OBJECTIVE -Approximately 15-20% of type 1 diabetic patients exhibit parietal cell antibodies (PCAs) targeting gastric H ϩ /K ϩ ATPase. We examined whether iron deficiency anemia, pernicious anemia, and autoimmune gastritis, which may predispose to gastric tumors, were more frequent in PCA ϩ than in PCA -patients. RESULTS -Autoimmune gastritis (AG) was present in 57% of PCA ϩ and 10% of PCA -cases (OR 12.5, P Ͻ 0.0001). PCA positivity (␤ ϭ 1.44; P ϭ 0.04) and hypergastrinemia (␤ ϭ 0.01; P ϭ 0.026), but not HP, age, diabetes duration, sex, and HLA-DQ type were risk factors for AG. Iron deficiency anemia (OR 3.9, P ϭ 0.015), pernicious anemia (OR ϭ 4.6, P ϭ 0.022), and hypochlorhydria (OR ϭ 20.0, P ϭ 0.0002) were more frequent in AG ϩ individuals. HP infection was present in 47 patients but did not influence corpus histology or gastrinemia. (Pre)malignant lesions were found in 26% of PCA ϩ subjects: ECL cell hyperplasia in 7 AG ϩ patients, comprising 1 with a gastric carcinoid tumor, and corpus intestinal metaplasia in 11 AG ϩ patients, including 1 with linitis plastica. RESEARCH DESIGN AND METHODS CONCLUSIONS -PCAϩ type 1 diabetic patients should be screened for autoimmune gastritis, iron deficiency, and pernicious anemia. Particularly hypergastrinemic PCA ϩ patients with autoimmune gastritis are at increased risk for (pre)malignant gastric lesions.

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Background: Fifteen to 20% of type 1 diabetic patients exhibit parietal cell antibodies (PCA), which are associated with autoimmune gastritis, hypochlorhydria, iron deficiency and pernicious anaemia. Aim: To examine whether Helicobacter pylori infection could explain the high prevalence of PCA and autoimmune gastropathy in diabetes. If so, H. pylori eradication could prevent autoimmune gastritis. Methods: In 229 type 1 diabetics (M/F: 135/94; age: 41 ± 12 years) PCA were measured. H. pylori infection was assessed by serology, urea breath test in all and by histology (updated Sydney system) in 88 subjects. Pentagastrin tests were performed in 42 patients. Results: Sixty‐nine patients were PCA‐positive. H. pylori infection was present in 72 patients and was negatively associated with HLA‐DQA1*0103‐B1*0603 (OR=0.12, P=0.015) and positively with DQA1*0501‐B1*0201 (OR=1.9, P=0.032). PCA‐positivity was linked to HLA‐DQA1*0501‐B1*0301 (OR=3.9, P=0.017). A link between H. pylori and PCA was observed when PCA‐positivity was defined as a titre ≥ 1/20 (OR=2.0, P=0.03), but not if ≥ 1/40 was the cut‐off point. PCA‐positivity, but not H. pylori infection, was associated with iron deficiency anaemia (OR=2.7, P=0.008), pernicious anaemia (OR= 33.5, P < 0.0001), hypochlorhydria (OR=12.1, P=0.0008) and autoimmune gastritis (OR=12.5, P < 0.0001). Conclusions: The HLA‐bound susceptibility of H. pylori and PCA differed. PCA‐positivity but not ongoing H. pylori infection is associated with autoimmune gastritis. Low titres of PCA might reflect H. pylori infection rather than autoimmune gastropathy.