Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Difficulties arise in the interpretation of liver tests in the pregnant subject, since some values increase (alkaline phosphatase) whilst others remain unchanged (transaminases) or fall during pregnancy. The diagnosis and management of some causes of jaundice in pregnancy, such as viral hepatitis, gall stones, benign intrahepatic cholestasis and acute fatty liver of pregnancy are discussed. Little is known about the commonest symptoms of pregnancy (nausea, vomiting and constipation) other than that they might be due to hormonally induced alteration of sphincter tone. However, pre-existing bowel disease has a greater effect on pregnancy. Fertility is reduced in poor nutritional states (e.g. coeliac and Crohn's diseases) and an increased occurrence of spontaneous abortion has been noted. For inflammatory bowel diseases, the time of onset is important in determining the outcome of pregnancy. Relapse in the disease is commonest in the first trimester and in the puerperium. Treatment of these conditions is essentially as in the non-pregnant subject. The controversial subject of sulphasalazine and steroid usage in pregnancy is discussed.
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PMID:Liver and gastrointestinal function in pregnancy. 38 67

The skin lesions seen in 10 patients who received parenteral nutrition during treatment of chronic enteropathy are described. All of these patients had a lowered serum zinc concentration. The skin lesions were similar to those seen in acrodermatitis enteropathica. After supplementation with zinc sulphate, the skin lesions disappeared completely. A decrease in the serum alkaline phosphatase level can be regarded as a sign of an impending zinc deficiency. Parenteral nutrition formulae should contain a sufficient amount of zinc.
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PMID:Skin lesions in acquired zinc deficiency due to parenteral nutrition. 41 40

The flat mucosal lesion of the small intestine is not pathognomonic of gluten-sensitive enteropathy (GSE). Frequently, the definitive diagnosis of this condition can only be established after three intestinal biopsies are performed: an initial one to show a flat mucosal lesion, one after a gluten-free diet to show morphological recovery, and one after a gluten challenge to show morphological deterioration. We used an organ culture model of GSE to determine the usefulness of this technique in establishing a diagnosis of GSE on the basis of the initial biopsy. Seventy-five patients with diarrhea, and/or malabsorption were evaluated prospectively; 40 had a flat mucosal lesion of variable degree; of these 26 were ultimately determined to have gluten-sensitive enteropathy by the above criteria. A rise in alkaline phosphatase activity of intestinal tissue from 22 of these 26 patients was inhibited when the tissue was cultured in gluten-containing medium as compared to enzyme activities of cultures in a gluten-free medium (108 +/- 69 versus 206 +/- 96, mean +/- SD, P less than 0.001). Mean enzyme values in the similarly cultured intestinal tissue from 13 of 14 patients ultimately shown not to have GSE were not affected by gluten (224 +/- 94 versus 201 +/- 109, P greater than 0.4). Examination of the data by stepwise discriminant analysis provided a function which correctly classified 35 of the 40 patients (88%). The false-positive and false-negative rate for establishing the diagnosis of GSE was 7% (1 of 14) and 15% (4 of 26), respectively. All patients with normal biopsies were classified correctly. The model can be used to establish prospectively the definitive diagnosis of GSE, obviate the need for additional diagnostic biopsies, and allow for the prompt pursuit of alternative diagnoses when gluten sensitivity is not shown.
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PMID:Definitive diagnosis of gluten-sensitive enteropathy. Use of an in vitro organ culture model. 71 Aug 38

Follow-up studies on 36 children, in whom celiac disease (gluten-sensitive enteropathy) was established by gluten challenge, were carried out after management on gluten-free diets for a mean of six years. Evaluations included measurement of height and weight, which for the group approximated normal distributions, and histologic examination of the duodenal or jejunal mucosa. Mucosal morphology was regarded as normal in 16, and there were minimal changes in 20. Epithelial cell height was within the normal range in all the children. Interepithelial lymphocytes were within normal range in the majority and lymphoid cells in the lamina propria were not different from those in control subjects. Mucosal lactase was significantly lower in patients than in control subjects in the duodenum and the jejunum, whereas sucrase and alkaline phosphatase values were significantly lower in the jejunum but not in the duodenum. Low content of mucosal lactase and increased numbers of interepithelial lymphocytes may be sensitive indicators of persisting ingestion of gluten in mucosa that is otherwise normal or approximately so in appearance.
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PMID:Mucosal recovery in treated childhood celiac disease (gluten-sensitive enteropathy). 95 66

A patient with ulcerative ileojejunitis was studied by determination of HL-A phenotype, by measurement of jejunal IgA synthesis using a labeled amino acid incorporation technique, and by in vitro organ culture. The patient carried the HL-A8 phenotype in common with 87.5% of patients with gluten-sensitive enteropathy. During a period of exposure to dietary gluten, jejunal tissue from the patient exhibited in high IgA synthetic rate. In organ culture of the jejunal biopsy specimen there was an increase in alkaline phosphatase activity in the absence, but not in the presence, of gluten peptides. The synthetic rate value and the organ culture behavior are similar to those observed in patients with gluten-sensitive enteropathy in exacerbation. During a period in which the patient was not exposed to dietary gluten, including prolonged period of intravenous alimentation, jejunal IgA synthesis and organ culture behavior were studied repeatedly. In contrast to patients with gluten-sensitive enteropathy in remission (i.e., on a gluten-free diet), jejunal IgA synthesis did not decline. However, in organ culture in the patients tissue now behaved like that of other patients with gluten-sensitive enteropathy in remission: alkaline phosphatase activity increased during culture in the presence and absence of gluten peptides. These studies support the concept that ulcerative ileojejunitis is a complication of gluten-sensitive enteropathy in which escape from control by gluten restriction has occurred. They suggest that ulcerative ileojejunitis due to a supervening pathological process which is, at least in part, immunological in nature.
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PMID:In vitro studies of ulcerative ileojejunitis. 111 60

Cortisol partially prevents the harmful effect of gluten on the jejunal mucosa of patients with gluten-sensitive enteropathy. To investigate further the pathogenesis of this disorder, we analyzed the effect of cortisol in cultures of jejunal specimens obtained by biopsy. Cultures were done with and without gluten or cortisol. Morphology and alkaline phosphatase activity were assessed before and after 24 hours. Biopsies from untreated patients cultured with gluten showed low enzyme values and cuboidal epithelial cells before and after culture. Biopsies cultured in a gluten-free medium showed a threefold increase in enzyme values (P less than 0.01) and morphologic improvement with change to columnar epithelial cells. Cultures with gluten plus cortisol showed rises in alkaline phosphatase and morphologic improvement indistinguishable from cultures without gluten. Cortisol and gluten had no effect on cultures from appropriate controls. Cortisol thus prevents the harmful effects of gluten on biopsies from patients with gluten-sensitive enteropathy in vitro.
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PMID:Gluten-sensitive enteropathy. Inhibition by cortisol of the effect of gluten protein in vitro. 127 29

Gluten sensitivity in a naturally occurring enteropathy of Irish setter dogs, and the effects of excluding dietary cereal from birth on the subsequent response to gluten challenge were investigated. Peroral jejunal biopsy specimens were obtained at 1 year of age for morphometric and biochemical examinations, and intestinal permeability was assessed using 51Cr-ethylenediaminetetraacetic acid. Affected setters, reared on a normal wheat containing diet, exhibited partial villus atrophy, intraepithelial lymphocyte infiltration, reduced brush border alkaline phosphatase activity, and increased intestinal permeability. Gluten sensitivity was shown by introduction of a gluten free diet, which resulted in resolution of morphological and biochemical abnormalities and decreased intestinal permeability, and subsequent gluten challenge, which resulted in relapse. In contrast, littermates reared exclusively on a cereal free diet showed minimal changes when challenged with gluten, apart from intraepithelial lymphocyte infiltration. These findings document a gluten sensitive enteropathy in Irish setters and indicate that exclusion of dietary cereal from birth may modify subsequent expression of the disease.
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PMID:Dietary modulation of gluten sensitivity in a naturally occurring enteropathy of Irish setter dogs. 134 79

Intestinal disease might contribute to osteopenia. Measurements of IgA antibodies to gliadin have been established as an accepted screening procedure for detection of coeliac disease. When we applied these measurements to 92 patients with verified osteoporosis, 11 subjects (12%) were found to have elevated levels. This is markedly higher than the incidence in healthy subjects (3%). However, the patients with raised levels of IgA antibodies displayed no clinical symptoms and no laboratory evidence of calcium malabsorption. Thus their values for serum calcium, phosphate, parathyroid hormone (PTH), alkaline phosphatase and osteocalcin, as well as the fasting urinary excretion of hydroxyproline and calcium, were similar to those found in other patients with osteoporosis. Intestinal biopsy verified coeliac disease in three patients and was normal in another three. This gives an incidence of verified coeliac disease in this patient group that is approximately tenfold higher than that in the healthy population. Subclinical coeliac disease appears to be unusually over-represented among patients with idiopathic osteoporosis, and screening for gliadin antibodies might therefore be a valuable addition to the routine assessment of the osteopenic patient. The mechanisms underlying the relationship are not clear, but calcium malabsorption is not evident.
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PMID:Screening for antibodies against gliadin in patients with osteoporosis. 158 66

Intestinal permeability to 51Cr-EDTA was examined during the development of gluten sensitive enteropathy in dogs bred from affected Irish setters and reared on a normal wheat containing diet. Comparisons were made with litter mates reared on a gluten free diet and with a control group of age matched, clinically healthy Irish setters reared on the normal diet. Studies at 4, 6, 8, and 12 months of age were correlated with morphometric and biochemical examinations of peroral jejunal biopsy specimens. Permeability was increased at all ages in the group fed gluten free diet compared with control dogs, although there were no differences in villus height, intraepithelial lymphocyte density, and alkaline phosphatase activity. At four months, permeability in the normal diet group was greater than in controls, although comparable with that in the gluten free diet group. Permeability in the normal diet group increased further in conjunction with the development of partial villus atrophy and reduced alkaline phosphatase activity, and by 12 months permeability was significantly greater than in their gluten free diet litter mates and the control dogs. The findings suggest that an underlying permeability abnormality may be involved in the pathogenesis of gluten sensitive enteropathy in Irish setter dogs.
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PMID:Abnormal permeability precedes the development of a gluten sensitive enteropathy in Irish setter dogs. 190 29

Biochemical changes in the small intestine during development of naturally acquired wheat-sensitive enteropathy of Irish Setters were investigated. To distinguish primary biochemical abnormalities from secondary effects of intestinal damage, progeny of affected dogs reared on a normal wheat-containing diet were compared with their own littermates reared on a cereal-free diet and with age-matched clinically normal Irish Setters fed the same wheat-containing diet. Peroral jejunal biopsy specimens were sequentially obtained between weaning and 1 year of age; specific activity and reorientating sucrose density-gradient distribution of organelle marker enzymes were determined. Major primary biochemical abnormalities were not detected in affected progeny. In affected dogs fed wheat, there was a selective, but secondary, loss of the brush border alkaline phosphatase and aminopeptidase N activities. This loss was associated with the development of partial villus atrophy, but represented a specific effect of dietary wheat on the brush border, not merely a nonspecific effect of mucosal damage, because other brush border enzymes, including disaccharidases, were not similarly affected. Increased soluble activities of lysosomal and peroxisomal marker enzymes late in the disease process may represent alterations in these 2 organelles as a secondary consequence of mucosal damage.
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PMID:Development of wheat-sensitive enteropathy in Irish Setters: biochemical changes. 197 61


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