Risks of interstitial cystitis among patients with systemic lupus erythematosus: A population‐based cohort study

Wen, Jen Yu; Lo, Tsia Shu; Chuang, Yao‐Chi; Ho, Chung‐Han; Long, Cheng‐Yu; Law, Kim-Seng; Tong, Yat Ching; Wu, Ming

doi:10.1111/iju.14065

Cited by 22 publications

(14 citation statements)

References 29 publications

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“…A nationwide population-based cohort study of 11,526 patients with primary Sjogrens syndrome in Taiwan revealed an increased risk of BPS/IC in this cohort, with a hazard ratio of 2.34 (95% CI 1.59-3.44, p < 0.01) [45]. A similar study revealed a higher incidence of BPS/IC in patients with systemic lupus erythematosus, with a hazard ratio of 2.45 (95% CI 1.57-3.27, p < 0.05) [46]. Further research is required to determine whether phenotypes of BPS/IC associated with autoimmune conditions could benefit from targeted immunomodulatory therapies [47].…”

Section: Phenotype Based On Co-existing Somatic Conditionssupporting

confidence: 60%

Phenotypes of BPS/IC

Malde

Sahai

2020

Curr Bladder Dysfunct Rep

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Purpose of Review The aim of this review is to summarise the latest research related to different phenotypes of BPS/IC, addressing the evidence for current well-defined phenotypes as well as identifying novel potential phenotypes and highlighting areas for future study. Recent Findings Two distinct phenotypes of BPS/IC are well-recognised: Hunner’s lesion disease and non-Hunner’s lesion BPS/IC. Recent studies have shown these phenotypes exhibit distinct clinical, pathological and cystoscopic features, and targeted treatment to Hunner’s lesions can prove effective. Recent studies have also identified new potential phenotypes based on biochemical, molecular and histological markers, pathophysiological mechanisms of disease, clinical features, cystoscopic findings, radiological features and urodynamic factors. This evidence has improved our understanding of the underlying mechanism of disease and may enable more personalised and targeted therapy in the future. Summary Novel phenotypes of BPS/IC relate to the presence of certain biomarkers, alterations in the urinary microbiome, the characteristics of pain and presence of co-existing somatic and psychosocial conditions, altered patterns of brain white matter changes and urodynamic features. Further study is required to evaluate whether these potential phenotypes are clinically useful based on their ability to guide treatment selection and predict outcome from therapy, and therefore optimise therapeutic outcomes.

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Section: Phenotype Based On Co-existing Somatic Conditionssupporting

confidence: 60%

Phenotypes of BPS/IC

Malde

Sahai

2020

Curr Bladder Dysfunct Rep

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“…Furthermore, the lower urinary tract symptoms in these patients resemble those in patients with IC/BPS with Hunner lesions 34,35 . In addition, female preponderance and an increased prevalence of comorbid systemic autoimmune disorders are well‐known epidemiological features of IC/BPS 36–38 . Collectively, this evidence strongly suggests the possible autoimmune nature of IC/BPS with Hunner lesions.…”

Section: Pathophysiology Of Ic/bpsmentioning

confidence: 75%

Interstitial cystitis/bladder pain syndrome: The evolving landscape, animal models and future perspectives

et al. 2020

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Abbreviations & Acronyms BPS = bladder pain syndrome CCL2 = C-C motif ligand 2 CNS = central nervous system DMSO = dimethyl sulfoxide EAC = experimental autoimmune cystitis ESSIC = International Society for the Study of BPS FSS = functional somatic syndrome GAG = glycosaminoglycan IC = interstitial cystitis IFN-c = interferon-gamma IL = interleukin MC = mast cell NGF = nerve growth factor OVA = ovalbumin TCR = T-cell receptor TNF = tumor necrosis factor TLR = Toll-like receptor UCPPS = urological chronic pelvic pain syndrome UPK = uroplakin Upo = unpublished observation VEGF = vascular endothelial growth factor WAS = water avoidance stress Correspondence: Yoshiyuki Abstract: Interstitial cystitis/bladder pain syndrome is a debilitating condition of unknown etiology characterized by persistent pelvic pain with lower urinary tract symptoms and comprises a wide variety of potentially clinically useful phenotypes with different possible etiologies. Current clinicopathological and genomic evidence suggests that interstitial cystitis/bladder pain syndrome should be categorized by the presence or absence of Hunner lesions, rather than by clinical phenotyping based on symptomatology. The Hunner lesion subtype is a distinct inflammatory disease with proven bladder etiology characterized by epithelial denudation and enhanced immune responses frequently accompanied by clonal expansion of infiltrating B cells, with potential engagement of infection. Meanwhile, the non-Hunner lesion subtype is a noninflammatory disorder with little evidence of bladder etiology. It is potentially associated with urothelial malfunction and neurophysiological dysfunction, and frequently presents with somatic and/or psychological symptoms, that commonly result in central nervous sensitization. Animal models of autoimmune cystitis and neurogenic sensitization might serve as disease models for the Hunner lesion and non-Hunner lesion subtypes, respectively. Here, we revisit the taxonomy of interstitial cystitis/bladder pain syndrome according to current research, and discuss its potential pathophysiology and representative animal models. Categorization of interstitial cystitis/bladder pain syndrome based on cystoscopy is mandatory to design optimized treatment and research strategies for each subtype. A tailored approach that specifically targets the characteristic inflammation and epithelial denudation for the Hunner lesion subtype, or the urothelial malfunction, sensitized/altered nervous system and psychosocial problems for the non-Hunner lesion subtype, is essential for better clinical management and research progress in this complex condition.

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“…The study indicated that twin similarity is suggestive of a genetic component to the etiology of IC/BPS in women. Further, IC/BPS has many features similar to those of autoimmune diseases, which display complicated gene-environment interactions [18][19][20] .The influence of environmental factors on IC/BPS and how to avoid such influence warrant further investigation. Further, the recruited patients with IC/BPS in this study had an average onset time of 6 years before their diagnosis was confirmed.…”

Section: Discussionmentioning

confidence: 99%

Lifestyle and behavioral modifications made by patients with interstitial cystitis

Lin

et al. 2021

Sci Rep

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Interstitial cystitis/bladder pain syndrome (IC/BPS) negatively affects the quality of life. In this study, we investigated the lifestyle behavioral changes patients with IC/BPS make to cope with their symptoms. This prospective study was conducted between August 2018 and June 2019. All patients had a primary symptom of suprapubic pain with a full bladder and other lower urinary tract symptoms for more than 6 weeks as well as cystoscopic findings. All participants completed our self-developed questionnaire, which included informations about their living and work environment, occupational garments, dietary habits, and personal habits. Continuous variables were compared using an independent sample t test, and categorical variables were compared using a chi-square test. We recruited 86 patients with IC/BPS and age-matched 86 controls without IC/BPS. In our study, patients with IC/BPS had more cranberry intake (45.34% vs. 5.81%, P < 0.05) than non-IC/BPS controls; the IC/BPS group had decreased consumption of coffee and spicy food; and wore less makeup or special work garments. In conclusion, patients with IC/BPS tend to make several lifestyle behavioral changes to cope with their symptoms.

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Risks of interstitial cystitis among patients with systemic lupus erythematosus: A population‐based cohort study

Cited by 22 publications

References 29 publications

Phenotypes of BPS/IC

Phenotypes of BPS/IC

Interstitial cystitis/bladder pain syndrome: The evolving landscape, animal models and future perspectives

Lifestyle and behavioral modifications made by patients with interstitial cystitis

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