The Study of Clinical and Biochemical Parameters in Assessing the Response to the Antiviral Therapy in the Chronic Viral Hepatitis B.

Background and Objectives: Hepatitis B virus infection remains a major public health concern. The interaction between hepatitis B virus (HBV) hepatitis B virus and the host inflammatory response is an important contributing factor driving liver damage and diseases outcomes. The management of chronic hepatitis B virus infection is an area of massive unmet clinical need worldwide. Our primary aim for this study was to evaluate biological response rates and sustained virological response in patients with chronic hepatitis B treated with Peg-IFN α-2a/b. The second aim of the study was the identification of metabolic changes and insulin resistance. Materials and Methods: We enrolled in this study 166 patients who fulfilled all inclusion and exclusion criteria. These treatment-naive patients with chronic HBV were treated with Pegylated Interferon α-2a/b. HBV infection was defined by the presence of HBV serological markers (HBsAg, anti-HBsAb, anti-HBcAb, HBeAg, anti HBeAb) by Enzyme-Linked Immuno Sorbent Assay (ELISA) and serum HBV-DNA levels were estimated by a commercially available quantitative polymerase chain reaction (PCR) assay. Results: Patients' recovery progress has been evaluated by determining the following: age, gender; biochemical tests; alanine aminotransferase, aspartate aminotransferase; serological assays for HBV serological markers (HBsAg, anti-HBsAc/Ab, anti-HBcAc/Ab, HBeAg, anti HBeAc/Ab); molecular tests to detect viral particles, testing for HBV DNA (PCR) to confirm the diagnosis and quantify the number of viral copies in the blood (viremia); liver ultrasound-performed through epigastric and intercostal approach (transversal and longitudinal sections). Conclusions: Our results indicated that only HOMA index values, that of fasting insulin, together with baseline HBV DNA, alanine aminotransferase values, mean blood glucose at the beginning of treatment may be predictive of the early viral response in chronic hepatitis B.