The viewpoint paper on prostate cancer screening in this issue of the New Zealand Medical Journal raises some interesting questions about the medical rights of individuals, and precisely what is unethical behaviour in medicine (Richardson A. Prostate cancer screening: is it possible to explain diametrically opposed views? URL: http://www.nzma.org.nz/journal/118-1209/1289).

The author immediately gets into difficulties by posing a question in the title of the paper, and then failing to address it in the subsequent text. The truth is that diametrically opposed views are rarely both right, and are often both wrong. The middle position, or moderate view, is usually shown in time to be the correct one. The extreme positions in prostate cancer screening are, at one end, that no one should be screened (the author’s position); and at the other end, that all men over the age of 50 years should be enrolled in systematic population-based screening programmes.

This latter extreme is a position unsupported by nearly all health professionals active in the treatment of prostate cancer. The middle position, which currently available evidence suggests is a reasonable one to hold, is that screening should be accessible to those younger men most likely to have the disease, and to those men most likely to benefit from early diagnosis, such as men aged 70 years or less.

In adopting a paternalistic approach to all prostate cancer screening, the author fails to recognise that there are important differences between population-based screening (PBS) and self-requested screening (SRS).1 The value of PBS is determined by measuring the net benefit for the population screened, and this requires levels I and II evidence from well designed randomised controlled trials (RCTs).

At present, such evidence is not available, but absence of evidence is not evidence of absence. Unless the biological behaviour of prostate cancer is completely different to that of other cancers, and we have no reason to believe that it is, then it is a reasonable premise that earlier detection and treatment of the disease will be associated with survival advantages for at least some patients. Backing this belief is the fact that, after treatment, the survival of patients presenting with locally advanced tumours extending through the prostate capsule falls to approximately 20% at 10 years, compared with 85% for early confined tumours.

Most clinicians do not believe that lead time bias can be the sole explanation for this difference, as the cancer control curves for patients presenting with non-metastatic tumours have reached a plateau by 10 years after treatment, indicating that patients who have not relapsed at this time are cured. If diagnosis as early as possible in the natural history is to be abandoned as one of the key goals for improving outcomes, RCTs will therefore need to produce some surprising results.

The situation with SRS is very different to PBS. Here it is the individual man who is making a value judgement on whether or not they perceive there are advantages in being screened. Given the uncertainties that currently exist, it is not appropriate for others to make this decision on his behalf. The individual does require access to adequate educational literature to make an informed decision, and this material is currently not freely available to the public of New Zealand.1 Most importantly, the public needs to know which people are most likely to develop prostate cancer, and which people are most likely to benefit from earlier diagnosis, as well as details of the screening process, and its side effects. Those who are found to have prostate cancer need additional information on the implications of their particular cancer,2,3 the management options open to them, and the possible side effects of treatment.4

Those men at particularly high risk of developing prostate cancer deserve a special mention. The risk of developing prostate cancer rises by up to 11 times that of the general male population when a man has one or more first-degree relatives with the disease.5 Surely these men with genetic risks comprise a group that should be actively encouraged to present for screening?

The utility of the prostate cancer screening process has been described in detail in a recent New Zealand publication.6 This paper addresses how the pathology report on prostate biopsies can be used to obtain a better understanding of whether or not the cancer is a clinically significant one. A recent Swedish report showed that unsuccessful treatment, or no treatment, of cancers considered ‘low risk’ at diagnosis led to a high mortality rate from cancer by the time 15 years follow-up had elapsed.7 The mortality rate was particularly high for those patients aged 70 years or less at diagnosis. The incidence of prostate cancer in the Finasteride Trial,8 referred to by the author of the opinion paper that follows, is certainly higher than might have been anticipated, but this is probably due to the inclusion of some low-grade tumours that most expert pathologists would regard as being of dubious clinical significance. The absence of any outcome data from this trial makes it impossible to interpret the data further.

The low mortality ratio (incidence/mortality) of prostate cancer seen in New Zealand9 and other Western countries is unlikely to be due solely to a high proportion of ‘trivial’ cancers allowing death from other causes to intervene. Effective treatment for early tumours is also probably a factor, but until the New Zealand Health Information Service (NZHIS) is able to monitor cohorts of patients with full clinical data, we will struggle to understand the relative contribution of treatment and natural history to patient outcomes.10

In conclusion, there are large gaps in our knowledge and understanding of prostate cancer, and we look to the results of large RCTs to fill these gaps. Until then, some assumptions have to be made based on the generic behaviour of cancer. Prostate cancer is a major cause of male death, so deserves the respect of all medical disciplines, as well as governments responsible for funding our health services.

Author information: David Lamb, Associate Professor; Brett Delahunt, Professor, Department of Pathology and Molecular Medicine, Wellington School of Medicine and Health Sciences, University of Otago, Wellington South

Correspondence: Associate Professor David Lamb, Department of Pathology and Molecular Medicine, Wellington School of Medicine and Health Sciences, PO Box 7343, Wellington South; email: David.Lamb@ccdhb.org.nz