Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0220723 (PCA)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoimmune thyroid diseases (AITD) can be associated with autoimmune gastritis (AIG), but the frequency of this association is poorly characterized. We performed a prospective study to: a) characterize the frequency of parietal cell (PCA) and intrinsic factor (IFA) autoantibodies in AITD patients; b) evaluate the development of histologically- and functionally-proven AIG after five years and to assess the predictive role of PCA for AIG at baseline; and c) analyze the trend of PCA levels in the course of the disease. We studied 208 consecutive adult patients affected by AITD (166 Hashimoto's thyroiditis, 42 Graves' disease). PCA, IFA and plasma gastrin levels were measured with ELISA methods at baseline and after 5years. At baseline, 51/208 (24.5%) AITD patients were positive for PCA and 10/208 (4.8%) for IFA. 25 out of 54 PCA/IFA-positive AITD patients (all without gastric or haematologic symptoms) agreed to participate in the follow-up study. After 5years, 6 (24%) of these 25 patients showed a histologically proven AIG, with lymphocytic infiltration and/or atrophy of body gastric mucosa. The trend analysis of PCA concentration showed that autoantibody levels rise progressively over time, reach a peak level and then fall, according to the progressive destruction of gastric mucosa and to the disappearance of the target autoantigen (proton pump). The presence of PCA predicts the development of autoimmune gastritis in AITD patients. Antibody levels measured with a sensitive quantitative immunometric method are useful for early diagnosis and early treatment of the disease.
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PMID:Autoantibodies to parietal cells as predictors of atrophic body gastritis: a five-year prospective study in patients with autoimmune thyroid diseases. 2069 84

Autoantibodies targeting the H+/K+-ATPase proton pump of the gastric parietal cell (parietal cell antibodies [PCA]) are diagnostic of atrophic body gastritis (ABG) leading to pernicious anemia (PA). PCA, ABG, and PA occur in increased frequency in patients with type 1 diabetes and their relatives and are considered "minor" components of forms of autoimmune polyglandular syndrome (APS). A customized radioimmunoprecipitation assay was applied to 6,749 samples from the Type 1 Diabetes Genetics Consortium to measure ATP4A autoreactivity. Autoantibody prevalence was correlated with variants in HLA class II, PTPN22, and CTLA4 genes. With an ATP4A radioimmunoprecipitation assay, PCA were detected in sera from 20.9% of affected individuals. PCA prevalence increased with age and was greater in females (25.3%) than males (16.5%) and among Hispanics (36.3%) and blacks (26.2%) compared with non-Hispanic whites (20.8%) and Asians (16.7%). PCA and other organ-specific autoantibodies GAD65, IA-2, thyroid peroxidase (TPO), 21-hydroxylase (21-OH), and transglutaminase (TG) clustered within families with heritability estimates from 71 to 95%. PCA clustered with TPO, 21-OH, and persistent GAD65 autoantibodies but not with celiac (TG) or IA-2 autoantibodies. PCA-positive subjects showed an increased frequency of DRB1*0404, DPB1*0201, and PTPN22 R620W (rs2476601-T) and a decreased frequency of DRB1*0101, DPB1*0301, and CTLA4 CT60 (rs3087243-T). Genetic variants accounted for 4-5% of the heritable risk for PCA. The same alleles were associated with other autoantibody phenotypes in a consistent pattern. Whereas most of the heritable risk for PCA and other antibodies reflects genetic effects that are tissue specific, parietal cell autoimmunity is a major pathogenetic contributor in APS2.
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PMID:ATPase4A Autoreactivity and Its Association With Autoimmune Phenotypes in the Type 1 Diabetes Genetics Consortium Study. 2640 69

This study aimed to investigate the intestinal microbiota in duodenal ulcer (DU) patients, effects of proton pump inhibitors,clarithromycin and amoxicillin, PCA) for Helicobacter pylori (H. pylori) and Bacillus subtilis and Enterococcus faecium (BSEF) on intestinal microbiota. DU patients were randomly assigned to receive either PCA (group TT) or PCA plus BSEF(group TP). The fecal microbiome was conducted using high throughput 16S rDNA gene and internal transcribed spacer sequencings. The diversity and abundance of intestinal bacteria in the DU were significantly lower than health check control (HC) group. In the TT group, the abundance and diversity of both intestinal bacteria and fungi decreased after PCA treatment, compared with those before treatment, whereas in the TP group no obvious changes were observed. In the TT group at all the time points, both the intestinal bacteria and fungi were different from those in the HC group. However, in the TP group, at 10w the bacterial flora abundance was close to that in the HC group. The results indicate that anti- H. pylori treatment induced significant decrease in the diversity of intestinal microbiota, while the combined therapy supplemented with BSEF could protect and restore the intestinal microbiota.
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PMID:Effects of anti-H. pylori triple therapy and a probiotic complex on intestinal microbiota in duodenal ulcer. 3149 12