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Although a rather benign course of chronic hepatitis B virus ( HBV) infection during childhood has been described, 3-5% and 0.01-0.03% of chronic carriers develop cirrhosis or hepatocellular carcinoma before adulthood. Considering the whole lifetime, the risk of hepatocellular carcinoma rises to 9-24% and the incidence of cirrhosis to 2-3% per year. The aim of this article is to review the current knowledge regarding the natural history and treatment of chronic hepatitis B in children and to focus on critical aspects and unresolved questions in the management of childhood HBV infection. A literature search was carried out on MEDLINE, EMBASE, and Web of Science for articles published in English in peer-reviewed journals from January 1980 to February 2013. The search terms used included 'Hepatitis B virus infection,' 'children,' ' HBV,' 'interferon,' 'lamivudine,' 'adefovir,' 'entecavir,' and 'tenofovir.' Articles resulting from these searches and relevant references cited in the articles retrieved were reviewed. The current goals of therapy are to suppress viral replication, reduce liver inflammation, and reverse liver fibrosis. Therapeutic options for children are currently limited, and the risk for viral resistance to current and future therapies is a particular concern. Based on the data available at this time, it is the consensus of the panel that it is not appropriate to treat children in the immune-tolerant phase or in the inactive carrier state. For children in the immune-active or reactivation phases, liver histology can help guide treatment decisions. Outside of clinical trials, interferon is the agent of choice in most cases; currently, available nucleoside analogs are secondary therapies. [ABSTRACT FROM AUTHOR]

Background and Aim: Oxidative stress is an important pathophysiological mechanism in non-alcoholic steatohepatitis, where hepatocyte apoptosis is significantly increased correlating with disease severity. Protein glutathionylation occurs as a response to oxidative stress, where an increased concentration of oxidized glutathione modifies post-translational proteins by thiol disulfide exchange. In this study, we analyzed the protein glutathionylation in non-alcoholic fatty liver disease (NAFLD) and evaluated a potential association between glutathionylation, fibrosis, and vitamin E treatment. Methods: Protein glutathionylation was studied in the livers of 36 children (mean age 12.5 years, range 4–16 years) subdivided into three groups according to their NAFLD activity score (NAS) by Western blot analysis and immunohistochemistry, using a specific monoclonal antibody. In addition, we identified the hepatocyte ultrastructures involved in glutathionylation by immunogold electron microscopy. Results: Our findings showed that protein glutathionylation increases in the livers of patients with NAFLD and it is correlated with steatohepatitis and liver fibrosis. Its increase appears mainly in nuclei and cytosol of hepatocytes, and it is reversed by antioxidant therapy with reduced fibrosis. Conclusion: Protein glutathionylation significantly increases in livers with NAFLD, strongly suggesting that oxidative injury plays a crucial role in this disease. Furthermore, the marked increase of protein glutathionylation, in correlation with collagen VI immunoreactivity, suggests a link between the redox status of hepatic protein thiols and fibrosis. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Fatal Fulminant Hepatitis in an Infant With Human Herpesvirus-6 Infection," by Y. Asano, T. Yoshikawa, S. Suga and colleagues in the 1990 issue.

The article reflects the opinion of the author on the significance of the measurement of advanced glycation end products (AGEs) in the changes on the management of non-alcoholic steatohepatitis. The author stressed that the discovery of nonenzygmatic AGEs and its receptors paved the way to new researches in medicine . Meanwhile, the author suggests that measurement of circulating AGEs can be a beneficial tool for discriminating patients with NASH.

A letter to the editor is presented in response to the article about the early effect of lifestyle changes on aminotransferase levels in non-alcoholic steatohepatitis (NASH) that was published in the February 2007 issue.

Comments on nutritional considerations in children with chronic liver disease. Indicators of protein and energy malnutrition; Mechanisms that can contribute to malnutrition; Pitfalls of malnutrition assessment.