lewis-y-antigen and Peptic-Ulcer

lewis-y-antigen has been researched along with Peptic-Ulcer* in 2 studies

Reviews

1 review(s) available for lewis-y-antigen and Peptic-Ulcer

Article	Year
Helicobacter pylori and gastric diseases. Nagoya journal of medical science, 2003, Volume: 66, Issue:3-4 Helicobacter pylori (H. pylori) infection is a pathogenic agent of gastric diseases, but their mechanisms are unclear. Effects of ammonia, tumor necrosis factor (TNF), and anti-Lewis autoantibodies induced after H. pylori infection on the development of gastric diseases were investigated. Ammonia disturbed the collagen metabolism in the ulcer base. Soluble TNF receptors regulate the action of TNF. The involvement of anti-Lewis autoantibodies in the development of peptic ulcer might be unlikely. Moreover, H. pylori-specific IgA in gastric juice and TNFalpha gene polymorphism in persons infected with H. pylori were studied. According to H. pylori-specific IgA titer in gastric juice, persons were divided into two histologically and endoscopically different states of disease. TNFA -857 single nucleotide polymorphism (SNP) may be associated with rugal hyperplastic gastritis and gastric carcinomas without severe atrophy. However, complete elucidation of pathogenic mechanisms of H. pylori-induced gastric diseases requires further research. Topics: Ammonia; Animals; Antibodies; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin A; Lewis Blood Group Antigens; Lewis X Antigen; Peptic Ulcer; Polymorphism, Genetic; Polymorphism, Single Nucleotide; Stomach Diseases; Tumor Necrosis Factor-alpha	2003

Article

Year

Helicobacter pylori and gastric diseases.

Nagoya journal of medical science, 2003, Volume: 66, Issue:3-4

Helicobacter pylori (H. pylori) infection is a pathogenic agent of gastric diseases, but their mechanisms are unclear. Effects of ammonia, tumor necrosis factor (TNF), and anti-Lewis autoantibodies induced after H. pylori infection on the development of gastric diseases were investigated. Ammonia disturbed the collagen metabolism in the ulcer base. Soluble TNF receptors regulate the action of TNF. The involvement of anti-Lewis autoantibodies in the development of peptic ulcer might be unlikely. Moreover, H. pylori-specific IgA in gastric juice and TNFalpha gene polymorphism in persons infected with H. pylori were studied. According to H. pylori-specific IgA titer in gastric juice, persons were divided into two histologically and endoscopically different states of disease. TNFA -857 single nucleotide polymorphism (SNP) may be associated with rugal hyperplastic gastritis and gastric carcinomas without severe atrophy. However, complete elucidation of pathogenic mechanisms of H. pylori-induced gastric diseases requires further research.

Topics: Ammonia; Animals; Antibodies; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin A; Lewis Blood Group Antigens; Lewis X Antigen; Peptic Ulcer; Polymorphism, Genetic; Polymorphism, Single Nucleotide; Stomach Diseases; Tumor Necrosis Factor-alpha

2003

Other Studies

1 other study(ies) available for lewis-y-antigen and Peptic-Ulcer

Article	Year
Are autoantibodies against Lewis antigens involved in the pathogenesis of Helicobacter pylori-induced peptic ulcers? Microbiology and immunology, 1999, Volume: 43, Issue:5 We examined whether anti-Lewis x (Le(x)) and y (Le(y)) autoantibodies affect the pathogenesis of Helicobacter pylori-induced peptic ulcers. Of 11 patients with peptic ulcers, 10 patients had both anti-Le(x) and -Le(y) immunoglobulin G (IgG) antibodies, and 1 patient had only anti-Le(x) antibody. After successful eradication, we measured the serum titer of anti-Le(x) and -Le(y) antibodies. Six patients had a reduction of the titers of anti-Le(x) and/or -Le(y) antibodies, whereas no notable changes were detected in 5 patients in the follow-up. This result suggests that anti-Le(x) and -Le(y) autoantibodies had no critical role in the development of H. pylori-induced peptic ulcer. Topics: Autoantibodies; Follow-Up Studies; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Lewis Blood Group Antigens; Lewis X Antigen; Lipopolysaccharides; Peptic Ulcer; Recurrence	1999

Article

Year

Are autoantibodies against Lewis antigens involved in the pathogenesis of Helicobacter pylori-induced peptic ulcers?

Microbiology and immunology, 1999, Volume: 43, Issue:5

We examined whether anti-Lewis x (Le(x)) and y (Le(y)) autoantibodies affect the pathogenesis of Helicobacter pylori-induced peptic ulcers. Of 11 patients with peptic ulcers, 10 patients had both anti-Le(x) and -Le(y) immunoglobulin G (IgG) antibodies, and 1 patient had only anti-Le(x) antibody. After successful eradication, we measured the serum titer of anti-Le(x) and -Le(y) antibodies. Six patients had a reduction of the titers of anti-Le(x) and/or -Le(y) antibodies, whereas no notable changes were detected in 5 patients in the follow-up. This result suggests that anti-Le(x) and -Le(y) autoantibodies had no critical role in the development of H. pylori-induced peptic ulcer.

Topics: Autoantibodies; Follow-Up Studies; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Lewis Blood Group Antigens; Lewis X Antigen; Lipopolysaccharides; Peptic Ulcer; Recurrence

1999