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)

The successful management of constipation depends on defining the patient's symptoms, excluding secondary causes, and characterizing the abnormality of defecation. Constipation without gut dilatation is found commonly in pregnancy, the elderly, and those with the irritable bowel syndrome. In addition, there is a group of patients that has intractable, severe idiopathic constipation. Some have 'slow transit' and open their bowels every 1-4 weeks. Others have a defecatory disorder with normal colonic transit. Constipation with gut dilatation is seen in Hirschsprung's disease, idiopathic megarectum and megacolon, chronic intestinal pseudo-obstruction and Chagas' disease. Constipation can also result from disturbance to the autonomic outflow of the gastrointestinal tract, and colonic function may be also affected by psychological factors. This review article discusses the presentation, investigation and management of patients with constipation.
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PMID:Review article: the management of constipation in adults. 828 Aug 17

In conclusion, it seems there has been a definite change in the epidemiology and course of IBD since earlier this century. Several points are worth emphasising: The diseases are relatively common, and there has been a general increase in their incidence, more so in some regions than others. The largest group affected is young adults, who will have their disease over several decades. This could potentially impact markedly on the workforce and on health care services. There is clearly a range of severity of this disease, and a greater number of mild cases have probably been diagnosed recently. This also helps to explain the differences in severity, need for surgery, and survival noted between community based studies and referral centre groups. Treatment has improved, particularly surgery (which usually takes place earlier on less critically ill patients), better operations, including continence surgery for most patients with UC and gut sparing procedures in Crohn's disease such as stricturoplasty. Medical management of acute disease has also improved which, in particular, has reduced mortality in elderly patients. Except for a subset of patients, life expectancy is close to normal, and time lost from the workforce, when considered in perspective over a working lifetime, is negligible. We can therefore be justifiably optimistic about the current long term outcome of IBD, and encourage our patients, their families and their employers to share in this outlook. With the promise of newer medical therapies on the horizon, prognosis may be further improved. Corticosteroids with little or no systemic side effects are currently in clinical trials and new anti-inflammatory agents are being examined for their efficacy through prostaglandin, leukotriene, or oxygen free-radical inhibition. Now that mortality from IBD is largely a thing of the past, we need to concentrate our attention more closely on the associated morbidity. It is to be hoped that future long term studies attempt the difficult clinical measurements of morbidity and quality of life.
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PMID:Inflammatory bowel disease--its history, current status and outlook. 830 96

The potential therapeutic applications of somatostatin and octreotide in gastroenterology involve gut neuro-endocrine tumours, bleeding varices, bleeding peptic ulcers, gastro-intestinal fistulae, pancreatic fistulae, dumping syndrome, pancreatic pseudocysts, short bowel syndrome, acute pancreatitis, AIDS-related diarrhoea, intestinal subacute obstruction, idiopathic 'diarrhoea', irritable bowel syndrome and GIT tumours. Octreotide has a longer duration of action than somatostatin and can be administered by subcutaneous injection, thus making it suitable for long-term administration. Many of the potential gastro-intestinal indications require long-term administration and thus octreotide would be the agent of choice.
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PMID:Potential indications for octreotide in gastroenterology: summary of workshop. 835 70

Patients with non-cardiac chest pain (NCCP) (n = 387) and cardiac chest pain (CCP) (n = 93) were compared with community controls (n = 81), using a symptom questionnaire that assessed the presence of irritable bowel syndrome (IBS), functional dyspepsia, and oesophageal dysfunction and chest pain characteristics. A significantly (p < 0.05) increased prevalence of symptoms compatible with IBS occurred in NCCP patients when compared with those with CCP and with controls. Dysphagia was more frequent in both those with non-cardiac and cardiac chest pain than in controls; this was not apparent, however, when patients with concomitant IBS were excluded. The presence of oesophageal or gastrointestinal symptoms did not enable discrimination with regard to the chest pain characteristics. We conclude that unselected referred patients with documented NCCP are more likely to have IBS and that the presence of oesophageal symptoms such as dysphagia may merely reflect the spectrum of the 'irritable gut'.
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PMID:Functional gastrointestinal disorders in unselected patients with non-cardiac chest pain. 836 9

The ill-understood complex of the irritable bowel syndrome comprises a group of intestinal motility disorders characterized by increased intraluminal pressures and decreased transit times. Elucidation of mechanisms which modulate gut motility may lead to the development of rational therapy for this prevalent problem. The purpose of this study was firstly to evaluate the interaction of cAMP-dependent agents (vasoactive intestinal polypeptide (VIP), norepinephrine (NE), and forskolin (FK)) on carbachol (Ca2+)-initiated motility and secondly to determine if a neural component of motility modulation existed by testing if the effect of cAMP-dependent agents was reversed by tetrodotoxin-induced neural blockade. Motility was measured in isolated segments of terminal ileum harvested from rabbits using perfusion manometry and quantitated by integration, expressed as mm Hg/min. Carbachol caused a concentration-dependent increase in measured motor activity (half-effective dose = 10(-7) M). VIP, NE, and FK each caused a concentration-dependent inhibition of carbachol-stimulated phasic contractions. TTX 10(-6) M failed to block the inhibitory actions of NE. In conclusion, these results suggest that cAMP-dependent mechanisms may inhibit gut motility induced by a cholinergic (Ca2+)-mediated agonist and that this process is mediated by a nonneural mechanism.
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PMID:Counterregulation of a prokinetic calcium-dependent mechanism by cAMP-dependent agents in isolated segments of terminal ileum. 838 83

Hyporesponsiveness to a universe of bacterial and dietary antigens from the gut lumen is a hallmark of the intestinal immune system. Since hyperresponsiveness against these antigens might be associated with inflammation, we studied the immune response to the indigenous intestinal microflora in peripheral blood, inflamed and non-inflamed human intestine. Lamina propria monocuclear cells (LPMC) isolated from inflamed intestine but not peripheral blood mononuclear cells (PBMC) of IBD patients with active inflammatory disease strongly proliferated after co-culture with sonicates of bacteria from autologous intestine (BsA). Proliferation was inhibitable by anti-MHC class II MoAb, suggesting that it was driven by antigen. LPMC from adjacent non-inflamed intestinal areas of the same IBD patients and PBMC or LPMC isolated from non-inflamed intestine of controls and patients with IBD in remission, in contrast, did not proliferate. PBMC or LPMC which had been tolerant to bacteria from autologous intestine, however, strongly proliferated after co-culture with bacterial sonicates from heterologous intestine (BsH). This proliferation was associated with an expansion of CD8+ T cells, increased expression of activation markers on both CD4+ and CD8+ lymphocyte subsets, and production of IL-12, interferon-gamma (IFN-gamma), and IL-10 protein. These results show that tolerance selectively exists to intestinal flora from autologous but not heterologous intestine, and that tolerance is broken in intestinal inflammation. This may be an important mechanism for the perpetuation of chronic IBD.
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PMID:Tolerance exists towards resident intestinal flora but is broken in active inflammatory bowel disease (IBD) 853 55

The role of motility tests in the evaluation of some common disorders in which motility has been assumed to play a role is reviewed. Three separate areas, non-cardiac chest pain, constipation and the irritable bowel syndrome are discussed. In each area, considerable difficulty in the clinical definition of these disorders persists and presents a major obstacle to the evaluation of diagnostic tests. With regard to non-cardiac chest pain, it is apparent that gastro-oesophageal reflux and sensory/perception abnormalities, rather than dysmotility, are the predominant factors, and investigations should take account of this. While studies of colonic and small intestinal motility have demonstrated various abnormal patterns in patients described as suffering from the irritable bowel syndrome, the specificity of any of these motor 'abnormalities' remains uncertain, and manometry cannot be recommended as a diagnostic tool in this context. Considerable advances have been made in our understanding of gut motor physiology and in our ability to accurately record motor function in man, the basic pathophysiology of many 'functional' gut syndromes remains unclear, and the role of dysmotility, in particular, poorly defined.
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PMID:Gastrointestinal motility testing--a personal perspective. 857 21

T cell hypersensitivity has been implicated in the tissue damage in Crohn's disease (CD). All studies to date have examined mucosal T cells, although much of the tissue damage occurs in the submucosa and muscle layers. The aim of this work was to study T cell proliferation throughout the intestinal wall in children with IBD. Surgical resection material from 19 children with CD (10 ileal, 10 colonic), seven with ulcerative colitis (UC), and 12 normal controls was studied. The distribution of dividing T cells was investigated by double-immunohistochemistry using Ki67 to identify proliferating cells, and CD3 to identify T cells. In ileal and colonic lamina propria virtually no Ki67+, CD3+ cells were seen in control, UC or CD tissue. In contrast, there were significantly more Ki67+, CD3+ cells within the lymphoid follicles of ileal and colonic CD than in the follicles in UC and controls. Increased numbers of Ki67+, CD3+ cells were present in the submucosa, muscle layers (M) and serosa in Crohn's ileitis and colitis compared with the lamina propria (LP), although only in the muscle of the colon was the difference statistically significant (LP, 0.4% (0-1%); M, 1.6% (0-5.2%); P = 0.03). Pooling data from ileal and colonic CD, however, did show significantly increased Ki67+, CD3+ cells in both serosa and muscle layers compared with the LP. Dividing T cells have been identified in the deeper layers of the gut wall in CD. These may contribute to the fibrosis and muscle hyperplasia characteristic of the condition.
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PMID:The distribution of dividing T cells throughout the intestinal wall in inflammatory bowel disease (IBD). 862 21

Recent studies strongly support the concept that gut and joint inflammation are closely related. Progress also has been made in identifying individual mechanisms that contribute to the pathogenesis of joint disease in IBD and in undifferentiated SpAs. However, the interrelationship of these mechanisms that result in chronic disease manifestations at a site distant from the initiating event remain to be elucidated. The local absence of homing molecule receptors in the gut wall combined with an expression of these receptors in target organs can be responsible for the transformation of the synovial membrane and/or the enthesis into an aberrant tertiary lymphoid organ of the gut.
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PMID:Spondylarthropathies: from gut to target organs. 867 44

In contrast with normal subjects where IgA is the main immunoglobulin in the intestine, patients with active inflammatory bowel disease (IBD) produce high concentrations of IgG from intestinal lymphocytes, but the antigens at which these antibodies are directed are unknown. To investigate the specificities of these antibodies mucosal immunoglobulins were isolated from washings taken at endoscopy from 21 control patients with irritable bowel syndrome, 10 control patients with intestinal inflammation due to infection or ischaemia, and 51 patients with IBD: 24 Crohn's disease (CD, 15 active, nine quiescent), 27 ulcerative colitis (UC, 20 active, seven inactive). Total mucosal IgG was much higher (p < 0.001) in active UC (median 512 micrograms/ml) and active CD (256 micrograms/ml) than in irritable bowel syndrome controls (1.43 micrograms/ml), but not significantly different from controls with non-IBD intestinal inflammation (224 micrograms/ml). Mucosal IgG bound to proteins of a range of non-pathogenic commensal faecal bacteria in active CD; this was higher than in UC (p < 0.01); and both were significantly greater than controls with non-IBD intestinal inflammation (CD p < 0.001, UC p < 0.01) or IBS (p < 0.001 CD and UC). This mucosal IgG binding was shown on western blots and by enzyme linked immunosorbent assay (ELISA) to be principally directed against the bacterial cytoplasmic rather than the membrane proteins. Total mucosal IgA concentrations did not differ between IBD and controls, but the IgA titres against faecal bacteria were lower in UC than controls (p < 0.01). These experiments show that there is an exaggerated mucosal immune response particularly in active CD but also in UC directed against cytoplasmic proteins of bacteria within the intestinal lumen; this implies that in relapse of IBD there is a breakdown of tolerance to the normal commensal flora of the gut.
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PMID:Mucosal antibodies in inflammatory bowel disease are directed against intestinal bacteria. 867 88


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