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)

In comparison to normal controls (n = 71) the activity of intestinal alkaline phosphatase in feces is reduced in chronic bowel disease using an immunoprecipitation method: patients with Crohns disease (n = 40) or inactive ulcerative colitis (n = 29) demonstrate small changes of fecal intestinal alkaline phosphate activity in comparison to normal controls. Intestinal alkaline phosphatase is reduced in patients with active ulcerative colitis (n = 11) to 50%, in patients with uraemic enteropathy (n = 18) to 30% and in patients with coeliac disease (n = 14) to 20% of the activity observed in normal controls. During cytostatic treatment of malignant tumors, fecal intestinal alkaline phosphatase activity increases as a sign of toxic damage of the intestinal mucosa.
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PMID:[Activity of small intestine alkaline phosphatase in the feces in chronic intestinal diseases]. 742 74

The intestinal alkaline phosphatase (I-AP) in feces was investigated in 16 patients with adult coeliac disease and 2 patients with gluten-sensitive enteropathy in dermatitis herpetiformis using an immunoprecipitation method. The mean concentration of I-AP activity in feces was reduced by 76% in patients with coeliac disease in comparison to normal controls (11.5 : 47.5 U/g). Patients with total villous atrophy (mean = 5.3 U/g) demonstrated a lower activity than patients with partial villous atrophy (mean = 14.3 U/g). Follow-up studies showed stable fecal I-AP-activities in symptom-free patients, whereas patients with relapses were characterized by fluctuating activities. The administration of a single oral dose of 31 g gluten is followed by a fecal I-AP-excretion pattern similar to toxic damage of the small bowel mucosa.
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PMID:Fecal intestinal alkaline phosphatase in coeliac disease. 742 78

OBJECTIVE To compare expression, activity, and fecal concentration of intestinal alkaline phosphatase (IAP) between healthy dogs and dogs with chronic enteropathy (CE). ANIMALS 9 healthy university-owned Beagles and 109 healthy client-owned dogs (controls) and 28 dogs with CE (cases). PROCEDURES Cases were defined as dogs with persistent (> 3 weeks) gastrointestinal signs that failed to respond to antimicrobials and anti-inflammatory doses of prednisolone or dietary trials, did not have mechanical gastrointestinal abnormalities as determined by abdominal radiography and ultrasonography, and had a diagnosis of lymphoplasmacytic enteritis or eosinophilic gastroenteritis on histologic examination of biopsy specimens. Duodenal and colonic mucosa biopsy specimens were obtained from the 9 university-owned Beagles and all cases for histologic examination and determination of IAP expression (by real-time quantitative PCR assay) and activity (by enzyme histochemical analysis). Fecal samples were obtained from all dogs for determination of fecal IAP concentration by a quantitative enzyme reaction assay. RESULTS For dogs evaluated, IAP expression and activity were localized at the luminal side of epithelial cells in the mucosa and intestinal crypts, although both were greater in the duodenum than in the colon. Active IAP was detected in the feces of all dogs. Intestinal alkaline phosphatase expression and activity were lower for cases than for controls, and fecal IAP concentration for dogs with moderate and severe CE was lower than that for dogs with mild CE. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that dogs with CE had impaired IAP expression and activity. Additional research is necessary to elucidate the role of IAP in the pathogenesis of CE.
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PMID:Comparison of the expression, activity, and fecal concentration of intestinal alkaline phosphatase between healthy dogs and dogs with chronic enteropathy. 2734 25