Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA.
Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA; Department of Medicine and Physiology, Enteric NeuroScience Program, 200 First Street Southwest, Rochester, MN 55905, USA.
Gastroenterol Clin North Am. 2021 Jun;50(2):445-461. doi: 10.1016/j.gtc.2021.02.007. Epub 2021 Apr 23.
Epidemiologic data support that acute gastrointestinal infection is one of the strongest risk factors for development of irritable bowel syndrome (IBS). Risk of post-infection IBS (PI-IBS) seems to be greater with bacterial and protozoal than viral enterocolitis. Younger individuals, women, and those with severe enterocolitis are more likely to develop PI-IBS. Disease mechanisms in animal models and humans involve chronic perturbation of intestinal microbiome, epithelial and neuronal remodeling, and immune activation. These mechanisms can lead to luminal (increased proteolytic activity, altered bile acid composition) and physiologic (increased permeability, transit changes, and visceral hypersensitivity) alterations that can mediate PI-IBS symptoms.
流行病学数据表明,急性胃肠道感染是导致肠易激综合征(IBS)的最强危险因素之一。与病毒性肠炎相比,细菌性和原虫性肠炎后发生 IBS(PI-IBS)的风险似乎更大。年轻人、女性以及患有严重肠炎的人更有可能患上 PI-IBS。动物模型和人类中的疾病机制涉及肠道微生物组的慢性紊乱、上皮和神经元重塑以及免疫激活。这些机制可导致腔(蛋白酶活性增加、胆汁酸组成改变)和生理(通透性增加、传输变化和内脏高敏性)改变,从而介导 PI-IBS 症状。