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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Though the pathophysiology of the irritable bowel syndrome (IBS) is commonly attributed to dysfunction of the large intestine, evidence exists to incriminate the small bowel. In order to further explore the role of the small bowel in IBS several stimuli were applied, in an attempt to unmask the dysmotility of the jejunum and ileum. These included infusions of cholecystokinin-octapeptide (CCK-OP), a high fat meal, neostigmine and balloon distension of the ileum. Three groups (n = 8) each of age and sex matched healthy volunteers were studied; patients with IBS complained of predominant constipation (n = 8) or diarrhoea (n = 8). Patients with IBS responded excessively to stimulation by CCK-OP, fatty meal, and ileal distension. In general patients with diarrhoea were more sensitive to stimuli than those with constipation. The ileum responded more to stimulation than the jejunum. As in the large bowel, stimuli appear to unmask intestinal dysmotility in patients with IBS. Motor abnormalities were often accompanied by abdominal symptoms, raising the possibility that dysfunction of the small bowel contributes to the symptoms of IBS.
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PMID:Dysmotility of the small intestine in irritable bowel syndrome. 319 98

We compared responses of the gallbladder to graded intravenous infusions of cholecystokinin octapeptide (CCK-OP) in normal controls (n = 8) and patients with irritable bowel syndrome (IBS) with predominant constipation (n = 8) or diarrhea (n = 8). The doses of CCK-OP ranged from subphysiological (negligible contraction of the gallbladder) to supraphysiological (90% contraction of gallbladder and abdominal side effects) amounts. All gallbladders contracted progressively in response to CCK-OP, and a Weibull model (power exponential function) described precisely the gallbladder's response to CCK-OP. Patients with IBS responded differently from normal patients; those with constipation contracted their gallbladders more and those with diarrhea contracted less in response to the peptide. Gallbladders were also stimulated with a high-fat, liquid meal; all patients' gallbladders contracted, but clear differences between groups could not be demonstrated postprandially. The results suggest that the smooth muscle of the gallbladder in IBS has an abnormal sensitivity to CCK-OP, and the results support the concept that IBS can be a generalized abnormality of the smooth muscle of the digestive tract.
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PMID:Altered sensitivity of the gallbladder to cholecystokinin octapeptide in irritable bowel syndrome. 331 95

So-called acalculous gallbladder disease is an ill-defined entity, mainly seen in young women, which could be due to a motility disorder of the biliary tract. Seven young women with relapsing pain in the right upper quadrant of the abdomen or in the epigastrium, with cholesterol crystals in the bile and with normal sonographic and radiologic findings as well as normal gastroscopy, were investigated by hepato-biliary scintigraphy with 99mTc-HIDA. This first group was compared with a second group of 6 young women suffering from irritable colon, and with a third group of 6 asymptomatic control subjects. The half emptying-time of the gallbladder after cholecystokinin injection was 104.36 +/- 43.93 minutes in the first group, 17.92 +/- 23.57 minutes in the second and 20.42 +/- 23.67 minutes in the third group (p less than 0.005). After 6 weeks of ursodeoxycholic acid treatment, regression of pain and a significant reduction in the half emptying-time from 104.36 +/- 43.93 to 74.35 +/- 52.79 minutes (p less than 0.01) was observed in the first group. These results, which need to be confirmed by further studies, show that in acalculous gallbladder disease there is a delay in gallbladder emptying which could explain the formation of cholesterol crystals by bile stasis as described by various authors.
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PMID:[Study of gallbladder emptying using 99m Tc-HIDA in acalculous cholecystopathy]. 367 67

Magnesium sulphate, a substance known to cause release of cholecystokinin (CCK) from the small intestinal mucosa, was given by mouth (dose 0.1g/kg in 150 ml water) to 20 patients with the irritable bowel syndrome. A rapid increase in colonic segmental motor activity (onset within two to six minutes in most cases) was seen (percentage activity increased from 16.2 to 23.7 p<0.05; mean wave amplitude from 7.1 to 9.1 cm H(2)O, NS; motility index from 144 to 259, p<0.01). This increase was most marked in 10 patients who complained of attacks of abdominal pain after food (16.1 to 29.8%, p<0.01; 6.8 to 9.6 cm H(2)O, p<0.05; 135 to 350, p<0.05), and after the magnesium sulphate three of these patients experienced an attack of their usual pain. These findings provide further evidence that ;functional' abdominal pain after food may in some cases be related to an exaggerated intestinal motor response to cholecystokinin.
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PMID:Effects of oral magnesium sulphate on colonic motility in patients with the irritable bowel syndrome. 478 87

The irritable bowel syndrome (IBS) is clinically characterized by a wide variety of symptoms, including dyspepsia, flatulence, nausea, cramping abdominal pain, constipation and/or diarrhea, and nonspecific symptoms, probably reflecting autonomic nervous system overreactivity. Physiologically, the colonic motor abnormality is characterized by an altered slow-wave rhythm, quantitative differences from normal in the repetitive contraction pattern of the rectosigmoid area, and increased colonic muscle responsiveness to hormones such as cholecystokinin and pentagastrin. The diagnosis of IBS involves practical and ethical considerations as well as the need for decisive reassurance of the patient through judicious examination. Treatment of IBS requires a thoughtful and sensitive approach to the patient, recognition of IBS as an important clinical problem, regularization of bowel function, relief of the abdominal discomfort, and intelligent emotional support.
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PMID:The irritable bowel syndrome. A clinical review and ethical considerations. 701 25

Motility disturbances of the large intestine, which appear in various conditions of a disease, are based on a reduction, the loss or an intensivation of the contractility as well as on a disorganization of the motor activity. Also in the region of the large intestine the normal motoricity can underlie such disturbances, such as retarded or accelerated passage, passage in wrong direction as well as increased turbulence or increased content. Retarded passage of the large intestine leads to obstipation and in advanced form to ileus. The leading symptom in accelerated passage is the diarrhoea. The passage in wrong direction disturbs the motoricity of the colon in the case of a lesion of the ileocaecal valves. Increased turbulence of the content of the large intestine is one of the causes of obstipation, particularly, when it appears in a retarded passage. The disturbances of the laminary flow are characteristic for a diverticulosis. The motor activity of the colon is influenced by many factors, mainly by the central nervous system, the gastrointestinal hormones (cholecystokinin, gastrin, serotonin, insulin and prostaglandins), the diet and the way of life. The motor disturbances are accompanied by bioelectric disturbances of the colon. In the second part of the lecture some pathogenetic and clinical aspects of the most frequently appearing motor disturbance of the large intestine, the irritable colon, are discussed.
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PMID:[Motility disturbances of the large intestine]. 722 37

Standard biliary manometry, including cholecystokinin (CCK) provocation, was performed on 42 consecutive patients (36 F, 6 M, median age 45 years) with postcholecystectomy syndrome (PCS) who had no evidence of organic disease but who had objective clinical features suggesting sphincter of Oddi dysfunction (SOD) (classes I and II). Patients were subdivided into those with (N = 14) and without (N = 28) irritable bowel syndrome (IBS) using a validated symptom questionnaire based on the modified Rome criteria. Resting sphincter of Oddi (SO) motor parameters (basal pressure, contractile amplitude and frequency, and proportion of retrograde contractions), the presence of abnormal manometry, and the presence of an abnormal response to CCK were compared in the two groups. No significant differences in resting parameters of SO motor activity between patients with and without IBS were observed, and abnormal biliary manometry as a whole was not more prevalent in either group (8/13 and 18/27, respectively). An abnormal response to CCK (failure of complete inhibition of phasic contractions), however, was demonstrated in five of 12 patients with IBS compared with only one of 23 patients without IBS (P = 0.01). In patients with postcholecystectomy SOD, an abnormal response of the SO to CCK thus appears to be an important feature of the subset of patients with concomitant IBS.
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PMID:Abnormal sphincter of Oddi response to cholecystokinin in postcholecystectomy syndrome patients with irritable bowel syndrome. The irritable sphincter. 772 79

Abnormalities of the autonomic nervous system function and cholecystokinin release have been described in patients with irritable bowel syndrome. Because the autonomic nervous system and cholecystokinin have an important role in the normal functioning of the gallbladder, we studied gallbladder contraction in response to a meal, using real time ultrasonography in irritable bowel syndrome patients (n = 20) and healthy controls (n = 15). The following parameters were studied: 1) fasting gallbladder volume, 2) residual volume after maximal contraction and at the end of 2 h, 3) maximum percent of gallbladder emptied, and 4) the time taken for maximal contraction. Fasting gallbladder volume (26.21 +/- 1.81 ml vs 15.21 +/- 1.63 ml, p < 0.001), and residual volume after maximal contraction (14.2 +/- 1.69 ml vs. 5.86 +/- 0.98 ml, p < 0.001) and at the end of 2 h (18.81 +/- 1.73 ml vs. 11.65 +/- 1.45 ml, p < 0.01) were significantly higher in the patient group, compared with controls. The maximum emptying was less (49.55 +/- 2.75% vs. 63.98 +/- 4.55%, p < 0.01) and the time taken for maximal contraction (59.25 +/- 3.8 min vs. 42.33 +/- 2.04 min, p < 0.001) was longer in the patient group than in the controls. Based on these observations, we conclude that patients with irritable bowel syndrome have significant abnormalities of gallbladder motor function.
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PMID:Abnormal gallbladder function in patients with irritable bowel syndrome. 836 36

Epidemiological studies indicate that irritable bowel syndrome represents the most frequent somatoforme disorder. Current pathogenetic concepts as well as newer results in pathophysiology, neurobiology and psychoendocrinology are described. As an example of the "brain-gut-link", the role of cholecystokinin (CCK) is discussed. The positive results of psychotherapeutic intervention studies are described in more detail. An intensified cooperation between the gastroenterologist and the psychotherapist is recommended.
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PMID:[Recent psychosomatic contributions to the pathogenesis and therapy of irritable colon (irritable bowel syndrome)]. 868 54

Over the last decade, the role of visceral sensitivity has been largely recognized in the pathophysiology of functional digestive disorders, particularly in the irritable bowel syndrome. These studies have highlighted the role of afferent pathways arising from the gut as a possible target for new treatments intended to relieve pain or modify altered reflexes present in such patients. These pharmacological targets have been identified mainly by studies on animal models of visceral hyperalgesia of various origins including local inflammation. Locally, several mediators are of paramount importance for sensitization of nerve endings: 5-hydroxytryptamine, bradykinin, tachykinins, calcitonin gene-related peptide, and neurotrophins. Selective antagonists to various subtypes of their receptors are currently available and have been shown to be active in these animal models. Other substances, such as somatostatin, opiold peptides, cholecystokinin, oxytocin, and adenosine, modulate the transmission of nociceptive inputs from the gut to the brain and are of clinical interest. This article reviews the current understanding of these mediators. Although these agents seem to be promising tools for the treatment of visceral hyperalgesia and its consequences (abdominal pain and disturbed reflexes), their clinical efficacy remains to be shown. A better understanding of the nature and the location of the defect in the sensory pathways may permit the selection of subgroups of patients for treatment according to the pharmacological properties of these new therapeutic agents.
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PMID:Mediators and pharmacology of visceral sensitivity: from basic to clinical investigations. 913 53


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