Disease relevance of Stomach Diseases

• Helicobacter pylori cagA status and s and m alleles of vacA in isolates from individuals with a variety of H. pylori-associated gastric diseases [1].
• Both cimetidine and antacids produced a near elimination of duodenal disease and markedly reduced the severity of gastric disease when compared to that of untreated historical controls [2].
• AIM: To investigate the usefulness of sucrose permeability test using serum in the diagnosis of gastric diseases, with special reference to early gastric cancer (EGC) [3].
• With methylene blue dye spraying endoscopy 392 Japanese outpatients with gastric diseases, and 253 Japanese and 84 Canadian outpatients free of gross findings in the stomach were investigated on chronic atrophic gastritis in special reference to intestinal metaplasia [4].

High impact information on Stomach Diseases

• The presence of three distinct serum markers of carcinoma, tumor-associated glycoprotein 72 (TAG-72; as measured by the CA 72-4 assay), CA 19-9, and carcinoembryonic antigen (CEA), was evaluated in 194 patients diagnosed with either malignant (n = 94) or benign (n = 100) gastric disease [5].
• In 46 patients with different gastric diseases no correlation between the serum gastrin concentrations and the labelling indices was found [6].
• The inhibition of gastric cell renewal by acetaldehyde may play a role in the pathogenesis of ethanol- and/or H. pylori-associated gastric diseases by inhibiting normal gastric mucosal protection and repair [7].
• Sera with IgG antibody to H. pylori from five children with culture-proven H. pylori gastric disease markedly enhanced complement-dependent phagocytosis of H. pylori in an assay using flow cytometry to measure uptake of fluorescent-labeled bacteria by PMNL [8].
• The aim of this study is to analyze the genetic and functional variability of cagA gene of clinical strains in relation to gastric diseases [9].

Chemical compound and disease context of Stomach Diseases

• Nitrite concentration increased with severity of gastric disease but the results were not significant (normal, 82.9 vs. CAG, 223.4 ng/ml, P = 0.069) [10].
• N-nitrosoproline excretion in the presence and absence of gastric disease [10].
• It is concluded that 150 mg of roxatidine daily would be adequate to treat patients with gastric diseases [11].
• All patients with gastric diseases who underwent combined T2-weighted single-shot echo train spin-echo and gadolinium-enhanced conventional and fat-suppressed spoiled gradient-echo imaging between October 1, 1996 and March 1, 1999, and who had histological or other imaging proof of disease, were included in this study [12].
• RESULTS: Serum sucrose levels started to increase 15 min after loading, and peaked at 60 min in the gastric disease groups [3].

Biological context of Stomach Diseases

• Association of cagA and vacA genotypes of Helicobacter pylori with gastric diseases in Estonia [13].
• Because deletion of cag PAI genes was found in the patients with all three gastric diseases that we studied, it was suggested that the pathogenicity of H. pylori might not be determined by cag PAI genes in those cases [14].

Anatomical context of Stomach Diseases

• We analyzed the expression of 17HSD type 1 and 2 enzymes which catalyze opposite reactions of estrogen metabolism, in normal gastric mucosa and various gastric diseases of 81 tissue specimens [15].
• Thus, we tested the hypothesis that omeprazole, a proton-pump inhibitor shown to reduce gastric acid secretion in dogs, would reduce the severity of exercise-induced gastric disease [16].
• Hoelen would thus appear useful for treating gastric disease by activating efferent activity of the gastric vagus nerve through the action of triterpenoid and polysaccharide [17].
• BACKGROUND: Helicobacter pylori is recognized as a primary etiologic factor in the development of gastric disease and the product of particular significance to the virulent action of the bacterium is its cell wall lipopolysaccharide [18].
• PECAM-1 stained tumor cells of 10 patients (27.8%), endothelial cells of 9 patients (25%) and inflammatory infiltrate of 4 patients (40%) with benign gastric disease [19].

Gene context of Stomach Diseases

• In conclusion, we have shown different patterns of mucin immunoreactivity in various gastric disease states [20].
• We investigated the topographic expression of MUC5AC and MUC6 in relationship with gastric diseases [21].
• CONCLUSIONS: GROalpha, IL-8 and IL-6 are increased early during acute H. pylori infection and may influence the development of gastric disease [22].
• In this study, we firstly characterized ZNRD1 expression in a wide spectrum of gastric diseases by immunohistochemistry and RT-PCR [23].
• The measurement of carcinoembryonic antigen (CEA) in serum and endoscopic brush specimens was evaluated for the differential diagnosis of malignant and nonmalignant gastric disease [24].

Analytical, diagnostic and therapeutic context of Stomach Diseases

• In patients with stomach diseases, gastrectomy resulted in decreases in the excretion of histamine and its metabolites in the urine, and patients subjected to intravenous hyperalimentation excreted less histamine and its metabolites in the urine than normal subjects [25].
• Adult patients with symptoms of gastric disease were randomly assigned to two treatment groups (roxatidine group, n = 115; famotidine group, n = 113) or untreated control group (placebo, n = 111) [26].

References