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)

A correlation was sought between changes in enzymes involved in gastric acid secretion (Mg-, NaK-, K- and HCO3-stimulated ATPases) and histological changes in gastric biopsies. Alkaline phosphatase was also studied. Mg- and NaK-stimulated ATPase activities increased significantly in biopsies from the pylorus and antrum which showed moderate or severe gastritis. NaK ATPase levels increased and HCO3 ATPase decreased in incisural, body and fundic mucosa which had intestinal metaplasia and atrophic gastritis. No K+ ATPase was found in normal mucosa. The total activity of alkaline phosphatase did not vary with histological changes in the gastric mucosa. Results indicate that the ATPase enzyme systems are sensitive indicators of gastric mucosal disease.
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PMID:Mucosal enzyme patterns in gastric epithelial disease. 21 78

Subcutaneous injection of W/Fu rat stomach antigen emulsified with an equal volume of Freund's complete adjuvant at 1 week interval for a total of 2 administrations induced atrophic gastritis in A/HeJ mice. From the second week after the last injection the parietal cell mass decreased. At the same time, Alcian blue-PAS positive cells and Paneth-like cells appeared. Furthermore, the activity of alkaline phosphatase and disaccharidase of the small intestinal mucosa was biochemically demonstrated in the atrophic glandular stomach.
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PMID:Morphological and biochemical changes in the gastric mucosa of A/HEJ mice injected with a xenogeneic stomach antigen. 60 98

Biopsy specimens from the antral and body part of the stomach were studied for a range of marker enzymes in 11 patients with superficial gastritis, 9 patients with atrophic gastritis, and 31 Billroth-II-resected patients and compared with activities found in controls with normal gastric mucosa. In the antral part of the stomach increased gamma-glutamyltransferase activity was found in superficial (p less than 0.01) and atrophic gastritis (p less than 0.05), whereas monoamine oxidase activity was decreased in superficial (p less than 0.01) and atrophic gastritis (p less than 0.05). In the body part, increased activity of gamma-glutamyltransferase (p less than 0.01) and acid-beta-glucuronidase (p less than 0.01) was found in superficial gastritis. In atrophic gastritis increased activities for lactase (p less than 0.01), alkaline phosphatase (p less than 0.05), leucyl-beta-naphthylamidase (p less than 0.05), gamma-glutamyltransferase (p less than 0.05), 5'-nucleotidase (p less than 0.01), N-acetyl-beta-D-glucosaminidase (p less than 0.05), and acid-beta-glucuronidase (p less than 0.01) were found. Specimens from the gastric remnant showed an enzyme activity pattern similar to that seen in the body in atrophic gastritis, apart from a significantly decreased monoamine oxidase activity (p less than 0.004). Specimens with dysplasia in the gastric remnant showed decreased monoamine oxidase activity when compared with specimens without dysplasia (p less than 0.01).
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PMID:Enzyme activities in human gastric mucosa in gastritis and resected stomachs. 381

Endoscopic diagnosis completed by biopsy achieved remarkable accuracy. New trends--endoscopy with the use of ultrasound orange red porphyrin fluorescence elicited by blue light e. g. krypton laser and strip biopsy not only greater accuracy of endoscopic methods but also open up new therapeutic possibilities. Histochemical and histoenzymatic methods allow to classify histological findings of the norm (presence of pepsinogen and neutral glycoprotein) of atrophic gastritis with intestinal metaplasia (acid glycoprotein, activity of sucrose, alkaline phosphatase-AP, leucin-aminopeptidase-LAP) and of dysplasia (presence of sulfomucin, decrease of AF, LAP, sucrose and trehalase activity) and to divide them into well defined groups. We are able to distinguish which mucosal changes are suspect, we know that malignant transformation can after a certain period of time be expected approximately 2-14% yet we still do not know whether the period from dysplastic change to malignant transformation is not longer than malignant change in resected stomach. Epidemiologic and experimental data gives us enough reasons for dietary and chemopreventive measures (apart of other treatment) especially in risk groups patients.
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PMID:[Early diagnosis of gastric cancer]. 850 56

Primary biliary cirrhosis is often associated with autoimmune diseases. However, its association with pernicious anemia has rarely been reported.We report a case of a 68-year-old woman who presented jaundice and pruritus. Mildly elevated serum levels of alkaline phosphatase and gamma-glutamyl transpeptidase were detected. The titer of anti-mitochondrial M(2 )anti-body was elevated. Histology of liver biopsy showed features of primary biliary cirrhosis. In addition, aregenerative macrocytic anemia was found in the full blood count. The diagnosis of pernicious anemia was established by megaloblastosis in bone marrow, atrophic gastritis without Helicobacter pylori, low level of vitamin B(12 )and good response to treatment regimen of vitamin B(12). The association of primary biliary cirrhosis and pernicious anemia is unlikely to be casual and may be explained by autoimmune mechanism commonly shared by the diseases.
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PMID:A case of primary biliary cirrhosis associated with pernicious anemia: a case report. 2014 39