Abstract

It is known that cytotoxic T lymphocytes are responsible for viral clearance in chronic hepatitis B (HBV) infection. Zinc deficiency affects development of acquired immunity by preventing certain functions of T lymphocytes. We investigated the serum zinc levels and the relationship to liver histopathology and response to interferon alpha (IFN-alpha) and lamivudine combination therapy in 28 children with chronic HBV infection. A course of IFN-alpha was injected as 5 million U/m2 subcutaneously, thrice a week for 6 months and lamivudine 4 mg/kg per day orally, for 1 year. Normalization of alanine aminotransferase (ALT), loss of HBV DNA, hepatitis B e antigen (HBeAg) seroconversion altogether was considered as end of therapy response (ETR). The ETR was achieved in eight (30.7%) patients. Serum zinc concentrations of 20 healthy children and patients was not significantly different (P>0.05). While pretreatment serum ALT, zinc, histological activity index (HAI) and portal inflammation scores were statistically higher in children who had ETR (P<0.005, P<0.05, P<0.05 and P<0.05, respectively), pretreatment serum HBV DNA was lower (P<0.005). Serum zinc level was correlated with HAI and portal inflammation scores (P<0.01 and P<0.01). This study showed the relationship of serum zinc status to liver histopathology and to the ETR and may be a preliminary study leading new studies focusing on zinc status in patients with chronic HBV infection.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.