IBS Is Linked to Bowel Defects

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Serotonin plays a critical role in the regulation of gastrointestinal (GI) motility, secretion, and sensation. Irritable bowel syndrome (IBS) is associated with clinical symptoms that include alterations in normal patterns of motility, secretion, and sensation. The role of serotonin in the pathophysiology of IBS, however, remains unclear.

In the June 2004 issue of Gastroenterology, researchers reported the results of a study aimed at testing whether enteric serotonin signaling is defective in patients with IBS and in patients with ulcerative colitis (UC). Key elements of serotonin signaling, including measures of serotonin content, release, and reuptake, were analyzed in rectal biopsy samples from patients with UC (n = 22), patients with IBS with diarrhea (IBS-D; n = 15), patients with IBS with constipation (IBS-C; n = 16), and controls (n = 34).

Results showed that mucosal serotonin, tryptophan hydroxylase 1 messenger RNA (mRNA), serotonin transporter mRNA, and serotonin transporter immunoreactivity were all significantly reduced in patients with UC, IBS-D, and IBS-C. The enterochromaffin cell population was reduced in samples from patients with severe UC but was unchanged in samples from patients with IBS. No changes were detected in any of the disease samples relative to the control samples when serotonin release was investigated under basal and mechanical stimulation conditions. The authors concluded that both UC and IBS are associated with molecular changes in serotonergic signaling mechanisms and that these data support the assertion that disordered GI function in IBS involves changes intrinsic to the bowel.