Neurogenic urogenital disorders in inflammatory bowel disease

Background. Experimental studies demonstrate shared afferent organization of the colon and urinary bladder, the presence of dichotomized neurons in dorsal root ganglia, and the development of cross-organ sensitization in colitis. TRPV1-positive visceral afferents, microglia, purinergic signalling, NK1/MAPK-p38 cascades, and brain-derived neurotrophic factor contribute to persistent neuroplasticity in spinal circuits. Clinical data confirm a high prevalence of urinary and sexual complaints in inflammatory bowel disease: the median BFLUTS score in women is 6, chronic prostatitis-like symptoms are present in 26.8% of men, and pooled prevalence of sexual dysfunction reaches 50.6%. At the same time, urinary symptoms in inflammatory bowel disease are heterogeneous and require differential assessment against urolithiasis, drug-related nephrotoxicity, pelvic floor dysfunction, chronic pelvic pain, and psychosocial factors. Current ECCO guidelines on extraintestinal manifestations and reproductive health do not define neurogenic urogenital disorders as a separate phenotype, and direct neurophysiological confirmation of neurogenic lower urinary tract symptoms in inflammatory bowel disease is still lacking.
Objective. To analyze current data on neurogenic mechanisms of urogenital disorders in inflammatory bowel disease, evaluate the clinical phenotype of lower urinary tract symptoms and sexual dysfunction, and define key evidence gaps.
Conclusion. A neurogenic mechanism of urogenital disorders in inflammatory bowel disease is biologically plausible and well supported by experimental evidence, but it has not yet been proven in humans by direct functional studies. Prospective studies incorporating urodynamics, pelvic floor electromyography, and neurophysiological testing are required; in current practice, active screening for urinary and sexual symptoms in patients with inflammatory bowel disease is warranted.

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