Copyright 2012 by ESPGHAN and NASPGHAN. Unauthorized reproduction of this article is prohibited. Introduction Carlos A. Velasco-Benı´tez I n the 35-year history of the Latin American Society for Pediatric Gastroenterology, Hepatology and Nutrition (LASPGHAN), this is the second supplement of the Journal of Pediatric Gastroenter- ology and Nutrition that we have edited. Within the framework of the XVIII Latin American Congress and the IX Iberoamerican Congress for our specialty, we used this opportunity to find articles written by the present presidents of the American society and the European society, as well as those responsible for this great event that was held November 19–21, 2011, in Punta Cana, Dominican Republic, and some other members of LASGPHAN. With this, the authors of the articles of charge allow their experiences are familiar to Latino and Iberian American peers and globally, leading again to the interaction between different societies that we are part of the Federation of International Societies of Pediatric Gastroenterology, Hepatology, and Nutrition. Management of Chronic Hepatitis B and C Virus Infection in Children: A 2011 Update Kathleen B. Schwarz B oth hepatitis B virus (HBV) and hepatitis C virus (HCV) are global health problems. Much has been written about these 2 infections in adults. Knowledge about epidemiology, pathogenesis, monitoring, natural history, and antiviral therapy of these infections in infants, children, and adolescents has emerged much more slowly than it has in adults. Nonetheless, in the last decade, much has been learned about the pediatric issues; this review updates these areas of knowledge for these 2 major pathogens. HBV The number of children with HBV infection is not known. However, it is reasonable to assume that a significant proportion of the 370 million individuals in the world with this infection are in the pediatric age group because maternal–fetal transmission remains the major mode of acquisition in much of the world. The infection is most common in Asia and Africa, but as many as 1 million adults in North America have the infection, which is considered an area of low endemicity. In Latin America, there are marked regional differences in prevalence rates. In the late 1990s, seropositive rates (positive for immumoglobulin [Ig] M or IgG anti-core antibody) were highest in the Dominican Republic (20%) and the Amazon basin and lowest in Chile (0.6%) (1). Prevalence rates increase in late adolescence, suggesting that sexual transmission is the major mode of trans- mission. HBV is a vaccine-preventable disease. Administration of active and passive vaccine within 12 hours of birth of an infant born to a mother known to have the infection is 95% protective if followed up with completion of the active vaccination series in the first 6 months of life. In infants born from high-risk mothers (those with HBV DNA >2 million cpm and/or those who had an infant previous who contracted the infection despite vaccination), however, as many as 30% of infants who are appropriately vaccinated still contract the infection. For this reason, there is active investigation about the utility of administering antiviral therapy during the third trimester of pregnancy to these high-risk mothers (2). There are several stages of HBV infection in children: immune active, immune tolerant, or inactive carriers. The immune active phase is characterized by elevated liver enzymes, detectable HBV DNA, and, usually, positive tests for HBeAg, although there are a few children with HBeAg-negative hepatitis. Individuals with immune active disease are always HBsAg positive. The immune- tolerant phase is characterized by a high viral load, normal liver enzymes, and positive tests for HBsAg and HBeAg. For inactive carriers, the only sign of infection is HBsAg positivity. They have seroconverted to HBeAb, have normal liver enzymes, and HBV DNA below the lower limit of detection. According to published articles on the long-term follow-up, the passage from tolerance to active and finally inactive phase would occur in >11% of infected children every year who are between ages 2 and 9 to 10 years (3,4). In these reports, >85% of children seroconverted before age 18 years from HBeAg positive/Anti–HBe negative to HBeAg negative/Anti– HBe positive (inactive phase), most of them with nondetectable HBV DNA in serum. Such passage from tolerance-active-inactive phases occurred similarly in treated or untreated children (5). A group of pediatric hepatologists experienced in monitoring and treating children with HBV infection recently published guide- lines on monitoring (6). The frequency of performing liver enzymes, hepatitis B serology, HBV DNA, a-fetoprotein, and liver ultrasound to screen for cancer was outlined in some detail. The same group also published detailed guidelines on whom to treat and what agents to consider (7). These recommendations are summar- ized briefly. It is clear that asymptomatic carriers require no XVIII Latin American Congress C.A. Velasco-Benı´tez, K.B. Schwarz, V. Discepolo, R. Troncone, C.A. Velasco-Benı´tez, R. Guerrero-Lozano, and W. Daza-Carren ˜o From the Department of Pediatrics, Division of Pediatric Gastroenterology and Nutrition, Johns Hopkins University School of Medicine, Baltimore, MD. The author reports no conflicts of interest. Copyright # 2012 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Supplement DOI: 10.1097/MPG.0b013e3182445059 From the Department of Pediatrics, University of Valle, Cali, Colombia. The author reports no conflicts of interest. JPGN  Volume 54, Supplement 1, May 2012 S1