High Rate of Helicobacter pylori Re-Infection in Patients Affected by Type 1 Diabetes

Patients affected by type 1 diabetes appear to be more prone to infection than healthy subjects (1).

Recently, it has been shown that Helicobacter pylori (H. pylori) infection is common in type 1 diabetes (2) and that the use of a standard antibiotic therapy obtains a significantly lower eradication rate than in non–insulin-dependent diabetic subjects (3,4). Our aim was to assess the incidence of H. pylori re-infection after a successful therapy in type 1 diabetic patients. A total of 74 subjects previously infected by H. pylori were enrolled, including 34 type 1 diabetic subjects (16 women and 18 men, 42 ± 9 years of age) and 40 nondiabetic control subjects (17 women and 23 men, 44 ± 8 years of age). Control subjects were matched for age and sex.

None of the type 1 diabetic patients had symptoms of gastroparesis, and none was treated with domperidone. All subjects previously treated for H. pylori infection and successfully eradicated, as assessed both by ¹³C-urea breath test (UBT) and histology (two biopsies in antrum, body, and fundus), were re-evaluated with UBT 12 months after eradication. Re-infected patients were also submitted to endoscopy to confirm the presence of the bacterium. Daily insulin requirement and HbA_1c (percent total hemoglobin) expressions of glycemic metabolic control were evaluated.

We found a significantly higher incidence of H. pylori re-infection in type 1 diabetic patients compared with nondiabetic control subjects. In particular, 13 of 34 (38%) type 1 diabetic patients compared with 2 of 40 (5%) control subjects were re-infected with H. pylori 1 year after successful eradication (P < 0.001).

Among type 1 diabetic patients, re-infection occurrence was not affected by sex, type 1 diabetes duration, or mean age. No differences in baseline values of daily insulin requirement and HbA_1c were observed between re-infected and not-infected diabetic patients (43 ± 8 vs. 38 ± 9 units and 7 ± 0.7 vs. 7 ± 0.8%, respectively). However, 12 months after eradication, significantly higher insulin requirement and HbA_1c were observed in re-infected patients compared with uninfected diabetic patients (43 ± 8 vs. 35 ± 8 units, P < 0.05; and 7.25 ± 1 vs. 6.8 ± 0.8%, P < 0.02). Interestingly, when compared with the enrollment value, patients who remained uninfected by H. pylori after 12 months from eradication showed a reduction trend of daily insulin requirement (38 ± 9 vs. 35 ± 8 units, P < 0.08).

This study shows that the incidence of H. pylori recurrence 12 months after a successful eradication is significantly higher in type 1 diabetic subjects compared with control subjects. Some mechanism could be hypothesized for the higher rate of re-infection observed in diabetic subjects, perhaps an increased susceptibility of the host to the infection as a result of reduced lymphocyte activity and neutrophil dysfunction with failure of chemiotaxis.

Better metabolic control in diabetic patients in whom H. pylori has been eradicated compared with re-infected subjects was observed, suggesting a trend of ameliorated metabolic control after H. pylori eradication. More studies are requested to investigate the mechanisms underlying the increased susceptibility of H. pylori re-infection in type 1 diabetic patients and the role of the bacterium in glycemic control. Vaccine development seems to be one possible effective long-term strategy for this subset of patients.