Pathophysiological mechanisms, diagnostic innovations, and multimodal therapeutic strategies for slow transit constipation

慢传输型便秘的病理生理机制、诊断创新和多模式治疗策略

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Abstract

BACKGROUND: Slow transit constipation (STC), a subtype of functional constipation characterized by delayed colonic transit (> 72 h), imposes substantial physical and psychological burdens. AIMS: This review synthesizes current evidence on STC epidemiology, pathophysiology, diagnostic innovations, and multimodal management. METHODS: A literature review was conducted using PubMed and China National Knowledge Infrastructure (CNKI) for all articles and trials with the following search terms: "Slow transit constipation" OR "Chronic constipation" OR "STC". The comprehensive literature search was conducted for relevant articles published up to June 2025. The search yielded approximately 1005 records from PubMed and 220 records from CNKI. The abstracts and titles of all retrieved articles were reviewed for relevance. Articles were included in this narrative review if they provided original insights, comprehensive summaries, or presented clinical trial data on the pathophysiology, diagnostic innovations, or therapeutic strategies for slow transit constipation. Both foundational and recent high-impact studies were prioritized. RESULTS: Key pathophysiological mechanisms involve: smooth muscle atrophy/fibrosis, interstitial cells of Cajal (ICC) depletion, enteric nervous system dysregulation, hormonal imbalances (thyroid/sex hormones), and gut microbiota dysbiosis. Diagnosis integrates: (1) Rome IV symptom criteria (≤ 3 spontaneous bowel movements/week, hard stools, straining); (2) Objective transit testing (scintigraphy, wireless motility capsule); (3) Exclusion of secondary causes. Conservative management emphasizes fiber intake, hydration, and physical activity. Pharmacotherapy includes osmotic laxatives (first-line), prokinetics (prucalopride; second-line), and microbiota modulators. For refractory cases, colectomy requires strict selection: failed conservative therapy, confirmed transit delay, and excluded pelvic floor dysfunction. Future research should prioritize genetic susceptibility, signaling pathway modulation, and personalized algorithms. CONCLUSIONS: The explicit pathogenesis of STC remains incompletely characterized. Besides referencing the Rome IV criteria, its diagnosis requires a comprehensive assessment integrating the clinical symptoms and various accessorial examinations. The management of STC also demands clinical gastroenterologist adopt a comprehensive approach, including appropriate lifestyle, pharmacological interventions, psychotherapy, and even surgical treatment. This review provides multidimensional ideas for gastroenterologists to treat patients grappling with STC.

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