Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021831 (enteropathy)
 4,403 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the aetiology of inflammatory bowel disease remains elusive, many agents are available for the control of symptoms and inflammation. Knowledge of drug pharmacology, indications and side effects is essential to ensure the best possible clinical care while minimising toxicity and inappropriate use. Sulfasalazine consists of sulfapyridine linked to mesalazine (5-aminosalicylic acid) via an azobond. Its use is indicated in the treatment of mild to moderately active ulcerative colitis and in the prevention of relapse in patients with quiescent disease. Patients with mild to moderate colonic or ileocolonic Crohn's disease also benefit from this drug, as do a proportion of patients with isolated small bowel disease. Sulfasalazine has not been uniformly effective in preventing relapse in Crohn's disease, although many clinicians continue its use in patients who respond initially. A high incidence of side effects which limit therapy include intolerance, hypersensitivity reactions and impairment of male infertility. The newer aminosalicylates offer targeted delivery of mesalazine to the bowel, with fewer side effects. Topical mesalazine has proved extremely effective in patients with distal ulcerative colitis; oral forms are effective in the treatment of mild to moderately active ulcerative colitis and in relapse. Both types appear to be effective in the treatment of Crohn's disease, and possibly in preventing relapse. There is no current clinical advantage of one mesalazine preparation over another, nor is there an indication for their use in sulfasalazine-treated patients who have satisfactory response without adverse effects. Corticosteroids are indicated for more severe disease activity where the aminosalicylates have limited efficacy-specifically to induce remission in patients with severe or refractory ulcerative colitis or Crohn's disease. They should not be used to maintain disease remission or in the prevention of postoperative recurrence. Topical corticosteroids allow their local use in distal colitis with minimal systemic side effects. Long term use is limited by side effects, many of which are dose related, although alternate-day therapy may lessen the incidence. Immunosuppressive agents are beneficial for the treatment of refractory inflammatory bowel disease unresponsive to other medications, and may also facilitate the withdrawal of steroids in refractory patients. Mercaptopurine has an added benefit in the treatment of Crohn's disease fistulae; the role of cyclosporin in bowel disease has not been established and its use cannot currently be recommended. The potential toxicity of immunosuppressive agents warrants careful consideration of their use by both physician and patient. Metronidazole is indicated for the treatment of mild to moderate Crohn's disease, including perineal disease. Common side effects include peripheral neuropathy and nausea.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Risk-benefit assessment of drugs used in the treatment of inflammatory bowel disease. 167 90

Interleukin-2 activity of intestinal lamina propria mononuclear cells is decreased in Crohn's disease and ulcerative colitis patients compared with control patients with noninflammatory bowel disease. Factors that might be responsible for this phenomenon were investigated. Most interleukin-2 activity was produced by helper (CD4+) T cells. These were present in comparable numbers in both inflammatory bowel disease and control cultures, but the frequency of interleukin-2-producing cells was significantly (3-4 times) lower among Crohn's disease and ulcerative colitis than control cells. In agreement with this finding, levels of interleukin-2 messenger RNA were substantially decreased in both forms of inflammatory bowel disease compared with controls. Mucosal CD8+ T cells and plastic-adherent cells were unable to suppress interleukin-2 activity by autologous or allogeneic CD4+ T cells. The rate of interleukin-2 absorption was similar for inflammatory bowel disease and control cells. Induction of interleukin-2 by different stimuli (phorbol ester, phytohemagglutinin, or anti-CD3 monoclonal antibody) before or after incubation under basal conditions ("resting") failed to normalize the capacity to generate interleukin-2 by Crohn's disease and ulcerative colitis cells. Prostanoids (prostaglandin E2 and 6-keto-prostaglandin F1 alpha) were produced in large amounts in cultures of inflammatory bowel disease cells, but inhibition by indomethacin failed to restore interleukin-2 activity to control levels. Finally, supernatants from Crohn's disease and ulcerative colitis cell cultures failed to suppress interleukin-2 production by control CD4+ T cells. Our results show that the low interleukin-2 activity detected in inflammatory bowel disease mucosa is not caused by activated suppressor cells, excessive lymphokine utilization or immune stimulation, a defective response to activation signals, or production of inhibitory substances. Rather, the low interleukin-2 activity appears to be related to a loss of interleukin-2-producing mucosal CD4+ T cells. It is concluded that abnormalities of intestinal CD4+ T-cell function are associated with the immunopathogenesis of Crohn's disease and ulcerative colitis.
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PMID:Loss of interleukin-2-producing intestinal CD4+ T cells in inflammatory bowel disease. 168 26

Nine patients with lymphoma occurring in association with inflammatory bowel disease were admitted to The Mount Sinai Hospital between 1960 and 1983. Five (two men and three women) occurred among 1156 patients (0.43%) with ulcerative colitis (UC) and four (men), among 1480 patients (0.27%) with Crohn's disease (CD), a strong male preponderance in the latter group. In all four of the patients with CD and in four of the five patients with UC, the lymphomas were extraintestinal. The mean age of onset of UC in these patients was late (46 years, 19 years older than in our overall series), with lymphomas occurring a mean of only 12 years later. By contrast, patients with CD had bowel disease much younger (mean age, 26 years), and their lymphomas appeared after a longer disease duration (mean, 24 years). The risk factors for the one patient with colonic lymphoma were similar to those with colitis-associated colorectal carcinoma: extensive and long-standing colitis and relatively young age when malignant disease developed. Four of the patients with lymphoma had associated colonic carcinoma; in three of them, the carcinoma appeared within the first decade of colitis, an unusual occurrence. A second malignant lesion also occurred in three patients with UC.
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PMID:Lymphoma in inflammatory bowel disease. 173 11

An 18-year review of 64 patients treated with 71 postoperative enterocutaneous fistulas of the stomach /4/, duodenum /21/, jejunum /9/ and ileum /37/ was carried out to identify the factors affecting morbidity and mortality. Age, localization, output, inflammatory or malignant bowel disease, nutritional status and associated sepsis were analysed. The administration of total parenteral nutrition (TPN) or/and enteral nutrition (EN) as adjuvant therapy in the management of gastrointestinal fistulas increased the fistula closure rate (64%) and decreased mortality (33%). In patients over 65 years a rise in mortality rate (69%) was found. TPN and EN support yielded the best results in duodenal and jejunal fistula patients (closure rate 83% and 71%; respectively). In patients with high-output fistulas, inflammatory bowel disease and malignancy good results could be achieved with nutritional treatment. The presence of malnutrition had an adverse effect on the outcome in the non-TPN group with a mortality rate of 49%. In 43 patients severe septic complications occurred and 21 died due to septic multiple organ failure proved by autopsy. The overall mortality rate was 39%. Timing of fistula surgery had little impact on the fistula closure rate, but better results were obtained when reconstructive surgery was deferred beyond 6 weeks from fistula onset. Mortality has decreased since 1980. While many factors influence the outcome of fistula disease, adequate antiseptic treatment is assumed of primary importance. The nutritional therapy facilitated the spontaneous fistula healing and allowed the elective intestinal reconstruction to be scheduled at an optimal time.
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PMID:Parenteral and enteral nutrition and the enterocutaneous fistula treatment. II. Factors influencing the outcome of treatment. 184 22

Gastrointestinal disease is a well recognized feature in patients with common variable immunodeficiency, and is often due to infection with a variety of organisms. Symptoms usually improve with appropriate antibiotic therapy and replacement gammaglobulin. We describe three middle-aged female patients with common variable immunodeficiency who had protracted diarrhoea and weight loss. Despite extensive investigation no infectious cause was found. All patients had granulomas distributed throughout the gastrointestinal tract, but no features of inflammatory bowel disease. There was a poor response to gammaglobulin replacement therapy, antibiotics or symptomatic treatment. We suggest that granulomatous enteropathy is another gastrointestinal manifestation of common variable immunodeficiency.
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PMID:Granulomatous enteropathy in common variable immunodeficiency: a cause of chronic diarrhoea. 185 60

Primary sclerosing cholangitis (PSC) is a syndrome of unknown etiology, characterized by fibrosis and inflammation of the intra- and extrahepatic bile ducts. PSC is usually seen in association with inflammatory bowel disease, particularly in younger patients with extensive ulcerative colitis. Crohn's disease is seen in more than 10% of all patients with PSC. The bowel disease may produce no symptoms in some patients, and the clinical course is usually silent. The development and widespread use of endoscopic retrograde cholangiopancreaticography (ERCP) have enabled us to diagnose the disease far more often than was possible only a decade ago, and also to recognize that PSC has a much wider clinical and pathologic spectrum than previously realized. Most patients with concomitant ulcerative colitis and persistently abnormal liver function tests are likely to have PSC. Patients with PSC usually have a cholestatic biochemical profile, whereas the histologic features of the liver biopsy are variable and often nonspecific. Cholangiography displaying strictures and beading is diagnostic of the disease. The prognosis is variable, with a benign clinical course in many patients. However, an increased rate of cholangiocarcinoma is found in PSC, as is an increased rate of colonic cancer in patients with PSC and ulcerative colitis.
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PMID:[Primary sclerosing cholangitis and inflammatory bowel disease]. 197 Jun 74

Four patients developed adrenal hemorrhage during treatment with intravenous adrenocorticotropic hormone (ACTH) for severe inflammatory bowel disease (IBD). This complication presented suddenly with upper abdominal and flank pain mimicking an acute surgical abdomen. In each patient the symptoms of the underlying bowel disease had subsided under the ACTH therapy. In our first patient the diagnosis was not made until laparotomy, but in the subsequent three patients the diagnosis was suspected by the strikingly similar clinical presentation. In each of these three latter patients the diagnosis was confirmed by sonography or computed tomography (CT) scan, and surgery was avoided. All four of our patients are doing well at 1-58 months of follow-up. Signs of adrenal insufficiency occurred only in the one of our four patients, and in those six of 11 previously reported patients, who had bilateral adrenal hemorrhage. ACTH-induced adrenal hemorrhage requires stopping ACTH and maintaining corticosteroid support. The diagnosis of adrenal hemorrhage should be considered in the patient treated with ACTH who develops unexplained acute abdominal or flank pain. Failure to recognize this complication of ACTH therapy can lead to unnecessary surgery or the dangerous continuation of the offending agent.
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PMID:ACTH-induced adrenal hemorrhage: a complication of therapy masquerading as an acute abdomen. 184 72

We have validated an established animal model of acute inflammatory bowel disease in indomethacin-treated rats. Studies in both in vitro and in vivo 51chromium-labelled ethylenediamine tetra-acetate (51Cr-EDTA) permeability and tissue myeloperoxidase activity, a marker of inflammatory cell invasion, showed increased permeability and enzyme levels, respectively, in treated animals compared to controls (in vitro 51Cr-EDTA permeability: (mean (SE] control 0.10 (0.02) microliter/mg per tissue, experimental 0.17 (0.02) (p < 0.01, 2 way analysis of variance); in vivo 51Cr-EDTA permeability: control 3.9 (1.3) (% dose recovered), experimental 12.1 (1.5) (p < 0.01); tissue myeloperoxidase: control 10.8 (0.4) mU/mg, experimental 17.2 (0.5) p less than 0.01). Pretreatment or simultaneous treatment of indomethacin-treated animals with glucocorticoids, sulphasalazine, or tetracycline reduced the permeability changes and the tissue inflammatory response (in vitro 51Cr-EDTA permeability: (mean (SE] sulphasalazine + indomethacin 0.11 (0.2) microliter/mg tissue (p < 0.01), prednisolone +/- indomethacin 0.12 (0.02) (p < 0.01), tetracycline + indomethacin 0.12 (0.02) (p < 0.01]. Glucocorticoids and sulphasalazine, but not tetracycline, administered after the indomethacin also partially corrected the permeability and inflammatory changes induced by indomethacin (in vitro 51Cr-EDTA permeability: sulphasalazine 0.15 (0.02) microliter/mg, p < 0.02; prednisolone 0.12 (0.02) microliter/mg, p < 0.01). This approach was used to investigate the effects of two different thromboxane synthetase inhibitors in indomethacin-treated animals. Simultaneous treatment with thromboxane synthetase inhibitors and indomethacin prevented the 51Cr-EDTA permeability and tissue myeloperoxidase increases induced by indomethacin alone (in vitro 51Cr-EDTA permeability: thromboxane synthetase inhibitors + indomethacin 0.11 (0.01) microliter/mg (p0.01); tissue myeloperoxidase: 11 (0.4) mU/mg, (p < 0.01). Thromboxane synthetase inhibitors administered after the indomethacin also partially corrected the permeability and inflammatory changes induced by indomethacin (in vitro 51Cr-EDTA permeability: thromboxane synthetase inhibitors 0.12 (0.02) mU/mg (p < 0.01); tissue myeloperoxidase 13.8 (0.5) (p < 0.01). These studies indicate that thromboxane synthetase inhibitors partially correct the intestinal lesion non-steroidal anti-inflammatory drug enteropathy and may therefore be of use in inflammatory bowel diseases in humans.
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PMID:Experimental non-steroidal anti-inflammatory drug-induced enteropathy in the rat: similarities to inflammatory bowel disease and effect of thromboxane synthetase inhibitors. 1128 36

Chronic undernutrition and high-dose daily corticosteroid therapy are well-accepted causes of growth failure in children with inflammatory bowel disease. Occasionally, children are seen with minimal gastrointestinal symptoms but in whom severe anorexia and profound growth impairment are evident. Recent observations that elevated serum levels of tumor necrosis factor-alpha (TNF) in cachexia associated with a number of disease states have suggested a similar possible role in inflammatory bowel disease. Accordingly, we determined TNF levels in 45 children and adolescents with inflammatory bowel disease (18 ulcerative colitis, 27 Crohn's disease) at varying times during their clinical course and compared them to values obtained from a group of 25 children with functional bowel disease. No differences were noted in serum TNF levels between the children with inflammatory bowel disease and the control population. Values were generally within the range of the lower limit of detection of the assay. In the children with inflammatory bowel disease, there was no significant correlation between TNF levels and disease activity or growth parameters. Our observations suggest that elevated TNF levels are not associated with inflammatory bowel disease in children.
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PMID:Tumor necrosis factor-alpha is not elevated in children with inflammatory bowel disease. 205 Dec 74

Serum levels of zinc, copper, and selenium, and alkaline phosphatase activity were prospectively studied in 29 patients with inflammatory bowel disease. Fifteen patients had extensive active colitis (active colitis group). Seven patients had active, and seven cases inactive small bowel or ileocecal Crohn's disease (small bowel disease group). Ninety-three healthy subjects acted as controls. Serum trace element levels were considered in relation to vitamin A and E levels, nutritional parameters, the activity of the disease, and the recent intake of steroids. The effect of total enteral nutrition on serum trace elements was studied in seven cases. Serum zinc levels were lower and serum copper levels higher in the active colitis group than in controls (p = 0.0007, and p = 0.02, respectively). More than 50% of patients with active colonic or small bowel disease showed zinc levels below the 15th percentile of the control group. Serum zinc levels correlated with plasma vitamin A in acute colitis (r = 0.67; p = 0.006), and with both serum albumin concentration (r = 0.76; p = 0.002) and disease activity score (r = -0.67, p = 0.009) in patients with small bowel disease. The copper:zinc ratio was higher in the active colitis group than in controls (p = 0.002). In spite of the increase in serum albumin levels and the decrease in disease activity, serum zinc levels remained low after total enteral nutrition. The implications of the abnormal trace element status in patients with inflammatory bowel disease are discussed.
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PMID:Serum zinc, copper, and selenium levels in inflammatory bowel disease: effect of total enteral nutrition on trace element status. 212 4


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