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Several metabolic (HbA1, HDL-C, triglycerides) and hemostatic (VIIIR: Ag, VIII:C, B-TG variables were investigated in 35 non-obese, insulin-dependent diabetics without clinically evident vascular complications. B-TG was high but did not correlate with other metabolic and hemostatic parameters, suggesting that elevated B-TG in diabetes might be an expression of in vitro platelet activation. VIIIR: Ag and the ratio of VIIIR: Ag to VIII: C were markedly increased. There was a significant correlation of the HbA1 and HDL-C levels with VIIIR: Ag, indicating that VIIIR:Ag is another reflection of metabolic control in diabetes. Additional pathogenic mechanisms, however, appear to be involved in causing the changes in VIIIR: Ag in diabetes.

In the literature there is no agreement on the prevalence of chronic liver disease (CLD) and the role of hepatitis B virus (HBV) infection in diabetics. We undertook an epidemiological case-control study of the prevalence of CLD and HBV infection in 394 diabetics and 265 healthy subjects from Seriate and Como. The results did not show any significant differences between: 1) the prevalence of CLD in the diabetic population and in controls (4.8% vs 4.5%); 2) the prevalence of HBV infection in diabetics (HBsAg+: 8.3%; HBVAb+: 55.8%) and in controls (HBsAg+: 8.6%; HBVAb+: 54.7%); 3) the prevalence of HBV infection in diabetics with CLD (HBsAg+: 21%; HBVAb+: 52.6%) and in controls with CLD (HBsAg+: 16.6%; HBVAb+: 50%); 4) the prevalence of HBV infection in diabetics with and without CLD (HBsAg+: 21% vs 7.7%; HBVAb+: 52.6% vs 56%); 5) the prevalence of HBV infection in diabetics treated by injection and orally (HBsAg+: 6.9% vs 8.6%; HBVAb+: 58.3% vs 55.2%). The relative risk of CLD for the factor HBsAg+ was 3.2 in the diabetic population vs 1.4 in controls. In view of the presence of antidelta antibodies (HDVAb) in 25% of HBsAg+ diabetics with CLD and the lack of HBV markers in 26.3% of diabetics with CLD, we assume that other viruses (Delta, nonA-nonB) may play roles. Probably the interaction of all possible etiopathogenetic factors (alcohol, viruses, glycometabolic derangement) is determinant for CLD in diabetics.