Post‐Coronavirus Disease ( COVID )‐19 Irritable Bowel Syndrome: What We've Learned So Far

ABSTRACT 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.