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Volume 3, Number 1—March 1997

Prostatitis and Benign Prostatic Hyperplasia: Emerging Infectious Diseases?

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To the Editor: In their excellent article, Molecular Approaches to the Identification of Unculturable Infectious Agents, Gao and Moore (1) point out that molecular approaches should be unleashed on diseases such as sarcoidosis, Kawasaki disease, and type I diabetes mellitus, which are thought but not proven to be infectious. The authors, however, are overlooking the more common and most likely infectious disease of unknown etiology today—prostatitis.

According to the pathologist McNeal, the prostate gland is the most commonly diseased internal organ of the human body (2). Prostatitis is the most common prostate disease, resulting in more physician visits than either benign prostatic hyperplasia or prostate cancer, according to the National Institutes of Health (3). Despite its frequency, prostatitis as a disease and as a histologic lesion is understudied (4).

By the Meares and Stamey culture localization procedure, in which the first voided urine, a midstream urine, the expressed prostatic secretions, and a final voided urine are compared, more than 90% of cases in patients with chronic pelvic symptoms are labeled as "nonbacterial" prostatitis or prostatodynia, both of which are thought to be incurable diseases (5).

The University of Washington has documented white blood cell counts as high as 38,000 per mm3, in "nonbacterial" prostatitis patients (6). According to urologist Thomas Stamey, up to 50% of all men experience symptoms of prostatitis during their lifetimes (7). The prostatitis lesion was found in 40 (44%) of 91 men at random autopsy (8). In another study of 100 consecutive autopsies on men who died suddenly in automobile accidents and from other causes, the prevalence of histologic signs of prostatitis increased with age and was highest when benign prostatic hyperplasia was also present. Prostatitis was present in 22% of men under 40 years of age and in 60% of those over 40 years of age (9).

In fact, the line between benign prostatic hyperplasia and prostatitis is blurred. Prostatitis as a histologic lesion has been found in 98% of patients with benign prostatic hypertrophy (10). Microbial tests on benign prostatic hyperplasia tissue have found significant rates of infectivity. In another study, more than 70% of transurethral resection of the prostate specimens showed clinical or laboratory signs of infection (11). Benign prostatic hyperplasia and prostatitis cannot be distinguished by symptoms, and some believe that they may be the same disease.

In these days of prostate specific antigen testing, more than 50% of men who undergo biopsies for prostate cancer have a prostatitis lesion whether they have cancer or not (Gottesman et al., unpublished data; McNeal, personal communication, 1995). Prostatitis occurs at an early age, and prostate cancer decades later, in the same part of the prostate gland, the peripheral zone.

Why aren't DNA techniques being unleashed on what is apparently the most common and most purulent unknown inflammatory disease in men—an inflammatory lesion that is associated with benign prostatic hyperplasia and prostate cancer? Surely, DNA microbial testing has important implications for all three major prostate diseases—prostatitis, benign prostatic hyperplasia, and prostate cancer.


Brad Hennenfent
Author affiliation: Director, The Prostatitis Foundation, Chicago, Illinois, USA



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  3. National Institutes of Health. The National Kidney and Urologic Diseases Advisory Board 1990 long-range plan. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, 1990.
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  7. Stamey  TA. Pathogenesis and treatment of urinary tract infections. Baltimore: Williams and Wilkins, 1980.
  8. McNeal  J. Regional morphology and pathology of the prostate. Am J Clin Pathol. 1968;49:34757.PubMedGoogle Scholar
  9. Bostrom  K. Chronic inflammation of the male accessory sex glands and its affect on the morphology of the spermatozoa. Scand J Urol Nephrol. 1971;5:133. DOIPubMedGoogle Scholar
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DOI: 10.3201/eid0301.970113

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