Helicobacter pylon: A Prostate Pathogen?

J Dimitrakov,¹ G Rawadi<sup>2

1</sup>Department of Nephrology and Urology, Higher
Medical Institute, Plovdiv, Bulgaria, ²Mycoplasma
Laboratory, Institut Pasteur, Paris, France

Background Helicobacter pylori is known to reside only in the stomach of humans, primates, and perhaps cats. In the stomach it lives beneath the mucous layer, adjacent to the surface and pit epithelial cells of the gastric antrum and body. Although H. pylori exhibits enormous genetic diversity, two basic phenotypes are widely recognized: one that produces vacuolating cytotoxin and one that does not. Cytotoxin expression correlates with the presence of a 40-kb segment of DNA termed the pathogenicity island. One of the genes in this island, the CagA gene, is a good, although imperfect, marker for the propensity of the strain to cause disease.

Material and Methods We PCR-analyzed prostate biopsy samples from 30 patients with symptoms and signs of chronic abacterial prostatitis/chronic pelvic pain syndrome with more than 10 WBC/hpf (Class IIIA- NIH). The diagnosis was based on the pre- and post-prostatic massage urine test as described by Nickel as well as on the expressed prostatic secretion (EPS). We also evaluated the detection of the putative virulence marker of H. pylori, the CagA gene, by PCR in biopsy samples as well as in corresponding H. pylori isolates following the protocol of Labigne et al. (1991). Prostate biopsy samples from 30 patients with prostate cancer served as controls. Levels of interleukin-8 (IL-8) were measured in EPS and/or post-prostatic massage urine as a marker of active H. pylori infection. All specimens tested negative for mycoplasma.

Results Three of the 30 patients (10%) with chronic prostatitis (Class IIIA- NIH) and none of the controls tested positive for the presence of H. pylori. The cagA gene was detected in all three H.pylori-positive specimens. All of the patients who tested positive for H. pylori had elevated levels of IL-8 as compared with the remaining 27 patients and the control prostate cancer patients. The differences between the groups were statistically significant (P<0.0001). The H. pylori-positive patients received triple combination anti-H. pylori therapy consisting of Omeprazole 40 mg bid, Metronidazole 500 mg bid, and Clarithromycin 500 mg bid for 3 weeks together with colloidal Bismuth subcitrate 240 mg bid for 4 weeks with favorable clinical outcome. At follow-up 3 and 6 months later, the leukocyte count was 10 WBC/hpf and the level of IL-8 was comparable to that of the patients in the non-H. pylori group.

Conclusion Our study raises some important questions about the pathogenic role of H. pylori in chronic abacterial prostatitis. It remains to be elucidated how the organism leaves its host and enters the environment; where (if anywhere) it persists in the environment; when and how people become infected (with circumstantial evidence favoring fecal-oral and oral-oral transmission); and why infection establishes itself in the prostate only in a proportion of exposed hosts.