Some forms of prostate pain are caused by environmental agents. Are other forms the result also of inherited predisposition: Do genetic factors cooperate with epigenetic factors to cause prostate pain?

The clinical phenotypes of prostatitis range from asymptomatic infiltration of inflammatory cells to a profoundly painful chronic illness. Along this spectrum there is an acute variant that is commonly associated with a clear-cut environmental pathogen: Bacteria. In acute bacterial prostatitis — characterized by fever, bleeding, sepsis, and tenderness — the disease resolves quickly with antibiotics. Acute bacterial prostatitis appears to be largely a disease of the environment, not the genome.

Based partly upon observations made in acute bacterial prostatitis, patients with chronic prostate pain are also treated with antibiotics, which are used excessively in that they are often ineffective in resolving the symptoms. In other words, if chronic prostate pain is caused by infectious agents alone, then those agents are either antibiotic-resistant bacteria, anatomically sequestered bacteria, or not bacteria at all. Alternatively, chronic prostate pain is not a disease of infectious agents alone.

Is it also possible that chronic prostate pain has multifactorial etiology and that this explains variations in clinical phenotypes? And that unidentified factors variably transform generally asymptomatic bacteria (and/or other environmental agents) into pain producers? Yes, because prostates are commonly, and usually asymptomatically, colonized with bacteria. Are there examples in which a prevalent infectious agent is variably expressed as highly painful disease? Sure: Varicella Zoster, the virus that causes Chicken Pox, is highly prevalent but only a small proportion of its hosts suffers the episodic chronic pain of Shingles. The concept of variably painful infection is known, even as the factors that explain the variations may not be.

Can genetic variations theoretically mark and/or causally explain why some men develop chronic prostate pain? Can they theoretically interact with generally asymptomatic but highly prevalent bacteria and/or other environmental agents to cause pain one one man but not another? News this week that susceptibility to chronic pain is associated with specific inherited genetic polymorphisms of CACNG2, the gene for stargazin , illustrate that the answer is affirmative. Specifically, the authors discovered that they are associated with the chronic pain following breast surgery.

This discovery of a genetic marker of chronic pain opens the door to constructing a multifactorial genetic and epigenetic model of chronic pain, including chronic prostate pain. One can only hope that from such lines of research the future will permit us to not only better mark patients at risk of chronic pain but also to develop more specific and effective clinical interventions. The Prostatitis Blog congratulates the authors on a terrific bit of research.