Prevalence and Psychosocial Correlates of Symptoms Suggestive of Painful Bladder Syndrome: Results From the Boston Area Community Health Survey

Link, Carol L.; Pulliam, Samantha J.; Hanno, Philip M.; Hall, Susan A.; Eggers, Paul W.; Kusek, John W.; McKinlay, John B.

doi:10.1016/j.juro.2008.04.009

Cited by 59 publications

(36 citation statements)

References 23 publications

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“…For instance, several studies administered surveys about prior diagnoses of IC/BPS or ‘prostatitis’, 1-6 or about current symptoms of IC/BPS 7, 8 or CP/CPPS. 2-6 Others have abstracted data from medical records.…”

Section: Introductionmentioning

confidence: 99%

The Prevalence and Overlap of Interstitial Cystitis/Bladder Pain Syndrome and Chronic Prostatitis/Chronic Pelvic Pain Syndrome in Men: Results of the RAND Interstitial Cystitis Epidemiology Male Study

et al. 2013

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Purpose As part of the RICE study, we previously developed validated case definitions to identify interstitial cystitis/bladder pain syndrome (IC/BPS) in women and chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) in men. Using population-based screening methods, we applied these case definitions to determine the prevalence of these conditions in men. Materials and Methods A total of 6,072 households were contacted by phone to screen for men who had symptoms of IC/BPS or CP/CPPS. An initial 296 men screened positive, of which 149 met the inclusionary criteria and completed the telephone interview. For IC/BPS, two case definitions were applied (one with high sensitivity and one with high specificity), while for CP/CPPS, a single case definition (with both high sensitivity and specificity) was used. These case definitions were used to classify subjects into groups based on diagnosis. Results The IC/BPS weighted prevalence estimate for the high sensitivity and specificity definition was 4.2% (3.1-5.3%), and 1.9% (1.1-2.7%), respectively. The CP/CPPS weighted prevalence estimate was 1.8% (0.9-2.7%). These values equate to 1,986,972 (95% CI 966,042- 2,996,924) men with CP/CPPS and to 2,107,727 (95% CI 1,240,485 – 2,974,969) men with the high specificity definition of IC/BPS in the U.S.. The overlap between men who met either the high specificity IC/BPS case definition or the CP/CPPS case definition was 17%. Conclusions Symptoms of IC/BPS and CP/CPPS are widespread among men in the US.. The prevalence of IC/BPS symptoms in men approaches that in women, suggesting that this condition may be underdiagnosed and undertreated in the male population.

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Section: Introductionmentioning

confidence: 99%

The Prevalence and Overlap of Interstitial Cystitis/Bladder Pain Syndrome and Chronic Prostatitis/Chronic Pelvic Pain Syndrome in Men: Results of the RAND Interstitial Cystitis Epidemiology Male Study

et al. 2013

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“…Those percentages translated into 3.3 to 7.9 million women 18 years old or older with IC/PBS symptoms [4]. Other studies have estimated the prevalence of IC/PBS among men to be 2 to 5 times lower than in women [5], [6]. Symptoms of IC interfere with employment, social relationships, and sexual activity.…”

Section: Introductionmentioning

confidence: 99%

Uroplakin Peptide-Specific Autoimmunity Initiates Interstitial Cystitis/Painful Bladder Syndrome in Mice

et al. 2013

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The pathophysiology of interstitial cystitis/painful bladder syndrome (IC/PBS) is enigmatic. Autoimmunity and impaired urothelium might lead the underlying pathology. A major shortcoming in IC/PBS research has been the lack of an appropriate animal model. In this study, we show that the bladder specific uroplakin 3A-derived immunogenic peptide UPK3A 65–84, which contains the binding motif for IAd MHC class II molecules expressed in BALB/c mice, is capable of inducing experimental autoimmune cystitis in female mice of that strain. A highly antigen-specific recall proliferative response of lymph node cells to UPK3A 65–84 was observed, characterized by selectively activated CD4+ T cells with a proinflammatory Th1-like phenotype, including enhanced production of interferon γ and interleukin-2. T cell infiltration of the bladder and bladder-specific increased gene expression of inflammatory cytokines were observed. Either active immunization with UPK3A 65–84 or adoptive transfer of peptide-activated CD4+ T cells induced all of the predominant IC/PBS phenotypic characteristics, including increased micturition frequency, decreased urine output per micturition, and increased pelvic pain responses to stimulation with von Frey filaments. Our study demonstrates the creation of a more specific experimental autoimmune cystitis model that is the first inducible model for IC/PBS that manifests all of the major symptoms of this debilitating condition.

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“…IC/PBS occurs mainly in women, with a prevalence estimated in different studies to be two to five times higher than in men (12,35). The most recent National Institutes of Healthfunded epidemiological study of IC/PBS in women in the United States (the Rand IC Epidemiology study) identified prevalences of 6.5% and 2.7% based on high sensitivity and high specificity criteria, respectively, for diagnosing IC/PBS (7).…”

mentioning

confidence: 99%

Chronic pelvic allodynia is mediated by CCL2 through mast cells in an experimental autoimmune cystitis model

Bicer

Altuntas

İzgi

et al. 2015

American Journal of Physiology-Renal Physiology

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The cause of chronic pelvic pain in interstitial cystitis/painful bladder syndrome (IC/PBS) remains unclear; autoimmunity is a possible etiology. We have recently shown that injection of a single immunogenic peptide of uroplakin 3A (UPK3A 65-84) induces experimental autoimmune cystitis (EAC) in female BALB/cJ mice that is unique among experimental models in accurately reflecting both the urinary symptoms and pelvic pain of IC/PBS. The aim of this project was to identify the roles of mast cells and mast cell chemoattractant/activator monocyte chemoattractant protein-1 [chemokine (C-C motif) ligand 2 (CCL2)] in the allodynia in this model. We immunized 6- to 8-wk-old female BALB/cJ mice with UPK3A 65-84 peptide and, 5–40 days later, observed increased responses to stimulation of the suprapubic abdominal and hindpaw surfaces with von Frey monofilaments compared with mice injected with adjuvant alone. Suprapubic and hindpaw tactile allodynia responses by EAC mice were blocked by instillation of lidocaine into the bladder but not by lidocaine in the uterus, confirming the bladder as the source of the hypersensitivity. Markedly increased numbers of activated mast cells and expression of CCL2 were found in the bladder after immunization with UPK3A 65-84. Hypersensitive responses were inhibited by mast cell stabilizer cromolyn sodium and antagonists of histamine receptors 1 and 2. Furthermore, BALB/cJ mice with deletion of the Ccl2 or chemokine (C-C motif) receptor 2 gene exhibited markedly reduced allodynia and accumulation of mast cells after UPK3A 65-84 immunization. These results show that UPK3A 65-84 immunization causes chronic visceral allodynia and suggest that it is mediated by CCL2-driven mast cell accumulation in the bladder.

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Prevalence and Psychosocial Correlates of Symptoms Suggestive of Painful Bladder Syndrome: Results From the Boston Area Community Health Survey

Cited by 59 publications

References 23 publications

The Prevalence and Overlap of Interstitial Cystitis/Bladder Pain Syndrome and Chronic Prostatitis/Chronic Pelvic Pain Syndrome in Men: Results of the RAND Interstitial Cystitis Epidemiology Male Study

The Prevalence and Overlap of Interstitial Cystitis/Bladder Pain Syndrome and Chronic Prostatitis/Chronic Pelvic Pain Syndrome in Men: Results of the RAND Interstitial Cystitis Epidemiology Male Study

Uroplakin Peptide-Specific Autoimmunity Initiates Interstitial Cystitis/Painful Bladder Syndrome in Mice

Chronic pelvic allodynia is mediated by CCL2 through mast cells in an experimental autoimmune cystitis model

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