Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence for autoimmunity in diarrhoeal disease is reviewed. Firstly, coeliac disease (CD) is considered. The incidence of tissue-reactive autoantibodies in both adults and children with CD (68% and 65%, respectively) is higher than the incidence of these autoantibodies in controls (6% in normal adults, and 14% and 9% in disease controls drawn respectively from adult and child populations). The R1 antireticulin antibody, when present, was found to disappear after several weeks on a gluten-free diet, but in contrast, other autoantibodies persisted. Secondly, a case is argued for a new disease category, namely "autoimmune enteropathy." Seven cases are reviewed in which patients presented with protracted diarrhoea, a small intestinal enteropathy which failed to heal during periods of total parenteral nutrition, and evidence of a predisposition to autoimmunity (namely, the presence of high titre autoantibodies including one specific for gut epithelium, and/or the presence of associated diseases regarded to be autoimmune). Thirdly, evidence for autoimmunity in inflammatory bowel disease is reviewed and includes discussion of serum goblet cell antibodies and of circulating T cells which participate in antibody-dependent cellular cytotoxicity in vitro using colonic epithelial cells as targets. Finally, an unusual child is described who presented with chronic diarrhoea and a flat small intestinal mucosa, who responded to gluten withdrawal but who later relapsed spontaneously during a strict gluten-free diet. Her mucosa healed only after a period of total parenteral nutrition and treatment with oral steroids. This child's enteropathy was also associated with thyrotoxicosis and a microscopic colitis.
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PMID:Autoimmunity in diarrhoeal disease. 402 May 70

Since beclomethasone dipropionate (BDP) is a very potent glucocorticoid and since small oral doses (1 mg) seem to be metabolised (possibly in the gut wall or liver) before they reach the systemic circulation, a study was conducted to find out whether patients with inflammatory bowel disease could be treated with enemas containing small doses of BDP without their acquiring Cushing's syndrome or hypothalamic pituitary adrenal (HPA) suppression. The BDP in the 100 ml enemas used was stable and present in a concentration likely to be therapeutic (0.5 mg/dl). Single overnight BDP enemas, unlike conventional betamethasone (5 mg) enemas, did not interfere with the HPA axis in 6 healthy volunteers. In the double-blind randomised part of the study 2-week courses of BDP or betamethasone enemas were assessed in 9 patients having exacerbations of distal inflammatory bowel disease. The clinical and sigmoidoscopic responses as well as adrenocortical function (judged by the 'Cosyntropin' test) were evaluated on the morning after the last day of a course of enemas. Both types of enemas had similar beneficial effects, but only BDP enemas did not interfere with HPA function. Over a prolonged period, a patient with distal ulcerative colitis had been completely dependent on regular treatment with betamethasone enemas to control his symptoms. Substitution with BDP enemas successfully controlled his bowel symptoms, whilst his cushingoid features and HPA suppression regressed.
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PMID:Beclomethasone dipropionate enemas for treating inflammatory bowel disease without producing Cushing's syndrome or hypothalamic pituitary adrenal suppression. 612 Nov 81

Deficiency of either folic acid or vitamin B12 may interfere with DNA synthesis and result in megaloblastic anemia or other conditions. These 2 vitamins have dissimilar molecular structures and are present in different foods; they are also absorbed and metabolized differently. In 201 consecutive cases of megaloblastic anemia, for 90% the cause was alcoholism and poor diet; 0.5% (1 case) was related to oral contraceptives (OCs). Megaloblastic anemia due to folate deficiency has occasionally been reported in patients with inflammatory bowel disease and has been attributed to poor diet, impaired absorption, and increased tissue utilization of folate. Sulfasalazine, a compound containing a sulfa drug and a salicylate that is broken down to its active components by the gut flora, is widely used in the treatment of inflammatory bowel disease and has been shown to impair the absorption of folic acid, polyglutamyl folate, and methyl-tetrahydrofolic acid in patients with these disorders. There is also evidence suggesting an interaction between anticonvulsant drugs and folate balance. A number of cases of megaloblastic anemia due to folate deficiency have been reported in women taking OCs. While in some cases no apparent cause for the megaloblastic anemia other than contraceptive therapy was demonstrated, in many patients other underlying disorders that were likely to disturb folate balance such as celiac disease, decreased dietary vitamin intake, and the administration of other drugs known to affect folate status have also been present. There is no convincing evidence that sex steroids affect folate absorption; about 20% of women taking OCs were found to have mild megaloblastic changes on Papanicolaou smears. These changes disappered after folic acid therapy, suggesting that OCs may cause an increased demand for folate limited to the reproductive system. Another finding is of low serum cobalamin levels in women using OCs; this appears however to be a laboratory abnormality of uncertain cause and of no clinical significance.
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PMID:Drugs and vitamin B12 and folate metabolism. 613 2

Lipid A is a component common to endotoxins of gram-negative bacteria. It has been suggested that the gut wall of patients with inflammatory bowel disease is more permeable to luminal bacterial macromolecules which may stimulate the gut-associated lymphoid tissue. We therefore investigated 40 patients with Crohn's disease (CD) and 23 patients with ulcerative colitis (UC) with respect to their lipid A antibody titers and presence of endotoxins (Limulus test). Both tests were performed simultaneously using peripheral venous blood. Systemic endotoxin was demonstrated in only two of the patients. The lipid A antibody titers in the CD patients were significantly higher than either in patients with UC or in 42 healthy controls. Lipid A titers of patients with UC did not differ from those of controls. Titers of lipid A were significantly higher in patients with active Crohn's disease than in patients with inactive disease. It is concluded that systemic endotoxemia occurs rarely in patients with inflammatory bowel disease; however, despite this virtual absence of endotoxins in their peripheral blood, patients with CD show an increase in antibody formation against lipid A. This is suggestive of an altered immunologic reactivity against endotoxins in patients with CD and may be relevant to the pathogenesis of this disease.
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PMID:Circulating lipid A antibodies despite absence of systemic endotoxemia in patients with Crohn's disease. 614 75

Electronmicroscopical studies have been carried out on colonic biopsies from patients with long-term laxative abuse, amyloidosis, diabetic autonomic neuropathy or chronic inflammatory bowel disease. The results of these investigations indicate that submucosal nerve fibres are damaged to an extent dependent upon the intensity of the toxic agent. The main pathological features range from distension or ballooning of axons, reduction of nerve-specific cell structures and increase in lysosomes to a total degeneration of whole nerve fibres. While the degenerative process is uniform, differentiation between disease states can be made on the basis of specific additional lesions such as the presence of typical amyloid fibrils, diabetic microangiopathy or the inflammatory process in inflammatory bowel disease. No changes were found in Whipple's disease or gluten-sensitive enteropathy. It is concluded that the structural alterations may provide a morphological explanation for the disturbances in gut motility, as an intact intramural nervous system is a necessary prerequisite for the regular coordination of normal peristalsis.
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PMID:Ultrastructural changes in the gut autonomic nervous system following laxative abuse and in other conditions. 617 11

Abnormalities in immune regulation at the gut level may be relevant to the pathogenesis of inflammatory bowel disease, but little is known about the immunoregulatory properties of intestinal mononuclear cells. Therefore, we wished to see if lymphoid cells derived from the lamina propria of surgically resected bowel specimens have any modulatory effect upon the immune response of peripheral blood mononuclear cells from patients with ulcerative colitis or Crohn's disease. When autologous peripheral blood and intestinal lamina propria lymphoid cells were mixed at different ratios and cultured in the presence of phytohaemagglutinin, we were able to show that intestinal mononuclear cells had the capacity to modify the mitogenic response of the cultured cells. These intestinal immunoregulatory cells, when obtained from mucosa affected by inflammatory bowel disease, express a significantly enhanced suppressor cell activity as compared with those from non-inflamed control mucosa. Such suppressor cell activity varies with cell concentration and requires cell proliferation, but it is independent of anatomical origin (small vs large bowel), type of inflammatory bowel disease (ulcerative colitis vs Crohn's disease) or immunosuppressive therapy. These findings point to an important functional difference between inflammatory bowel disease and control intestinal mucosa mononuclear cells. The enhanced suppressor activity of lamina propria mononuclear cells may be associated with impairment of cell-mediated immunity at the gut level. This may be related to the pathogenesis of inflammatory bowel disease by leading to defective intestinal immune regulatory events, which may not be detectable at the peripheral level.
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PMID:Immunoregulatory function of human intestinal mucosa lymphoid cells: evidence for enhanced suppressor cell activity in inflammatory bowel disease. 622 62

Antigen presenting veiled cells have recently been described in cell suspensions prepared from the gut wall of patients with chronic idiopathic inflammatory bowel disease (CIBD). The normal gut wall is virtually devoid of these cells. In this report we describe a phenomenon known as peripolesis studied by phase contrast cinematography. This is a process in which lymphocytes are seen to wander around larger target cells. These could be identified ultrastructurally as Ia positive veiled cells. In most cases peripolesis was followed by lysis of the target cell. Peripolesis was recorded in cell suspensions of three out of seven patients with ulcerative colitis and in three out of nine patients with Crohn's disease; furthermore peripolesis was observed in one out of two patients with non-classifiable CIBD. In four cell suspensions showing peripolesis, cell lysis could be recorded and was especially striking in ulcerative colitis. Peripolesis involving veiled cells was previously described in delayed hypersensitivity reactions. This study lends support to the concept that delayed allergic reactivity plays a part in chronic inflammatory bowel disease. The antigens involved are, however, completely unknown.
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PMID:Peripolesis followed by cytotoxicity in chronic idiopathic inflammatory bowel disease. 638 Aug 39

An unclassified Mycobacterium species has been isolated from two patients with Crohn's disease (CD). Antibodies to the unclassified mycobacteria cross-reacted with Mycobacterium paratuberculosis. Because of this cross-reactivity, an enzyme-linked immunosorbent assay (ELISA) was used to examine the sera of inflammatory bowel disease (IBD) patients, both CD (N = 56), and ulcerative colitis (UC) (N = 34), for antibodies to M. paratuberculosis, Mycobacterium kansasii, and Mycobacterium tuberculosis. Controls consisted of healthy, PPD-negative individuals (N = 67), and from PPD-positive patients (N = 41). Eighteen resected CD patients were also examined. CD patients had a statistically significant increase in antibody titer (P = 0.0003) to M. paratuberculosis compared to healthy controls. Although patients with positive PPD had elevated titers to this organism, the positive response of CD patients was not related to PPD responsiveness, area of involvement in the gut, nor to activity of the disease process.
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PMID:Possible role of mycobacteria in inflammatory bowel disease. II. Mycobacterial antibodies in Crohn's disease. 643 75

We investigated suppressor cell activity in the peripheral blood of 39 patients with inflammatory bowel disease (30 Crohn's disease and 9 ulcerative colitis) by the short-lived suppressor cell assay. There was a significant decrease in the suppressor cell activity in patients with inflammatory bowel disease (IBD), compared to 26 healthy subjects studied simultaneously. Five other patients with acute bacterial infections had normal suppressor activity. A group of 14 IBD patients was also investigated for concanavalin A-induced suppressor cell activity and decreased suppressor function was confirmed. A significant positive correlation was found between the two assays. A defect in suppressor cell activity may permit the expression or maintenance of immunologically mediated damage to the gut in IBD.
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PMID:Spontaneous suppressor cell function in inflammatory bowel disease. 645 77

Symptoms of 50 patients with the irritable bowel syndrome were compared with those of 49 with endoscopically proven peptic ulcer disease and 49 with radiologically or endoscopically proven inflammatory bowel disease using a questionnaire which was administered after the diagnosis was made. Symptoms of bowel dysfunction including pain related to bowel movements were more likely to occur in the irritable bowel syndrome than peptic ulcer disease. Only abdominal distension, straining at stool and scybala, however, were significantly more likely in the irritable bowel syndrome than inflammatory bowel disease. Four symptoms previously shown to be more common in irritable bowel syndrome than in organic abdominal disease were combined. The more of these symptoms that were present, the more likely were the patients to have the irritable bowel syndrome than peptic ulcer disease. Symptoms of gut dysfunction are highly discriminating between irritable bowel syndrome and peptic ulcer disease but less so between irritable bowel syndrome and inflammatory bowel disease.
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PMID:Gastrointestinal symptoms in the irritable bowel compared with peptic ulcer and inflammatory bowel disease. 647 83


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