High viral load and mild liver injury in children with hemophilia compared with other children with chronic hepatitis C virus infection.

BACKGROUND: In adults with hepatitis C virus (HCV) infection, the severity of liver disease may be influenced by the mode of transmission. The purpose of this study was to evaluate whether the mode of transmission affects liver injury and viral load in children with chronic HCV infection, independent of duration of infection and/or HCV genotype. METHODS: Thirty-nine anti-HCV (EIA-2) positive patients, were divided into three groups: group 1, children with a history of blood transfusion (n = 9; age, 13.3+/-1.3 years), group 2, children with hemophilia (n = 19; age, 11.6+/-0.8 years); and group 3, children with maternal-fetal transmitted disease (n = 10; age, 4.7+/-1.1 years). Serum alanine aminotransferase, HCV viral load, HCV genotype, and liver histology were assessed. RESULTS: Serum HCV viral load was higher in group 2 (4.27+/-1.0x10(6) copies/ml; p = 0.006) than in group 1 (0.73+/-0.3x10(6) copies/ml) and in group 3 (0.83+/-0.2x10(6) copies/ml). Conversely, group 2 had less severe liver injury compared with children of similar age in group 1 (p = 0.022). Despite a shorter duration of infection, group 3 had liver injury similar to that in group 1. Hepatitis C virus genotype did not influence the level of viremia or liver injury. CONCLUSIONS: Although children with hemophilia exhibited a high HCV viral load, liver histopathology was less severe than in children who had acquired HCV by blood transfusion or maternal-fetal transmission. These observations support the need to investigate the role of host immune response rather than the virus per se in the pathogenesis of HCV infection in children.     

Prospective study of mother-to-infant transmission of hepatitis C virus

BACKGROUND: Mother-to-infant transmission of hepatitis C virus (HCV) could become the main route of HCV infection in the future because there are no methods available to prevent vertical infection. The aim of this study was to determine the incidence of mother-to-infant transmission in infants born to mothers who tested positive for anti-HCV antibodies and to elucidate associated risk factors for transmission. METHODS: Screening was conducted for 16,800 pregnant women with an anti-HCV antibodies test, and 154 mothers were positive. From the positive group 141 mothers were enrolled in the study and their 147 infants were followed from birth for serum alanine aminotransferase activity, anti-HCV antibodies and HCV RNA. HIV infection was tested in 73 of 141 mothers, all of whom were negative. RESULTS: Thirty-three infants were dropped from the study because they were followed for <6 months or were not tested adequately. Of the 114 infants finally evaluated 9 (7.8%) had detectable HCV RNA. The transmission rate was not influenced by the mode of delivery [vaginal delivery, 8 of 90 vs. cesarean section, 1 of 24 (P = 0.396)] or by the type of feeding [9 of 98 for breast-fed infants vs. 0 of 16 for formula-fed infants (P = 0.243)]. All infected infants were born to mothers who had HCV viremia at the delivery (P = 0.040) and to those with a high viral load (P = 0.019). CONCLUSIONS: Our prospective study showed that the transmission rate of mother-to-infant HCV infection was 7.8% in anti-HCV antibody-positive mothers. Risk was related to the presence of maternal HCV viremia at delivery and a high viral load in the mothers.     

Liver histology and alanine aminotransferase levels in children and adults with chronic hepatitis C infection

BACKGROUND: Chronic hepatitis C is often a mild disease in children, but whether this is related to younger age or shorter duration of infection is unclear. Histologic severity has been shown to correlate with duration of infection regardless of age. OBJECTIVES: We compared histologic findings in children and adults with chronic hepatitis C while controlling for sex, duration of infection, hepatitis C virus (HCV)-RNA level, and genotype. METHODS: Twenty-one children and 52 adults whose infection was less than 20 years in duration and who had undergone a liver biopsy were included. Two blinded liver pathologists reviewed the liver biopsies and scored inflammatory activity and fibrosis using the modified Knodell scoring system. RESULTS: The groups were the same with respect to HCV-RNA level (P=0.8), and genotype (P=0.6) but differed in duration of disease (P=0.01) and sex composition (P=0.005). Covariate analysis showed no influence of genotype, duration of infection, or HCV-RNA level on outcome. In controlling for sex, children had significantly milder liver disease and alanine aminotransferase (ALT) elevations. CONCLUSIONS: With equal duration of infection, HCV-RNA level, and genotype, children have lower serum ALT levels and less severe liver disease than adults infected with HCV.     

Treatment of chronic hepatitis C in children

Since the discovery of hepatitis C virus (HCV) in 1989, significant advances have been made in our understanding of this important viral pathogen. Children at risk for HCV infection include recipients of potentially contaminated blood products and organ transplants, and infants born to HCV-infected mothers. Chronic HCV infection is usually asymptomatic in children but active hepatitis, cirrhosis and hepatocellular carcinoma can occur. The development of treatment strategies for chronic hepatitis C in children has directly evolved from clinical trials in adults. Sustained virologic response, defined by undetectable HCV RNA in serum 24 wk after completion of treatment, occurs in approximately 36% of children treated with conventional interferon alone and in about 50% of those given conventional interferon in combination with ribavirin. Pegylated interferon-based treatment regimens are better than those based on conventional interferon in adults but little is known about pegylated interferon in children. Factors associated with a favorable response to antiviral therapy in children are similar to those in adults and include infection with HCV genotype 2 or 3 and low pretreatment serum HCV RNA levels. Treatment related adverse events in children include 'flu-like' syndrome, fatigue, anorexia, weight loss, depression, anemia, leukopenia and thrombocytopenia.     

The prevalence of GB virus C/hepatitis G virus RNA among healthy and HCV-infected Catalan children

GB virus C (GBV-C) is a blood-borne flavivirus. The prevalence of GBV-C viremia among healthy adults is 0.5% to 4% and, to date, no disease has been definitely associated with GBV-C infection. We conducted a cross-sectional study to evaluate GBV-C viremia prevalence in a group of 327 healthy children with normal alanine amino transferase (ALT) levels (Group A) and elevated ALT levels (Group B) of unknown origin, and among 38 pediatric patients with mother-to-child-transmitted hepatitis C virus (HCV) infection (Group C). No statistically significant differences were observed between prevalences in Groups A and B (2.2% vs 6.7%, p = 0.06). None of the children in Groups A or B who tested positive for GBV-C RNA showed any clinical symptoms. The prevalence of GBV-C viremia in Group A was lower than for patients in Group C (2.2% vs 13.2%, p = 0.007); no differences were observed in HCV infection characteristics between those patients who were co-infected with GBV-C and those who were not. In conclusion, while GBV-C viremia is more frequent among HCV-infected pediatric patients, it is neither associated with liver disease nor has any influence on HCV-related chronic hepatitis.     

Impact of human immunodeficiency virus coinfection on the progression of mother-to-child transmitted hepatitis C virus infection

Data on mother-to-child transmitted human immunodeficiency virus/hepatitis C virus (HIV/HCV) coinfection are scarce. A prospective observational study with a cohort of 70 HCV-infected children (13 of whom were HIV/HCV-coinfected; mean follow-up: 7.3 years) is presented. In our series, surrogate markers of disease progression (HCV viremia, maximum alanine aminotransferase values, and spontaneous HCV infection clearance) suggest that the evolution of liver disease in HIV/HCV-coinfected pediatric patients is more aggressive than it is in HCV-only infected children.     

Chronic viral hepatitis

Among hepatitis A to E viruses, hepatitis B, C, and D viruses can cause chronic hepatitis, in both children and adults. Hepatitis B virus (HBV) infection is the most prevalent and important one. Perinatal transmission accounts for about 40–45% of chronic HBV infection in hyperendemic areas. Horizontal transmission through intramuscular injection using non-sterile needles and intrafamilial spread accounts for the other half of carriers. During the natural course of HBV infection, the host gradually clears HBV and hepatitis B e antigen (HBeAg), liver damage and elevation of aminotransferases occur during the process of HBV clearance. The most effective way to eliminate HBV infection is immunoprophylaxis starting since birth. It can prevent both HBV and hepatitis D virus (HDV) infections. Hepatitis C virus (HCV) infection in children occurs mainly in high risk children, such as those who received blood product or injection using non-sterile needles, or infants of HCV viremic mothers, etc. Screening of blood product reduced markedly the prevalence of post-transfusion HCV infection, but the prevention of sporadic cases requires HCV vaccination which is still under investigation.     

Chronic non-A, non-B hepatitis: role of hepatitis C virus.

Thirty three consecutive children with chronic non-A, non-B hepatitis (NANBH) were studied during a four year period to evaluate clinical and histological features and the role of hepatitis C virus (HCV). All patients were asymptomatic. Thirteen (39%) of them were anti-HCV positive. A history of parenteral exposure was significantly more frequent among anti-HCV positive (69%) than anti-HCV negative patients (15%). Aminotransferase serum values were not statistically different between anti-HCV positive and anti-HCV negative patients. Unlike adults, cirrhosis was never found in the children studied. Our results suggest that chronic NANBH is, during childhood, an asymptomatic disease and that the prevalence of HCV infection is lower than in adults. As the majority of the children with chronic NANBH showed no evidence of HCV infection, it seems unwarranted to identify NANBH with HCV infection in children. The lack of cirrhosis in paediatric patients is probably related to a shorter duration of liver disease.     

Update on prevention and treatment of viral hepatitis in children.

Viral hepatitis is a persisting concern. Outbreaks of hepatitis A occur in developed countries where only 10% to 20% of the population is seroprotected. The disease may cause fulminant liver failure and death. People who are targeted for vaccination include intravenous drug users, homosexuals, and chronic hepatitis patients. Secondary prophylaxis of household contacts is an efficient way to prevent secondary cases. Universal vaccination is now in progress for hepatitis B. Vaccination failure may occur in low birth weight infants, or in infants infected in utero. Chronic carriers of viral hepatitis may progress to cirrhosis and hepatocarcinoma, the latter risk being most important for men infected at birth. Alcohol intake should be avoided in carrier adolescents. Interferon is able to triple the rate of hepatitis B e antigen loss and decouple the rate of hepatitis B s antigen loss after one year, shortening disease evolution and, it is to be hoped, decreasing the risk of unfavorable outcome. Similarly, lamivudine increases by four times the rate of hepatitis B e antigen loss in adults. However, precore mutants may be selected by immune pressure after seroconversion in children, and tyrosine-methionine-aspartate-aspartate (YMDD) mutations appear in 15% of patients treated with lamivudine after 1 year. Hepatitis C is mainly acquired during childhood via true vertical transmission. The risk of acquiring Hepatitis C is related to the presence and amount of RNA for hepatitis C virus in mothers at the time of birth. The infection rate for the hepatitis C virus is higher in children from mothers who have tested positive for HIV, and higher if these children are themselves coinfected with HIV. Treatment with interferon alone has a poor rate of efficiency, although pediatric studies remain scarce. Combination treatment using ribavirin plus interferon yield a higher rate of success in eradicating viral infection in adults.     

Histologic activity of childhood chronic hepatitis B related to viremia levels,genotypes, mutations,and epidemiologic factors

BACKGROUND: Despite high viral load, children with chronic hepatitis B virus (HBV) infection may lack significant biochemical signs of liver dysfunction. Failure to develop abnormal liver chemistriesis is probably due to immunologic hyporeactivity. Despite the absence of biochemical abnormalities in these patients, there is still a risk for long-term complications. The pathogenic importance of viral load and genetic variability is less well studied in children than in adults. METHODS: We evaluated viremia levels, genotypes, and mutations related to histologic evidence of liver damage in 71 HBV carriers, aged 2 to 18 years, all of non-Swedish origin. RESULTS: None of the of 22 children who were hepatitis B e antigen (HBeAg) negative had severe liver disease or had HBV DNA levels greater than 10 copies/mL (mean 10 ); 3 (14%) of them had increased alanine aminotransferase (ALT). The 49 HBeAg-positive children had a mean HBV DNA level of 10 copies/mL, and increased ALT was seen in 28 (55%). Core promoter mutations (at nt 1764) or precore mutations (at codon 1, 2, or 28) were rare; they were seen in four and one HBeAg-positive children, and in four and nine HBeAg-negative children, respectively, without association to liver damage. C-1858 was associated with more liver inflammation. Genotype did not significantly influence liver damage. Children with horizontal transmission had a faster rate of seroconversion and more inflammation of the liver. CONCLUSIONS: Severe HBeAg-negative hepatitis with high HBV DNA levels and mutations in the core promoter or precore regions seems to be less common in children than in adults. C-1858 strains may be more pathogenic, but this requires further study. Epidemiologic factors influence the course of infection.     

Vertical transmission of hepatitis C virus in a cohort of 2,447 HIV-seronegative pregnant women: a 24-month prospective study.

BACKGROUND: Mother to infant transmission of hepatitis C virus (HCV) has been extensively studied in mothers with human immunodeficiency virus (HIV) infection, whereas fewer data are available on the vertical HCV transmission in HIV-negative women. METHODS: Between January 1995 and June 1997, 78 consecutive HCV-positive/HIV-negative women with their offspring entered this prospective study aimed to define the prevalence of and risk factors for HCV vertical transmission. Risk factors for HCV were carefully sought, and HCV viral load and genotype were determined in all positive mothers. The infants were tested for alanine aminotransferase (ALT) and HCV-RNA at birth and at 4, 8, 12, 18, and 24 months of age. RESULTS: Eight of 60 (13.3%) infants born to HCV-RNA positive mothers acquired HCV infection, but only 2 (3,3%) were still infected by the end of follow-up. Infants' genotypes matched that of the mothers. ALT levels were in the normal range in all study subjects throughout the follow-up. High maternal viral load (P < 0.05), possession of HCV risk factors (P < 0.004), and history of blood transfusion (P < 0.05) were associated with increased risk of HCV vertical transmission. CONCLUSIONS: This long-term prospective study shows that, although vertical transmission from HIV-negative mothers occurs in 13% of cases, there is a high rate of spontaneous viral clearance (75%). High maternal viral load and mothers belonging to HCV risk categories were the only variables predictive of the vertical transmission.     

High rate of maternal-infant transmission of hepatitis G virus in HIV-1 and hepatitis C virus-infected women

The prevalence of hepatitis G virus (HGV) infection was investigated in 56 mothers with both human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) infection. Thirty-three (58.8%) women had markers of HGV infection, including 7/15 (46.6%) with no history of parenteral exposure to blood. Sixteen (48%) had HGV RNA in serum by a polymerase chain reaction assay, and 17 (52%) had antibody to E2 viral protein. No woman was positive for both markers. Of 20 infants born to the 16 mothers with HGV viremia, 9 (45%, 95% CI 34-56%) acquired the infection. No infected child seroconverted to HGV during the first year of life. At the latest visit (mean: 37.1 mo, range: 9-89 mo) 7 children were still seronegative HGV RNA carriers, 1 was both RNA- and antibody-negative, while 1 RNA-negative child had developed the E2 antibody. Of the 20 HGV-exposed infants, 2 contracted HCV and 1 HIV-1 (all 3 with HGV coinfection). No abnormalities in clinical findings and ALT levels were observed throughout the follow-up period in the six children with HGV infection alone. Our findings show that HGV infection is widespread among HIV-1- and HCV-infected women. Maternal-infant transmission of HGV is common and occurs independently from that of HIV-1 and HCV in women with triple infection. Most perinatally HGV-infected children develop persistent infection with no clinical or biological signs of liver damage, at least in the first years of life.     

Spontaneous clearance of hepatitis C virus in vertically infected children

Spontaneous viral clearance of hepatitis C virus (HCV) has been reported to occur in children with vertical HCV infection. However, factors which are associated with or predispose for clearance are largely unknown. In this case series we retrospectively analyzed laboratory parameters associated with spontaneous clearance of HCV in vertically infected children. The charts of six patients with documented spontaneous viral clearance by the age of 5 years were reviewed regarding clinical course, liver function tests (LFTs) and trend of HCV gene copy numbers. Spontaneous viral elimination was observed between the 25th and 52nd months of age. All patients had elevated LFTs, which peaked before 20 months of life. Peak LFT elevation was followed by normalization of LFTs and decline in viral load. These findings suggest that, in vertically HCV-infected children, a potent inflammatory response in the liver precedes viral clearance. Therefore, temporarily elevated LFTs, followed by a decline of viral load may be indicative of a near viral clearance in early childhood. Conclusion: Further investigations regarding the development of optimal treatment algorithms should take into account factors, which are associated with possible spontaneous viral resolution, such as viral genotype, favourable host factors as well as direct and indirect parameters of antiviral immunity, and the individual course of viral replication.     

Hepatitis B and C viruses in infants and young children

Advances during the past 20 years have led to a better understanding of the prevention, diagnosis, and treatment of acute and chronic hepatitis B (HBV) and hepatitis C (HCV) infections in the pediatric population. Universal vaccination and prenatal testing for HBV have decreased the incidence rate of acute HBV infections from more than 3/100,000 to 0.34/100,000 in all children. Diagnosis of chronic HBV is confirmed with positive serologic testing on two occasions at least 6 months apart. Current approved therapies with interferon alpha and lamivudine for children with chronic HBV infection have shown some efficacy, but results have been variable. In contrast, the lack of an effective HCV vaccine and the risk of mother-to-child transmission may increase the number of children with vertically acquired HCV that ultimately go on to develop liver fibrosis or cirrhosis. Diagnosis of HCV in the neonate should be postponed until after the child reaches 1 year of age because infants may have transient viremia. Treatment for HCV infected children has not been studied extensively. Peginterferon alpha-2a and Ribavirin are not currently approved for pediatric use; however, recent studies in children have shown potential benefit. More effective and less toxic therapies for young patients with HBV and HCV are needed, as are methods to interrupt perinatal transmission of HBV and HCV.     

Increased risk of chronic hepatitis in children with cancer

BACKGROUND: There is a risk of viral hepatitis for children with cancer. Both hepatitis B virus (HBV) and hepatitis C virus (HCV) infections in countries with high prevalence cause major problems in the management of cancer patients. In this study, we evaluated the incidence and chronicity of HBV and HCV infections in children with malignant diseases receiving chemotherapy. PROCEDURE: One hundred ninety-eight children with cancer (mean age = 7.5 +/- 2.5 years) and 100 healthy children as a control group were screened for HBV and HCV. Liver function tests, the number of transfusions, HBV and HCV serology were regularly monitored. In seropositive children, HBV-DNA and HCV-RNA were measured. Chronic hepatitis was defined as having an alanine aminotransferase (ALT) level three times of upper normal limit, positive HBV and HCV antigenemia for longer than 6 months. Liver biopsies were performed in all children with chronic hepatitis. The relationship between the chronic hepatitis and study parameters was statistically analyzed. RESULTS: HBsAg positivity, anti-HCV, and mixed (HBV and HCV) infection were found in 11.6, 5.5, 2% of children, respectively. Most HBV infected children developed chronic hepatitis (48%) while 26 and 21.7% became carriers and immune, respectively. One died of acute fulminant HBV hepatitis. Of HCV infected children, 63.6% also had positive HCV-RNA. Four children with mixed infection (100%) all progressed to chronic hepatitis. In this setting, chronic hepatitis was observed in 22 of 38 infected children (57.8%). The majority had leukemia and lymphoma. Children with HBsAg antigenemia developed chronic hepatitis in shorter time than HCV positive children (median 13 months vs. 51 months, P < 0.001). CONCLUSION: We observed an increased incidence of chronic hepatitis and even mortality due to HBV infection. This suggests that HBV and HCV infections are serious causes of morbidity and mortality in children with cancer.     

Hepatitis C virus infection and interferon therapy in patients with Down syndrome.

BACKGROUND: The clinical features of hepatitis C virus (HCV)-associated liver diseases, or the efficacy of interferon (IFN) therapy in children with Down syndrome (DS) remain to be elucidated. The purpose of the present paper was to survey the features of liver diseases in this subset of children and evaluate the efficacy of IFN treatment in those patients. METHODS: A questionnaire was sent to 41 members of the Japan Society of Pediatric Hepatology. Ten of them reported on 11 patients with DS who had concomitant chronic HCV infection, providing information on liver disease and the response to IFN treatment. RESULTS: Interferon therapy of 24 weeks duration using natural IFN-alpha was instituted in six of the 11 patients with DS, but none of the six patients cleared HCV-RNA from their serum. Among 12 age- and sex-matched control children who were treated with IFN using the same regimen against chronic HCV infection, half of them had a favorable response to IFN therapy with a sustained clearance of HCV-RNA from their serum. The major baseline features including alanine aminotransferase levels, HCV genotype and viral load were not apparently different between the six patients with DS and the 12 controls. CONCLUSIONS: IFN therapy for HCV infection in patients with DS may be unfavorable as compared with non-DS children.     

Hepatitis C virus infection and related liver disease in children of mothers with antibodies to the virus

Objective: To evaluate the clinical, biochemical, and virologic features associated with hepatitis C virus (HCV) infection acquired early in life from mothers with antibodies to HCV (anti-HCV).Study design: Multicenter prospective-retrospective study in Italian children.Patients: Two groups of children were investigated. Group 1 included 14 infants, born to mothers with anti-HCV but without human immunodeficiency virus infection, who became seropositive for HCV RNA during the first year of life and were thus considered infected. Group 2 included 16 children with chronic hepatitis C, aged 1 ½ to 14 years, whose mothers were the unique potential source of infection. Both groups were followed for 12 to 48 months.Methods: Alanine transaminase (ALT), anti-HCV, and HCV RNA were investigated by the polymerase chain reaction on entry to the study and during follow-up.Results: All children in group 1 had anti-HCV throughout follow-up, and all had ALT abnormalities, ranging from 1.5 to 10.5 times the normal value during the first 12 months. During further follow-up, 5 of 10 children had HCV RNA with abnormal ALT values, 3 had a return to normal of the ALT values but continued to have viremia, and 2 eventually had normal ALT values and clearance of HCV RNA. Of the 16 children in group 2, all were free of symptoms and 62% had only slight ALT elevations; 7 who underwent liver biopsy had histologic features of minimal or moderate hepatitis.Conclusions: HCV infection acquired early in life from mothers with anti-HCV is usually associated with biochemical features of liver damage during the first 12 months of life. Progression to chronicity seems to occur in the majority of cases, although HCV-associated liver disease is likely to be mild throughout infancy and childhood. (J Pediatr 1997;130:990-3)     

SEN virus infection in children in Taiwan: transmission route and role in blood transfusion and liver diseases

BACKGROUND: SEN virus (SENV) is a newly discovered DNA virus. We conducted this study to evaluate potential modes of SENV transmission and the pathogenic effect of SENV on liver diseases in children. METHODS: Polymerase chain reaction was used to detect 2 SENV variant (SENV-D and SENV-H) DNA in sera from healthy individuals and diseased children. Nucleotide sequence of SENV was determined by direct sequencing. RESULTS: SENV infection was assessed in healthy individuals, including 50 newborns (sera collected from the umbilical cord), 24 infants, 46 preschool children (aged 1-6 years), 42 school children of an age before that of the first sexual experience (aged 7-12 years), 62 adolescents (13-18 years), 72 young adults (19-30 years) and 32 adults (>30 years). The prevalence of SENV-D and/or SENV-H (SENV-D/H) viremia in each group was 0%, 17%, 24%, 24%, 27%, 33% and 40%, respectively. The prevalence of SENV-D/H viremia in 18 children with non-A to E hepatitis, 64 thalassemic children, 80 children transfused during cardiac surgery, 30 children with chronic hepatitis B, 9 children with chronic hepatitis C and 32 infants with biliary atresia was 11%, 61%, 80%, 83%, 67% and 50%, respectively. SENV was found more frequently in all patient groups than in 174 age-matched controls (P < 0.01), with the exception of non-A to E hepatitis (11% versus 24% in the control group; P = 0.27). In 2 infants with proven intrauterine hepatitis B viral infection, identical SENV-D nucleotide sequence existed in both the maternal and neonate serum. Elevated alanine aminotransferase concentrations were rarely observed in children who acquired isolated SENV viremia because of transfusion for surgery. Infection with SENV in children with chronic hepatitis C virus or hepatitis B viral infection was not associated with higher peak alanine aminotransferase values. CONCLUSION: SENV is transmitted mainly via nonparenteral daily contact and frequently occurs early in life. Transfusion can significantly increase the rate of SENV viremia. SENV does not appear to cause hepatitis in children.     

NASPGHAN practice guidelines: Diagnosis and management of hepatitis C infection in infants, children, and adolescents

Hepatitis C virus (HCV) is an RNA virus that affects >180 million individuals worldwide with a high propensity for chronic infection. Children with HCV infection differ from adults in several ways including some modes of transmission, rates of clearance, progression of fibrosis, and the duration of potential chronic infection when acquired at birth. Since the discovery of HCV in 1989, there have been significant advances in the understanding of the virology and natural history of chronic HCV infection in children. In addition, there are now several treatment options for children with chronic hepatitis C infection and many new therapies on the horizon. As a consequence, the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition brought together experts in pediatric hepatology to review the available data in children and provide clinicians with approaches to the diagnosis, management, and prevention of HCV infection in children and adolescents. The guideline details the epidemiology and natural history of HCV infection in children, the diagnostic workup, monitoring and treatment of disease, and provides an update on future treatment options and areas of research.     

乙型肝炎病毒母婴传播影响因素探讨

目的：探讨乙型肝炎病毒(HBV)母婴传播的影响因素,寻求降低婴儿HBV感染率的方法。方法：HBV携带及慢性乙型肝炎孕妇共635例,分别比较不同血HBV DNA滴度,不同分娩方式（剖宫产或自然分娩）,以及不同肝功能状态孕妇所生婴儿出生时及3月龄时HBV的感染率。新生儿生后12 h内肌注乙肝免疫球蛋白200 U 及重组酵母乙肝疫苗10 μg;生后即刻显示血清HBV感染存在者,14 d时再肌注乙肝免疫球蛋白200 U。结果：孕妇高滴度组（HBV DNA>105拷贝/mL）所生新生儿出生时（14.4% vs 4.1%,P<0.01）与3月龄时（4.7% vs 0,P<0.01）HBV感染率均高于低滴度组（HBV DNA ≤105拷贝/mL）。两组新生儿3月龄时HBV感染率均低于出生时（P<0.05）。自然分娩的孕妇其婴儿出生时HBV感染率明显高于剖宫产组（P<0.01）,但3月龄时,两组感染率接近。HBV携带孕妇所生婴儿出生时HBV感染率明显高于慢性乙型肝炎孕妇所生婴儿（P<0.01）,但3月龄时两组婴儿HBV感染率亦接近。结论：孕妇血清HBV DNA水平与新生儿HBV宫内感染密切相关,故降低孕妇血清HBV DNA水平可能成为减少新生儿HBV感染的一种有效途径。在乙肝免疫球蛋白及重组酵母乙肝疫苗的双重保护下,孕妇的分娩方式与肝功能状态对HBV母婴传播无影响。