Endocrine Abstracts

Background and aims: Earlier we reported, that GADA and ICA revealed more often in HBV and HCV infected type 2 diabetic patients, than in noninfected. The goal was to determine the role of HBV- and HCV-infections in insulin insufficiency mechanisms in type 2 diabetic patients.

Materials and methods: 173 patients with type 2 DM (41 male, 132 female, middle age 57.5±0.8 year, average diabetes duration 8.55±0.53 years) were surveyed. Markers of a viral hepatites B and C, glutamic acid decarboxilase antibodies (GADA), islet cells antibodies (ICA) and basal C-peptide level were studied by immune-enzyme assay.

Results: In HBV and HCV infected, GADA and/or ICA-positive diabetic patients (n=18, patients with 0 pmol/l C-peptide level were excluded) the C-peptide median was essentially lower, than in GADA and/or ICA-negative diabetic patients (n=10) (0.84 vs 1.49 pmol/l respectively; P=0.027, Mann-Whitney U test). The survival analysis (Kaplan–Meier product limit method with use of Cox F-test) has been lead before an outcome (decrease C-peptide) depending on duration DM. It is revealed, that in HBV- and HCV-infected type 2 diabetic group a share of persons, which are not having C-peptide level decrease, was less, than in noninfected; the difference made from 8 up to 13% (F (158.66)=1.59, P=0.016).

Conclusion: In HBV and HCV infected patients with type 2 DM, with increase in duration of disease, decrease of insulin secretion faster progress than in noninfected. One of the pathogenetic mechanisms of insulin secretion decrease can be autoimmune aggression directed to pancreatic β-cells, initiated by HBV- and HCV-infection.