Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Certain ejaculate infections can be traced back to sexually transmitted microorganisms, such as Neisseria gonorrhoeae, Chlamydia trachomatis, Ureaplasma urealyticum and Trichomonas vaginalis. To varying extents, these microorganisms cause such classical genital infections as urethritis, epididymitis and prostatitis as well as subclinical genital tract infections. Several different pathomechanisms are under discussion for infection of the ejaculate: reduction of spermatogenesis resulting from testicular damage, autoimmune processes induced by inflammation, direct influence on the spermatozoal function, disturbances in spermatozoal transport, secretory dysfunction of the male accessory sex glands and leukocytospermia with secondary influence on ejaculate parameters. The relevance of these microorganisms for the localization of the inflammatory process within the genital tract are discussed in detail. Their importance for male fertility is a matter of debate. In particular, the significance of C. trachomatis and U. urealyticum, both of which are detectable in the urethra, is still uncertain and cannot be assessed conclusively. Further information allowing delimitation of an infection resulting from bacterial colonization may be provided, on the one hand, by biochemical markers for an inflammatory reaction and indicators of an immune response in the ejaculate, e.g. PMN elastase, complement C3, or coeruloplasmin, and on the other hand, by secretion markers such as alpha-glucosidase, PSA and phosphatase. Whether the assessment of these markers and indicators can help to clarify the inflammatory origin of infertility in individual cases remains doubtful.
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PMID:[Infections of the ejaculate by sexually transmissible pathogens]. 751 3

Secretory leucocyte protease inhibitor, SLPI, is a low-molecular-weight, acid-stable protein present in the liquid part of fresh human ejaculate but not demonstrable in the gel structure. No fragmentation of SLPI occurred during gel dissolution, but a slow proteolytic cleavage of SLPI was seen on incubation of the liquified semen at 37 degrees C. The same pattern of degradation products was seen after incubation of SLPI with prostatic secretion and also with purified prostate-specific antigen, PSA. We could identify Arg 20-Tyr 21 and Met 73-Leu 74 to be the primary cleavage sites upon proteolytic modification of SLPI by purified PSA. However, we did not find any inhibition of the enzymatic activity of PSA by SLPI, even at a 100-fold molar excess of the inhibitor. The slow degradation of SLPI facilitated sampling and the reliable determination of the normal level of SLPI in seminal plasma, which was about 20 mg/L. We investigated the glandular origin of SLPI in the genital tract by immunocytochemistry. A strong immunostaining for SLPI was demonstrated in epithelial cells within the glandular lumina of the prostate gland, seminal vesicles, and epididymis but not in the stromal parts of these glands. In addition the immunostaining was also detected in the deferent ducts and the germinal epithelium of the testes. Taking into account that SLPI is a strong inhibitor of several proteases, including leukocyte elastase and cathepsin G, the results suggest that SLPI has a local protective function against proteolytic degradation of the male reproductive tract tissues during inflammation.
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PMID:Secretory leucocyte protease inhibitor in the male genital tract: PSA-induced proteolytic processing in human semen and tissue localization. 753 15

Though detailed cytological and microbiological diagnostic procedures are routinely carried out in male genital tract infection, the correct diagnosis and localization of inflammation or infection is often difficult. In this prospective study, the relevance of the seminal plasma markers PMN elastase, complement C3, CRP, fructose, PSP 94, PSA, and alpha-glucosidase was investigated in 13 patients with chronic prostatitis, 31 patients with significant leukocytospermia, and 58 patients with non-inflammatory diseases (controls). Statistically relevant results were obtained for PMN elastase when comparing chronic prostatitis with controls, leukocytospermia with controls (P < 0.001) and chronic prostatitis with leukocytospermia (P < 0.05); for complement C3 chronic prostatitis and leukocytospermia vs. controls (P < 0.05) and for fructose/ejaculate leukocytospermia vs. controls (P < 0.05). No statistically relevant differences were found for C-reactive protein, alpha-glucosidase, PSA and prostatic secretory protein (PSP 94). To delimit genital tract inflammation from non-inflammatory patients, cutpoint levels for PMN elastase of 230 ng ml-1 and for C3c of 0.01 g l-1 were suggested. PMN elastase was shown to possess the strongest discriminating power. The assessment of a cutpoint for fructose to indicate seminal vesicle dysfunction is not possible as the significance level is weak (P < 0.05).
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PMID:Evaluation of seminal plasma parameters in patients with chronic prostatitis or leukocytospermia. 962 42

The new classification of prostatitis syndromes by the National Institutes of Health clearly defines the diagnostic criteria for categorization according to the clinical symptoms. In addition to the validated symptom scores, the four-glass test demonstrating increased numbers of leukocytes and/or bacteria serves for differentiating between the symptoms. Increased levels of leukocytes and/or increased bacterial count in expressed prostatic excretion (EPS) are typical of prostatitis, although there is a high degree of correspondence with the VB3 fraction (urine voided after prostatic massage). The detection of peroxidase cells (granulocytes) and of an increased concentration of polymorphonuclear (PMN) leukocyte elastase in the ejaculate are indicative of uroadnexitis. Nonbacterial forms of prostatitis (NIH III) and increased PSA levels require intensive clinical diagnosis.
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PMID:[Diagnosis of chronic prostatitis]. 1122 37