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Gastritis autoimmune

Gastritis, autoimmune. Autoimmune-mediated destruction of the gastric mucosa that may result in the development of pernicious anaemia. Autoimmune gastritis is associated with autoantibodies to H+/K+-ATPase of gastric parietal cells as well as autoantibodies to the intrinsic factor produced by these cells. [Pg.236]

Alderuccio F, Gleeson PA, Berzins SP, Martin M, Van Driel IR (1997) Toh BH Expression of the gastric H/K-ATPase alpha-subunit in the thymus may explain the dominant role of the beta-subunit in the pathogenesis of autoimmune gastritis. Autoimmunity 25 167-175... [Pg.46]

Hematologic diseases autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, pernicous anemia Kidney disease Goodpasture syndrom, lipoid nephroses, minimal change glomerulonephritis Diseases of the gastrointestinal tract autoimmune chronic active hepatitis, autoimmune atrophic gastritis, Crohn s disease, ulcerative colitis... [Pg.241]

Advanced Hp gastritisd Peptic ulcer surgery Autoimmune atrophic gastritis Maximum increase 108-9 CFU/ml URT URT (10-50% GNB) URT (20-30% GNB)... [Pg.7]

Heneghan, M.A., McCarthy, C.F., Janulaityte, D., Moran, A.P. Relationship of anti-Lewis x and anti-Lewis y antibodies in serum samples from gastric cancer and chronic gastritis patients to Helicobacter py/on -mcdiated autoimmunity. Infect Immun 69 (2001) 4774 1781. [Pg.234]

Other causes of gastric atrophy, such as those due to Helicobacter pylori,AIDS, or radiation injury, can lead to a similar outcome but from different pathogenic mechanisms. Therefore, vitamin B12 deficiency, resulting in neurological, psychiatric, metabolic, and hematological disorders, can arise from any one of the many causes listed in Table 28-1. For this reason, the term pernicious anemia (PA) is used here to describe only the classical disease that is associated with IF deficiency due to autoimmune gastritis. [Pg.303]

Parietal cells also secrete intrinsic factor, which is necessary for the absorption of vitamin B12. Vitamin B12 is a cofactor of enzymes which synthesise tetrahydrofolic acid, which in turn is needed for the synthesis of DNA components. An impairment of DNA synthesis will affect rapidly dividing cell populations, among them the haematopoietic cells of the bone marrow, which may result in pernicious anaemia. This condition may result from a destruction of the gastric mucosa by, for example, autoimmune gastritis or the resection of large parts of the lower ileum, which is the main site of vitamin B12 absorption, or of the stomach. [Pg.65]

Suri-Payer E, Cantor H Differential cytokine requirements for regulation of autoimmune gastritis and colitis by CD4 +)CD25(+) T cells. J Autoimmun 2001 16 115-123. [Pg.157]

In cases of suspected autoimmune gastritis, gastrin immunohistochemistry can be used to distinguish antral from atrophic body or fundic mucosa synaptophysin and chromogranin immunohistochemistry is useful in the detection of enterochromaffin-like cell hyperplasia, a characteristic feature of autoimmune gastritis. [Pg.505]

Torbenson M, Abraham SC, Boitnott J, et al. Autoimmune gastritis distinct histological and immunohistochemical findings before complete loss of oxyntic glands. Mod Pathol. 2002 15 102-109. [Pg.533]

Stolte M, Baumann K, Bethke B, et al. Active autoimmune gastritis without total atrophy of the glands. Z Gastroenterol. 1992 30 729-735. [Pg.533]

The least well characterized autoimmune polyglandular syndrome is the type 3 syndrome. This syndrome is defined by the presence of autoimmune thyroid disease with another autoimmune disease, such as diabetes mellitus type l, autoimmune gastritis, or myasthenia gravis, but in the absence of Addison disease. APGS type 3 primarily involves females (the female to male ratio is 7 1) who have HLA-DR3-associated autoimmune disease and is probably the most common of the autoimmune polyglandular syndrome disorders. Since different and multiple clinical combinations can be found, the classification of this type of autoimmune polyglandular syndrome is probably more complicated than originally anticipated. [Pg.72]

Pernicious anaemia. End stage of 10-15% of autoimmune gastritis due to vitamin B12 malabsorption caused by depletion of gastric parietal cells and autoantibodies against intrinsic factor. Associated with a variety of autoimmune endocrine diseases (e.g. -Hashimoto thyroiditis, Addison disease) and autoimmune myasthenic syndromes. [Pg.248]

Toh BH, Gleeson PA, Simpson RJ, et al. The 60- to 90-kDa parietal cell autoantigen associated with autoimmune gastritis is a beta subunit of the gastric H /K -ATPase (proton pump). Proc Natl Acad SdUSA 1990 87 6418-6422. [Pg.40]

Autoimmune gastritis special form of H. pylori gastritis probable no possible not known 52... [Pg.136]

Autoantibodies against gastric epithehal cells are detectable in up to 50% of patients with chronic, active H. pylori gastritis. However, attempts to relate these autoantibodies to Lewis antigens have failed so far [12], Therefore, epitopes other than Lewis antigens are the autoimmune targets, and the pathogenic mechanism may be other than molecular mimicry between H. pylori and the host. [Pg.2060]


See other pages where Gastritis autoimmune is mentioned: [Pg.505]    [Pg.505]    [Pg.33]    [Pg.1]    [Pg.164]    [Pg.209]    [Pg.211]    [Pg.222]    [Pg.223]    [Pg.303]    [Pg.305]    [Pg.180]    [Pg.1102]    [Pg.921]    [Pg.152]    [Pg.1819]    [Pg.505]    [Pg.506]    [Pg.519]    [Pg.519]    [Pg.48]    [Pg.70]    [Pg.145]    [Pg.240]    [Pg.286]    [Pg.348]    [Pg.101]    [Pg.137]    [Pg.250]   
See also in sourсe #XX -- [ Pg.33 ]




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