Personal Views

Are we promoting stress and anxiety?

BMJ 1997; 315 doi: (Published 06 December 1997) Cite this as: BMJ 1997;315:1549
  1. Peter Whelan, is a consultant urologist in
  1. Leeds

    In 1989 carcinoma of the prostate was a decidedly provincial, indeed, almost homely type of disease. It had been known for more than 30 years to have a high latent prevalence, varying between 1:3 and 1:2 of all men, depending on their age, but it seemed to have a relatively small, clinical incidence. The diagnosis was made in most patients during their eighth decade, usually by the pathologists, following a prostatectomy for relief of obstructive urinary symptoms. In at least half the patients metastases were present at diagnosis. As this tumour, since the Nobel prize winning work of Huggins and Hodges in 1940, was known to be androgen dependent, all these patients were placed on either female hormones or underwent bilateral orchidectomy. Their median survival was a couple of years.

    In patients with localised disease many were treated by observation only, some had radiotherapy, some radical surgery, and some were started on hormone treatment immediately. Given the apparently slow nature of disease progression and competing mortalities in this age group, it was a perception, supported by the scientific literature, that all treatments had broadly similar survival curves. The concept in this group was that more men died with their prostate cancer rather than of it. At least half the men who died from prostate cancer were over 75, but, more importantly, less than 5% were under 60 at diagnosis.

    Science has also enabled us to know quite a lot about this 1989 version of carcinoma of the prostate. The latent cancer prevalence seemed to be similar worldwide, whereas there were marked racial and geographical differences in the clinical incidence of the disease. The rate for men in east Asia being apparently only a tenth of that of Afro-Americans. Interestingly, we also knew that when Asians migrated to the west coast of the United States the incidence increased and by the next generation was nearing the average for Caucasian Americans. Clearly there seemed to be both dietary and environmental as well as genetic factors which contributed to the development of clinical prostate cancer. We also knew, from initial reports in the 1960s, that there seemed to be a familial form of the disease which was diagnosed in younger men and was apparently more aggressive.

    In general, however, this disease was not perceived as a major public health problem. In Britain there were approximately 8000 deaths from prostate cancer each year; this represented approximately 8% of all cancer deaths and just over 2% of all male deaths. Cancer of the pancreas, a decidedly uncommon tumour, accounted for over 6000 deaths in Britain at this time, although they were appearing obviously in both sexes.

    What then has happened to invent or produce new prostate cancer? How and why has it occurred? The why is simple: prostate specific antigen (PSA). The how is more complex and may take social historians many years to understand and explain. We can, however, identify some factors that seem to have contributed.

    One was the presence of an obviously superior marker to those that have gone before. The limits of this marker had not been fully explored. The second was the presence of effective drug treatment for benign prostatic hyperplasia and the natural concern that patients would not take these tablets because of the risk of masking prostate cancer. Perhaps there was a subliminal male desire to have a disease all of our own, even if it had to be a cancer. There was an obvious desire on the part of the urological community to see whether this disease could be diagnosed earlier and by intervention influence its outcome.

    The rush to introduce PSA testing has produced the antithesis of a paradigm of how a marker should be used for either case finding or so called screening. Where are the identifiable at risk groups? Where is the minimal effective interventional treatment? Where are the randomised and longitudinal studies showing that the use of this marker early is necessary and helpful?

    There is only one paper of a prospective randomised trial comparing radical surgery with observation, and no difference in survival in this much criticised paper was shown. Indeed, exhaustively perusing more than 12 000 articles on localised prostate cancer, an expert committee in 1995 was unable to define the best method of treating localised prostate cancer comparing observation, radical surgery, or radical radiotherapy. These issues, thanks to current prospective randomised trials, are likely to be answered within the next few years. Answers were not available six years ago when PSA testing started.

    Although cancer societies recommend that all men over 50 should have an annual PSA test, the vast majority of men will never get prostate cancer. PSA means prostate specific antigen, not prostate cancer specific antigen, and we know that many of the values are arbitrary and that most men taken as a group with minor elevations of their PSA will not have prostate cancer. Investigation is not a benign process. A recent audit of transrectal ultrasound biopsy of the prostate published by the Royal College of Surgeons of England has shown that there is a 0.4% mortality rate for the test and 2% of patients need to stay in hospital.

    Despite observation being a successful valid treatment no patient who has been found to have prostate cancer on the basis of a blood test will accept this. Patients will rightly expect to be treated, and treated effectively, although there remains as yet no scientific validity for any interventional treatment. We have to be wary of the many reports which genuflect vaguely in the direction that this work should have been validated by a randomised prospective trial, but then go on to give us an anecdotal observational study with actuarial survival and end up trying to persuade us that it is Holy Writ.

    There is no turning the clock back. A whole generation of men are probably more aware of their current PSA state than anything else. Whether this will do more than worry a large number of people to no good purpose is something that only the ongoing observational studies will actually tell us, but surely, after the fiasco of mass radiography for lung cancer, a much more serious and prevalent disease which kills people in large numbers prematurely, we should have learnt our lesson. Perhaps it may come as no surprise that new prostate cancer is the same as the old 1989 version of prostate cancer, plus PSA, which merely Promotes Stress and Anxiety.

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