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)

In inflammatory bowel disease (IBD), mucosal damage and loss of colonic function are regarded as major consequences of inflammation. Decreased colonic (Na+ + K+)-ATPase activities with diminished reabsorption of sodium and water have been found in active stages of ulcerative colitis. In this study, we report an inverse relationship between colonic (Na+ + K+)-ATPase activity and the degree of mucosal inflammation in 19 patients with IBD of mild to moderate disease activity. Various macroscopic and histologic types of mucosal lesions were differently associated with the (Na+ + K+)-ATPase activities. 5'-nucleotidase activity was not associated with the degree of mucosal inflammation or the kind of macroscopic or histologic lesions. Our findings support the view that, in contrast to 5H-nucleotidase, (Na+ + K+)-ATPase activity may better reflect the severity of mucosal damage and the degree of inflammation in IBD.
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PMID:Inverse relationship between colonic (Na+ + K+)-ATPase activity and degree of mucosal inflammation in inflammatory bowel disease. 283 38

The effects of lipoxygenase products (5-, 12-, 15-HETE, LTB4) and superoxide radicals on human colonic (Na+ + K+)-ATPase and specific ouabain binding were measured. No significant inhibition in concentrations up to 3 x 10(-5) M was observed. The results are discussed with regard to a possible role of lipoxygenase products and radicals in the pathogenesis of water and electrolyte disturbances in various diarrheal states including inflammatory bowel disease.
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PMID:Human colonic (Na+ + K+)-ATPase and specific ouabain binding are not influenced by lipoxygenase products or superoxide radicals. 285 Apr 5

Sulphasalazine (SASP), used in the treatment of inflammatory bowel disease, is split into sulphapyridine (SP) and 5-aminosalicylic acid (5-ASA) in the colon. Lower plasma levels of SASP and 5-ASA as compared to those of SP may be due to different absorption rates from the colon because of different pK values and pH dependent lipid-water partition coefficients. In this study we determined the pK values of 5-ASA and its major metabolite, N-acetyl amino-salicylic acid (AcASA), by 13C-NMR spectroscopy and compared the pH dependent apparent benzene-water partition coefficients (Papp) of SASP, SP and 5-ASA with respect to their different plasma levels. The COOH group of 5-ASA had a pK value of 3.0, the -NH3+ group had 6.0, the -OH group 13.9; the -COOH group of AcASA had 2.7 and the -OH group 12.9; The Papp of SASP (0.042 +/- 0.004) and 5-ASA (0.059 +/- 0.01) were significantly lower than that of SP (0.092 +/- 0.03) (at pH 5.5).
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PMID:Determination of the pK values of 5-aminosalicylic acid and N-acetylaminosalicylic acid and comparison of the pH dependent lipid-water partition coefficients of sulphasalazine and its metabolites. 286 70

Antibody to rat liver metallothionein prepared by the method of Brady and Kafka (1979) was used to localise immunoreactive metallothionein using a sensitive DNP hapten sandwich technique applied to formalin fixed wax embedded tissues. Rat tissues examined were liver, kidney and small intestine, taken from normal animals, from animals fasted after receiving either an oral dose of water, or 1 ml zinc acetate solution either orally or by intraperitoneal injection, (3-4 mg Zn++/Kg body weight). Human tissues examined were 6 histologically normal liver biopsies and small intestine including histologically normal jejunal biopsies and samples of ileum obtained at operation. Pathological tissue including liver from cases of Indian childhood cirrhosis with copper retention and ileum from cases of inflammatory bowel disease were also examined. Immunoreactive metallothionein (IMT) was found in both rat and human liver localised in the hepatocyte cytoplasm, nucleus, sinusoids and canaliculi. In some livers IMT was found in the portal and hepatic veins. In the small intestine the IMT was localised consistently in the enterocyte cytoplasm and nucleus, and in the basement membrane region. The rat kidney IMT was localised in the cytoplasm of the distal convoluted tubules the collecting tubules and the ducts of Bellini. The distribution of IMT in rat tissues showed changes associated with fasting, stress and zinc administration. In man, inflammatory bowel disease appeared to decrease the intestinal IMT and no significant difference was seen when patients had received steroid therapy. The greatest amounts of IMT were seen in the control group of patients. The distribution of IMT in human liver in Indian childhood cirrhosis did not correspond with that of copper associated protein.
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PMID:Histological demonstration of immunoreactive metallothionein in rat and human tissues. 295 45

The sodium pump, (Na+ + K+)-ATPase, which is involved in the transport of cations and water movement by the colonic mucosa, may be decreased in various diarrhoeal states. In this study, we have measured 3H-ouabain binding and (Na+ + K+)-ATPase activity in human colonic biopsy homogenates and the influence of various inflammatory and antiinflammatory compounds on these parameters. 3H-ouabain binds to one site of high affinity (KD 1.9 +/- 0.2 X 10(-9) mol/l) with a maximal binding capacity of 7.5 +/- 0.8 X 10(14) binding sites/g protein. Both arachidonic and linoleic acid inhibited (Na+ + K+)-ATPase activity (IC50 arachidonic acid: 7.5 X 10(-5) mol/l, linoleic acid: 6.5 X 10(-5) mol/l) and Mg2+-ATPase activity (IC50 arachidonic acid: 9 X 10(-5) mol/l, linoleic acid: 4 X 10(-5) mol/l). Arachidonic acid inhibited 3H-ouabain binding, (IC50 3.2 X 10(-5) mol/l). The following antiinflammatory compounds, at concentrations up to 1 X 10(-3) mol/l, did not influence ATPase activity directly nor reverse the arachidonic acid-induced inhibition: indomethacin (cyclooxygenase inhibitor), nordihydroguaiaretic acid (lipoxygenase inhibitor), sulphasalazine and its metabolites: 5-aminosalicylic acid, N-acetylaminosalicylic acid and sulphapyridine. These results indicate that human colonic (Na+ + K+)-ATPase is inhibited by the prostanoid precursors, arachidonic and linoleic acid. From a therapeutic point of view (effect on colonic (Na+ + K+)-ATPase and perhaps diarrhoea), the suppression of the production of these prostanoid precursors by drugs may, therefore, be beneficial in the treatment of inflammatory bowel disease.
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PMID:Inhibition of human colonic (Na+ + K+)-ATPase by arachidonic and linoleic acid. 301 58

The short and long-term effects of postoperative total parenteral nutrition (TPN) on body composition were studied in a randomised series of patients undergoing major colorectal surgery. Ninety-two patients (colorectal cancer: 50, ulcerative colitis or Crohn's disease: 42) were grouped according to diagnosis and clinical inflammatory activity. TPN was given for 9.7 +/- 1.1 days. The complication rate was not changed by the TPN. Nitrogen balance was studied during the first week. Body weight, total body potassium, triceps skinfold, serum albumin and body water were measured before and at intervals up to 24 weeks after the operation. Cumulative nitrogen balance in control patients at 7 days after surgery was -47.3 g. Patients given TPN balanced nitrogen intake and output (cancer patients and patients with quiescent inflammatory bowel disease, IBD) or were in positive balance (patients with active IBD). Weight loss at 1 week after surgery was less in TPN patients compared to controls and this difference remained statistically significant up to 6 months after termination of the nutritional treatment. A similar, although not statistically significant, difference was noted in total body potassium and triceps skinfold. Patients with active IBD regained pre-operative body composition earlier than cancer patients and patients with quiescent IBD. It is concluded that TPN after major colorectal surgery reduces postoperative weight loss and that this effect lasts after termination of the nutritional treatment. In the absence of increased body potassium and increased body water, we conclude that the long-term effect of TPN on body weight is most likely due to preservation of fat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The immediate and long-term effects of postoperative total parenteral nutrition on body composition. 311 32

Eight malnourished patients (5 men and 3 women, mean age 26.5 +/- 0.4 years) suffering from Inflammatory Bowel Disease were prospectively included at admission to study the effect on protein-energy and vitamin status of a specially designed enterally tube fed formula diet. Eighty nine healthy individuals (36 men and 53 women, mean age 34 +/- 2 years) were used as controls. All but one patient were on steroids. The mean caloric supply was 58.2 +/- 2.4 kcal/kg/day with a mean nitrogen content of 0.37 +/- 0.02 gN/kg/day. The mean Total Enteral Nutrition period lasted 20.8 +/- 2.3 days (range 12 to 28 days). Fat- and water-soluble vitamins were studied at admission and after the nutritional period. Likewise both the protein-energy nutritional status and the activity of the disease were evaluated. At admission, plasma levels of folate, biotin, beta-carotene and vitamins A, C and E were significantly lower in patients than in controls. Tocopherol/cholesterol ratio, and vitamin B1, B2, B6, and B12 status were normal. At the end, plasma values of folate, biotin and vitamin C remained unchanged. However, the protein-energy nutritional status and the activity of the disease significantly improved. At admission, 4 out of 8 patients were at risk of developing hypovitaminosis for vitamins A, C, biotin, beta-carotene, and folate. At the end, a similar percentage remained at risk for these vitamins except for vitamin A. The content of some vitamins in the best designed formula diets does not meet the needs for patients with Inflammatory Bowel Disease.
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PMID:The effect of total enteral tube feeding on the vitamin status of malnourished patients with inflammatory bowel disease. 314 27

To determine if organic anions contribute to the diarrhea of inflammatory bowel disease, we measured osmolality, electrolytes, short-chain fatty acids, lactic acid, and some Krebs cycle anions in 24-hr fecal collections from 18 patients with chronic ulcerative colitis, 20 with Crohn's disease of the colon, and 16 normals. Mean lactic acid concentration was significantly elevated in ulcerative and Crohn's colitis, but values correlated with fecal weight only in the former syndrome. In ulcerative colitis, concentrations of each short-chain fatty acid, especially butyrate, were decreased compared with those from normals or Crohn's disease. Lactate and short-chain fatty acids accounted for nearly half the variability in fecal weight in ulcerative colitis. Crohn's patients had elevated mean fecal water osmolality and osmotic gap not observed in ulcerative colitis. Increased lactic acid and/or deficient short-chain fatty acids may modulate the diarrhea of ulcerative colitis. This mechanism seems less important in Crohn's colitis where an additional osmotic component may be significant.
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PMID:Organic anions and the diarrhea of inflammatory bowel disease. 318 Sep 70

An epidemiologic study of inflammatory bowel disease was conducted in Regio Leiden, the Netherlands, between 1979 and 1983. Archives of endoscopy, radiology, pathology, and specialist letters were reviewed for suspected patients with inflammatory bowel disease, together with a survey of all general practitioners to verify completeness of data. One thousand forty patients were identified and each diagnosis was reviewed. Two hundred ten patients had Crohn's disease and 257 had ulcerative colitis. Of the other 573 patients, the largest proportion (21%) had incomplete data for disease classification. Others had irritable bowel syndrome, diverticulitis, or ischemic or irradiation colitis; some were nonresident patients with inflammatory bowel disease treated within the region and others were out of the period for inclusion in this investigation. The incidence of Crohn's disease was 3.9 per 10(5) per year and the period prevalence was 48 per 10(5). The sex-specific incidence was similar, although the disease was significantly more common in women aged 20-29 yr. The prevalence in the city municipalities of Leiden and Alphen on the Rijn (63 per 10(5)) was similar but significantly greater than in suburban (39 per 10(5)) or agarian areas (40 per 10(5)). This may be partially due to urban density but not to differences in water supply. The lack of cases in the migrant population almost reaches significant levels, but studies in locations with a higher migrant population may clarify the issue.
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PMID:Epidemiology of Crohn's disease in Regio Leiden, The Netherlands. A population study from 1979 to 1983. 349 61

Mutagenicity testing can be used to assay faeces for genotoxic substances and the results are reported to correlate with population risk for colorectal cancer (Ehrich et al., 1979). It has been suggested that histidine in faeces may cause false positive results (Venitt and Bosworth, 1983). To determine the relationship between histidine and false positive mutagenicity assays aliquots of non-mutagenic faecal extract and saline were supplemented with histidine and subjected to the Ames Salmonella/mammalian microsome mutagenicity assay (Ames et al., 1975). Using high-pressure liquid chromatography the analytical recovery of histidine from water and faecal extract supplemented with histidine was equivalent (r = 0.998, p less than 0.001). Histidine was measured in faecal extracts (1 in 10 dilutions) from 35 volunteers, 10 patients with inflammatory bowel disease and 4 with rectal cancer. These extracts were also assayed for mutagens using the Salmonella/mammalian microsome mutagenicity assay. None of the faecal extracts gave mutagenicity ratios above 2. Faecal extracts from volunteers were free of detectable histidine. Although 9 of those from inflammatory bowel disease patients contained histidine (mean +/- SEM 255 +/- 34 mumoles l-1) as did 1 extract from a rectal cancer patient (50 mumoles l-1), none contained sufficient histidine to give a false positive Salmonella/mammalian microsome mutagenicity assay result (800 mumoles l-1 in test solution). Our results do not implicate histidine as a cause of error in faecal mutagenicity testing by the Salmonella/mammalian microsome mutagenicity assay.
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PMID:What is the role of histidine in studies of faecal mutagenicity? 351 71


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