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Screening for prostate cancer
Peter Davidson
The article ‘Screening for prostate cancer: a survey
of New Zealand general practitioners’ by Durham, Low and McLeod appears in
this issue of the NZMJ.1 This important paper
looks at New Zealand general practitioners’ attitudes, habits and
understanding around this complex issue. In so doing, a number of areas are
highlighted where there are discordant views between GPs and the evidence from
the literature.
Of the GPs surveyed, 42.3% would screen men between the ages
of 70 and 79 years and 12.3% would screen men of 80 years or greater. Most
recommendations on screening would not advise the screening of men over the age
of 75 years and many would not recommend screening men over the age of 70 years.
Risk factors for carcinoma of the prostate are a family history, advancing age,
a diet high in animal fat and, to a lesser degree, a family history of breast
cancer. Also implicated have been low UV sunlight exposure and low selenium
intake. Benign prostatic hyperplasia is not a risk factor for carcinoma of the
prostate and indeed prostate cancer is detected in no greater frequency in men
with symptoms than men without symptoms of bladder outflow obstruction.
Nevertheless, if one is considering treatment of benign prostatic hyperplasia,
exclusion of malignancy is important, as that may alter the treatment
administered. As far as ethnicity is concerned, African-Americans seem to have
the highest incidence and Asians the lowest incidence. Little is known about the
relative risk in Maoris. It should be noted, however, that Asians who live in a
Western environment start to develop a risk more akin to that of a Western
population.
This article highlights the fact that there is wide
variation in the screening tests used to detect prostate cancer. The most common
combination, however, is digital rectal examination (DRE) and prostate specific
antigen (PSA) testing. This would remain the recommendation of the urological
community if a PSA cut-off point of 4 were to be used as the threshold for
advancing to prostate biopsies. There is evidence, however, that lowering the
cut-off point to 3 may negate the need for the rectal examination in an
organised screening programme.2 Further, a
number of urologists have recommended the screening cut-off point to be lowered
as far as 2.5. To date, there is no evidence that the outcomes in men who have a
PSA between 2.5 and 4 are any worse than in men with a PSA between 4 and 10.
Thus, it is generally recommended that a PSA of 4 be a trigger point for further
investigation. The role of free-to-total PSA is still debated. As pointed out by
Durham et al, while this may reduce the probability of having prostate cancer on
a biopsy, it is unlikely to result in a difference sufficient to persuade men
not to have a biopsy. This paper points out that there is a 90-day spontaneous
variation of up to 1ng/ml. With fully automated testing this may be greater and
certainly in clinical practice it is not uncommon to find greater spontaneous
variations of PSA. Accordingly, repeating the PSA is preferable prior to
proceeding to biopsy of the prostate, as recommended in a recent publication by
Eastham et al.3 The majority of GPs
overestimated the positive predictive value of both the PSA and DRE. These
positive predictive values are around 35%.
In discussing the results, Durham et al state that
‘These reviews have consistently concluded that there is no evidence that
screening for prostate cancer will reduce mortality, and that radical treatment
of prostate cancer has risk of significant increased morbidity.’ To date,
there are no results from randomized controlled trials of screening. The results
of the American and European screening studies should be available within the
next five years. Until these results are available the question of whether or
not prostate cancer screening will reduce mortality remains unanswered.
Nevertheless, there is a considerable body of evidence, including the Quebec
study, the Tyrolia study, and the Olmstead County study, as well as the analysis
of the SEER data, which would suggest a possible effect, without being
conclusive.4 Furthermore, in Western countries,
where widespread PSA testing has become common, the age-adjusted mortality rate
of prostate cancer is falling. Thus, to date, whilst there is no proof that
prostate cancer screening will reduce mortality, there is also no proof that it
will not!
Finally, the findings of the controlled trial performed in
Sweden by Holmberg et al, comparing radical prostatectomy with watchful waiting,
require comment.5 This trial was reported after
eight years of follow up and there was no statistically significant difference
in overall mortality between the two groups. There is, however, a statistically
significant difference in prostate cancer mortality between the two groups. It
is widely expected that as the trial matures this may translate into a
difference in overall mortality. Thus, it seems highly likely that an effective
treatment is available for the treatment of prostate cancer.
The question of prostate cancer screening remains complex
and requires discussion between GP and the individual patient. The study by
Durham et al highlights some of the deficiencies in the understanding of GPs
around a number of issues related to the discussion about screening. An
understanding of these issues should help GPs to better advise their patients
about the benefits and risks associated with prostate cancer screening, and in
so doing help them in making their individual decisions.
Author information:
Peter Davidson, Urologist, Department of Urology, Christchurch Hospital,
Christchurch
Correspondence: Dr
Peter Davidson, Department of Urology, Christchurch Hospital, Private Bag 4710,
Christchurch. Fax: (03) 364 0936; email: peter@urology.co.nz
References:
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