A possible correlation of inflammatory bowel diseases (IBDs) with interstitial cystitis/ bladder pain syndrome (IC/BPS) has been studied in animal models, demonstrating a bidirectional neural cross-sensitization between colon and lower urinary tract [1][2]. However, clinical trials have not provided yet adequate evidence for a direct correlation in the era of clinical manifestations. Also, the use of monoclonal antibodies as treatment modalities in IBDs and IC/BPS has aroused the question of potent common strategies in these situations, although evidence is low, especially for the IC/BPS [3]. The aim of our study is to evaluate any possible clinical correlation between IBDs and IC/BPS, as well as to overview any effect of monoclonal treatment for IBDs in the clinical manifestations of IC/BPS.

This is a clinical observational study enrolling female patients with inflammatory bowel disease under treatment with monoclonal antibodies from the Gastrointestinal Department of our hospital. All women with an at least three months therapeutic scheme were regarded as eligible for the study. Exclusion criteria were any recent or concurrent treatment for any lower urinary tract disease, previous treatment for IC/BPS, a medical history of recurrent urinary tract infections, bladder cancer, bladder stones, pelvic surgery, radiotherapy, pregnancy and a known gynecological disease. The evaluation of lower urinary tract symptoms (LUTS) has been performed with the Incontinence Quality of Life Questionnaire (I-QoL), International Consultation on Incontinence Questionnaire-Female Lower Urinary Tract Symptoms (ICIQ-FLUTS) and International Consultation on Incontinence Questionnaire Female Sexual Matters Associated with Lower Urinary Tract Symptoms Module (ICIQ-FLUTSsex). Bladder pain measurement has been based on Visual Analogue Scale (VAS). All women underwent a cystoscopy at least three months after the beginning of monoclonal treatment, independent of reporting bladder pain or LUTS.

18 women with a mean age of 42.7 years old have been enrolled and finished the study. 11 (61.1%) of them suffered for Crohn’s disease, while 7 (38.9%) of them had Ulcerative Colitis. All patients reported symptoms related to IBDs; 6 (33.3%) mucus or blood in stool, 3 (16.7%) diarrhea, 1 (5.6%) abdominal pain and 8 (44.4%) combination of the above. The vast majority (94.4%) received treatment with infliximab, while the 5.6% received vedolizumab with a mean duration of 95 months. Additionally, all women were complaining about LUTS. However, only 2 (11.1%) of them documented in ICIQ-FULTS that these symptoms were bothersome affecting negatively their quality of life. The mean I-QoL score was 102.1, with only 4 patients (22.2%) under the cut point of 100. The mean I-QoL for the subgroup of those 4 women was equal to 92. 6 women (33.3%) localized pain mainly in the bladder area with a mean VAS score of 6.5. Moreover, the same 6 patients reported pain and limitations during sexual intercourse and all of them had a cystoscopy with diffusible bladder inflammation without Hunner’s lesions. Only one patient documented improvement of LUTS or pain during monoclinal treatment for the underlying IBD.

The clinical investigation for the correlation between IBDs and IC/BPS has a lot do in the way of proving a possible common pathophysiological mechanism. In our study, a co-existence of an already diagnosed IBD with lower urinary tract symptoms and cystoscopic findings has been found, implying a potent relationship between them. On the other hand, a possible therapeutic benefit of the monoclonal antibodies, been used for IBDs, on IC/BPS has been investigated without a positive message. The limitations of our study were the small recruitment, the short-term follow-up and lack of bladder biopsies in order to specify the number of macrophages in patients with IC/BPS.

Inflammatory bowel diseases and interstitial cystitis/ bladder pain syndrome may have common pathophysiological pathways and parallel clinical manifestations. Our study suggests that basic research investigation and more clinical trials are needed to definite and highlight this correlation.

Malykhina AP, Qin C, Greenwood-Van MB, et al. Hyperexcitability of convergent colon and bladder dorsal root ganglion neurons after colonic inflammation: Mechanism for pelvic organ cross-talk. Neurogastroenterol Motil 2006, Oct;18(10):936-48.
Malykhina AP. Neural mechanisms of pelvic organ cross-sensitization. Neuroscience 2007, Nov 9;149(3):660-72.
Peyronnet B, Pape DM, Michel MC, et al. Treatment of Bladder Pain Syndrome: One Size May Not Fit All. Eur Urol. 2018 Nov;74(5):631-632

Continence 2S2 (2022) 100454
DOI: 10.1016/j.cont.2022.100454