[Post-infectious irritable bowel syndrome. A review based on current evidence]

Pathophysiology of irritable bowel syndrome (IBS) is multifactorial. Recent investigations have associated episodes of infectious gastroenteritis with development of IBS. This condition is named post-infectious IBS (PI-IBS). The role of inflammation-infection in IBS pathogenesis is not well understood.

To review published scientific evidence on PI-IBS regarding risk factors, causal agents, histopathological changes, and treatment.

An electronic search in MEDLINE and abstracts presented at national and international GI meetings was performed, looking for information published in the past 50 years including animal studies, cohort studies, case-control studies, and series of cases and case reports, using the key words post-infectious enteritis, post-dysenteric or post-infectious irritable bowel syndrome (PI-IBS), and post-infectious colitis.

Fifty one papers were included. These studies were classified according to pathophysiologic mechanisms, infectious agents involved, animal or human studies, and treatment.

Current evidence shows a strong association between colonic infection and inflammation with development of IBS. Approximately 25% of patients with IBS have a history of infectious enteritis. Microbial agents related with PI-IBS include bacteria (Campylobacter, Salmonella) and parasites (Trichinella spiralis). Increased number of enteroendocrine cells, CD3 lymphocytes and mast cells within the colonic muscle wall, release of pro-inflammatory substances, and increased number of inflammatory cells with intestinal nervous endings are the most common histopathologic findings. Patients developing PI-IBS have a higher frequency of psychological disorders and stressful events prior to the gastroenteritis episode. Therapeutic interventions with steroids, COX-2 inhibitors, antibiotics and probiotics require further investigation.