Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of the unusual presentation of pernicious anemia in many black women, a further characterization of this disease among the different racial groups was undertaken. The following were found. (1) Black women under the age of 50 years had a significantly lower prevalence of anti-parietal cell antibody than did "European" and Latin-American patients or even older black women. The disease in the younger black women resembles juvenile pernicious anemia in this respect. Blacks in general had a lower prevalence of anti-parietal cell antibody than did "Europeans" and Latin Americans, though the difference was not statistically significant. A particularly striking finding was that anti-parietal cell antibody occurred much less often than anti-intrinsic factor antibody among black patients. (2) An analysis of all published HLA data for patients of European origin indicated a weak association of pernicious anemia with HLA-B7. However, no antigen association among the black and Latin-American patients studied was found. HLA-DR typing, not previously reported even for whites, also showed no association. (3) Lymphocytotoxic antibody was equally increased in frequency in all racial groups. (4) Serum gastrin levels did not follow a racial pattern; however, women with pernicious anemia had much higher levels than did men. (5) Pernicious anemia was not associated with blood group A.
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PMID:Profiles of black and Latin-American patients having pernicious anemia. HLA antigens, lymphocytotoxic antibody, anti-parietal cell antibody serum gastrin levels, and ABO blood groups. 721 50

Helicobacter pylori infection is associated with duodenal and gastric ulcer disease, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma. Although more than half the world's population harbors H. pylori, only a proportion will develop clinically significant disease. The specific clinical outcome of an individual can be examined as the modulation of host factors by H. pylori infection. Host acid-secretory status and sensitivity to gastrin can be modulated by H. pylori infection. Once H. pylori has established itself in the stomach, virtually everyone develops gastritis, and variations in gastritis patterns have been associated with different gastric acid responses to H. pylori infection. The patterns of gastritis are important because they seem to determine disease outcome. Blood group antigens have been implicated in studies of ulcer disease. Receptors to Lewis antigens in gastric mucosa indicate that host mucosal factors influence H. pylori attachment. Conversely, H. pylori strains express Lewis antigen-like molecules, suggesting an autoimmune component for some H. pylori-associated diseases. HLA genotypes may influence the host response to H. pylori infection, and those of H. pylori-infected individuals have been correlated with histological features. The clinical outcome of H. pylori infection is most likely a result of complex interactions among host, bacterial, and environmental factors. The mechanisms by which these diverse factors influence the pathogenesis of different clinical outcomes remain under investigation.
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PMID:What are the host factors that place an individual at risk for Helicobacter pylori-associated disease? 939 54