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)

Functional disroders are the most important cause for complaints in the gastrointestinal tract. Dysfunction may concern one or more physiologic properties like tonus, motility, secretion, sometimes also resorption and digestion, or their interaction. Functional disorders of the esophagus (esophagospasm and achalasia) become manifest as dysphagia. Halitosis, bad taste, burning tongue, and flatulent abdomen are frequent symptoms of functional disorders of the gastrointestinal tract. Irritable bowel syndrome is probably the functional disorder most freqently found in the gastrointestinal tract. Characteristic symptoms are pain in the lower and upper middle abdominal region, obstipation and/or diarrhea, flatulent abdomen, mucous discharge with the stools and urgent defecation with cramps relieved after discharge. Prognosis quoad vitam is good, the course, however, is subject to many changes. Therapie is symptomatic. Diagnostic and psychotherapeutic measures are intended to help remove carcinophobia and to overcome conflicts and fears.
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PMID:[Functional disorders of the gastrointestinal tract (author's transl)]. 68 14

Gastrointestinal motility is greatly influenced by both the autonomic nervous system (ANS) and the enteric nervous system (ENS). Dysfunction of ANS and/or ENS produces various kinds of dysmotility from the esophagus to the colon. Generalized autonomic dysfunction, often seen in diabetics, causes abnormal peristaltic waves in the esophagus, abnormal electrical activity of the stomach, delayed gastric emptying and delayed intestinal transit. Localized disorders of the enteric nervous system is seen in patients with achalasia and Hirschsprung's diseases. Functional disorders, without evidence of organic disorders, like non-cardiac chest pain, non-ulcer dyspepsia, irritable bowel syndrome, can be partly caused by abnormal function of autonomic nervous system.
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PMID:[Gastrointestinal motility and autonomic nerve dysfunction]. 161 54

The enteric nervous system (ENS) can be thought of as the third component of the autonomic nervous system. It is a vast network of neurons widely dispersed throughout the gut. The ENS is a dominant regulator of gut function through the action of peptide and non-peptide neurotransmitters. The most intensively studied roles of the ENS have been the regulation of secretory processes, such as gastric acid secretion, and motility. It is clear, however, that the ENS plays a broader role in the regulation of other gut functions, including mucosal defense, the gut immune response, and sphincter function. Alterations in the regulation of gut function by the ENS are likely or suspected in a number of conditions, including achalasia, Hirschsprung's disease, inflammatory bowel disease, Chagas' disease, chronic intestinal pseudoobstruction, biliary dyskinesia, tachygastria, and irritable bowel syndrome. Improved knowledge of the pathophysiology of these troublesome conditions makes effective therapy more likely in the future.
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PMID:Neuroendocrine design of the gut. 167 22

The author gives an account of clinical syndromes which develop as a result of overproduction of gastrointestinal hormones. From the various diagnostic approaches, which are not always available or are expensive, the author summarizes the importance of thin-needle biopsy under sonographic control, the argentaffine technique (Grimelius) and histoenzymatic examination for neuron specific enolase. In addition to surgical treatment treatment with streptozotocine, 5-FU, dimethyl triazenoimidazole carboxamide and somatostatin is possible. The author draws attention to the possibility of using somatostatin not only in the treatment of apudomas but also of haemorrhage into the gastrointestinal tract and in the treatment of fistulae. Neuroendocrine factors probably play a significant role in the pathophysiology of irritable colon, Crohn's disease, achalasia and Hirschsprung's disease.
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PMID:[Gastrointestinal hormones--clinical significance]. 273 95

Nonesophageal, gastrointestinal symptoms were sought from consecutive patients referred for esophageal manometry in order to determine the prevalence of such symptoms in relation to manometric diagnosis. Reports by 103 patients with esophageal contraction abnormalities, a cluster of manometric findings which includes the "nutcracker esophagus" and diffuse esophageal spasm, were compared to those by patients with the achalasia pattern (21 patients) and scleroderma esophagus (19 patients). A history of persistent (greater than 3 months) bowel habit abnormality requiring medical attention was reported by 19% of those with contraction abnormalities and 26% of those with scleroderma esophagus but by no patient with achalasia (P less than 0.05 for both compared to achalasia). Patients with contraction abnormalities had complained to physicians of more gastrointestinal symptoms and had more often been diagnosed as having the irritable bowel syndrome than those with achalasia. We conclude that, with regard to gastrointestinal symptoms, patients with esophageal contraction abnormalities more closely resemble patients with a motility disorder which has the potential for diffuse symptomatic gastrointestinal involvement (scleroderma) than those with a motility disorder restricted to the esophagus (achalasia). These findings add support to the argument that functional gastrointestinal syndromes may be representative of diffuse neuromuscular derangement in the gastrointestinal tract.
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PMID:Gastrointestinal symptoms of patients with esophageal contraction abnormalities. 394 27

In the last 20 years considerable progress has been achieved--among others--in motility associated disorders, in chronic inflammatory bowel diseases (ulcerative colitis, Crohn's disease) and in the treatment and prophylaxis of bleeding from esophageal varices. The motility associated diseases achalasia, functional dyspepsia, irritable bowel syndrome and intestinal pseudoobstruction can be better treated now with drugs which either promote or inhibit motility. In chronic-inflammatory bowel diseases controlled studies have defined the role of salazosulfapyridine, 5-aminosalicylic acid, glucocorticoids, azathioprine and metronidazole. The bleeding from esophageal varices is handled nowadays successfully with a combination of mechanical treatment (sclerosing and banding) and lowering the portal pressure by vasoactive substances or the somatostatin analogue octreotide. The prophylaxis of bleeding with noncardioselective betablockers is also introduced on the base of controlled trials.
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PMID:[Gastroenterology. I: General gastroenterology]. 949 75

Acupuncture has been used for various gastrointestinal (GI) conditions. Voluminous data support the effect of acupuncture on the physiology of the GI tract, including acid secretion, motility, neurohormonal changes, and changes in sensory thresholds. Much of the neuroanatomic pathway of these effects has been identified in animal models. A large body of clinical evidence supports the effectiveness of acupuncture for suppressing nausea associated with chemotherapy, postoperative state, and pregnancy. Prospective randomized controlled trials have also shown the efficacy of acupuncture for analgesia for endoscopic procedures, including colonoscopy and upper endoscopy. Acupuncture has also been used for a variety of other conditions including postoperative ileus, achalasia, peptic ulcer disease, functional bowel diseases (including irritable bowel syndrome and nonulcer dyspepsia), diarrhea, constipation, inflammatory bowel disease, expulsion of gallstones and biliary ascariasis, and pain associated with pancreatitis. Although there are few prospective randomized clinical studies, the well-documented physiological basis of acupuncture effects on the GI tract, and the extensive history of successful clinical use of acupuncture, makes this a promising modality that warrants further investigation.
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PMID:Acupuncture for gastrointestinal and hepatobiliary disorders. 1010 29

* The enteric nervous system has sensory neurons, interneurons and motor neurons and functions as a brain-in-the-gut. * Smooth muscles of the digestive tract are autogenic in the absence of neural control. * Enteric inhibitory motor neurons control excitability of the autogenic musculature. * The neuropathic form of chronic intestinal pseudo-obstruction is a form of disinhibitory motor disease linked with neuropathic degeneration in the enteric nervous system. * Patients with inflammatory degenerative neuropathy may progress from irritable bowel syndrome (IBS)-like symptoms to chronic pseudo-obstruction. * Detection of anti-enteric neuronal antibodies may be a useful diagnostic test for early stages of inflammatory degenerative neuropathy in patients with symptoms of a functional gastrointestinal disorder. Awareness is increasing that autoimmune attack targeted to neuronal elements of the enteric nervous system may underlie irritable bowel-like symptoms that progress to chronic pseudo-obstruction. The inflammatory neuropathy disrupts the integrative functions of the brain-in-the-gut, including reduction in the population of inhibitory motor neurons to the musculature. Extreme loss of inhibitory motor neurons is manifest as disinhibitory motor disease characterized by achalasia in smooth muscle sphincters and hyperactive, disorganized contractile behaviour of intestinal circular muscle which results in pseudo-obstruction. Detection of anti-enteric neuronal antibodies in the serum of patients with early symptoms of a functional gastrointestinal motility disorder may prove to be a useful diagnostic test for inflammatory enteric neuropathy.
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PMID:Neuropathy in the brain-in-the-gut. 1091 73

The functioning of enteric neuronal circuitries has been elucidated in the recent past. Evidence is now gathering to explain how dysfunction of the enteric nervous system (ENS) may lead to human gastrointestinal motor disorders. These conditions include achalasia, congenital hypertrophic pyloric stenosis, chronic intestinal pseudo-obstruction, Hirschsprung's disease, chronic idiopathic constipation, and probably irritable bowel syndrome. Degenerative, inflammatory and genetic mechanisms exert a critical role in ENS dysfunction underlying gut dysmotility. The study of the ENS abnormalities in gut dysmotility provides a framework to better understand the mechanisms involved in degeneration and neuronal loss and fosters the development of targeted therapeutic options.
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PMID:New insights into human enteric neuropathies. 1506 21

Despite the extensive impact of autonomic function on the gastrointestinal system, there is little understanding of the mechanisms by which specific autonomic abnormalities translate into particular gastrointestinal complaints. Three logical alternatives include: (1) the underlying disorder affects the autonomic and gastrointestinal systems independently; (2) autonomic dysfunction alters gastrointestinal processing directly; (3) gastrointestinal manifestations arise as a delayed, indirect consequence of autonomic dysfunction. The major gastrointestinal manifestations of dysautonomia include esophageal dysmotility such as achalasia, gastroparesis, and small bowel bacterial overgrowth in the upper tract. Lower tract disorders include diarrhea, fecal incontinence, and constipation. Sorting through the varied causes of these disorders requires a careful history and examination in each patient. Supportive diagnostic studies may include radionuclide imaging, motility examination, and electrogastrography. Autonomic studies can (1) distinguish a purely enteric from a more generalized dysautonomia; (2) provide surrogate information about motility; (3) differentiate primary (e.g., multiple system atrophy) from secondary (e.g., irritable bowel syndrome) dysautonomias as the etiology of gastrointestinal symptoms. Several new strategies are available for the treatment of gastroparesis, constipation, irritable bowel, and sphincteric incontinence.
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PMID:Evaluation and treatment of autonomic disorders of the gastrointestinal tract. 1508 66


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