What Is Prostatodynia?

Background
The term prostatodynia, or chronic pelvic pain syndrome (CPPS), is used to designate unexplained pelvic pain in men; this pain is associated with irritative voiding symptoms and/or pain located in the groin, genitalia, or perineum in the absence of pyuria and bacteriuria (no pus cells or bacteria seen on microscopic analysis of the urine). However, excess WBCs(white blood cells) or bacteria seen on Gram stain and culture of expressed prostatic secretions (EPS) may be found.

The use of the term prostatodynia is not encouraged in current practice. This term carries the negative historical connotation of being a "wastebasket" designation for a melange of psychosomatic symptoms and suggests that the source of the patient's symptoms invariably lies within the prostate gland itself. Current research has provided evidence of numerous extraprostatic considerations, including neuropathic and other systemic pathologies.

An academic distinction is currently made between
(1) patients with excess WBCs in their prostatic secretions (chronic nonbacterial prostatitis, class IIIa) and
(2) those with normal prostatic secretions (prostatodynia, class IIIb). However, the clinical value of this distinction is now being challenged. The sole parameter is the number of WBCs seen within a smear of prostatic secretions. However, this number may vary widely within the same specimen and even more so from sample to sample taken from the same patient. Furthermore, asymptomatic control patients devoid of any evidence of pelvic pathology have also been found to have a significant number of WBCs in their prostatic secretions. At present, the distinction seems to provide no meaningful differential with respect to either etiology or treatment options.

Pathophysiology
Pontari and Ruggieri's comprehensive 2004 update reviews the numerous pathophysiologic mechanisms implicated as the potential etiology of CPPS. After surveying all of the relevant articles on this topic published from 1966-2003, these researchers reached the following conclusions:
The etiology (or etiologies) of CPPS remains unknown.

  The number of WBCs (pus cells) found in the prostatic fluid under microscopic examination—long considered the hallmark of this disease process—does not correlate with the degree of pain or with other symptoms experienced by patients with CPPS. Histological signs of inflammation were found in only one third of all patients diagnosed with CPPS who underwent prostatic biopsy, further suggesting an extraprostatic etiology for CPPS. Perhaps CPPS—so-called chronic prostatitis (CP)—is not directly associated with the prostate or with inflammation within it, at least in some cases.

Special signaling molecules called cytokines, which are produced by WBCs (and by other cells), may play a role. While certain cytokines stimulate an inflammatory reaction, others inhibit inflammation. Moreover, the same cytokine may act as either an inciting influence or an inhibiting influence at different sites under varying conditions. Tissue necrosis factors, interleukins, interferons, and epithelial neutrophil-activating factors are but a few of these cytokines. To complicate matters, each of these terms indicates a whole, separate family of closely related molecules, not a single agent. An imbalance in this complex network of cytokines (ie, of proinflammatory cytokines and endogenous cytokine inhibitors) has been linked to the development of pelvic inflammation and pain in patients with CPPS.
Genetic predisposition to CPPS may be the result of differences in DNA sequences at chromosomal sites that regulate the production and action of these various cytokines.
Autoimmunity, the abnormal tendency of the body to react against itself, has long been thought to play a role in the development of CPPS. In this context, immunity refers to the body's ability to reject foreign material, such as bacteria or toxins. This process can sometimes turn on itself and lead to rejection of the body's own healthy tissues. In CPPS, the body may be attempting to reject its own prostate.
Testosterone has been shown to protect against inflammation within the prostate. Perhaps a low testosterone level (or, more likely, a breakdown in the mechanism whereby testosterone inhibits prostatic inflammation) may be at work in some men with CPPS.
Abnormal functioning of the nervous system, at the local level and/or within the CNS, may also play a role in the development of CPPS. For example, a substance known as nerve growth factor (NGF) can cause an increase in the number and the sensitivity of the pelvic nerves that transmit pain. An increase in NGF has been correlated with the development of CPPS symptoms.
Each of the above factors has been individually identified as a culprit in the causation of CPPS; additionally, at least in some cases, they may interact with each other to cause CPPS. For instance, cytokines may adversely affect the suppression of NGF, which, in turn, leads to a flare of CPPS symptoms.
Psychological stress and depression have long been associated with CPPS flare-ups. This observation has led some researchers to mistakenly conclude that CPPS is "all in your head” or that such mental stress results in a lower psychological threshold for the same objective degree of pain. More recent data, however, suggest that psychological stress and depression may measurably influence the local production of cytokines (eg, interleukin 10, interleukin 6) in the pelvis, thus directly exacerbating CPPS inflammation.
Some cases of "abacterial" prostatitis may not actually be abacterial. Recent data suggest that gram-positive bacteria, which have traditionally been dismissed as normal florae in prostatic fluid cultures, may not be so normal in men with CPPS. Normal defense mechanisms allow healthy men to render these bacteria harmless as mere microbial "hitchhikers." However, these defense mechanisms may be defective in men with CPPS. This theory helps explain why prolonged courses of antibiotics sometimes provide symptomatic relief for men with CPPS despite the absence of bacteria that are traditionally considered pathogenic.
Pontari and Ruggieri conclude that "To what degree these factors interact in a given patient and to what degree there is a common pathway or several pathways that lead to the end point of pelvic pain remains to be determined." Clearly, the final answer (or answers) is not yet determined. Opportunities abound for clinical and basic science research in this area.

Frequency
United States
CP is the most common urological diagnosis in men older than 50 years and is the third most common diagnosis in men younger than 50 years. This diagnosis results in at least 2 million office visits per year. The average urologist sees approximately 10 patients with prostatitis per month, 30% of whom are new patients. Specific urinary pathogens are detected infrequently after culture. The vast majority of these patients are categorized as having chronic nonbacterial prostatitis or prostatodynia, otherwise known as CPPS in the male.

Age
CP most commonly affects men older than 50 years. It is only slightly less common in men younger than 50 years.

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