***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: This r and omized , double-blind , placebo-controlled study evaluated whether lamivudine given during late pregnancy can reduce hepatitis B virus ( HBV ) perinatal transmission in highly viraemic mothers . Mothers were r and omized to either lamivudine 100 mg or placebo from week 32 of gestation to week 4 postpartum . At birth , infants received recombinant HBV vaccine with or without HBIg and were followed until week 52 . One hundred and fifty mothers , with a gestational age of 26 - 30 weeks and serum HBV DNA > 1000 MEq/mL ( bDNA assay ) , were treated . A total of 141 infants received immunoprophylaxis at birth . In lamivudine-treated mothers , 56 infants received vaccine + HBIg ( lamivudine + vaccine + HBIg ) and 26 infants received vaccine ( lamivudine + vaccine ) . In  placebo-treated mothers , 59 infants received vaccine + HBIg ( placebo + vaccine + HBIg ) . At week 52 , in the primary analyses where missing data was counted as failures , infants in the lamivudine + vaccine + HBIg group had a significant decrease in incidence of HBsAg seropositivity ( 10/56 , 18%vs 23/59 , 39 % ; P = 0.014 ) and in detectable HBV DNA ( 11/56 , 20%vs 27/59 , 46 % ; P = 0.003 ) compared to infants in the placebo + vaccine + HBIg group . Sensitivity analyses to evaluate the impact of missing data at week 52 result ing from a high dropout rate ( 13 % in the lamivudine + vaccine + HBIg group and 31 % in the placebo + vaccine + HBIg group ) remained consistent with the primary analysis in that lower transmission rates were still observed in the infants of lamivudine-treated mothers , but the differences were not statistically significant . No safety concerns were noted in the lamivudine-treated mothers or their infants . Results of this study suggest that lamivudine reduced HBV transmission from highly viraemic mothers to their infants who received passive/active immunization The purpose of this study was to investigate the efficacy and safety of lamivudine ( LAM ) in stopping the vertical transmission of hepatitis B virus ( HBV ) . Pregnant women with normal alanine transaminase ( ALT ) ( n = 100 ) and with abnormal ALT ( n = 100 ) who were positive for hepatitis B e antigen ( HBeAg ) , and with HBV DNA ( deoxyribonucleic acid ) levels ≥1.0 × 107 copies/ml were enrolled in this study . One hundred volunteers ( 50 with normal ALT , 50 with abnormal ALT ) received 100 mg of LAM daily from the 24th to 32nd week of gestation and the untreated 100 volunteers served as controls . All infants received passive-active immunoprophylaxis . Compared to the control group , the study group got a marked reduction in serum levels ( P < 0.001 ) and high negativity ( P < 0.001 ) of HBV DNA before delivery . They also got normalization in ALT levels as much as controls received general medication ( P > 0.05 ) . The prenatal transmission rate in the study group was significantly lower than that of the control group ( P < 0.05 ) . There were no differences in incidences of congenital malformation between the two groups ( P > 0.05 ) . LAM treatment can effectively and safely stop vertical transmission of HBV and normalize the ALT levels of pregnant women BACKGROUND & AIMS Fetal safety of antiviral therapies is important given the long-term treatment of women with chronic hepatitis B ( CHB ) infection who may become pregnant . We analyzed neonatal safety data from the Antiretroviral Pregnancy Registry ( APR ) , the largest safety data base in pregnancy for antivirals used for HIV and CHB . METHODS Data were extracted from APR cases prospect ively enrolled between 1989 and 2011 . Primary outcomes were major birth defects rates with exposure to all antivirals , individual classes , and drugs compared to population -based controls . Relevant to CHB , only lamivudine ( LAM ) and tenofovir disoproxil fumarate ( TDF ) had sufficient individual data for review ( ≥200 cases ) . RESULTS Of 13,711 cases analyzed , the overall birth defect prevalence ( 2.8 % , 95 % CI 2.6 - 3.1 % ) was comparable to Centers for Disease Control population -based data ( 2.72 % , 2.68 - 2.76 % , p=0.87 ) and two prospect i ve antiretroviral exposed newborn cohorts ( 2.8 % , 2.5 - 3.2 % , p=0.90 and 1.5 % , 1.1 - 2.0 % , p<0.001 ) . The birth defects prevalence between first and second/third trimesters exposure was similar ( 3.0 % vs. 2.7 % ) . No increased risk of major birth defects with LAM or TDF exposure compared to population -based controls was observed . No specific pattern of major birth defects was observed for individual antivirals or overall . CONCLUSIONS No increased risk of major birth defects including in non-live births was observed for pregnant women exposed to antivirals relevant to CHB treatment overall or to LAM or TDF compared to population -based controls . Continued safety and efficacy reporting on antivirals in pregnancy are essential to inform patients on their risks and benefits during pregnancy OBJECTIVE To determine the rate of perinatal hepatitis B virus ( HBV ) transmission in an Australian setting and to identify maternal virological factors associated with highest risk of transmission . DESIGN , PARTICIPANTS AND SETTING A prospect i ve , observational study of perinatal transmission of HBV . Participants were pregnant women attending Sydney South West Area Health Service antenatal clinics who tested positive for hepatitis B surface antigen ( HBsAg ) , and their babies . All babies were routinely offered hepatitis B immunoglobulin ( HBIG ) and HBV vaccination . Babies positive for HBsAg at 9-month follow-up underwent further virological testing , including HBV DNA sequencing . The study was conducted between August 2002 and May 2008 . MAIN OUTCOME MEASURES HBV DNA levels and demographic characteristics of HBsAg-positive pregnant women ; proportion of their infants with active HBV infection at 9-month follow-up ; maternal characteristics affecting transmission rate ; HBV DNA sequencing of infected infants and their mothers . RESULTS Of 313 HBsAg-positive pregnant women , 213 ( 68 % ) were HBV DNA-positive and 92 ( 29 % ) were positive for hepatitis B " e " antigen ( HBeAg ) ; 138 babies born to HBV DNA-positive mothers were tested for HBV infection ( HBsAg positivity ) at about 9 months of age . Four cases of transmission were identified . All four mothers had very high HBV DNA levels ( > 10(8 ) copies/mL ) and were HBeAg-positive . Three of the four infants were infected with wild-type HBV strains , with identical maternal/infant isolates . The fourth mother-infant pair had an S gene variant , HBV D144E , which has been previously reported in association with vaccine/HBIG escape . ( Unfortunately , HBIG was inadvertently omitted from the immunisation schedule of this infant . ) Transmission rates were 4/138 ( 3 % ) from HBV DNA-positive mothers overall , 4/61 ( 7 % ) from HBeAg-positive mothers , and 4/47 ( 9 % ) from mothers with very high HBV DNA levels . No transmission was seen in 91 babies of mothers with HBV DNA levels < 10(8 ) copies/mL. CONCLUSION In this cohort , HBV perinatal transmission was restricted to HBeAg-positive mothers with very high viral loads OBJECTIVE To investigate the efficacy of telbivudine on intrauterine hepatitis B virus ( HBV ) infection during the last stage of pregnancy . METHODS 61 pregnant chronic hepatitis B ( CHB ) patients were enrolled and 31 patients were treated by telbivudine 600 mg once daily , 30 patients in the control group were not received antiviral treatment .  Maternal HBV DNA level and the HBsAg positive rate in newborns were investigated . RESULTS The levels of serum HBV DNA in patients treated with Telbivudine were significantly reduced ( t = 19.09 , P less than 0.01 ) . Compared with the control group , serum HBV DNA levels were significantly lower in telbivudine treated patients than those in the control group before parturition ( t = 23.64 , P less than 0.01 ) . The infection rate of 7-month newborns were 0 and 13.33 % ( 4/30 ) , in telbivudine group and control group , respectively ( x2 = 4.29 , probability value less than 0.05 ) . CONCLUSIONS Telbivudine treatment can block intrauterine infection in pregnant chronic hepatitis B patients OBJECTIVE To investigate the effect of high viral loads ( HBV DNA concentration in blood > 2.0 copy/ml ) on the vertical transmission of hepatitis B virus in mothers with HBV DNA positivity . METHOD Forty pregnant women with HBV DNA positivity were divided r and omly , double-blindly into 2 groups : at 28 weeks of pregnancy , one group received oral lamivudine ( 100 mg/d ) and the other received oral placebo . The serum HBV DNA loads were tested at 28 and 40 weeks ' gestation in mothers , and serum HBV DNA , HBsAg , HBeAg and anti-HBs were examined in infants at 12 month follow up . RESULT Thirty-nine infants finished ( one twins ) the follow up , and 2 infants lost ( 5 % ) . Among them 4 infants were confirmed to be HBV infection ( 10 % , 4/39 ) , 2 in the treatment group ( 10 % , 2/20 ) and 2 in the control group ( 11 % , 2/19 ) ( P > 0.05 ) . The serum HBV DNA levels of 40 weeks ' gestation in the treatment group , compared with the levels of 28 weeks ' gestation in the treatment group and 40 weeks ' gestation in the control group , showed a significant decline ( P < 0.01 ) . The HBV DNA levels of the mothers whose infants were infected , were ( 3.1 + /- 3.4 ) copy/ml , ( 3.1 + /- 3.2 ) copy/ml during 28 and 40 weeks ' gestation , and for mothers whose infants were non-infected , the levels were ( 3.4 + /- 2.2 ) copy/ml , ( 2.6 + /- 1 . 5 ) copy/ml respectively ( P > 0.05 ) . The mean values of anti-HBs of 18 infants in the treatment group showed no significant difference as compared to 17 infants in the control group , ( 594 + /- 416 ) U/L vs ( 458 + /- 398 ) U/L ( P > 0.05 ) . CONCLUSION The pregnant women 's HBV DNA loads could be obviously decreased from high viral loads ( HBV DNA concentrations in blood > 2.0 copy/ml ) after they take lamivudine from 36 weeks ' gestation . But it might not reduce the maternal-fetal vertical transmission of HBV infection Little observational data exist describing telbivudine ( LdT ) or lamivudine ( LAM ) use in late pregnancy for preventing hepatitis B mother-to-child transmission ( MTCT ) in real-world setting s. During the period of January 2009 to March 2011 , we enrolled hepatitis B e antigen – positive mothers with HBV DNA > 6 log10 copies/mL in China . At gestation week 28 , the mothers received LdT or LAM until postpartum week 4 or no treatment ( NTx ) . The study endpoints were the safety of LdT/LAM use and MTCT rates . Of the 700 mothers enrolled , 648 ( LdT/LAM/NTx  = 252/51/345 ) completed the 52-week study with 661 infants  ( LdT/LAM/NTx = 257/52/352 ) . On treatment , viral rebound occurred in 1.6 % of mothers , all result ing from medication noncompliance . There was no genotypic mutation detected . At delivery , significantly lower HBV DNA levels were noted in mothers who received LdT or LAM versus NTx . Alanine aminotransferase flares were observed in 17.1 % of treated mothers versus 6.3 % of untreated mothers ( P < 0.001 ) . At birth , hepatitis B surface antigen ( HBsAg ) was detected in 20 % and  
    Output:
    
No significant differences were found in the congenital malformation rate , prematurity rate , and Apgar scores .
Compared to control , lamivudine or telbivudine improved maternal HBV DNA suppression at delivery and during 4 - 8 weeks ' postpartum follow-up .
Tenofovir showed improvement in HBV DNA suppression at delivery .
No significant differences were found in postpartum hemorrhage , cesarean section , and elevated creatinine kinase rates .
CONCLUSIONS Antiviral therapy improves HBV suppression and reduces MTCT in women with chronic HBV infection with high viral load compared to the use of hepatitis B immunoglobulin and vaccination alone ; the use of telbivudine , lamivudine , and tenofovir appears to be safe in pregnancy with no increased adverse maternal or fetal outcome