MON-175 Glycemic Impairment in Chronic Hepatitis C: Does the Virus Reduce B-Cell Function? An Amazonic Brazilian Study

In the course of chronic hepatitis C, extrahepatic manifestations are frequent, with important glycemic alterations, occurring approximately three times more than in the general population. In order to study this glycemic impairment in patients with Hepatitis C virus (HCV), we developed a cross-sectional and observational study with 72 patients living in State of Pará, Amazon region of Brazil, which has an endemic prevalence of HCV infection, both sexes, over 40 years of age, with a history of chronic infection by HCV and without co-infection with the Hepatitis B virus or HIV. The glycemic variables evaluated were fasting glycemia, glycemia after 2 hours of overload with glucose, insulin, HbA1c, HOMA-B and HOMA-IR, relating them to aspects of liver disease. The fibrosis grade was estimated by the FIB-4 value (FIB-4 ≥ 3.25 vs < 3.25). Of the total of 72 participants, 52.8% were women. The mean age was 61.5 ± 8.4 years. Glycemic alterations were found in 40% of the patients: 26.4% were diabetic and 13.6% with pre-diabetes. The main genotype was type 1 (78%), followed by type 3 (22%). The glycemic variables behaved in a similar way among the genotypes. When we evaluated the glycemic profile according to the degree of fibrosis, patients with higher fibrosis (n=17) presented a double prevalence of Diabetes Mellitus (41% vs 22%; p=0.51) and higher 2h glycemia (9.5 ± 4.5 mmol/L vs 6.8 ± 2.9 mmol/L, p=0.028), however and in a contrary way than expected, caused by a lower HOMA-B (111.7 ± 63.4 vs 192.8 ± 182.4; p=0.009), with equal levels of HOMA-IR, and without association with metabolic syndrome or obesity. Diabetic patients (n=19) showed a tendency for a worse response to treatment: virological sustained response (SVR) was achieved in 80% of diabetics (vs 92.3% in non-diabetics, p>0.05), especially those with genotype 3, that only 66% achieved SVR. Cirrhotic patients presented no more glycemic alterations than non-cirrhotic patients, however, diabetics showed a higher frequency of hepatocarcinoma compared to non-diabetics (10.5% vs 1.9%, p>0.05). We conclued that the frequency of glycemic changes was high in the studied population, but without association with the traditional components of the metabolic syndrome and obesity. It is suggested, therefore, that HCV infection may compromise insulin secretion and that patients diagnosed with DM may require specific treatment because they present a poorer response to antiviral treatment and have greater chronic complications of the disease.