Changing face of irritable bowel syndrome

Abstract

Recent years have witnessed tremendous progress in our understanding of irritable bowel syndrome (IBS). It is evident that this is a truly global disease associated with significant symptoms and impairments in personal and social functioning for afflicted individuals. Advances in our understanding of gut flora-mucosal interactions, the enteric nervous system and the brain-gut axis have led to substantial progress in the pathogenesis of symptoms in IBS and have provided some hints towards the basic etiology of this disorder, in some subpopulations, at the very least. We look forward to a time when therapy will be addressed to pathophysiology and perhaps, even to primary etiology. In the meantime, a model based on a primary role for intestinal inflammation serves to integrate the various strands, which contribute to the presentation of IBS.

Figure 1

Interactions between the gut, the brain and the external and internal environments in IBS; the Iinflammation hypothesis (a personal view). Bacterial or viral infection, a disturbed flora or an abnormal response to a normal flora leads to mucosal Iinflammation which in turn can disrupt motility and augment visceral sensation. Centrally, perception is abnormal, thereby, contributing to symptom development. Central output can in turn influence motor events in the periphery. While not central to causation, psychological factors, either spontaneously or in response to environmental stressors, can influence motor and sensory events and immune activity in the gut.