Association between maternal hepatitis B virus carrier and gestational diabetes mellitus: a retrospective cohort analysis

Introduction Given that many pregnant women have chronic hepatitis B virus (HBV) infection and that gestational diabetes mellitus (GDM) is linked to poor maternal and neonatal outcomes, we looked into the relationship between the hepatitis B surface antigen (HBsAg) and GDM to see if a high HBV DNA load is linked to a higher risk of GDM in chronic maternal HBsAg carriers. Materials and methods Our study included 39,539 pregnant women who gave birth at the Third Affiliated Hospital of Guangzhou Medical University in Guangzhou, China, between January 1, 2009, and December 31, 2019. The patients were divided into two groups: HBsAg negative (36,500) and positive (3039). The viral load levels of 1250 HBsAg-positive women who had tested their HBV DNA load during pregnancy were separated into three groups. We utilized univariate and multivariable logistical regression analysis to determine the relationship between maternal chronic HBsAg carrier and GDM. Results Being HBsAg positive was discovered to be an independent risk factor for GDM.Pre-pregnancy Obesity and advanced age were linked to an increased incidence of GDM. Those with a high HBV DNA load (> 106 IU/mL) had a higher risk of GDM than HBsAg-positive women with a low viral load (< 103 IU/mL). Pre-eclampsia and intrahepatic cholestasis of pregnancy (ICP) appeared to be more common in HBsAg-positive women than in uninfected women. Conclusions Being HBsAg positive, advanced age, and pre-pregnancy obesity were all revealed to be independent risk factors for GDM in our study. In HBsAg carrier, pregnant women, a high HBV DNA burden was linked to a greater risk of GDM. Furthermore, being an HBsAg carrier during pregnancy raised the risk of ICP and pre-eclampsia.

Study on the Relationship Between Hepatitis B Virus Infection in Pregnant Women and Adverse Pregnancy Outcomes

Objective: Aim to the relationship between adverse pregnant outcomes with chronic hepatitis B virus (HBV) infection in pregnant women. Simultaneously, assess the incidence of adverse pregnancy outcomes (APO) among different serum HBV status in pregnant women. Method: From 2017 to 2019, we studied HBsAg (+) pregnant women and HBsAg (-) who gave birth at our hospital in Guangzhou City, China. We compared of the incidence of pregnant women with HBsAg(+) or HBsAg(-). Further, among HBsAg(+) pregnant women, We compared of the incidence of pregnant women with HBeAg(+) group or HBeAg(-) group, high HBV DNA loads (HBV DNA≥2×10^5IU/mL) group or low HBV DNA loads (HBV DNA＜2×10^5IU/mL) group, respectively. Finally, multivariate logistic regression analysis was used to evaluate the independent association between HBV infection and the risk of developing APO.Result: First, Our research Indicates that the rates of gestational diabetes mellitus (GDM), intrahepatic cholestasis of pregnancy (ICP), premature rupture of membrane (PROM), Fetal distress (FD), Oligohydramnios, Premature delivery (PD), Low birth weight (LBW), Meconium contamination (MC), Neonatal hyperbilirubinemia(NH) in HBsAg(+) group were higher than those in HBsAg(-) group (P<0.05). Second, among 711 HBsAg(+) pregnant women, the rates of GDM and ICP in high loads of HBV DNA were higher than those in low loads of HBV DNA group (P<0.05). Similarly, The rates of ICP in HBeAg(+) group were higher than those in HBeAg(-) group. Further, through multivariable logistical regression model analysis, we observed maternal HBsAg carrier (OR, 6.758; 95% CI, 2.358-19.369) had an independent risk for ICP. Similarly, HBsAg carrier(OR, 1.101; 95% CI, 1.066-1.137) ,advanced age (OR, 1.407; 95% CI,1.016-1.137) and abortion(OR,1.446; 95% CI, 1.062-1.969) had independent risk for GDM. Conclusions: Chronic HBV infection can increase the rate of host adverse pregnancy outcomes (APO). The maternal viral load and HBeAg status were significantly associated with the incidence of GDM and ICP. Maternal HBsAg carrier had an independent risk for GDM and ICP.

Course of HBV-infection in HIV-infected and HIV-non-infected Pregnant women

The objective of the work – is to study the course of HBV-infection in pregnant women, infected and uninfected with HIV, based on the analysis of clinical-laboratory parameters. Materials and methods. HBV-infection was diagnosed in 5.6% of women with negative HIV-status and in 9.4% positive with HIV. To verify the diagnosis of HBV-infection, the data of anamnesis, clinical examination, laboratory tests: general clinical, biochemical, EIA, PCR, and VL in each trimester of pregnancy were used. Research. In HIV-negative pregnant women, 71.6% of the patients were diagnosed with HBsAg carrier status and 28.4% – the replication stages. Replication stages were only in HIV-positive patients. The frequency of clinical manifestations of CHB is higher in HIV-positive women – it is 33.33% vs 10.00% in HIV-negative (p<0.05), in a significantly lower rate of cytolysis – 11.11% vs 45.00% (p< 0.001), which did not increase up to the childbirth. The rate of VL of HBV increased before the childbirth in 63.3% of pregnant women without HIV-infection, and in 36.7% it did not change. Thus, in 83.3% of HIV-infected, it decreased to the threshold, and in 16.7% it hasn’t changed (p<0.01). During pregnancy, the immunotolerant phase of CHB in women of both groups was not transformed into immunoactive, and in HIV-negative pregnant women – the carrier status of HBsAg to the replicative form. Conclusion. In pregnant women with HIV-infection the incidence of replicative forms of HBV-infection is 3.5 times than in pregnant women without HIV-infection, the HBsAg carrier status is not determined. HIV-immunosuppression is accompanied by the prevalence of the immunotolerant phase of CHB (88.9%) with subclinical course without disturbance of pigmentary metabolism and cytolysis increase against the background of a decrease of VL HBV up to the threshold in 83.3% (p<0.01). The inverse weak correlation between the level of CD4 + T-lymphocytes and VL HBV was determined. In HIV-negative pregnancies, latent forms of HBV-infection prevail (71.6%). Replicative forms are characterized by a low degree (80.0%) of HBV viremia (p<0.05) with minimal cytolysis in 43.3% of women (p<0.001), which did not change during pregnancy.

Hepatitis B e Antigen Seroconversion Is Related with the Function of Dendritic Cells in Chronic Hepatitis B Virus Infection

Aim. To investigate the relationship between hepatitis B e antigen seroconversion and the function of dendritic cells (DC) in patients with hepatitis B virus.Methods. The peripheral blood mononuclear cells (PBMC) from 21 chronic HBV patients in immune tolerance state, 23 patients in inactive HBsAg carrier state, and 10 healthy HBV-naive blood donors were incubated and induced into DC in presence of granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-4 (IL-4), respectively. The expressions of surface markers on DC were detected by flow cytometry, and the stimulatory capacity of DC in allogenic mixed leukocyte reaction (MLR) was tested by CCK-8, and the level of cytokines released by DC was analyzed by enzyme-linked immunosorbent assay (ELISA).Results. DC from patients in immune tolerance showed a remarkably lower surface expression of CD80, CD86, and HLA-DR and exhibited an impaired stimulatory capacity in MLR and reduced secretion of IL-12, as compared to the patients in inactive HBsAg carrier state. There was no significant difference between the indicators from the patients in inactive HBsAg carrier state and healthy subjects. There was a significant difference of HBV DNA level between immune tolerance and inactive HBsAg carrier group (P<0.01) and a negative correlation between HBV DNA level and the expressions of dendritic cells in both groups, respectively (P=0.01).Conclusion. DC from patients in inactive HBsAg carrier state shows stronger function in comparison with patients in immune tolerance, the expressions of dendritic cells correlate with HBV DNA level, and the function stage of DC may play an important role in HBeAg seroconversion.