BACKGROUND: The COVID-19 pandemic has unveiled a hidden epidemic of disorders of gut-brain interaction (DGBIs), notably post-infection irritable bowel syndrome (PI-IBS), driven by SARS-CoV-2 GI tropism and pandemic stressors.
PURPOSE: This review synthesizes and critically appraises current evidence on the prevalence, clinical spectrum, and predictors of post-COVID-19 IBS, integrating mechanistic insights. Topics discussed in this review will advance understanding of pathophysiological mechanisms, identify therapeutic targets, inform phenotype-tailored management and clinical care, and outline research priorities for post-COVID-19 IBS.
METHODS: A narrative review was performed by the authors.
KEY RESULTS: Recent evidence indicates that approximately 7.2% of individuals develop IBS after SARS-CoV-2 infection, with 2.6-fold higher odds vs. non-infected controls. At the population level, a nationally representative U.S. survey (> 160,000 adults) showed a pandemic-era surge in IBS prevalence (predominantly IBS-M) and a modest increase in chronic idiopathic constipation (CIC), while other Rome IV DGBIs remained stable. Mechanisms are multifactorial, involving ACE2-linked epithelial/neuromuscular effects, persistent low-grade inflammation, microbiota dysbiosis with reduced short-chain fatty acids, altered serotonin signaling, barrier dysfunction, and psychosocial stress acting along the gut-brain axis. Emerging data indicate dyspnea and depression further mediate the COVID-19-to-IBS pathway, underscoring biopsychosocial endotypes.
CONCLUSIONS AND INFERENCES: This review indicates that following infection with SARS-CoV-2, DGBI, particularly IBS, occurs in 7.2% patients on follow-up. Clinically, a positive diagnosis framework and phenotype-tailored, multidisciplinary care are recommended. Future studies on post-infection IBS including post-COVID-19 IBS should be undertaken using upcoming Rome V criteria, controlling for confounding factors, and defining mechanistic endotypes to unlock precision therapies.
