Colonic motility abnormality in patients with irritable bowel syndrome exhibiting abdominal pain and diarrhea

Citation
Wy. Chey et al., Colonic motility abnormality in patients with irritable bowel syndrome exhibiting abdominal pain and diarrhea, AM J GASTRO, 96(5), 2001, pp. 1499-1506
Citations number
23
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
AMERICAN JOURNAL OF GASTROENTEROLOGY
ISSN journal
00029270 → ACNP
Volume
96
Issue
5
Year of publication
2001
Pages
1499 - 1506
Database
ISI
SICI code
0002-9270(200105)96:5<1499:CMAIPW>2.0.ZU;2-C
Abstract
OBJECTIVES: Although colon dysmotility is recognized as a pathophysiologica l factor in irritable bowel syndrome (IBS), it has not been characterized. We have investigated motility patterns in IBS patients with abdominal pain and frequent defecation or diarrhea and in healthy volunteers. METHODS: A recording catheter that had six polyvinyl tubes with infusion po rts was placed in the transverse, descending, and sigmoid colon under fluor oscopy. After 2-h basal recordings, motility responses to cholecystokinin o ctapeptide (CCK-8) and a meal were studied for 3 h. The motility index (MI) and number of high amplitude propagating contractions (HAPCs) in 10 IBS pa tients were compared with those of 10 controls. HAPCs were correlated with abdominal pain, and colon transit time using radio-opaque markers was deter mined. Using human colon muscle strips, the effect of CCK-8 on muscle contr actions was also studied. RESULTS: The MI and mean number and peak amplitude of HAPCs in IBS patients were significantly greater than in controls. These abnormalities parallele d markedly shortened colonic transit time. Abdominal pain coincided with > 90% of HAPCs. Dose-dependent muscle contraction by CCK-8 was profoundly sup pressed both by loxiglumide and atropine. CONCLUSIONS: The dysmotility in this subset of IBS patients was characteriz ed by significantly increased occurrences of powerful HAPCs that paralleled rapid colon transit and were accompanied by abdominal pain. Thus, it is su ggested that this powerful contraction is one of the causes of abdominal pa in. The action of CCK-8 seems to be mediated via the colon enteric nervous system.