ArticleInternational urogynecology journal2026
Etiology of Hunner Lesions: Linking Immune Dysregulation and Chronic Inflammation in Interstitial Cystitis/Bladder Pain Syndrome.
Article in International urogynecology journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introduction and hypothesisHunner lesions (HL) are distinctive ulcerative bladder lesions characterized by a central scar and surrounding erythema. Traditionally, HL has been used as a clinical diagnostic tool for a subset of patients with interstitial cystitis/bladder pain syndrome (IC/BPS); however, emerging evidence supports a unique pathophysiology for IC/BPS with HL (HIC) that is distinct from IC/BPS without HL (NHIC). This review is aimed at synthesizing current literature on the etiology of HL/HIC and evaluate whether HIC and NHIC warrant classification as separate clinical conditions with distinct management strategies.
methodsA comprehensive literature review using PubMed was conducted to identify literature surrounding HL etiology and pathophysiology. Case-control studies, cohort studies, experimental studies, case reports, and animal studies were included; editorial comments and literature reviews were excluded from this review.
resultsEmerging data suggest that a subset of patients might be predisposed to HIC, including alteration in major histocompatibility complex (MHC) molecules, HLA amino acid positions, and additional protein expression alterations detected by RNA sequencing. Hypoxia-inducible factor activation and chronic ischemia have also been shown to play a role in HL development. Both local and systemic inflammation are seen in HIC, with clonal B-cell expansion influencing the upregulation of inflammatory cytokines, chemokines, and lymphoplasmacytic cells. With additional validation these biomarkers have the potential to serve as a diagnostic tool.
conclusionHunner lesion with IC/BPS is a chronic condition likely caused by an upregulation of humoral immunity leading to an overexpression of inflammatory markers within the urothelium, suggesting an autoimmune-mediated pathology for this patient subgroup.
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