Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An analysis was made of the prognosis over a one-year follow-up period of a consecutive series of 86 out patients with irritable bowel syndrome (SII) who were treated randomly with an antispasmodic (otilonium) or a tranquilizer (clobazam), and the existence of factors, mainly psychological, that could worsen it was determined with the Zung anxiety test and the Hamilton depression scale. We confirmed that irritable intestine syndrome is a chronic disease, with a mean course of 13 +/- 12.5 years at the time of consultation. A large proportion of patients had permanent problems (58.1%) and did not experience important changes in the intensity of symptoms throughout evolution (68.6%). Although most improved initially with the treatment instated (76.7%), the improvement was rarely complete (11.8%). A year after beginning treatment, 61.6% were the same or worse than before the index consultation. In the group of patients with a good course, the proportion of those that correctly followed medical treatment and of those who had experienced more or less lengthy asymptomatic periods before consultation was significantly larger. In the group of patients with poor evolution, the scores on the Zung anxiety test and Hamilton depression scale were significantly higher than in those who evolved favorably. Neither consultation of a specialist nor the treatment used in this study seem to have contributed to an evident improvement in the prognosis.
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PMID:[Prognosis of patients with irritable intestine syndrome. A prospective study with 1 year follow-up]. 233 79

Visceral pain processing is abnormal in a majority of irritable bowel syndrome (IBS) patients. Aberrant endogenous nociceptive modulation and anticipation are possible underlying mechanisms investigated in the current study. Twelve IBS patients and 12 matched healthy controls underwent brain fMRI scanning during the following randomised stimuli: sham and painful rectal distensions by barostat without and with simultaneous activation of endogenous descending nociceptive inhibition using ice water immersion of the foot for heterotopic stimulation. Heterotopic stimulation decreased rectal pain scores from 3.7+/-0.2 to 3.1+/-0.3 (mean+/-SE, scale 0-5) in controls (p<0.01), but not significantly in IBS. Controls differed from IBS patients in showing significantly greater activation bilaterally in the anterior insula, SII and putamen during rectal stimulation alone compared to rectal plus heterotopic stimulation. Greater activation during rectal plus heterotopic versus rectal stimulation was seen bilaterally in SI and the right superior temporal gyrus in controls and in the right inferior lobule and bilaterally in the superior temporal gyrus in IBS. Rectal pain scores were similarly low during sham stimulation in both groups, but brain activation patterns differed. In conclusion, IBS patients showed dysfunctional endogenous inhibition of pain and concomitant aberrant activation of brain areas involved in pain processing and integration. Anticipation of rectal pain was associated with different brain activation patterns in IBS involving multiple interoceptive, homeostatic, associative and emotional areas, even though pain scores were similar during sham distension. The aberrant activation of endogenous pain inhibition appears to involve circuitry relating to anticipation as well as pain processing itself.
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PMID:Cortical effects of anticipation and endogenous modulation of visceral pain assessed by functional brain MRI in irritable bowel syndrome patients and healthy controls. 1684 94

The irritable bowel syndrome (IBS) is a frequent gastrointestinal disorder (10 -15% of the population). It is characterized by chronic abdominal pain with modification in the bowel habits. The diagnosis is based of ROME II criteria. The pathophysiology of the SII remains unknown . It result from visceral hypersensitivity with anomalies of the digestive motility. These anomalies are secondary of dysfunction of the brain - gut axis modulated by environmental and the psychosocial factors. The understanding of the pathophysiological mechanisms of the SII and in particular the function of the brain-gut axis will permit a better handling of the patients. Indeed, the present knowledge of the neurotransmitter implied in the communication between the central nervous system and the digestive tract are currently the basis of the new therapies aimed to modulate the mechanisms implicated in the causation of the several symptoms of IBS. These novel pharmacotherapy should reduce the indirect societal and costs of IBS.
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PMID:[The pathophysiology of irritable bowel syndrome]. 1691 74