Helicobacter pylori, parietal cell antibodies and autoimmune gastropathy in type 1 diabetes mellitus

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 DQAl*0501-B1*0201 (OR = 1.9, P = 0.032). PCA-positivity was linked to HLA-DQAl*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 greater than or equal to 1/20 (OR = 2.0, P = 0.03), but not if greater than or equal to 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.