IJE Advance Access originally published online on January 13, 2005
International Journal of Epidemiology 2005 34(1):197-198; doi:10.1093/ije/dyh403
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IJE vol.34 no.1 © International Epidemiological Association 2005; all rights reserved.
Commentary |
Commentary: Is prostate cancer an infectious disease?
Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA. E-mail: correa{at}lsuhsc.edu
In this issue, Leticia Fernandez and her fellow epidemiologists from Cuba, Barcelona, and Lyon report interesting findings of their case–control study in Havana, Cuba.1 The report adds relevant information supporting the causal relationship between chronic inflammation and cancer development. The list of infections and chronic inflammatory states aetiologically linked to cancer is increasing and includes major human burdens such as carcinomas of the cervix, stomach, colon, liver, and bladder as well as some lymphomas. Although the cancer risk attributable to infections has been quoted as 
15.6%,2 that estimate does not take into account the risk enhancement effect of chronic inflammation in multifactorial causal associations in common cancers such as those of the breast and colon. It is also well accepted that chronic inflammation affects the prognosis of cancer by as yet unclear mechanisms. This knowledge has led to many ongoing intervention trials of inhibitors of inflammation such as the non-steroidal anti-inflammatory drugs and the cyclooxygenase (Cox-2) inhibitors in dozens of cancer sites, with convincing beneficial effects on prognosis.
Prostatic cancer is the second most frequent malignant neoplasia worldwide, accounting for 542 990 new cases and 204 313 deaths in 2000.3 The incidence has been increasing recently in many countries, but the extent of confounding by the recent introduction and generalization of the PSA test for screening is difficult to evaluate. The experience in Cuba, where PSA testing is not done, clearly shows that the increasing trend is real.
Most epidemiological studies have shown that sexual activity and prostatic cancer are causally associated. Indicators of sexual activity vary in their association with prostatic cancer in different studies, but the trend for a risk increase is clear and consistent.4–6 The association with venereal diseases is also significant and consistent. These two sets of aetiological factors are obviously interrelated: greater sexual activity increases the chances of infection. It seems clear, however, that androgen secretion, which increases the sexual drive, has an independent risk-enhancing effect. Men whose testicles are never developed or are removed, never develop prostatic cancer.7–9 The beneficial effects of chemical or surgical castration in the prognosis of advanced prostatic cancer are well known.
It is not clear which of the venereal diseases or which combination of them are responsible for the increase in risk. The most consistent finding refers to gonorrhoea, but syphilis and herpes have also been implicated.4 Human papilloma virus infections have been suggested, but no good evidence supporting the association has been found.5 The determinant factors may be related to the potential of the infection to establish a chronic active inflammation. In that scenario, the prospects for gonorrhoea are more plausible since the bacteria can survive in the secretion of the prostatic glands, where they can escape the effects blood-borne antibiotics and at the same time induce an indolent, but active, chronic inflammatory state which attracts neutrophilic leukocytes and macrophages carrying mutagenic agents such as myloperoxidase and nitric oxides. Chronic prostatitis may be clinically silent but is a frequent cause of elevated blood PSA levels.
The Cuban study clearly contributes to our understanding of the complex host–environment interactions in cancer causation, and in particular of the role of chronic inflammation.
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1 Fernandez L, Galan Y, Jimenz R et al. Sexual behaviour, history of sexually transmitted diseases and risk of prostate cancer: a case-control study in Cuba. Int J Epidemiol 2005;34:193–97.
2 Pisani P, Parkin DM, Muñoz N et al. Cancer and infection: estimates of the attributable fraction in 1990. Cancer Epidemiol Biomarkers Prev 1997; 6:387–400.[Abstract]
3 Ferlay J, Bray P, Pisani P, Parkin DM. GLOBOCAN 2000: Cancer Incidence, Mortality and Prevalence Worldwide, version 1.0. IARC Cancer Base No. 5. Lyon, France: IARC Press, 2001.
4 Key T. Risk factors for prostate cancer. Cancer Surv 1985; 23:63–77.
5 Dennis LK, Dawson DV. Meta-analysis of measures of sexual activity and prostate cancer. Epidemiology 2004; 13:72–79.
6 Rosenblatt KA, Wicklund KG, Stanford JL. Sexual factors and the risk of prostate cancer. Am J Epidemiol 2001; 12:1152–58.
7 Ross BK, Shimizu H, Paganini-Hill A et al. Case-control studies of prostate cancer in blacks and whites in Southern California. J Natl Cancer Inst 1987; 78:869–74.[Web of Science][Medline]
8 Perez CA, Fair WR, Ihde DC. Carcinoma of the Prostate. In: Devita VT, Hellmann S, Rosenberg SA (eds). Cancer: Practices and Principles of Oncology. Philadelphia: JB Lippincott Co, 1989.
9 Wilson JD. Recent studies on the mechanism of action of testosterone. N Engl J Med 1972; 287:1284–91.[Web of Science][Medline]
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