Helicobacter pylori seroprevalence in patients with chronic prostatitis: a pilot study.
ABSTRACT This study investigated the possible relationship between Helicobacter pylori infection and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). The rate of seropositivity for antibodies against H. pylori was determined in a cohort of subjects with CP/CPPS and prostatitis-free control subjects.
Sixty-four consecutive patients with CP/CPPS and 55 randomly selected asymptomatic men were recruited to the study. Blood samples from enrolled patients and control subjects were analysed using an enzyme-linked Immulite analyser immunoglobulin G serological test for H. pylori diagnosis. Prostate volume, prostate-specific antigen level, maximum urinary flow rate, and International Prostate Symptom Score (IPSS) and National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) score of the subjects were also determined. The results were analysed with chi-squared and Student's t test and statistical analysis was carried out using SPSS software.
There were no significant differences in age and social status between the CP/CPPS and control groups (p > 0.05). Total NIH-CPSI score was significantly higher in the CP/CPPS group. Seropositivity for antibody against H. pylori was higher in the CP/CPPS than the control group (p < 0.05).
This pilot study supports the hypothesis that H. pylori may play a role in CP/CPPS. The infection may be related to the immune response and increased cytokines in seminal plasma and/or expressed prostatic secretion. However, no study has investigated the relationship between CP/CPPS and H. pylori stool antigen positivity. This study showed that H. pylori seropositivity is high in CP/CPPS patients, but this needs to be confirmed by other studies.
[Show abstract] [Hide abstract]
ABSTRACT: PURPOSE: To review the etiology and pathogenesis of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). METHODS: A literature review for the years 1985-2012 was performed using the MEDLINE database of the United States National Library of Medicine. RESULTS: The evidence for ongoing infection in men with CP/CPPS is lacking. However, men with CP/CPPS are twice as likely to have had a sexually transmitted disease (STD), and bacteria from men with CP/CPPS may be phenotypically different from those that cause cystitis or acute prostatitis. Evidence continues to support an alteration in both the afferent and efferent autonomic nervous systems. Functional brain imaging suggests changes in the gray matter as well as the importance of the anterior insula and anterior cingulated gyrus in pain processing. Neural function can be modulated by immune and endocrine factors. Alterations in cytokine function and autoimmunity appear to play a role in the immune dysfunction. Alterations in the hypothalamic-pituitary-adrenal axis can mediate the endocrine effects, similar to many other chronic pain conditions. Genetics may play a role in who may develop chronic pain after an initial insult. Finally, any biological changes must then be processed through the psychosocial environment, including the tendency to catastrophize, and degree of spousal support, to produce a given individual patient's pain experience. CONCLUSIONS: Infection with atypical bacteria or sequelae of an STD may lead to CP/CPPS in some men. Such a biological insult in the context of alterations in psychoimmunoneurendocrine factors produces the chronic pain experience.World Journal of Urology 04/2013; 31(4). DOI:10.1007/s00345-013-1061-z · 3.42 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Helicobacter pylori (H. pylori) is a atypical gram-negative bacteria preferring gastric mucosa which also have bizarre multisystem effects extended to some malignancies, hematologic and vascular disorders through some not well defined pathophysiologic pathways. Our pioneer data was pointing that the urinary system stone existence was seemed to be high in the group of H. pylori+cases. While the explanation of the reason of the coincidence of renal-gall bladder stones, it was previously suggested that there may be a shift mechanism of intestinal microbial flora, from Oxalobacter formigenes that may reduce the risk of renal stone by consuming intestinal oxalate, to H. pylori which is known to induce gallstone by unknown mechanism. This hypothesis is an indirect one and highly controversial for the effect of H. pylori in the renal stone formation because intestinal absorption of oxalate is not significant when it is compared with the endogen oxalate. The present preliminary unique data in connection with our hypothesis claimed that a possible relation between H. pylori and renal stones. We think that this detrimental effect is due to the possible systemic influence such as vascular and/or endoluminal sickness due to the H. pylori other than directs bacteriologic colonization. There is strong evidence that H. pylori have some role in the atherosclerotic procedure. The vascular theory of Randall plaque formation at renal papilla and subsequent calcium oxalate stone development that suggests microvascular injury of renal papilla in an atherosclerotic-like fashion results in calcification near vessel walls that eventually erodes as a calculus format into the urinary system. Briefly, theories of stone and atherosclerosis seemed to be overlap and H. pylori is one of the factor of both processes. In addition to our hypothesis, we claimed that H. pylori might have same detrimental effect on endoluminal surfaces of urinary and genital systems and resulting in some special pathologies as Hunner's ulcers in interstitial cystitis and even posttesticular infertility. The accumulating knowledge about extragastric sequelae of H. pylori may open new aspects on therapeutic and the prevention strategies of urolithiasis and even this progress may reach to chronic pelvic pain syndromes and idiopathic infertility. Copyright © 2014 Elsevier Ltd. All rights reserved.Medical Hypotheses 10/2014; 83(6):677-680. DOI:10.1016/j.mehy.2014.09.016 · 1.15 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: The cause of chronic pelvic pain syndrome (CPPS) has yet to be established. Since the late 1980s, cytokine, chemokine, and immunological classification studies using human samples have focused on identifying biomarkers for CPPS, but no diagnostically beneficial biomarkers have been identified, and these studies have done little to deepen our understanding of the mechanisms underlying chronic prostatic pain. Given the large number of men thought to be affected by this condition and the ineffective nature of current treatments, there is a pressing need to elucidate these mechanisms. Prostatitis types IIIa and IIIb are classified according to the presence of pain without concurrent presence of bacteria; however, it is becoming more evident that, although levels of bacteria are not directly associated with levels of pain, the presence of bacteria might act as the initiating factor that drives primary activation of mast-cell-mediated inflammation in the prostate. Mast cell activation is also known to suppress regulatory T cell (Treg) control of self-tolerance and also activate neural sensitization. This combination of established autoimmunity coupled with peripheral and central neural sensitization can result in the development of multiple symptoms, including pelvic pain and bladder irritation. Identifying these mechanisms as central mediators in CPPS offers new insight into the prospective treatment of the disease.Nature Reviews Urology 04/2014; DOI:10.1038/nrurol.2014.63 · 4.52 Impact Factor