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Functional esophageal disorders / Irritable bowel syndrome
Irritable bowel syndrome
Colonic and rectal hypersensitivity (also called "visceral hyperalgesia") are also important factors in the causation of symptoms. Patients with IBS have a n increased visceral sensitivity to stimuli which causes pain and abdominal discomfort. Studies involving balloon distension of the rectosigmoid colon have shown that patients with IBS experience pain and bloating at pressures and volumes much lower than control subjects(12).
It has been noticed that gastroenteritis or dysentery plays a role in pathogenesis of irritable bowel syndrome, and antibiotics can increase functional abdominal symptoms, both of which may be partly due to intestinal flora disorders. The intestinal flora disorders in IBS patients, may be involved in triggering the IBS-like symptoms(13). Clinicians have for many years recognized that the onset of IBS often follows an episode of acute gastroenteritis.
Some studies have shown that abnormal colonic fermentation subsequent to damaged gut flora by antibiotics or gastroenteritis may be an important factor in the development of symptoms in some patients with IBS(13).]
Enteric inflammatory cells may also play an important role in the pathophysiology of IBS. Inflammation may alter intestinal cytokine milieu and motility, both of which can result in an increase in a patient's pain sensation.
Stress is known to alter gastrointestinal function. "Approximately 40-60% of patients with IBS who seek medical care also report psychiatric symptoms, such as depression, anxiety, or somatization(11)
There is some data available on that the limbic system (the area of the brain where stress is perceived) is involved in IBS(11). Moderate stress in rats causes the release of corticotropin-releasing factor (CRF), and this endogenous CRF may mediate stress-induced changes in colonic function. Patients with IBS have an exaggerated colonic response to corticotropin-releasing, and results in the abdominal symptons present in the syndrome(11).
There is also some indices that in IBS the regulatory conduit between the central and enteric pathway may be impaired at any of its three anatomical levels:
- Prevertebral ganglia.
- Spinal cord.
- Brainstem.
"End organ sensitivity, stimulus intensity changes or receptive field size of the dorsal horn neuron and limbic system modulation are the mechanisms involved in visceral hypersensitivity(11)."
Enteric propulsion and sensation are, in part, mediated by acetylcholine and serotonin (5HT). Recent studies associate neurotransmitters with IBS. Serotonin is located in the central nervous system (5%) and the gastrointestinal tract (95%), and when it is released into the body it results in the stimulation of intestinal secretion and peristaltic reflex and in symptoms such as abdominal pain, bloating, nausea, and vomiting. These preliminary studies suggest increased serotonin levels in the plasma and in the rectosigmoid colon of patients with IBS(7).
2. Longstreth G.F., Thompson W.G., Chey W.D. Functional bowel disorders. Gastroenterology 2006; 130: 1480-1491.
5. O'Donnell L.J., Virjee J, Heaton K.W. Detection of pseudodiarrhoea by simple clinical assessment of intestinal transit rate. BMJ 1990; 300: 439-440.
6. Kellow J.E., Phillips S.F. Altered small bowel motility in irritable bowel syndrome is correlated with symptoms. Gastroenterology 1987; 92 (6): 1885-1893.
7. Horwitz B.J., Fisher R.S. The irritable bowel syndrome. N Engl J Med 2001; 344 (24): 1846-1850.
8. King T.S., Elia M, Hunter J.O. Abnormal colonic fermentation in irritable bowel syndrome. Lancet 1998; 352: 1187-1189.
9. Si J.M., Yu Y.C., Fan Y.J. Intestinal microecology and quality of life in irritable bowel syndrome patients. World J Gastroenterol 2004; 10 (12): 1802-1805.
