and the peak was higher in Perth. However, by 1996, Perth and the rest of Western Australia had similar recorded incidences of prostate cancer. Within Perth, the changes were greatest in areas of high SES. Most observers have attributed the increases in recorded incidence of prostate cancer during the 1980s to improved case detection, particularly following transurethral resection of the prostate for benign prostatic hypertrophy.1,13 The sudden rise in incidence figures in about 1993 was observed in all Australian States.1 In the United States, similar dramatic increases were observed first in 1989.3 These increases are almost certainly the result of the introduction of screening by PSA testing.1,3 In Western Australia, free PSA testing during Prostate Awareness Week would have contributed to the increase. Each October from 1993, about 1100 men attended Prostate Awareness Week in Perth for PSA tests (Mr M D'Antuono, Biostatistician, Urological Research Centre, University of Western Australia, personal communication). These tests do not appear in the Medicare figures, although the peaks in Medicare-funded PSA tests in November 1994 and November 1995 might be the result of publicity surrounding Prostate Awareness Week. However, substantially fewer tests were performed at the screening venues than were reimbursed by Medicare each month in Western Australia. Thus, Prostate Awareness Week is unlikely to have greatly increased the recorded incidence in Western Australia. Rapid declines in recorded incidence, such as we found in Western Australia since 1994, have also been reported in some US States.4,6,7,14 Part of the Western Australian decrease is probably the result of reduced screening activity. The most likely explanation for the decrease in Medicare reimbursements that started in 1995 is a reduction in PSA testing for screening. In fact, the reduction in screening tests is probably greater than Figure 3 suggests, because PSA testing is also used for surveillance of men with prostate cancer. Therefore, its overall use will decline less rapidly than its use for screening. Widespread publicity in the media about the controversy surrounding screening for prostate cancer may have contributed to this decline, and the greater declines seen in the oldest men may be because of concerns that screening is unlikely to benefit those with a short expectation of life.15 Recorded incidence is expected to decrease even if screening activity remains constant. After the introduction of screening, recorded incidence increases because the time of diagnosis is advanced and some cases may be diagnosed that would not have become symptomatic. When all prevalent cases are detected, incidence figures will fall until new cancers develop, whereupon they will rise again. If screening detects only those cancers that would eventually have been diagnosed anyway, the recorded incidence will stabilise at its pre-screening level. Otherwise, it will stabilise at a higher level.16 Before 1980, the mortality rate from prostate cancer in Australia was stable for some time.17 Since then it has increased, but more slowly than recorded incidence, indicating that short-term survival, at least, has improved over time. Increasing diagnosis of disease with low potential for metastasis is one explanation for the discrepancy. What changes in mortality rate can we expect? Gann has argued that if screening is effective and covers enough of the population, the mortality rate should eventually decrease.16 It is too early for any effect of screening on mortality rate to be seen, and by the end of 1996 there had been no new trend in the mortality rate in Western Australia. Because of the effect of lead time (the time by which screening advances diagnosis), changes may not occur for some years. We have witnessed extraordinary changes in the recorded incidence of prostate cancer in Western Australia, and we have strong evidence that these changes are the result of medical practice rather than intrinsic changes in the incidence. Surveillance of incidence and mortality rates may help answer the question of whether screening has benefit, although more rigorous scientific evaluations are also needed. References McCredie M. A rising incidence of prostate cancer in Australia: effect of "screening" or more disease? Cancer Forum 1995; 19: 7-12. McCaul KA, Luke CG, Roder DM. Trends in prostate cancer incidence and mortality rates in South Australia, 1977-1993. Med J Aust 1995; 162: 520-522. Lu-Yao GL, Greenberg ER. Changes in prostate cancer incidence and treatment in USA. Lancet 1994; 343: 251-254. Gilliland FD, Welsh DJ, Hoffman RM, Key CR. Rapid rise and subsequent decline in prostate cancer incidence rates for New Mexico, 1989-1993. Cancer Epidemiol Biomarkers Prev 1995; 4: 797-800. Merrill RM, Brawley OW. Prostate cancer incidence and mortality rates among white and black men. Epidemiology 1997; 8: 126-131. Polednak AP. Trends in prostate carcinoma incidence in Connecticut (1988-1994) by age and race. Cancer 1997; 79: 99-103. Newcomer LM, Stanford JL, Blumenstein BA, Brawer MK. Temporal trends in rates of prostate cancer: declining incidence of advanced stage disease, 1974 to 1994. J Urol 1997; 158: 1427-1430. Australian Bureau of Statistics. Estimated Resident Population by age and sex in statistical local areas, Western Australia. Canberra: AGPS, 1996. (Catalogue No. 3203.5.) Parkin DM, Muir CS, Whelan SL, et al, editors. Cancer incidence in five continents. Vol VI. IARC Scientific Publications No. 120. Lyon: International Agency for Research on Cancer, 1992. Australian Bureau of Statistics. Information Paper: 1991 Census socioeconomic indicators for areas. Canberra: AGPS, 1993. (Catalogue No. 2912.0.) MapInfo [computer program]. Version 3. New York: MapInfo Corporation, 1995. EGRET [computer program]. Version 1.02. Seattle: Statistics and Epidemiology Research Corporation, 1995. Potosky AL, Kessler L, Gridley G, et al. Rise in prostatic cancer incidence associated with increased use of transurethral resection. J Natl Cancer Inst 1990; 82: 1624-1628. Stephenson RA, Smart CR, Mineau GP, et al. The fall in incidence of prostate carcinoma. On the down side of a prostate specific antigen induced peak in incidence -- data from the Utah Cancer Registry. Cancer 1996; 77: 1342-1348. Chodak GW, Thisted RA, Gerber GS, et al. Results of conservative management of clinically localized prostate cancer. N Engl J Med 1994; 330: 242-248. Gann PH. Interpreting recent trends in prostate cancer incidence and mortality. Epidemiology 1997; 8: 117-120. Holman CD, James IR, Segal MR, Armstrong BK. Recent trends in mortality from prostate cancer in male populations of Australia and England and Wales. Br J Cancer 1981; 44: 340-348.(Received 30 Sep 1997, accepted 31 Mar 1998) Addendum Since this article was submitted in September 1997, data on the recorded incidence and mortality rate of prostate cancer in the first eight months of 1997 have become available. The age-adjusted recorded incidence of prostate cancer was 64 per 100000 person-years, while the mortality rate was 16 per 100000 person-years. Thus, the recorded incidence was almost the same as in 1992, before the rapid rise and fall. In 1997, men aged 50-69 years had higher recorded incidences of prostate cancer than in 1992, but older men had lower recorded incidences. Authors' details Health Department of Western Australia, East Perth, WA. Timothy J Threlfall, MB BS, MPH, Senior Medical Officer, Western Australian Cancer Registry; Ian L Rouse, PhD, General Manager, Health Information Centre. Department of Public Health, University of Western Australia, Nedlands, WA. Dallas R English, PhD, Senior Lecturer. Reprints: Dr D R English, Department of Public Health, University of Western Australia, Nedlands, WA 6907. E-mail: dallasATdph.uwa.edu.au Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>
Timothy J Threlfall · Dallas R English · Ian L Rouse
Self-reported prevalence of prostate-specific antigen testing in South Australia: a community study
Self-reported prevalence of prostate-specific antigen testing in South Australia: a community study Carole B Pinnock, David P Weller and Villis R Marshall MJA 1998; 169: 25-28 For editorial comment, see McCredie & Cox Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objective: To determine the prevalence and other characteristics of self-reported blood testing (prostate-specific antigen [PSA]) for prostate cancer in the community. Design: Interview-based prevalence study. Participants and setting: 695 men aged 40 years and over in the Spring 1996 South Australian Health Omnibus survey of a probability sample of 3011 households, weighted to reflect the age and sex distribution of the South Australian population. Outcome measures: Number of men who had a PSA test in the preceding 12 months; number of first tests; the person initiating and performing the test; knowledge of the next step if test result abnormal; number of men visiting doctor for lower urinary tract symptoms in the preceding 12 months. Results: 20.3% of participants reported having a PSA test in the preceding 12 months; 62.1% were first tests. Prevalence of testing was highest in the age group 70-79 years (35.8%). Most tests were initiated by the general practitioner (41.2%) and by patients (35.7%). Of those tested, 45.3% had inadequate knowledge of the next step. Visiting a doctor for urinary symptoms was significantly associated with PSA testing (P < 0.001): 47.7% of men who visited a doctor for urinary symptoms had been tested compared with only 17.4% of those who did not visit the doctor for this problem. Only age and visiting a doctor for urinary symptoms were significant independent predictors of having a PSA test. Conclusions: Investigation of lower urinary tract symptoms contributed substantially to PSA testing, and those tested did not adequately understand the consequences. Our findings suggest a need for a better framework for PSA testing in general practice, including all important elements of decision-making, such as evidence and patient preference, as well as the means to ensure adequate patient counselling before testing. Introduction Screening for prostate cancer remains a topic of widespread debate. Recent systematic reviews have concluded that there is currently insufficient evidence to establish an overall benefit of prostate cancer screening, and major health agencies have issued conflicting recommendations.1-3 Randomised controlled trials examining this question have begun in the United States and Europe,4,5 but results will not be available for some years. Nevertheless, prostate-specific antigen (PSA) testing of asymptomatic men is thought to be common in Australia,6,7 and the recent doubling in recorded incidence of prostate cancer in this country8,9 has been attributed to PSA testing. Little is known about the circumstances of such testing -- whether it occurs in general practice or other specialties, whether men are truly asymptomatic, whether the test is initiated by the patient or the doctor, and how much information about the test is provided to the patient. Most authors agree that men seeking a test should be informed about the risks as well as the benefits of taking the test,10,11 and that individual preferences should be taken into account.12-15 A community survey of self-reported participation in PSA testing confirmed high rates in the community (25% of men 40 years and over with no history of prostate cancer) and an even higher rate of intention to test (53.9%).16 The strongest predictor of past testing was a visit to a doctor for urinary tract symptoms, and the strongest predictor of intention to test was perceived vulnerability to prostate cancer.16 This study was undertaken in 1996 to expand these findings by establishing the prevalence of self-reported prostate cancer testing (PSA testing) over the preceding 12 months, the incidence of PSA testing (first tests), who initiated the test, who performed it, the association with investigation for urinary symptoms, and whether participants had understood the immediate consequences of taking the test. Methods Survey Questions were included in the Spring 1996 South Australian Health Omnibus survey, a multiple-user household interview survey undertaken on behalf of a number of healthcare organisations in South Australia. The sampling method provides a probability sample of the South Australian population.17,18Participants were asked whether they had visited the doctor for troublesome urinary symptoms in the past 12 months (as in a previous survey17), ever been diagnosed with prostate cancer or had a blood test for prostate cancer (PSA test) in the previous 12 months. Those who had been tested were asked who had initiated the test, who performed it and what they understood to be the next step if the test were abnormal. Question alternatives were derived from a previous qualitative study (who initiated test)19 and expert clinical opinion (who performed it, next step). Questions were tested for comprehensibility and acceptability in 50 pilot interviews before the survey. Analysis Data were weighted by household size, age, sex and geographical region to benchmarks derived from the estimated resident population at 30 June 1995 (Australian Bureau of Statistics). Because of the clustered nature of the sample, confidence limits were calculated after allowing for a design effect of 1.1, calculated using the method of Kish,20 which inflates the standard error. We analysed data for men aged 40 years or older who had not had a diagnosis of prostate cancer, using SPSS for Windows.21 Statistical significances were determined by Pearson c2 tests or Fisher's exact test, and logistic regression by the forced entry method (the contribution is evaluated after removal of effects of all other variables). The contribution of demographic and urinary symptom variables was examined in a logistic regression model to identify independent predictors of having a PSA test in the preceding 12 months. Results Sample In unweighted numbers, from the sampling frame of 4081 households, 3011 interviews were conducted, giving a response rate of 73.8%. The reasons for not participating were refusal (548), no contact could be established (301), selected respondent away for duration of study (108), illness/mental incapacity (65) and respondent unable to speak English (48). Of the 3011 people interviewed, 695 were men 40 years or older and 642 of these had not had a diagnosis of prostate cancer. The average age of these 642 men was 58.3 years (SE, 0.50 years; range, 40-91 years). After weighting, 6.0% (95% confidence interval [CI], 4.45%-7.86%) of men aged 40 years or more reported being diagnosed with prostate cancer. The weighted sample size of men aged 40 years and over with no reported diagnosis of prostate cancer was 716. PSA testing and demographic factors Overall, 20.3% of men older than 40 years reported having a blood test for prostate cancer (PSA test) in the preceding 12 months (Table 1). This varied with age (chi-squared = 48.1; df = 4; P < 0.001), with the highest proportion (35.8%) being in the age group 70-79 years. Nearly two-thirds of tests (62.1%) were first tests, and this proportion was high across all age groups. Men were slightly more likely to be tested if they lived in metropolitan (20.8%; 95% CI, 17.5%-24.1%) than in rural (19.0%; 95% CI, 15.8%-22.1%) areas, but the difference was not significant. Educational attainment was not associated with testing. Lifetime occupation also showed no clear trends (eg, drivers and plant operators had similar rates to managers and administrators), nor did marital status and country of birth. Lower urinary tract symptoms Of 715 men aged 40 years and over who had not had a diagnosis of prostate cancer, 65 (9.1%) had visited a doctor for troublesome lower urinary tract symptoms (LUTS) in the preceding 12 months (46 visited their general practitioner). Of these 65 men, 31 (47.7%) had had a PSA test, compared with only 113/650 (17.4%) of those who did not visit the doctor for such a problem (P < 0.001, Fisher's exact test). A first visit to a doctor for LUTS was significantly associated with a first PSA test (P = 0.018, Fisher's exact test): 15/17 (88.2%) men who had a first visit for LUTS in the previous 12 months also had a first test in that time, compared with only 6/14 (42.9%) men for whom it was not the first visit. Who initiates and performs the test Most testing (70.6%) was performed in general practice, and most tests were initiated by the general practitioner (Table 2). However, patients initiated 35.7% of tests. Tests performed by "other doctor" may reflect those done by pathology services, but could also have been included in other types of medical assessments. Doctors initiated 25 (80.6%) of the tests on the 31 men who visited for LUTS and were tested, but initiated only 51 (45.1%) of the tests on the 113 who were tested but had not visited a doctor for LUTS (chi-squared = 12.3; df = 1; P < 0.001). Knowledge of the "next step" There was wide variability in understanding of the next step if the test were abnormal. The most frequent response was "do not know" (34.0%). Other responses were "operation on the prostate" (10.7%), "no further action" (0.6%), "referral to a specialist" (27.2%), "repeat the test" (6.3%), "biopsy of the prostate" (4.8%) and "other" (16.7%). The first three (do not know, operation on the prostate, no further action), totalling 45.3%, may be considered to reflect poor understanding. Independent predictors of testing The logistic regression model (chi-squared = 89.8; df = 22; P < 0.001) included age, rural/metropolitan residence, country of birth, educational attainment, marital status, lifetime occupation, and doctor visit for LUTS in the past 12 months. Of these, only age and visit to a doctor for LUTS were significant independent predictors of having had a PSA test in the past 12 months (Table 3). Discussion We found a high level of self-reported PSA testing among men in South Australia. Testing was associated with lower urinary tract symptoms and was initiated by the patient or his GP. Nearly half the respondents had an inadequate knowledge of the appropriate next step if the test result were abnormal. Our study was a community-based survey of self-reported testing. Such studies suffer from limitations in that individual recall of past events and comprehension of the research questions may vary. Nevertheless, representative community sampling makes it possible to derive estimates of incidence and prevalence, a benefit over general practice-based studies. The level of self-reported rates of PSA testing observed in this study is higher than that reported in New South Wales across all age groups.7 This may result from a real difference between South Australia and New South Wales or from differences in survey method. The sampling method differed between the two studies (probability sample weighted to reflect age and sex structure of South Australian population versus random telephone number selection from Sydney metropolitan white pages). Older men were under-represented in the New South Wales study compared with 1991 Census data. The interview method (face to face in South Australia versus telephone in New South Wales) may also have contributed to the differences. In our study, the number of men tested increased with age and peaked in the age group 70-79 years, with nearly half the tests in this age group being first tests. The choice to begin PSA testing at this age is of concern, as those least likely to benefit are men who can anticipate less than a decade of life.1 We found no association between PSA testing and socioeconomic factors such as education and occupation, although in the United States participation in prostate cancer screening is reported to be sensitive to socioeconomic factors.22,23 However, our result is consistent with other Australian data.7,16 It is also consistent with the view that testing is initiated more by doctors than patients in this community. There was only a small difference between rural and metropolitan testing rates, which suggests that access to services does not influence the number of men seeking or being offered testing. The role of LUTS in prompting testing for prostate cancer has been reported previously,7 and is important because of the high prevalence of such symptoms in the community. In a recent South Australian survey, 26.4% of men over 18 years reported experiencing troublesome urinary symptoms in the past 12 months, and 10.2% had visited a doctor for this reason. A similar number (8.6%) were substantially dissatisfied with their urinary function.17 The relative proportions of men and their doctor initiating prostate cancer testing have not been reported previously. We found that, in the absence of urinary symptoms, this is roughly equal. However, among those men who had visited a doctor for LUTS, 80% of tests were doctor-initiated. This strong association between doctor as test initiator and LUTS suggests that, while testing may be for case-finding or screening purposes in asymptomatic men, its use may be investigational for those with LUTS. We cannot know, from these and other data,7 whether other indicators for investigational PSA testing (such as abnormal or suspicious digital rectal examination, family history of prostate cancer, or complicated LUTS) were present, and therefore whether testing was appropriate in these cases. The current clinical guidelines for uncomplicated LUTS do not recommend testing for prostate cancer.24 The American College of Physicians maintains that, as no association between LUTS and prostate cancer has been demonstrated, testing in men both with and without LUTS consistent with benign prostatic enlargement constitutes screening.10 Current guidelines focus on when not to use the PSA test, but not when it is appropriate.24 There is no framework for doctors and patients which includes all the important elements of decision-making in this area, including evidence, patient preference and medicolegal issues. PSA testing in general practice is driven in part by concern of patients and in part for investigational purposes. In addition, there is anecdotal evidence that general practitioners are concerned that if a PSA test is not offered, and prostate cancer is later diagnosed, they may be seen as negligent. Clinical guidelines or other measures promoting the appropriate use of the PSA test in general practice need to give consideration to all of these factors. Undoubtedly, providing information about testing for prostate cancer is more complex than for breast cancer or cervical cancer screening. The finding that a large proportion of men tested did not understand the immediate consequences of testing is thus not surprising, but of concern. We cannot tell from these data whether information was not given, not understood, or not recalled. Nevertheless, it is reasonable to assume that if this very basic information is not understood effectively, then more complex information (such as the likelihood of a false positive result, side effects of a biopsy, effectiveness of treatment for early-stage prostate cancer, and the risks of impotence and incontinence resulting from radical surgery for localised cancer) would also not have been understood. Yet this has been suggested as basic information needed by a patient to understand the implications of a PSA test.11,14,15 We therefore see a need for closer examination of the exchange and uptake of information in consultations that result in a PSA test, and the provision of resources for GPs which aid effective counselling. Such resources may need to include longer consultations. Acknowledgements The study was funded through a collaboration of Repatriation General Hospital, Daw Park, the Anti-Cancer Foundation of Australia, and the Department of Evidence Based Care and General Practice, Flinders University of South Australia, under the auspices of the Collaborative Centre for Prostate Health. References Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. National Health Service. Screening for prostate cancer: effectiveness matters. York, UK: NHS Centre for Reviews and Dissemination, 1997. Mettlin C, Jones G, Avarette H, et al. Defining and updating the American Cancer Society guidelines for cancer-related checkup: prostate and endometrial cancers. CA Cancer J Clin 1993; 43: 42-46. Denis L, Middelheim A. To screen or not to screen? Prostate 1992; Suppl 4: 63-70. Gohagan J, Prorok P, Kramer B, et al. The prostate, lung, colorectal and ovarian screening trial of the National Cancer Institute. Cancer 1995; 75: 1869-1873. Parkes A, Killer G. Prostate-specific antigen -- is it already being used as a screening test? [letter]. Med J Aust 1994; 161: 722-733. Ward JE, Hughes A-M, Hirst GHL, Winchester L. Men's estimates of prostate cancer risk and self-reported rates of screening. Med J Aust 1997; 167: 250-253. McCredie M. A rising incidence of prostate cancer in Australia: effect of "screening" or more disease? Cancer Forum 1995; 19: 7-12. McCaul K, Luke C, Roder D. Trends in prostate cancer incidence and mortality rates in South Australia. Med J Aust 1995; 162: 520-522. American College of Physicians. Screening for prostate cancer. Clinical Guideline: Part III. Ann Intern Med 1997; 126: 480-484. Hirst GH, Ward JE, Del Mar C. Screening for prostate cancer: the case against. Med J Aust 1996; 164: 285-288. Hahn DL, Roberts RG. PSA screening for asymptomatic prostate cancer: truth in advertising. J Fam Pract 1993; 37: 432-436. Woolf SH. Should we screen for prostate cancer? Men over 50 have a right to decide for themselves [editorial]. BMJ 1997; 314: 989-990. Flood AB, Wennberg JE, Nease RF Jr, et al. The importance of patient preference in the decision to screen for prostate cancer. Prostate Patient Outcomes Research Team. J Gen Intern Med 1996; 11: 2342-2349. Wolf AM, Nasser JF, Wolf AM, Schorling JB. The impact of informed consent on patient interest in prostate-specific antigen screening. Arch Intern Med 1996; 156: 1333-1336. Weller D, Pinnock C, Silagy C, et al. Prostate cancer testing in South Australian men: influence of sociodemographic factors, health beliefs and lower urinary tract symptoms. Aust N Z J Public Health 1998; 22: 400-402. Pinnock C, Marshall V. Troublesome lower urinary tract symptoms in the community: a prevalence study. Med J Aust 1997; 167: 72-75. Wilson D, Wakefield M, Taylor A. The South Australian Health Omnibus Survey. Health Prom J Aust 1992; 2: 47-49. Pinnock C, O'Brien B, Marshall V. Older men's concerns about their urological health: a qualitative study. Aust N Z J Public Health 1998; 22: 368-373. Kish L. Estimates of unit variance: design effect. In: Survey sampling. New York: John Wiley and Sons, 1965; 257-263. SPSS for Windows [computer program]. Version 7.5. Chicago, Ill: SPSS Inc, 1996. Robinson SB, Ashley M, Haynes MA. Attitudes of African Americans regarding screening for prostate cancer. J Natl Med Assoc 1996; 88: 241-246. Diefenbach PN, Ganz PA, Pawlow AJ, Guthrie D. Screening by the prostate-specific antigen test: what do the patients know? J Cancer Educ 1996; 11: 39-44. National Health and Medical Research Council. Clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: Commonwealth of Australia, 1997. (Received 7 Nov 1997, accepted 7 May 1998) Authors' details Division of Surgery, Repatriation General Hospital, Daw Park, SA. Carole B Pinnock, PhD, Principal Research Scientist. Flinders University of South Australia, SA. David P Weller, FRACGP, FAFPHM, Senior Lecturer, Department of Evidence Based Care and General Practice; Villis R Marshall, MD, FRACS, Professor of Surgery, Department of Surgery, Flinders Medical Centre, and Head, Division of Surgery, Repatriation General Hospital, Daw Park, SA. Reprints will not be available from the authors. Correspondence: Dr C R Pinnock, Division of Surgery, Repatriation General Hospital, Daws Rd, Daw Park, SA 5041. E-mail: spinncbATrgh.edu.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>
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