Crohn’s disease is a very common inflammatory disease, and as the disease progresses, it can easily endanger the patient’s life. Its pathogenesis and mechanisms are still unclear [8]. The common suspected causative factors and pathogenesis currently include geographical and food factors, intestinal cell injury, intestinal flora dysbiosis, pathophysiological changes in the intestinal mucosa or related tissues, and immune dysfunction [9]. A gold standard method for diagnosis is lacking, and diagnosis currently requires comprehensive and integrated analysis of symptoms in combination with the findings of relevant examinations, mainly colon features on endoscopy and histopathological characteristics. Crohn’s disease is characterized by transmural inflammation, and intestinal ulcers penetrating the serosal layer can form intestinal fistulas, which can be categorized as extraintestinal and intraintestinal fistulas according to their location; intraintestinal fistulas include enteroenteric fistulas and intestinal vesicovaginal fistulas [10].

Cystitis glandularis is a chronic inflammatory disease of the bladder caused by epithelial metaplasia [11]. There are three theories regarding the pathogenesis of cystitis glandularis, namely, the embryonic origin theory, the Pund degeneration theory and the epithelial metaplasia theory [12]. Epithelial metaplasia is widely accepted as a defence mechanism in which migratory metaplastic epithelium becomes glandular epithelium under the action of chronic irritants and achieves self-protection by secreting mucus [13]. Chronic irritants include but are not limited to infections, obstructions (female urethral syndrome, prostatic hyperplasia, urethral strictures, etc.), physical irritants (stones, foreign bodies), and chemical carcinogens. The clinical manifestations are mostly nonspecific, such as varying degrees of discomfort, urinary frequency, difficulty in holding urine, and lower abdominal distension. In severe cases, acute urinary retention, bladder contracture and upper urinary tract fluid accumulation may occur [14]. The confirmation of the diagnosis is mainly based on cystoscopy and pathological examination, and biopsy results are the gold standard for the diagnosis of cystitis glandularis [15]. There have been no reports of a vesicovaginal fistula after a cystoscopic biopsy in the literature on cystitis glandularis, which does not affect the bladder muscle. Vesicovaginal fistulas occur mainly after hysterectomy, caesarean section, radiotherapy and pelvic surgery [16] and are mainly caused by local ischemia and fibrosis. The cause of the vesicovaginal fistula in this patient is unclear; cystitis glandularis mainly occurs in the mucosal layer of the bladder, and further research is needed to determine the mechanism by which the tissue between the muscle layer of the bladder and the vagina is destroyed.

Crohn’s disease and cystitis glandularis in this patient were confirmed by pathology, and our searches of the PubMed® and Sci-Hub® databases using the two keywords “cystitis glandularis” and “Crohn’s disease” failed to retrieve any relevant studies. To identify common causative genes or signalling pathways for both diseases, considering that both diseases are correlated with tumorigenesis, we conducted bioinformatics-related searches through six databases, namely, TCGA, GEO, ICGC, HPA, CGGA, and DisGeNET [17], and failed to find common causative genes or signalling pathways. Considering that both cystitis glandularis and Crohn’s disease are also inflammatory diseases [18, 19], we searched the NCRI database with the keywords “Crohn’s disease” and “cystitis glandularis” [20], and no common inflammatory causative factors were found. In terms of potentially relevant biomarkers, we searched the SC2disease database [21] and found no common biomarkers for the two diseases. Therefore, the cause of the co-occurrence of the two diseases in this patient is unclear. This patient developed an intestinal fistula after laparoscopic surgery, and we analysed the possible factors as follows: (1) Intraoperative pulling could have led to damage to the intestinal canal. The patient was found to have multiple intestinal fistulas upon dissection, but some of the intestinal fistulas could have resulted from pulling during nonlaparoscopic repair of the intestinal canal; however, most fistulas were less likely to be caused by external physical stimulation. (2) The patient experienced a paroxysm; the release of specific factors, such as TNF-α, IL-1β, IL-6, and TGF-β, in the body after the stress of surgery could have accelerated the Crohn’s disease paroxysm and resulted in an intestinal fistula. During the formation of the vesicovaginal fistula in the patient, there was a transient increase in abdominal pain at the time of cystoscopic biopsy, and it is possible that the release of these pathogenic factors in the body had already been initiated or accelerated at this time. (3) After repair of the intestinal fistula and reappearance of the small intestinal fistula with a large amount of bloody stool and abdominal bleeding, the disease continued to progress, which is a highly unfavourable clinical finding and portends the ultimate outcome of the patient.