Aims/Introduction: Helicobacter pylori infection is associated with insulin resistance and glycemia in non-diabetes. However, the relationship between H. pylori infection and glycemia in diabetes remains inconclusive. Therefore, we explored the effect of H. pylori infection status and its eradication on glycemic control and antidiabetic therapy in type 2 diabetes patients. Materials and Methods: A total of 549 diabetes patients were recruited for sequential two-step approach (immunoglobulin G [IgG] serology followed by 13C-urea breath test [UBT]) to discriminate “active” (IgG+ and UBT+) from “non-active” (UBT− or IgG−) H. pylori infection, and “past” (IgG+ but UBT−) from “never/remote” (IgG−) infection. The differences in hemoglobin A1c (A1C) and antidiabetic regimens between groups were compared. In the “active” infection group, the differences in A1C changes between participants with and without 10-day eradication therapy were compared after 3 months. Results: Despite no between-group difference in A1C, the “active” infection group (n = 208) had significantly more prescriptions of oral antidiabetic drug classes (2.1 ± 1.1 vs 1.8 ± 1.1, P = 0.004) and higher percentages of sulfonylurea use (67.3% vs 50.4%, P < 0.001) than the “non-active” infection group (n = 341). There were no differences in A1C and oral antidiabetic drug classes between “past” (n = 111) and “never/remote” infection groups (n = 230). Compared with the non-eradication group (n = 99), the eradication group (n = 98) had significant within-group (−0.17 ± 0.80%, P = 0.036) and between-group (−0.23 ± 0.10%, P = 0.024) improvements in A1C. Conclusions: Diabetes patients with active H. pylori infection need higher glycemic treatment intensity to achieve comparable glycemia. Furthermore, H. pylori eradication decreases A1C, and thus improves glycemic control.
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