Men's health

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 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 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/>

Carole B Pinnock · David P Weller · Villis R Marshall

Abstract Objective: To determine the health-related quality of life (HRQOL) of Australian men after radical prostatectomy. Design: Cross-sectional study. Setting: Private and public practices of three urologists in south-east Queensland, July 1989 to June 1995. Participants: 140 men with no evidence of disease recurrence 1 to 6 years after radical prostatectomy. Main outcome measures: Voiding and erectile potency and HRQOL. Recall of preoperative status and status at survey were established by an independently administered multi-item questionnaire. Results: 112 men (80%) completed the study questionnaire. Difficulty with bladder control before the operation was reported by 25 (22%; 95% confidence interval [CI], 15%-31.2%), and the incontinence rate after treatment was 22/112 (20%; 95% CI, 12.7%-28.2%). Men with incontinence after operation were more likely to recall preoperative urinary symptoms. Eighty-four (75%) men were happy or coping with their sexual function after radical prostatectomy despite an erectile potency rate of only 12% (95% CI, 7%-20%). Twenty-eight (25%) had tried penile injections and three have had penile prostheses since their operation. Impotence was reported more frequently (40%) as the treatment-related problem most affecting life, followed by "concern about cancer" (12%) and incontinence (8%). Impotence was also the most common cause given for diminished HRQOL. Conclusions: Loss of sexual function after radical prostatectomy is more commonly perceived as a major problem and is more likely than urinary incontinence to adversely affect HRQOL. Loss of sexual function and its effect on HRQOL needs to be given greater emphasis in counselling before radical prostatectomy. MJA 1998; 168: 483-486 Introduction Prostate cancer is the second most common cause of cancer-related death in Australian men, and in 1989 became the most common cancer in men in New South Wales.1 This increase may be partly attributed to a more health-conscious, ageing population, as well as greater use of "routine" digital rectal examination (DRE) and prostate-specific antigen (PSA) tests.2 PSA tests, together with DRE and transrectal ultrasound-guided prostatic biopsies, have enabled the diagnosis of potentially curable early-stage prostate cancer.3 In particular, increased efforts have been made to identify early-stage prostate cancer in men under 70 years of age, even though a significant survival advantage has yet to be demonstrated. Screening and case detection remain controversial. There is argument about whether the tests are sufficiently sensitive and specific for effective screening, and whether screening affects outcomes enough to be cost effective.4,5Opinions also differ regarding the optimal management of localised prostate cancer.6 In men over 70 years of age, or in those with appreciable co-morbidity, a conservative approach is generally accepted. Healthy younger men are more likely to live long enough to experience progression of their disease, so radical prostatectomy and radiotherapy, as well as "watchful waiting", are options in this group. Judging by current published studies, these options may provide similar outcomes in selected patients: up to 10 years after diagnosis, similar survival rates are seen in patients treated immediately with surgery or radiotherapy, and in patients initially watched and then treated with androgen ablation, transurethral resection or radiotherapy if the disease progresses.7 This has created a significant dilemma for both doctor and patient when selecting appropriate treatment.6 The lack of a clearly superior treatment option makes the impact of treatment on health-related quality of life (HRQOL) of greater importance. The difficulty in selecting appropriate treatment is compounded by a lack of Australasian data on the effect of treatment on HRQOL. Radical prostatectomy has been increasingly used in treating patients with localised prostate cancer and is considered an appropriate option for men who have a life expectancy in excess of 15 years.8 Despite improved surgical technique, postoperative impotence and incontinence may still occur, although the reported incidence varies considerably.9 Our study was undertaken to record patients' perception of HRQOL after radical prostatectomy, to assist patients, families and doctors in their discussions about treatment expectations and outcomes. Methods Sample Surgical audit data were collected prospectively on all patients having radical prostatectomy between July 1989 and June 1995. Three of us (P S H, A N J and L C T) performed the operations. We all receive referrals from other specialist urologists, and perform most of the radical prostatectomies in Queensland. We believe that the patients studied are likely to be representative of the Australian population, although there are no data currently available from other States or Territories. We selected for review patients who had no evidence of recurrent or residual disease to avoid any effect treatment failure may have had on HRQOL. No evidence of disease was defined as a PSA level less than 0.1 µg/L and no abnormal signs and symptoms at the last clinic visit. Men operated on less than a year before the survey were excluded as complications may still resolve during this period.9 As complications are likely to remain stable after one year, we believe the cohort to be homogeneous for the purposes of studying the effects of radical prostatectomy on HRQOL. To minimise recall bias, we included only patients operated on less than six years earlier. Non-surgical factors, such as co-morbidity and ageing, were thought to be unlikely modifiers of HRQOL during this period, so that most of the changes seen could be attributed to the prostatectomy. We decided that post-hoc subgroup analysis of a cross-sectional study with small numbers was of limited value so we included patients in the survey regardless of whether nerve sparing (which may affect postoperative potency) was contemplated or performed. Comparisons with non-surgical therapies may be facilitated by this approach. Definitions We defined urinary incontinence as the need to wear incontinence pads regularly, and defined erectile potency as the ability to achieve an erection firm enough for sex more than once a month. Questionnaire As higher complication rates are usually reported in studies in which patients are reviewed independently of their treating physician,10 our questionnaire was administered independently (by R J B). Each patient was telephoned before the questionnaire and a letter of explanation was mailed. They were assured of confidentiality, that the questionnaire was being administered independently of their treating doctor and that their answers would have no impact on management of their condition. Patients who had not replied within one month were sent one reminder. As there is no current internationally validated HRQOL questionnaire for patients with prostate cancer,11 two of us (D L N and R J B) developed the questionnaire. The initial questions collected demographic data; there were 16 items about bladder and sexual function, with similar questions to check for internal consistency; and another five items assessed postoperative therapies (such as penile injections and prostheses) and satisfaction with treatment. As our questionnaire is a new tool, only some sections have been validated.10,12-14 The questionnaire assessed men's perceptions of their urinary, sexual and overall function during the month before receipt of the questionnaire. (This is a recognised method used in other validated scoring systems.15,16) Urinary symptoms and erectile function, at the time of the survey and before surgery, were assessed on a five-point scale and included severity, effect and bothersomeness of symptoms. Satisfaction with treatment and willingness to have the same treatment again were also assessed on a five-point scale. An edited version of the Functional Assessment of Cancer Therapy Scale was used to assess health, social life and satisfaction with life.14 Statistical analysis We calculated exact confidence intervals (CI) and Fisher's exact tests using the STATA statistics package.17 Results Respondents Of 185 men having radical prostatectomy, 140 had no evidence of disease at last review. One of these 140 died in a motor vehicle accident and three more were lost to follow-up. Completed questionnaires were received from 112 (80%) men whose ages at the time of survey were normally distributed around the mean of 64 years (range, 54-73). Urinary incontinence There were 22 (20%; 95% CI, 12.7%-28.2%) respondents with postoperative urinary incontinence (Box). Those with more severe incontinence were more likely to report urge incontinence or mixed stress and urge incontinence. Twenty-five respondents (22%; 95% CI, 15%-31.2%) recalled "trouble with bladder control" before surgery, although none required pads. Seventeen of the 25 (68%; 95% CI, 46.5%-85%) were incontinent after the operation, compared with only 5 of the 87 (6%; 95% CI, 2%-13%) who did not recall having problems before surgery. That is, men with urinary incontinence after radical prostatectomy were much more likely to recall preoperative urinary symptoms. There was no statistically significant association between age and postoperative continence, nor was there any association with level of education or area of residence (Fisher's exact test). Urinary symptoms did not interfere with daily activities in 93 (83%; 95% CI, 75%-85%) respondents, and 89 (79%; 95% CI, 71%-86%) were either very happy or happy with their present bladder function. Erectile potency Of the 112 respondents, 99 (88%; 95% CI, 81%-94%) recalled preoperative erectile potency, but only 14 (12%; 95% CI, 7%-20%) described erectile potency at survey. Although only 14 were potent, 23 (20.5%; 95% CI, 13.5%-29%) were happy and 61 (54.5%; 95% CI, 45%-64%) were coping with their level of sexual function. Since surgery, 28 of the respondents (25%) have tried penile injections and three (2.7%) now have a penile prosthesis. Of the 13 men who were impotent before surgery, two have tried penile injections and one has had a penile prosthesis. There was no statistically significant association between postoperative impotence and age, level of education or place of residence (Fisher's exact test). Health-related quality of life Most respondents enjoyed a high HRQOL -- 104 (93%) were satisfied with their life and with their social life. Nearly all respondents reported good general health. The most common problem affecting their lives was impotence (44 men; 40%), followed by "concern about cancer" (13 men; 12%) and "bladder problems" (9 men; 8%). Despite the high prevalence of impotence, 104 (93%; 95% CI, 80.5%-97%) respondents were satisfied with their treatment and 98 (88%; 95% CI, 80%-93%) would opt for the same treatment again. Impotence was the most common reason given for treatment dissatisfaction (7/8) and reluctance to have the same treatment again (8/14). A final section asked about "any other problems related to your surgery which affects your quality of life". One man had a problem with a lack of pad-disposal facilities in golf club toilets, and one, although potent, said that loss of ejaculation left him unsatisfied. Discussion Our questionnaire was designed to examine specific problems of incontinence, impotence and patients' perception and satisfaction with treatment and feeling of well-being after radical prostatectomy. We found impotence to be the most common cause of diminished HRQOL, followed by "concern about cancer" and then incontinence. The preoperative urinary difficulty and impotence rates in our study are similar to those in other published prospective series,18,19 and our postoperative results lie within the range of the results of other published studies,10 suggesting that our questionnaire and study design are valid. Differences between our results and those of others may be explained by our case selection and independent data collection. In Australia, initial presentation of men with prostate problems during the study period was usually prompted by lower urinary tract symptoms. Men with troublesome urinary symptoms are more likely to have detrusor instability, a factor that commonly predisposes them to incontinence after radical prostatectomy.20 Our respondents reported a 20% incontinence rate and 22% recalled preoperative urinary difficulties. In contrast, Steiner et al reported an 8% incontinence rate after radical prostatectomy,21 but the more widespread screening for prostate cancer in the United States2-5 makes it likely that their patients were referred after screening and may not have had incontinence problems. The methods by which data are collected may also affect reporting of incontinence. Other studies that also used independent data collection15,22 have reported higher rates of incontinence (31% and 47%, respectively). We found that men with postoperative incontinence were much more likely to recall preoperative symptoms. However, we advise caution in interpreting this apparent strong association because of the limitations of cross-sectional studies (such as only measuring subjects' status once and not taking account of variation in patients' condition, including only those with successful treatments, and not yielding true relative risks) and the potential effects of recall bias. Patients with incontinence after surgery may have thought more about their predicament and been more likely to recall preoperative urinary symptoms; and, conversely, those continent after the operation may have had urinary symptoms before the operation but did not recall being troubled by them. Nevertheless, specific enquiry regarding urinary symptoms is advised when discussing treatment options with patients with localised prostate cancer, and those with urinary symptoms need to be informed of the association with urinary incontinence after radical prostatectomy. Lack of preoperative symptoms, however, does not guarantee postoperative continence as 6% of this group were incontinent after the operation. The preoperative impotence rate in our patient group is similar to that reported by Jonler et al. Men in their study were of similar age, and data were collected prospectively in a community setting.19 After the operation 12% of our respondents were potent, which is similar to the rates Jonler et al22 and Fowler et al10 reported (16% and 11%, respectively), but lower than the 70% found by Quinlan et al.23 Recall bias, case selection and independent data collection, as discussed for incontinence, are also plausible explanations for these differences. Impotence was much more likely to be reported as a major quality-of-life problem than incontinence, which is consistent with other series.12,24 Loss of potency as a cause of diminished HRQOL is not specific to radical prostatectomy, as Jonler et al concluded in their study of 1680 men attending a cancer screening program "impotent men have a lower QOL than potent men".19 Many men are prepared to trade off survival for sexual potency,25 so some men may choose a treatment with possibly lower long-term survival to increase their chance of remaining potent. The impact of radical prostatectomy and other treatments on potency should be discussed in detail when counselling patients with localised prostate cancer before therapy. However, erectile potency and a happy sex life do not go hand-in-hand, as 75% of respondents were happy or coping with their sexual function but only 12% claimed postoperative potency. This may be because people who have made a treatment decision are likely to believe, and want others to believe, that they have made the right choice,24 especially if they are disease free, as this group were. References Coates M, McCredie M, Armstrong BK. Cancer in New South Wales. Incidence and mortality, 1993. Sydney: NSW Cancer Council; 1996. McCredie M, Coates M, Churches T, Rogers J. The rising incidence of prostate cancer in Australia -- a result of "screening"? J Epidemiol Biostat 1996; 1: 99-105. McCaul KA, Luke CG, Roger DM. Trends in prostate cancer incidence and mortality rates in South Australia, 1977-1993. Med J Aust 1995; 162: 520-522. Hirst GHL, Ward JE, Del Mar CB. Screening for prostate cancer: the case against. Med J Aust 1996; 164: 285-288. Kaye KW. Prostate cancer: enthusiasm for screening. Med J Aust 1995; 162: 540-541. Whitmore WF Jr. Management of clinically localized prostatic cancer -- an unresolved problem [editorial]. JAMA 1993; 269: 2676-2677. 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. Freedman G, Hanlon M, Lee W, Hanks G. Young patients with prostate cancer have an outcome justifying their treatment with external beam radiation. Int J Radiat Oncol Biol Phys 1996; 35: 243-250. Madsen F, Bruskewitz R. Functional results of radical prostatectomy. Curr Opin Urol 1995; 5: 246-248. Fowler JF Jr, Barry MJ, Lu-Yao G, et al. Patient-reported complications and follow-up treatment after radical prostatectomy. The National Medicare Experience: 1988-1990 (updated June 1993). Urology 1993; 42: 622-629. Borghede G, Karlsson J, Sullivan M. Quality of life in patients with prostate cancer: results from a Swedish population study. J Urol 1997; 158: 1477-1486. Brickman AL, Soloway MS. Quality of life 12 months after radical prostatectomy. Br J Urol 1995; 75: 48-53. Herr HW. Quality of life of incontinent men after radical prostatectomy. J Urol 1994; 151: 652-654. Cella DF, Tulsky DS, Gray G, et al. The Functional Assessment of Cancer Therapy Scale: development and validation of the general measure. J Clin Oncol 1993; 11: 570-589. O'Leary MP, Barry MJ, Fowler FJ Jr. Hard measures of subjective outcomes: validating symptom indexes in urology. J Urol 1992; 148: 1546-1548. Barry MJ, Fowler FJ Jr, O'Leary MP, et al. Correlation of the American Urological Association symptom index with self-administered versions of the Madsen-Iversen, Boyarsky and Maine medical assessment program symptom indexes. J Urol 1992; 148: 1558-1563. STATA statistics package [computer program]. Version 5.0. Texas: Stata Corp; 1996. Diokno A, Brock BM, Brown M, Herzog A. Prevalence of urinary incontinence and other urological symptoms in the non-institutionalised elderly. J Urol 1986; 136: 1022-1025. Jonler M, Moon T, Brannan W, et al. The effect of age, ethnicity and geographical location on impotence and quality of life. Br J Urol 1995; 75: 651-655. Goluboff E, Chang D, Olsson C, Kaplan S. Urodynamics and the etiology of post prostatectomy urinary incontinence: the initial Colombia experience. J Urol 1995; 153: 1034-1037. Steiner MS, Morton RA, Walsh PC. Impact of radical prostatectomy on urinary continence. J Urol 1991; 145; 512-515. Jonler M, Messing EM, Rhodes RR, Bruskewitz RC. Sequelae of radical prostatectomy. Br J Urol 1994; 74: 352-358. 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. Litwin MS, Hays RD, Fink A, et al. Quality of life outcomes in men treated for localized prostate cancer. JAMA 1995; 273: 129-135. Singer PA, Tasch E, Stocking C, et al. Sex or survival: trade-offs between quality and quantity of life. J Clin Oncol 1991; 9: 328-334. (Received 7 Apr 1997, accepted 24 Feb 1998) Authors' details Princess Alexandra Hospital, Brisbane, QLD. Peter S Heathcote, FRACS, Urologist; Peter N Mactaggart, FRACS, Urologist; Robyn J Boston, MB BS, Urology Registrar; Leslie C Thompson, FRACS, Urologist; David L Nicol, FRACS, Urologist. Royal Brisbane Hospital, Brisbane, QLD. Anthony N James, FRACS, Urologist. Reprints will not be available from the authors. Correspondence: Dr D L Nicol, Department of Urology, Princess Alexandra Hospital, Ipswich Road, Brisbane, QLD 4102. E-mail: D. NicolATmailbox.uq.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 ".

Peter S Heathcote · Peter N Mactaggart · Robyn J Boston · Anthony N James · Leslie C Thompson · David L Nicol

Rugby and spinal injury: what can be done? We cannot be complacent -- we must continue an expanding injury database MJA 1998; 168: 372-373 In the early 1980s, staff in Australian hospital spinal units became aware of a serious increase in the incidence of young football players in both codes of rugby -- union and league -- admitted with serious or permanent cervical spinal cord injury. By 1983 the two spinal units in Sydney were admitting 10 or more young players in a season.1 By 1984, I had introduced the Spinal Awareness and Prevention Program at the Royal North Shore Hospital, Sydney, for audiovisual presentation to schoolchildren in independent and public schools in New South Wales. Lecturers in this program, themselves disabled from spinal cord injury, highlighted how spinal cord injury could occur. By 1987, documentation from injured players had been presented in a report to the International Rugby Board, and changes to the scrum formation had been recommended. In 1987, in a review of 107 footballers in Australia who had suffered a spinal cord injury between 1960 and 1985, scrummaging in rugby union was identified as particularly dangerous, with illegal tackles (eg, "spear tackling" -- with a player being driven head-first into the ground, or a "stiff-arm" impact to a player's head and neck) identified as the most serious problem in rugby league.2 Administrators of both codes had already acknowledged these problems, particularly in "schoolboy" football. There were also lectures by sports medicine specialists to coaches and selectors of teams, with identification of the particular danger for young players in their mid teens beginning to participate in a contact sport. During the second half of the 1980s, coaches for both schoolboy and more senior grades of rugby union and rugby league were emphasising adequate preparation for the game and careful selection of players for particular positions of play, and encouraging the reporting of injuries. Some heads of independent schools in Sydney were initially reluctant to accept that many boys are genetically and psychologically destined to be unsuitable for participation in competitive contact sport! Some administrators were reluctant to consider changes of rules necessary to reduce the forces generated on the necks and shoulders of players involved in scrums and mauls and to ensure the absolute necessity of playing according to the rules. In 1997, Armour et al confirmed an increased frequency of serious spinal cord injuries in rugby union and league players over the 20-year period 1976 to 1995 in New Zealand.3 One hundred and forty-one players were admitted to New Zealand's two spinal injury units, and 47 remained permanently paralysed. The authors noted that, although studies of cervical spinal cord injury in rugby football had been presented to medical and rugby authorities within the previous five years, no action appeared to have been taken to reduce the unacceptable incidence of this grave injury. Professor Timothy Noakes, from Cape Town, South Africa, lamented in an editorial in the British Medical Journal in 1995 that "nearly 20 years after the BMJ first drew attention to the issue, we still do not know the true incidence of either spinal cord or cervical injuries in rugby players in any rugby-playing country".4 He emphasised that changes in rules of the game and player preparation could not be supported without sufficient accurate epidemiological data. More recently, Scher reported that the incidence of serious rugby spinal injuries in South Africa had not decreased over the past 10 years, with an average of 5.4 players per year admitted to one of the world's largest spinal cord injury centres, in Cape Town.5 Of interest, therefore, is the finding of Rotem et al, reported in this issue of the Journal, of a "small but significant decline in the number and approximate incidence of cases [of permanent neurological deficits leading to tetraplegia] associated with rugby union but no change in rugby league", from their survey of the spinal units at Royal North Shore Hospital and Prince Henry's Hospital.6 Further collection of data will allow a more detailed study of the statistics and will, one hopes, confirm the apparent trend towards reduction in injury incidence. In the 18 months since the New Zealand Rugby Union instituted compulsory nationwide safety seminars for coaches early in 1996, no cases of spinal cord injury from scrums have been reported in that country, although one player sustained tetraplegia in a tackle.3 During 1997, the spinal unit at Royal North Shore Hospital had no admissions of patients with serious cervical spinal cord injury from playing either rugby union or league (Dr Sue Rutkowski, Medical Director, personal communication), although this encouraging statistic could be a continuation of the variability seen in Rotem et al's study. In 1995, the National Health and Medical Research Council released a handbook7 with Guidelines for prevention and management of head and neck injuries in football. Compiled by medical specialists with knowledge and interest in neurotrauma from sporting injuries, this useful guide should be in the hands of all referees, umpires, coaches and players. The handbook highlights important first-aid principles and assessment of injured players before returning them to play, to prevent aggravation of a potentially serious injury. The laws for under-19 players, with the 1993 variations (such as rules eliminating "crotch binding" in scrums) introduced to rugby union in New South Wales, must also be maintained. The cost to the community of spinal cord injuries cannot be overemphasised. In Australia, 300 new patients with spinal cord injuries are expected every year; the lifetime cost is one million dollars for each paraplegic casualty and five million dollars for a tetraplegic casualty, as confirmed by awards in Australian courts. Our pessimism should be balanced by remembering Davidson's 1987 findings that, among 1444 schoolboys injured in interschool rugby from 1969 to 1986, there were two clinically "serious" injuries -- a skull fracture and a fracture dislocation of the cervical spine. The "severe" injury rate was 14 per 10 000 player-hours, or 0.12 per 100 player-games.8 Rotem et al have confirmed the impression of a reduction in the incidence of spinal cord injury in some contact sports following rule changes, as well as increasing our understanding of how cervical spinal cord injury occurs. Further epidemiological studies are essential for the adequate re-assessment of rule changes and of techniques to prepare players for contact sports. We must also further our knowledge of how injuries occur, and remain in close consultation with physicists, sports medicine clinicians and biomedical engineers. There must be no complacency in the future. Continuing vigilance is imperative to avoid the devastating personal and societal costs. John D Yeo, AO Associate Professor, and Consultant in Spinal Injuries Royal North Shore Hospital, Sydney, NSW Yeo JD, Walsh J. Prevention of spinal cord injuries in Australia. Paraplegia 1987; 25: 221-224. Taylor TKF, Coolican MRJ. Spinal cord injuries in Australian footballers, 1960-1985. Med J Aust 1987; 147: 112-118. Armour KS, Clatworthy BJ, Bean AR, et al. Spinal injuries in New Zealand rugby and rugby league -- a 20-year survey. N Z Med J 1997; 110: 462-465 . Noakes T, Jakoet I. Spinal cord injuries in rugby union players. BMJ 1995; 310: 1345-1346. Scher AT. Rugby injuries to the cervical spine and spinal cord -- a 10-year review. Clin Sports Med 1998; 17: 195-206. Rotem T, Lawson JS, Wilson SF, et al. Severe cervical spinal cord injuries related to rugby union and league football in New South Wales, 1984-1986. Med J Aust 1998; 168: 379-381. Newcombe R, et al. Football injuries of the head and neck. National Health and Medical Research Council Report, January 1995. Canberra: AGPS, 1995. Davidson RM. Schoolboy rugby injuries, 1969-1986. Med J Aust 1987; 147: 119-120. Lewis CS. The problem of pain. London: Collins Fontana Books, 1940: 141. - 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/>

John D Yeo

Patient preference and prostate cancer screening Fully informed men should be free to exercise their personal preference regarding screening MJA 1997; 167: 240-241 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/>". - ©MJA1997 Every year in Australia it is estimated that more than 2500 men die of disseminated prostate cancer and many more suffer the consequences of advanced metastatic disease.1 In New South Wales in 1994, the chance of men in the age group 0-74 years developing clinically apparent prostate cancer was 13.2% (2908 new prostate cancer cases were reported in men aged 45-74 years).2 However, because of ageing of the Australian population (many men live beyond 74 years of age) the lifetime risk is actually considerably higher. The use of prostate specific antigen (PSA) screening for early detection of prostate cancer has been the subject of considerable debate. The screening may be of the general population, or limited screening of "at risk" populations, or, finally, case finding, with the screening being part of a routine medical check-up. Currently, for all three types of screening there are no randomised trials to determine whether PSA screening does more good than harm, or the converse. In particular, there is little evidence to support general population screening.3 In the current climate of uncertainty, it is mandatory to include the patient in any screening decision. What is the stance of national professional bodies in the face of this uncertainty? The American Cancer Society recommends annual PSA testing starting at age 50 for men with average risk for prostate cancer.4 Their guidelines, however, are not recommendations for public programs of mass screening, but are intended to help individual doctors and patients select the best early detection protocol for their personal needs. The American Urological Association also recommends annual screening with both digital rectal examination and PSA for men aged 50-70 years.5 On the other hand, the US Preventive Services Task Force recommends against screening,6 and in Europe the consensus is that widespread population screening cannot be recommended as a public health policy at present.7 What are the recommendations in Australia? The Australian Cancer Society8 and the Australian Health Technology Advisory Committee3 recommend against screening.4 The Urological Society of Australasia's current position is to recommend against population screening of asymptomatic men. However, they recommend that asymptomatic men aged 50-70 years (or between 40 and 70 years with a positive family history of the disease) who wish to be tested should be able to do so after appropriate counselling. They suggest that it is up to individual doctors to decide whether to advocate screening for a man not requesting it.9 What are the arguments for and against screening? Those in favour of screening argue that even small tumours will eventually progress to metastatic disease if the patient lives long enough.10 In addition, most cancers detected by PSA-based screening are largely cancers expected from their volume and histological grade to progress.11 There is also strong evidence to suggest that disease confined to the prostate is curable.12 Furthermore, a recent population study with long term follow-up of almost 60 000 patients with clinically localised prostate cancer provided evidence that treatment in moderate and poorly differentiated tumours is superior to observation alone.13 Finally, PSA will detect organ-confined disease, and therefore potentially curable cancer, more frequently than digital rectal examination alone.11 Critics of screening contend that the sensitivity and specificity of PSA screening are too low to make it an ideal screening test. Furthermore, only one cancer will be found for every three men having a biopsy after a PSA-positive test result.11 This leaves a proportion of patients with the stress of being PSA positive and biopsy negative, until it is ultimately discovered whether the PSA test result is a false positive or the biopsy result a false negative. Furthermore, the potential for slow non-life-threatening growth of untreated prostate cancer, particularly in the older age group, means that more men will die with prostate cancer than of it, not to mention the morbidity and mortality associated with the biopsy and the treatment.14 In this climate of uncertainty what are our general practitioners (GPs) doing? The Royal Australian College of General Practitioners recommends against screening.15 However, in a recent questionnaire survey of New Zealand GPs, most indicated that they currently screen at least some men aged 50 or more by digital rectal examination or PSA regardless of beliefs about test efficacy.16 This is probably explained by GPs' direct clinical responsibility and their greater concern with their patients' individual needs rather than with recommendations of public health and professional bodies. What then is the community perspective? In this issue of the Journal, Ward et al. address the subject of male awareness of prostate cancer.17 In a randomly selected group of 340 men aged between 40 and 80, they showed that 22% of those aged 50 or more had been screened for prostate cancer within the previous 12 months. They also found that the men in this population overestimated their lifetime risk of developing and dying of prostate cancer. This is no doubt due in part to the widespread incidence of the disease, as well as a general fear of cancer and raised awareness resulting from increased media coverage. From a public health viewpoint, the significant cost of prostate cancer screening would need to be offset by pos sible cost savings from an eventual mortality rate decrease. From an individual viewpoint, the detection of an asymptomatic organ-confined cancer (case finding) may be of substantial benefit. While the international medical community remain divided on this issue, and there is evidence for and against case finding, we believe that each man must participate in the screening decision and decide for himself. This decision is complex and must be made with full knowledge of the risks of contracting and dying from prostate cancer. The decision will be affected by the man's age and general health, and his particular risk category for developing prostate cancer. The opinions of his general practitioner and even the wishes of his spouse will affect his decision. He must be aware of the potential side effects of diagnosis and treatment, and understand that, in conservatively managed patients, if hormone therapy fails there is no further reliably effective treatment. Ward et al. have shown that screening is occurring in the community, and they argue that accurate information is not being received by the community at large. They recommend that public health initiatives to discourage prostate cancer screening should focus particularly on men with bothersome urinary symptoms and those who worry about prostate cancer.17 While we agree that public education is essential, we believe this must neither discourage nor encourage screening by case finding, but rather give accurate, unbiased information to all men. The information must be balanced, as it has now been shown in several studies that patient preference regarding screening and treatment is greatly affected by this information.18 In the current climate of uncertainty, it is mandatory to include the patient in any screening decision. This is the recommendation of the Australian Health Technology Advisory Committee3 and the Urological Society of Australasia.9 When fully informed, men should be free to exercise personal preference regarding prostate cancer screening. Phillip D Stricker Urologist, St Vincent's Clinic, Sydney, NSW David R Eisinger Urologist, Concord Hospital, Sydney, NSW Australian Bureau of Statistics. Causes of death, Australian, 1994. Canberra: ABS, 1995. (Catalogue No. 3303.0.) Coates MS, Armstrong BK. Cancer in New South Wales. Incidence and mortality, 1994. Sydney, NSW Cancer Council, June 1997. Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. Mettlin CJ, Jones GW, Avarette H, et al. Defining and updating the American Cancer Society guidelines for the cancer related checkup; prostate and endometrial cancer. CA Cancer J Clin 1993; 43: 42-46. American Urological Association Policy Statement on early detection of prostate cancer. Am Urol Assoc Today 1994; 7: 16. US Preventive Services Task Force. Screening for prostate cancer. Guide to clinical preventive services. 2nd ed. Baltimore, Md: Williams & Wilkins, 1996: 119-134. Flemish Advisory Committee on Cancer Prevention, Belgium. Report of the consensus workshop on screening and global strategy for prostate cancer. Denis LJ, Murphy GP, Schroder FH, editors. Cancer 1995; 75: 1187-1207. Australian Cancer Society. Prostate cancer screening: guidelines for health professionals. Cancer Forum 1995; 19: 47-50. Urological Society of Australasia. Prostate screening, a personal choice: surgeons. Media release, 27 August, 1996. Hugosson J, Aus E, Bergdahl D, et al. Prostate cancer mortality in patients surviving more than 10 years after diagnosis. J Urol 1995; 154: 2115-2117. Catalona WJ, Richie HP, Ahmann FR, et al. Comparison of digital rectal examination and serum PSA in the early detection of prostate cancer: results of a multicenter clinical trial of 6,630 men. J Urol 1994; 151: 1283-1290. Walsh PC, Partin AW, Epstein JI. Cancer control and quality of life following anatomical radical retropubic prostatectomy: results at 10 years. J Urol 1994; 152: 1831-1836. Lu-Yao GL, Yao Siu-Long. Population-based study of longterm survival in patients with clinically localised prostate cancer. Lancet 1997; 349: 906-910. Hirst GHL, Ward JE, Del Mar CB. Screening for prostate cancer: the case against. Med J Aust 1996; 164: 285-288. Royal Australian College of General Practitioners. Preventive and Community Medicine Committee. Kable B, chair. Guidelines for preventive activities in general practice. 3rd ed. Sydney: RACGP, Oct 1996. Morris J, McNoe B, Adam H. Screening for prostate cancer: what do general practitioners think? N Z Med J 1997; 110: 178-182. Ward JE, Hughes AM, Hirst GHL, Winchester L. Men's estimates of prostate cancer and self-reported rates of screening. Med J Aust 1997; 167: 250-253. Flood AB, Wennberg JE, Nease RF Jr, et al. The importance of patient preference in the decision to screen for prostate cancer. J Gen Intern Med 1996; 11: 342-349. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Phillip D Stricker · David R Eisinger

Men's estimates of prostate cancer risk and self-reported rates of screening Jeanette E Ward, Ann-Maree Hughes, Geoffrey H L Hirst and Lorraine Winchester For editorial comment, see Stricker & Eisinger 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/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - ©MJA1997 Abstract Objective: To determine rates of prostate cancer screening and predictors of men's participation in this screening in the light of national recommendations against prostate cancer screening. Design: Community-based study (computer-assisted telephone survey). Setting: Central Sydney Area Health Service. Participants: Randomly selected men aged 40-80 years. Results: 340 men participated (65% response rate). While the true lifetime (0-74 years) risk of developing or dying from prostate cancer is reported to be one in 18 (6%) and one in 65 (1.5%), respectively, 37% of respondents thought that at least one in five men (20%) would develop prostate cancer before the age of 75 years and 11% that one in five (20%) would die from it. Twenty-two per cent of men aged 50 years or over had been screened for prostate cancer within the previous 12 months. Ever worrying about prostate cancer and bothersome urinary symptoms independently predicted the probability of screening within the previous year. Sociodemographic characteristics such as age, occupation and country of birth were not associated with screening. Conclusions: Public health initiatives to discourage prostate cancer screening should focus particularly on men with bothersome urinary symptoms and those who worry about prostate cancer. Accurate information about the low risks of dying from prostate cancer needs to be communicated, and the speculative nature of current evidence in support of screening as a means of reducing this risk should be emphasised. MJA 1997; 167: 250-253 Introduction Despite repeated advice to the contrary, screening for prostate cancer is being requested by patients and conducted by doctors. Advice against screening has come from a policy statement for health professionals released in 1995 by the Australian Cancer Society,1 and a 1996 report of a multidisciplinary committee convened by the Australian Health Technology Advisory Committee on the basis that the evidence did not meet accepted criteria for benefits, risks and costs.2 In addition, the National Health and Medical Research Council (NHMRC) evidence-based guidelines for the management of men with uncomplicated lower urinary tract symptoms (LUTS)3 state that there is no evidence that prostate specific antigen (PSA) tests are required for men with uncomplicated LUTS as men with these symptoms are at no greater risk of prostate cancer than asymptomatic men.4 Data indicating that screening is occurring come from the Department of Veterans' Affairs,5 as well as surveys of urologists6 and general practitioners (unpublished data). In describing this "conundrum", Horner identified a pressing need for research to support educational programs for men, focusing on "strategies to combat uninformed patient demand".7 While the Australian Health Technology Advisory Committee guidelines advocate national action involving the NHMRC,2 the need for health services to intervene actively at a local level to discourage prostate cancer screening has also been recognised in New South Wales.8 In the absence of more recent data, we used the opportunity of a large population-based study about men's health to determine the prevalence and predictors of participation in screening for prostate cancer in the area defined by the Central Sydney Area Health Service. Methods The study was approved by the Royal Prince Alfred Hospital Ethics Review Committee. Community sampling Two thousand names, addresses and telephone numbers within the 35 postcodes constituting the Central Sydney area were randomly selected from the Electronic White Pages.9 To maximise participation rates, each household received a one-page letter outlining the Men's Health Study and anticipating telephone contact, supported by a media release to further publicise the study. The initial sample size of 2000 was estimated to be sufficient to provide between 250-350 completed surveys given an estimated prevalence of 38%10 of eligible male respondents in contacted households and a conservative consent rate. Computer-assisted telephone interview survey A market research company with computer-assisted telephone interview facilities contacted all 2000 households between 26 November and 12 December 1996 on weekdays between 1500 and 2100. Where the first contact was unsuccessful, a further five attempts were made at different times and on different days. Men aged between 40 and 80 years residing in the household and fluent in English were eligible to participate. If there was more than one man in the household meeting these criteria, the one with the most recent birthday was asked to participate. Due to the sensitive nature of the survey, all telephone interviewers were mature females with previous experience in conducting health-related surveys. A briefing session for interviewers was conducted to address potential difficulties with medical jargon, to ensure sensitivity towards the issues and to standardise the interviews. Survey instrument At the beginning of the interview, respondents were asked standard sociodemographic questions, as well as whether they had ever been diagnosed with a urological condition and questions modified from the International Prostate Symptom Score11 to assess the presence of and degree of "bother" attributable to urinary symptoms. We then asked respondents five questions about prostate cancer. 1. "Have you ever worried that you might have prostate cancer?" Those answering "yes" were asked "For what reasons?". 2. "Have you had any test to detect prostate cancer in the last 12 months?" Those answering "yes" were asked to name the test(s). 3. "Have you heard of any tests for prostate cancer?" 4. "Out of 100 Australian men, how many or what percentage do you think will get prostate cancer before the age of 75?" If the respondent was unable to quantify his response, the interviewer was instructed to establish a range by saying "Would it be more or less than 1%? Less than 5%? Between 5% and 9%? More than 10% or more than 20%?" until an answer was given. 5. "Out of 100 Australian men, how many or what percentage do you think will die from prostate cancer before the age of 75?" If necessary, an answer to this question was prompted in the same way as Question 4. For Questions 4 and 5, interviewers were unaware of the correct answers. Questions 4 and 5 were modelled on previous research. 12 Data analysis Data were analysed using SAS13 and Epi Info.14 We used chi-squared tests to examine associations between knowledge of prostate cancer screening tests and eight respondent characteristics: age (40-49, 50-59, 60-69, 70-80 years); country of birth (Australia v. other); socioeconomic status based on occupation (manager/ administrator and professional/para-professional combined v. all other categories [tradesperson/clerk/salesperson and personal service worker/plant and machine operator/driver and labourer]);15 education (up to and including Intermediate or School Certificate [Year 10] v. Leaving or Higher School Certificate [Year 11 or 12] and beyond); moderate or severe "bother" from urinary symptoms (a score equal to or greater than six from a possible range of 0-18); ever worrying about prostate cancer (yes v. no); estimate of risk of developing prostate cancer (correct or lower estimate v. overestimate); and estimate of risk of death from prostate cancer (correct or lower estimate v. overestimate). Jelfs et al. report a lifetime risk of developing prostate cancer of one in 18 (6%).16 We considered an estimate of 10% or greater to be an overestimate of incidence risk. Using the Jelfs data,16 we calculated the lifetime risk of dying of prostate cancer as one in 65 (1.5%). We considered an estimate of 5% or greater as an overestimate of mortality risk. For the sample of men 50 years and over, we used chi-squared tests to determine associations between the outcome variable -- having had either a prostate specific antigen test, a digital rectal examination, or both, within the previous 12 months -- and these eight variables as well as knowledge of prostate cancer tests. Logistic regression analysis was performed, using significant univariate variables and any plausible non-significant variable. Results Response rate and characteristics of the sample Of 2000 randomly selected households, 1481 (74%) were ineligible. Of the remaining 519 households with an eligible male resident, 340 agreed (65% response rate). Men who refused were significantly older than those who participated (t27.49 = 4.19; P < 0.01). Compared with 1991 Census data12 (Box 1), the sample under-represented older men. No respondent indicated a past history of prostate cancer. Respondents' worry about prostate cancer, estimates of risk and knowledge of tests Ninety-nine men (29%) indicated they had ever worried about prostate cancer. The three most frequently cited reasons were: presence of urinary symptoms (36 men [11%]), age (26 men [8%]), and media publicity (24 men [7%]). Of the sample, 216 men (63%) overestimated lifetime risk of developing prostate cancer (Box 2). Respondents were significantly more likely to overestimate the risk of death from prostate cancer than the risk of developing it (McNemar's test, 10.800; df = 1; P = 0.001). Ever having worried about prostate cancer was not associated with correctly estimating the risk of developing it or the risk of dying from it. Of the total sample, 237 (70%) and 228 (67%) required no prompting to estimate lifetime risk of developing or dying from prostate cancer, respectively. One hundred and seventy-two men (51%) reported they had heard of one or more tests for prostate cancer. Respondents who had heard of any test were more likely to be managers or professionals than to have other occupations (chi-squared = 4.04; df = 1; P = 0.044) or were educated to Year 12 or beyond (chi-squared = 5.49; df = 1; P = 0.019). Knowledge of tests was unrelated to age, country of birth, perception of risk, "bother" from urinary symptoms or anxiety. Rates and predictors of prostate cancer screening within the previous 12 months Of the total sample, 52 men (15%) had had at least one prostate cancer screening test within the previous 12 months (Box 3). Almost all tests (97%) were reported by men 50 years or older, yielding an annual screening rate of 22% for this older group. For the subsample of 186 men aged 50 years or over, univariate analyses revealed only two variables to be significantly associated with having had a prostate cancer screening test within the past year: moderate or severe "bother" from urinary symptoms (chi-squared = 13.41; df = 1; P < 0.001), and "ever worrying" about prostate cancer (chi-squared = 18.38; df = 1; P < 0.001). Knowledge of available tests and other sociodemographic variables were not associated with having had a test within the past year. However, as age was a potential confounder, it was included with the two significant univariate associations in the logistic regression analysis. After adjustment, "bother" and "anxiety" remained independent predictors (Box 4). Discussion Just over one in five of the men in our study 50 years or over had had a prostate cancer screening test within the previous 12 months, a rate almost double that given in an earlier report of national claims data.5 Screening was significantly more likely among those who had ever worried about prostate cancer or were bothered by urinary symptoms. In contrast to research in other countries demonstrating that economic and ethnic factors influence participation in prostate cancer screening,17,18 our study showed no association between screening and men's occupation, education or country of birth. As a priority for public campaigns, men who experience uncomplicated LUTS -- nocturia, frequency, dribbling, urgency, hesitancy or reduced stream -- in the absence of haematuria need to be reassured that there is no empirical evidence of a relationship between such symptoms and early prostate cancer.3 Men's anxiety about prostate cancer may also be explained, in part, by their overestimation of the actual risks of prostate cancer. More than a third of respondents thought that at least one in five men would develop prostate cancer before the age of 74 years, and 11% thought that one in five would actually die from this disease before that age. Reasons for consistent overestimation of risk remain speculative but might reflect extensive media coverage of prostate cancer, possibly fuelled by commercial interests, which increases men's anxiety, and, in turn, raises their perception of risk.19 In contrast, McCormick20 has argued that informed public participation in screening should be founded on clear messages about absolute risk, the evidence from rigorous randomised trials for reduction in risk, the costs and adverse outcomes. Our study is the first to quantify a considerable gap between men's perceptions of risk and the actual risk. When provided with impartial information on an individual basis about the risks and unknown benefits of prostate cancer screening, men are less inclined to have a screening test.21 Given our collective failure to convey accurate health risk information to the public about risks for other cancers,9 risk reduction22 or screening,23 a systematic approach to the development, implementation and evaluation of a public health initiative to discourage prostate cancer screening is required. The recent release of the guidelines for the management of uncomplicated LUTS in men3 provides a focus for such an initiative. Our study suggests that men who are anxious about prostate cancer or have bothersome urinary symptoms represent priority target groups for educational messages via general practice, men's service and recreation clubs, mass media and peak groups such as the Council of the Ageing and the Consumers' Health Forum. Because of the limitations of our study, we also recommend that a dedicated survey about prostate cancer be conducted which examines in depth men's knowledge of indolent and aggressive cancer types, their health beliefs and attitudes towards early detection, their awareness of the speculative and controversial nature of screening, and their knowledge of treatment options and their effectiveness. Men's recall of the recommendations of their GP in either promoting or discouraging prostate cancer screening could also be ascertained. As female partners represent a key source of health information for men,24 a concurrent survey of partners of men in these age groups is also recommended. Acknowledgements The Men's Health Study was conducted for the NHMRC Working Party developing guidelines for the management of lower urinary tract symptoms in men with funds from the Commonwealth Department of Health and Family Services. We thank members of the Working Party for comments on survey protocols; the men who participated in the computer-assisted telephone interview and the Hunter Valley Research Foundation for diligent administration of the survey; Jo Williams and the Central Sydney Area Health Service Public Relations Unit for assisting with the media release; and Neil Donnelly for statistical advice. References Australian Cancer Society. Prostate cancer screening: guidelines for health professionals. Cancer Forum 1995; 19: 47-50. Australian Health Technology Advisory Committee. Prostate cancer screening. Canberra: AGPS, 1996. NHMRC clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: AGPS, 1996. Catalona W, Ritchie J, Ahmann F, et al. Comparison of digital rectal examination and serum prostate specific antigen in the early detection of prostate cancer: results of a multicenter clinical trial of 6,630 men. J Urol 1994; 151: 1283-1290. Parkes A, Killer G. Prostate-specific antigen -- is it already being used as a screening test? Med J Aust 1994; 161: 722. Urological Society of Australasia. Prostate screening, a personal choice: surgeons. Media release, 27 August 1996. Horner D. Prostate cancer: a challenge for health promotion. Health Promot J Aust 1996; 6: 3-7. Cancer Expert Working Group. Cancer control NSW goals and targets. North Sydney: NSW Health, August 1995. Oz On Disc. Sydney: Read Only Memory Pty Ltd, May 1996. Rissel C, Winchester L, Hodge W, et al. Health outcome indicators for Central Sydney. Sydney: Needs Assessment & Health Outcomes Unit, Central Sydney Area Health Service, August 1996. Cockett A, Aso Y, Denis L, et al. Recommendations of the International Consensus Committee. In: Proceedings of the International Consultation on Benign Prostatic Hyperplasia (BPH). Paris: SCI, June 1991: 279-281 (ISBN 2-905744-11-1). Clover K, Redman S, Boyle K, et al. Community knowledge of cancer. Health Promot Int 1991; 6: 93-101. SAS [computer program], version 6. 3rd ed. Cary, NC: SAS Institute, 1990. Dean AG, Dean JA, Burton AH, Dicker RC. Epi Info, version 5: a word processing database, and statistics program for epidemiology on microcomputers. Stone Mountain, Ga: USD Inc, 1990. Australian Bureau of Statistics. Australian standard classification of occupations. 1st ed. Canberra: AGPS, 1992. Jelfs P, Coates M, Giles G, et al. Cancer in Australia 1989-1990 (with projections to 1995). Canberra: Australian Institute of Health and Welfare, 1996 (Cancer Series No. 5). Schwartz K, Kau T, Severson R, Demers R. Prostate-specific antigen in a community screening program. J Fam Pract 1995; 41: 163-168. Williams R, Boles M, Johnson R. Use of prostate-specific antigen for prostate cancer screening in primary care practices. Arch Fam Med 1995; 4: 311-315. Wasson J. Prostate cancer fears and facts. In: Proceedings of the National Men's Health Conference; 10-11 August 1995. Canberra: AGPS, 1996: 69-72. McCormick J. Medical hubris and the public health: the ethical dimension. J Clin Epidemiol 1996; 49: 619-621. Wolf A, Nasser J, Wolf A, Schorling J. The impact of informed consent on patient interest in prostate-specific antigen screening. Arch Intern Med 1996; 156: 1333-1336. Hancock L, Sanson-Fisher RW, Redman S, et al. Knowledge of cancer risk reduction practices in rural towns of NSW. Aust N Z J Public Health 1996; 20: 529-537. Cockburn J, Redman S, Hill D, Henry E. Public understanding of medical screening. J Med Screen 1995; 2: 224-227. Norcross W, Ramirez C, Palinkas L. The influence of women on the health care-seeking behaviour of men. J Fam Pract 1996; 43: 475-480. (Received 24 Feb, accepted 22 May 1997) Subsequently cited in Prostate-specific antigen testing in Australia and association with prostate cancer incidence in New South Wales by David P Smith and Bruce K Armstrong, Med J Aust 1998; 169: 17-20 Authors' details Central Sydney Area Health Service, Needs Assessment & Health Outcomes Unit, Sydney, NSW. Jeanette E Ward, PhD, FAFPHM, Director; Ann-Maree Hughes, BEd, GradDipAppSci(Nursing), Research Assistant; Lorraine Winchester, BSocSc(Hons), Data Manager. Taylor Medical Centre, Brisbane, QLD. Geoffrey H L Hirst, MB BS, FRACS, Urologist. Reprints: Associate Professor J E Ward, Central Sydney Area Health Service, Needs Assessment & Health Outcomes Unit, PO Box 374, Camperdown, NSW 2050. E-mail: jward AT nah.rpa.cs.nsw.gov.au ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Jeanette E Ward · Anne-Maree Hughes · Lorraine Winchester

Urinary symptoms as men age: the reassurance of an evidence-based approach Medical intervention is not usually necessary for men with uncomplicated lower urinary tract symptoms if quality of life is not affected MJA 1997; 167: 62-63 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/>". Make a comment - - ©MJA1997 A high prevalence of uncomplicated lower urinary tract symptoms (LUTS) in an Australian community-based population is reported in this issue of the Journal, although the authors, Pinnock and Marshall, note that despite these symptoms many men and women do not experience substantive dissatisfaction with their quality of life.1 This study is timely, as it follows the recently launched National Health and Medical Research Council (NHMRC) evidence-based Clinical practice guidelines for the management of uncomplicated lower urinary tract symptoms in men.2 Developed by a multidisciplinary working party, the NHMRC Guidelines and two derivative documents, ". . . is it my prostate Doc?" A guide for general practitioners3 and " To pee . . . or not to pee". A guide for men about their urinary symptoms,4 emphasise the need to assess not only the presence of symptoms but also their nature and the "bother" they cause. The distinction between symptoms alone and their impact on quality of life is an important one. There is strong evidence that uncomplicated urinary symptoms in a man are very unlikely to represent any serious threat to his health. For example, the incidence of unsuspected and clinically significant upper-tract obstruction secondary to lower-tract abnormality in these men is very low (0.8%-2.5%).2 Accordingly, the outcome of interest for men (as typified by Pinnock and Marshall's study) is an improvement in their quality of life as related to urinary symptoms, not avoidance of a serious threat to life itself. Thus, measurement of quality of life becomes the key. Only men themselves can assess how bothered they are by their uncomplicated urinary tract symptoms and how much they subsequently improve. How do we encourage men whose quality of life is severely compromised by their urinary symptoms to consult their medical practitioners? Pinnock and Marshall provide another important finding -- that the prevalence of LUTS is similar in men and women aged 55 or more. The factors responsible for LUTS remain to be fully determined -- while urine outflow obstruction in men and pelvic floor dysfunction in women are possible causes, it is probable that many of the changes are simply age related.2 Unfortunately, the use of terms such as "benign prostatic hyperplasia or hypertrophy" (BPH) and "prostatism" inadvertently imply that enlargement of the prostate is the definitive cause of the symptoms. However, the severity of urinary symptoms does not correlate with the presence of BPH or the degree of prostatic enlargement.2 Accordingly, the acronym "LUTS" is preferable to other terminology,5 as it permits a pragmatic definition of the symptom complex without necessarily implying a full understanding of its underlying pathology.2 When is intervention warranted for uncomplicated LUTS? The strongest predictor of the outcome of intervention for uncomplicated LUTS in men is the degree of "bother" the symptoms cause.6 If a man is not particularly bothered by his symptoms, he can be reassured they are unlikely to represent a health threat and that intervention is unlikely to improve his outcome. If he is moderately or significantly bothered, then medical and surgical interventions are more likely to improve his quality of life. While it has been argued that urodynamic parameters or residual urine volume can predict clinically significant differences in the outcome of surgical treatment, this assertion has not been validated in the literature.2 Pinnock and Marshall found that men with high levels of dissatisfaction with the symptoms did not necessarily complain or seek help. Conversely, a smaller, but still substantial, proportion of men who were "not dissatisfied" with their symptoms did visit their doctor because of these symptoms. These findings present a dual challenge. How do we encourage men whose quality of life is severely compromised by their urinary symptoms to consult their medical practitioners? And, because there is little need for or benefit from treatment of symptoms causing minimal bother, how do doctors reassure most men that medical care is unnecessary? We argue that the most effective means of achieving this balance will be via the dissemination and implementation of the NHMRC Guidelines for consumers and their practitioners.7 Of increasing concern to us is the insistence of detractors of the NHMRC Guidelines that early prostate cancer must be excluded as a cause of LUTS and, accordingly, that men must be fully investigated for this malignancy.8,9 Men with uncomplicated LUTS are at no greater risk of early prostate cancer than are their asymptomatic counterparts.2,10 As the evidence to date for prostate cancer screening does not yet meet rigorous public health criteria,11 we believe that the testing of men with LUTS for early prostate cancer is equally unjustified and has the potential to undermine an evidence-based approach to health care. In our view, prostate-specific antigen testing is ethical only when a man has been fully informed of the facts, uncertainties and consequences.12 The NHMRC Guidelines provide eight specific recommendations for further research to clarify those issues poorly supported by empirical evidence. Two priorities were larger randomised trials of the newer urological interventions (such as prostatic heating) against conventional surgical treatments, and methodological research to develop more robust outcome measures. The need for better research is self-evident, especially as the Guidelines are scheduled for review in two years. In the interim, it is our view that, in the absence of strong evidence supporting particular investigations or specific treatments, responsible guidelines should err on the side of conservatism; they should not support a more interventionist position in anticipation of some as yet unidentified future benefit. Men's health will not improve with an unquestioning acceptance of intervention for its own sake. We need to pursue an evidence-based approach with both confidence and compassion, finding new ways to accelerate rigorous, yet relevant, clinical research in areas of need. Concurrently, we need to share the empirical uncertainties of everyday clinical practice more widely with our patients, their partners, our fellow practitioners, and politicians. Geoffrey H L Hirst Urologist, Mater Hospitals, Brisbane, QLD Jeanette E Ward Associate Professor; Director, Needs Assessment and Health Outcomes Unit Central Sydney Area Health Service, Sydney, NSW Pinnock CB, Marshall VR. Troublesome lower urinary tract symptoms in the community: a prevalence study. Med J Aust 1997; 167: 72-75. National Health and Medical Research Council clinical practice guidelines. The management of uncomplicated lower urinary tract symptoms in men. Canberra: AGPS, 1996. National Health and Medical Research Council ". . . is it my prostate Doc?". A guide for general practitioners. Canberra: AGPS, 1996. National Health and Medical Research Council "To pee . . . or not to pee". A guide for men about their urinary symptoms. Canberra: AGPS, 1996. Abrams P. New words for old: lower urinary tract symptoms for "prostatism" [editorial]. BMJ 1994; 308: 929-930. Wasson JH, Reda DJ, Bruskewitz RC, et al. A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia. The Veterans Affairs Cooperative Study Group on Transurethral Resection of the Prostate. N Engl J Med 1995; 332: 75-79. Thomson R, Lavender M, Madok R. How to ensure that guidelines are effective. BMJ 1995; 311: 237-242. Royal Australasian College of Surgeons media release: Urological Society of Australasia. Men shouldn't ignore urinary symptoms: urologists. April 9, 1997. Royal Australasian College of Surgeons media release: Urological Society of Australasia. Prostate screening, a personal choice: surgeons. August 27, 1996. Rietbergen JB, Kranse R, Boeken Kruger AE, et al. Additional value of the AUA7 symptom score in prostate cancer (PC) detection. J Urol 1997; 157: 467. Commonwealth Department of Health and Family Services prostate cancer screening. Australian Health Technology Advisory Committee (a standing committee of NHMRC). Canberra: AGPS, 1996. Hirst GH, Ward JE, Del Mar CB. Screening for prostate cancer: the case against. MJA 1996; 164: 285-288. To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia. We appreciate your comments.

Jeanette E Ward

A recent study has provided evidence that testosterone increases muscle strength, but does this translate to enhanced performance? 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". strength increased considerably in subjects who received placebo, but who were told they were receiving anabolic steroids For almost half a century, athletes have believed that use of anabolic-androgenic steroids can improve sporting performance. The United States physician John Zeigler was so convinced of their positive effects that on his return from the World Powerlifting Championships in Vienna in 1954 he worked on the development of methandrostenolone as a means of enhancing sporting performance. 1 This belief has persisted, leading to the widespread and much-publicised use of these drugs at all levels of sport (professional and amateur). It has been promoted by the banning of these drugs by sporting bodies to ensure fair competition. 2 Media reports and "underground" guides to anabolic steroids have also propagated the use of anabolic-androgenic steroids, which has spread from elite athletes to recreational bodybuilders, amateur athletes and adolescents. 3 Are the athletes and their coaches mistaken in their belief? Theoretically, anabolic-androgenic steroids should improve athletic performance by increasing muscle mass (via increased protein synthesis, nitrogen retention and antiglucocorticoid actions), as well as by increasing aggression and motivation. Moreover, recent isotope uptake studies in humans indicate that androgens may increase muscle protein synthesis, possibly through stimulation of intramuscular insulin-like growth factor-I (IGF-I) gene expression. 4 However, clinical studies have, in general, been inconclusive, partly because of the many unique methodological problems in studying the effects of anabolic-androgenic steroids (see below). In 1991, 16 randomised, placebo-controlled studies that used objective measures of performance were analysed by Elashoff et al. 5 They concluded that, while the possibility of anabolic-androgenic steroids improving sporting performance could not be excluded, "the data are insufficient to allow any firm conclusion about the efficacy of anabolic steroids in enhancing overall athletic performance". Since then, apart from a non-placebo-controlled study that showed an increase in lean body mass in healthy male volunteers receiving weekly injections of testosterone enanthate, 6 there were few real developments in the area until Bhasin et al. 7 published their study in July 1996. This study will probably become, in time, one of the most-cited articles on drugs and sport. Funded by the National Institutes of Health (US), the study examined the effect of high doses of testosterone enanthate in sesame oil (600 mg/week intramuscularly for 10 weeks); the authors made every attempt to remove confounding variables (such as diet, training, and weightlifting experience), and used standardised measures. Forty-three experienced weightlifters were randomly assigned to one of four groups (placebo with or without exercise, or testosterone with or without exercise). Strength was measured by two single weightlifts -- upper-body strength by benchpress, and lower-body strength by squatting. Fat-free body mass was measured by underwater weighing, and muscle size by magnetic resonance imaging. Forty subjects completed the study. Body weight increased only in the two testosterone-treated groups, and fat-free body mass only in the exercise groups, with the greatest change in fat-free mass in the testosterone plus exercise group (increase, 6.1 kg). Percentage body fat did not change in any group. Muscle size increased more in the testosterone groups than in either placebo group. Strength increased in both testosterone groups, as well as in the exercise group receiving placebo, but was greater in the exercise group with testosterone than in the exercise group with placebo. No significant adverse drug reactions were reported. Hence, for the first time, in a well designed study, supraphysiological testosterone did appear to increase muscle strength. One other placebo-controlled study has used higher doses of anabolic steroids (methandrostenolone, 100 mg/day for six weeks). 8 Reported 20 years ago, it used a crossover design, with attempts to control for most variables. The active drug was found to be no better than placebo in increasing strength. However, some caveats should be considered in assessing Bhasin et al.'s data. A placebo response has not been completely eliminated. It was not stated that the placebo was identical to the active drug in terms of pH, viscosity and other factors that may have allowed the code to be broken by either the administrator or recipient of the drug. Indeed, in a controlled study of oral anabolic steroids, all subjects correctly identified the active drug when directly asked. 9 The importance of the placebo response was shown by Ariel and Saville, who found that strength increased considerably in subjects who received placebo, but who were told they were receiving anabolic steroids. 10 Bhasin et al.'s subjects were experienced weightlifters. Although they reported that they had not taken anabolic steroids, these medications are illicit, and thus self-reporting may not be reliable. As 38%-58% of bodybuilders and weightlifters have been reported to use anabolic steroids, 11,12 some of Bhasin et al.'s subjects may well have been able to identify the active drug. Before generalising these results to athletes who use anabolic-androgenic steroids in the community, it should be remembered that they receive and use their supplies in very different ways to the controlled circumstances of Bhasin et al.'s study. Street supplies are often veterinary or illegally manufactured preparations, often combined with other medications such as diuretics and stimulants. Doses and duration are often well in excess of those used in this study. Although no major side effects were reported, the well documented long-term adverse effects of anabolic-androgenic steroids on cardiovascular risk, gynaecomastia, carcinogenesis, prostate and sexual function would not have been evident in a study of this duration. 13 On considering the available evidence, it appears that anabolic steroids definitely increase muscle size, and probably strength, but the mechanism is unknown. Further studies, using a crossover design, including inexperienced as well as experienced weightlifters, and the same drug vehicle for both placebo and active drug, with confirmation of subject blinding, should probably be conducted to confirm these findings. In addition, whether androgen-induced muscle hypertrophy translates into improved performance in sports that require skill as well as strength remains to be determined. But such studies should not overshadow the need for significant research into the prevention of anabolic-androgenic steroid abuse. Michael C Kennedy Department of Clinical Pharmacology and Toxicology, St Vincent's Hospital; and Manly Hospital, Sydney, NSW. Anthony J O'Sullivan Departments of Medicine and Endocrinology, St George Hospital, Sydney, NSW. Wade N. Anabolic steroids: Doctors denounce them, but athletes aren't listening. Science 1972; 176: 1399-1403. Skolnick AA. Tougher drug tests for Centennial Olympic Games. JAMA 1996; 275: 348-349. Buckley WE, Yesalis CE, Friedl KE, et al. Estimated prevalence of anabolic steroid use among male high school seniors. JAMA 1988; 260: 3441-3445. Urban RJ, Bodenburg YH, Gilkison C, et al. Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis. Am J Physiol 1995; 269: E820-E826. Elashoff JD, Jacknow AD, Shain SG, Braunstein GD. Effects of anabolic-androgenic steroids on muscular strength. Ann Int Med 1991; 115: 387-393. Forbes GB, Porta CR, Herr BE, Griggs RC. Sequence of changes in body composition induced by testosterone and reversal of changes after drug is stopped. JAMA 1992; 267: 397-399. Bhasin S, Storer TW, Berman N, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996; 335: 1-7. Hervey GR, Hutchinson I, Knibbs AV, et al. "Anabolic" effects of methandienone in men undergoing athletic training. Lancet 1976; 2: 699-702. Freed DLJ, Banks AJ, Longson D, Burley DM. Anabolic steroids in athletics: crossover double-blind trial on weightlifters. BMJ 1975; 2: 471-473. Ariel G, Saville W. Anabolic steroids: the physiological effects of placebos. Med Sci Sports 1972; 4: 124-126. Perry HM, Wright D, Littlepage BNC. Dying to be big: a review of anabolic steroid use. Br J Sports Med 1992; 26: 259-261. Delbeke FT, Desmet N, Debackere M. The abuse of doping agents in competing body builders in Flanders (1988-1993). Int J Sports Med 1995; 16: 66-70. Kennedy MC. Anabolic steroid abuse and toxicology. Aust N Z J Med 1992; 22: 374-381. Reprints: Dr M C Kennedy, Manly Non-Invasive Cardiac Laboratory, Level 4, 22 Darley Road, Manly, NSW 2095.

Michael C Kennedy · Anthony J O'Sullivan