Updates on the epidemiology, pathogenesis, diagnosis, and management of postinfectious irritable bowel syndrome

With its impact on quality of life and increasing awareness, postinfectious irritable bowel syndrome (PI-IBS) is now gaining attention as one of the major health problems commonly encountered in gastrointestinal practice. Literature investigating the various pathogenic mechanisms involved is rapidly emerging. The objective of the current review is to provide an update on recent evidence published in the past 2 years describing advances in our understanding of the epidemiology, pathogenesis, diagnosis, and treatment of PI-IBS.

Significant proportion of research in the recent past was preclinical in nature. Epidemiological studies continue to highlight the risk of IBS after infection, with recent studies documenting postprotozoal effects. Advances in pathogenic mechanisms included clinical studies, which documented micro-RNA down-regulation and Peroxiredoxin-1 up-regulation in colonic mucosa of PI-IBS patients. Protease-activated receptor-2 (PAR-2) activation in PI-IBS mice models resulted in increase in epithelial permeability, mucosal inflammation, visceral hypersensitivity. Moxibustion and rifamycin reduced intestinal inflammation by inhibiting cytokine and chemokine release via different mechanisms. Miltefosine reduced mast cell degranulation and TRPV1 activation, thereby reducing visceral hypersensitivity.

At present, generalization of limited diagnostic and therapeutic strategies across a heterogeneous prevalent patient population impedes the ability to provide effective personalized care in PI-IBS. Further development in pathogenesis discovery, diagnostic tool development are needed in order to design well tolerated and effective therapies that guide treatments based on distinct pathways of disease.