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Objective@#To investigate the efficacy of 200IU hepatitis B immunoglobulin (HBIG) injection at 1 month after birth to interrupt the mother-to-children transmission (MTCT) of hepatitis B virus (HBV).@*Methods@#Infants born to mothers who were hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) positive, with HBV DNA load ≥1.0×106 IU/ml and who did not receive antiviral drug treatment during pregnancy, were randomly divided into 2 groups. Infants in the control group were treated with standard immunoprophylaxis: 200 IU HBIG and 10 μg recombinant hepatitis B vaccine injection within 2 h after birth and a vaccine booster at 1 and 6 months after birth. For infants in the HBIG group the standard immunoprophylaxis and an additional 200 IU HBIG were administered at 1 month. HBsAg, the antibody to HBsAg (anti-HBs), and HBV DNA load were measured at birth and after 7 months. later.Immunoprophylaxis failure was defined as the presence of HBV DNA and HBsAg positivity or the presence of HBV DNA and HBsAg negativity at 7 months.@*Results@#In this prospective cohort study, of the 280 infants enrolled, 14 infants (HBIG/control: 6/8) were lost to follow-up and 266 subjects (HBIG/control: 134/132) completed the 7-month study. The log10HBV DNA load of mothers in the HBIG group and control group were (7.31±0.66) log10IU/ml and (7.32±0.74) log10IU/ml, respectively (P=0.92). The MTCT rate of the two groups was similar (5.97% vs. 7.58%, P=0.63). At 7 months, the HBsAg positive rate and the level of anti-HBs in the two groups were 94.03%(126/134)vs. 91.67% (121/132) and 623.60±412.93 mIU/mL vs. 620.38±399.10 mIU/ml, respectively with no significant difference (P=0.48 and P=0.95, respectively). The log10 HBV DNA load of mothers in immunoprophylaxis failure group and success group was similar (P=0.09). The number of infants who were serum HBsAg positive and HBV DNA positive at birth in the immunoprophylaxis failure group were higher than those in the success group (100% and 100% vs. 35.89% and 31.85%, P<0.01, respectively). The serum HBsAg levels in infants at birth was the only independent relevant factor for HBV MTCT, with risk rates of 11.18 (95% Confidence interval (CI), 1.23-101.88), 352.00 (95%CI, 15.82-7833.20), and 968.00 (95%CI 81.35-11519.19) for HBsAg levels of 0.05-< 1, 1-< 10, and ≥ 10 IU/ml, respectively, compared to infants with HBsAg levels < 0.05 IU/ml.@*Conclusions@#Administering 200IU HBIG injection at 1 month did not reduce the risk of HBV MTCT.
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Objective To establish a clinical cytokine test method based on flow multiple microarray technology,and discuss its clinical significance by observing the change of cytokines level in the early stage of influenza.Methods 54 cases of influenza A virus positive and 20 cases of influenza A virus negative influenza like patients were selected as influenza group.Among them,influenza A virus positive patients were divided into mild group and severe group,influenza A virus negative influenza like patients were as neg-ative group.In addition,35 healthy people were selected as the control group,and the cytokine of all the whole blood samples was detected and statistically analyzed.Results Interleukin-6(IL-6),interleukin-21(IL-21),interleukin-12p70(IL-12p70),interleukin-1 β(IL-1 β)and interleukin-10(IL-10),chemokine-10(IP-10),interleukin-2(IL-2),monocyte chemoattractant protein-1(MCP-1)lev-els were significantly higher in the patients with early onset of influenza,and the difference was statistically significant(P<0.05). The difference of interferon-γ(IFN-γ)between the influenza group and the control group was not statistically significant(P> 0. 05).The levels of IL-6 and IP-10 in the severe group were higher than that of the mild group and the negative group,and the differ-ence was statistically significant(P<0.05).Conclusion IL-6,IL-21,IL-12p70,IL-1 beta,IL-10,IP-10,IL-2 and MCP-1 levels can be used as clinical biological evaluation indicators of patients with fever,of which IL-6 and IP-10 can be used as important indicators for disease progression assessment.
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Objective To discuss the relationship between hepatitis B virus (HBV) genotype and HBV DNA ,liver fibrosis ,liver function and HBeAg .Methods HBV genotypes ,HBV DNA ,liver fibrosis indicators and alanine aminotransferase(ALT ) ,aspartate aminotransferase(AST ) ,total bilirubin(TBIL) ,albumin(ALB) and HBV e antigen(HBeAg) were detected in patients with serum hepatitis .All data were statistically analyzed .Results There was no significant difference of HBV DNA ,ALT ,AST ,TBIL ,ALB , procollagen- Ⅲ -peptide ,type Ⅳ collagen ,hyaluronic acid and laminin between patients with B and C genotype infection (P> 0 .05) . However ,HBeAg level in patients with C genotype infection was higher than that in patients with B genotype infection (P< 0 .05) . Conclusion There might be no significant difference of HBV DNA ,liver function and liver fibrosis between patients with B and C genotype infection ,but HBeAg level in patients with C genotype infection could be higher than patients with B genotype infection .
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<p><b>BACKGROUND</b>To study etiology of clinically diagnosed non A-E hepatitis.</p><p><b>METHODS</b>HBV, TTV, human parvovirus B19, SENV DNA were detected by nested polymerase chain reactions (nPCR), while HGV, HCV RNA were tested by reverse transcription nested polymerase chain reactions (RT-nPCR).</p><p><b>RESULTS</b>Of 60 patients with clinically diagnosed non A-E hepatitis, 30 (50.0%) were HBV DNA positive alone, 10 (16.7%) HBV and TTV DNA positive, 6 (10.0%) HBV and B19 DNA positive; 1 (1.7%) HBV, SENV DNA and HCV RNA positive, 1 (1.7%) HCV RNA positive alone, 1 (1.7%) HCV RNA and B19 DNA positive, 2 (3.3%) B19 DNA positive alone, 1 (1.7%) TTV DNA positive alone, and the remaining 8 (13.3%) negative for all viruses. All the 60 patients were HGV RNA negative. There were no differences in serum biochemical markers of hepatitis B patients with or without TTV or B19 virus infection.</p><p><b>CONCLUSIONS</b>HBV is a major etiologic agent for the clinically diagnosed non A-E hepatitis. HGV, TTV, B19 and SEBV may not be associated with nonA-E hepatitis.</p>