Hepatitis: Mohan N

Murray KF, Shah U, Mohan N, Heller S, González-Peralta RP, Kelly D, Chang MH, Mieli-Vergani G, Jara P, Fujisawa T, Anonymous00091. · Hepatobiliary Program, Seattle Children's Hospital and Regional Medical Center, Seattle, WA 98105, USA. · J Pediatr Gastroenterol Nutr. · Pubmed #18664880 No free full text.

This publication has no abstract.

Shah U, Kelly D, Chang MH, Fujisawa T, Heller S, González-Peralta RP, Jara P, Mieli-Vergani G, Mohan N, Murray KF. · Harvard Medical School Dubai Center, Dubai Health Care City, Dubai, UAE. · J Pediatr Gastroenterol Nutr. · Pubmed #19322053 No free full text.

Abstract: Hepatitis B virus (HBV) infection is a worldwide problem and can cause acute liver failure, acute hepatitis, chronic hepatitis, liver cirrhosis, and liver cancer. In areas of high prevalence such as in Asia, Africa, southern Europe, and Latin America, the hepatitis B surface antigen positive rate ranges from 2% to 20%.In endemic areas, HBV infection occurs mainly during infancy and early childhood. Mother-to-infant transmission accounts for approximately half of the chronic HBV infections. In contrast to infection in adults, HBV infection during early childhood results in a much higher rate of persistent infection and long-term serious complications such as liver cirrhosis and HCC.Three phases of chronic hepatitis B have been identified: the immune-tolerant phase, the immune-active phase, and the inactive hepatitis B phase. These phases of infection are characterized by variations in viral replication, hepatic inflammation, spontaneous clearance, and response to antiviral therapy.The optimal goal of antiviral therapy for chronic HBV infection is to eradicate HBV and to prevent its related liver complications. However, due to the limited effect of available therapies in viral eradication, the goal of treatment is to reduce viral replication, to minimize liver injury, and to reduce infectivity. In this review the current recommendations for monitoring and treating chronic HBV infection in children are reviewed.

Radhakrishnan S, Upadhyay A, Mohan N, Dhar A, Walia HK, Zubaidi G. · Department of Gastroenterology, The Royal Hospital, Muscat, Oman. · Med Princ Pract. · Pubmed #15961942 No free full text.

Abstract: OBJECTIVE: To report the late development of immune-mediated diabetes mellitus after completion of alfa-interferon therapy for hepatitis C in an Asian patient. CLINICAL PRESENTATION AND INTERVENTION: A 50-year-old male with chronic hepatitis C received treatment with alfa-interferon and ribavirin for 52 weeks. He developed immune-mediated diabetes mellitus with low C-peptide and positive antiglutamic acid decarboxylase antibody after completion of therapy. The hepatitis C infection was eradicated, but he continued to be diabetic requiring insulin therapy during the follow-up. CONCLUSION: This report shows thatimmune-mediateddiabetes mellitus can occur as a late complication of alfa-interferon therapy.