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. 1997 Nov;41(5):619–623. doi: 10.1136/gut.41.5.619

Antigastric autoantibodies in Helicobacter pylori infection: implications of histological and clinical parameters of gastritis

G Faller 1, H Steininger 1, J Kranzlein 1, H Maul 1, T Kerkau 1, J Hensen 1, E Hahn 1, T Kirchner 1
PMCID: PMC1891571  PMID: 9414967

Abstract

Background—It has recently been shown that humoral antigastric autoreactivities occur in a substantial number of Helicobacter pylori infected patients. 
Aims—To analyse the relevance of such antigastric autoantibodies for histological and serological parameters of the infection as well as for the clinical course. 
Methods—Gastric biopsy samples and sera from 126 patients with upper abdominal complaints were investigated for evidence of H pylori infection using histology and serology. Autoantibodies against epitopes in human gastric mucosa were detected by immunohistochemical techniques. Histological and clinical findings of all patients were then correlated with the detection of antigastric autoantibodies. 
Results—H pylori infection was significantly associated with antigastric autoantibodies reactive with the luminal membrane of the foveolar epithelium and with canalicular structures within parietal cells. The presence of the latter autoantibodies was significantly correlated with the severity of body gastritis, gastric mucosa atrophy, elevated fasting gastrin concentrations, and a decreased ratio of serum pepsinogen I:II. Furthermore the presence of anticanalicular autoantibodies was associated with a greater than twofold reduced prevalence for duodenal ulcer. 
Conclusion—The data indicate that antigastric autoantibodies play a role in the pathogenesis and outcome of H pylori gastritis, in particular in the development of gastric mucosal atrophy. 



Keywords: gastritis; Helicobacter pylori; autoimmunity; gastric atrophy

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Figure 1 .

Figure 1

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: Antiluminal antigastric reactivity against the apical membrane of foveolar epithelium cells in the human gastric antrum and body (original magnification ×40). 


Figure 2 .

Figure 2

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: Anticanalicular antigastric autoreactivity against canaliculi within parietal cells of the human gastric body (original magnification ×40). 


Figure 3 .

Figure 3

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: Fasting serum gastrin concentrations in healthy controls, patients with H pylori gastritis with and without anticanalicular autoantibodies, and patients with type A gastritis. 


Figure 4 .

Figure 4

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: Fasting pepsinogen I:II ratio in healthy controls, patients with H pylori gastritis with and without anticanalicular autoantibodies, and patients with type A gastritis. 


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