A Nomogram for Predicting Non-Rebound in HBV-Infected Pregnant Women With Mother-to-Child Transmission Prevention

Wang, Chunrui; Zhong, Guo‐Chao; Chen, Zhiwei; Hu, Peng

doi:10.3389/fmed.2021.746759

Cited by 2 publications

(2 citation statements)

References 38 publications

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“…Although patients treated with NA often have undetectable serum HBV DNA, most of them still have detectable cccDNA, which could explain why most pregnant patients infected with HBV experienced virological relapse after treatment cessation postpartum. This phenomenon was confirmed in our previously published article [ 23 ]. These findings support the conclusions of other studies that serum pgRNA or HBcrAg levels are useful for monitoring antiviral effects.…”

Section: Discussionsupporting

confidence: 88%

Profiles of HBcrAg and pgRNA in Pregnant Women With Chronic HBV Under Different Disease Phases and Antiviral Prophylaxis

Wang,

Liu,

Shen

et al. 2024

Open Forum Infectious Diseases

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Objectives Pregnant women with chronic hepatitis B (CHB) exhibit unique clinical features in terms of postpartum immune system reconstitution and recovery from pregnancy-related changes. However, current studies focus primarily on the outcomes of maternal-infant transmission and postpartum hepatitis flares. We aimed to evaluate the profiles of HBcrAg and pgRNA in pregnant women with CHB. Methods This retrospective analysis included treatment-naïve pregnant women with CHB who were followed up regularly in an outpatient clinic from 2014 to 2021. Baseline HBcrAg and pgRNA levels were compared in patients with different disease phases. Changes in these parameters were examined in a subset of patients receiving anti-viral prophylaxis. HBcrAg and pgRNA levels were measured before treatment, at 32 weeks of gestation, and postpartum. Results The final analysis included a total of 121 patients, 100 of whom were HBeAg-positive (96 and 4 in the immune-tolerant and -indeterminate phases, respectively) and 21 of whom were HBeAg-negative (6 and 15 in the immune-active and -inactive carrier phases, respectively). The HBeAg-negative vs. HBeAg-positive groups had lower levels of baseline HBcrAg [median (interquartile range): 3.7 (3.0-5.9) vs. 8.6 (8.4-8.7) log10U/mL; P < 0.01] and pgRNA [(0.0 (0.0-2.5) vs. 7.8 (7.6-8.1) log10copies/mL; P < 0.01)]. The serum levels of HBcrAg and pgRNA were the highest in immune-tolerant carriers and the lowest in immune-inactive carriers. In HBeAg-positive patients, the correlation coefficients of HBcrAg and pgRNA with HBV DNA were 0.40 and 0.43, respectively; in HBeAg-negative patients, they were 0.53 and 0.51, respectively (all P < 0.05). The correlation coefficients with HBsAg were 0.55 and 0.52 (P < 0.05) in HBeAg-positive patients, respectively, while in HBeAg-negative patients, they were 0.42 and 0.37, respectively (P > 0.05). Among 96 patients receiving antiviral prophylaxis, we detected a rapid decrease in HBV DNA to an undetectable level during treatment but relatively stable levels of pgRNA and HBcrAg. Conclusions HBcrAg and pgRNA levels are lower in HBeAg-negative patients than in HBeAg-positive patients. These two markers are significantly associated with HBV DNA irrespective of HBeAg status, while they are significantly associated with HBsAg only in HBeAg-positive patients.

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Section: Discussionsupporting

confidence: 88%

Profiles of HBcrAg and pgRNA in Pregnant Women With Chronic HBV Under Different Disease Phases and Antiviral Prophylaxis

Wang,

Liu,

Shen

et al. 2024

Open Forum Infectious Diseases

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“…HBeAg positivity and gestational diabetes were associated with postpartum hepatitis ( 123 ). When oral AVT is used in late pregnancy and stopped after delivery, the prediction model of postpartum hepatitis includes the decrease of HBsAg and HBV DNA from baseline to gestation 32 weeks or delivery, respectively ( 127 ).…”

Section: Postpartum Hepatitis and Maternal Changesmentioning

confidence: 99%

Postpartum hepatitis and host immunity in pregnant women with chronic HBV infection

et al. 2023

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In order to develop immune tolerant to the fetal, maternal immune system will have some modification comparing to the time before pregnancy. Immune tolerance starts and develops at the maternal placental interface. In innate immunity, decidual natural killer (dNK) cells, macrophages and dendritic cells play a key role in immue tolerance. In adaptive immunity, a moderate increase of number and immune inhibition function of regulatory T cells (Treg) are essential for immune tolerance. The trophoblast cells and immune cells expressing indoleamine 2,3-dioxygenase (IDO), the trophoblast cells expressing HLA-G, and Th1/Th2 shifting to Th2 dominant and Th17/Treg shifting to Treg domiant are in favor of maternal fetal immune tolerance. Steroids (estrogen and progesterone) and human chorionic gonadotropin (HCG) also participate in immune tolerance by inducing Treg cells or upregulating immunosuppressive cytokines. Most of the patients with chronic HBV infection are in the “HBV immune tolerance period” before pregnancy, and the liver disease is relatively stable during pregnancy. In chronic HBV infection women, after delivery, the relative immunosuppression in vivo is reversed, and Th1 is dominant in Th1/Th2 and Th17 is dominant in Th17/Treg balance. After delivery, the number of Treg decrease and NK cells increase in quantity and cytotoxicity in peripheral blood. Liver NK cells may cause liver inflammation through a non-antigen specific mechanism. After delivery, the number of CD8+ T cells will increase and HBV specific T cell response recovers from the disfunction in pregnancy. Under the background of postpartum inflammation, the rapid decrease of cortisol after delivery, and especially the enhancement of HBV specific T cell response induced by HBV DNA and cytokines, are the main reasons for postpartum hepatitis. HBeAg positive, especially HBeAg<700 S/CO, and HBV DNA>3-5Log10IU/ml are risk factors for postpartum hepatitis. Antiviral treatment in late pregnancy can reduce the incidence of mother to child transmission (MTCT) in chronic HBV infection women. Chronic HBV infection women have hepatitis both during pregnancy and more often in 12 weeks postpartum. It is generally agreed that postpartum hepatitis is mild symptoms and self-limited. Delaying drug withdrawal to 48 weeks can increase the seroconversion rate of HBeAg in delivery women with elevated alanine aminotransferase (ALT) in pregnancy.

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A Nomogram for Predicting Non-Rebound in HBV-Infected Pregnant Women With Mother-to-Child Transmission Prevention

Cited by 2 publications

References 38 publications

Profiles of HBcrAg and pgRNA in Pregnant Women With Chronic HBV Under Different Disease Phases and Antiviral Prophylaxis

Profiles of HBcrAg and pgRNA in Pregnant Women With Chronic HBV Under Different Disease Phases and Antiviral Prophylaxis

Postpartum hepatitis and host immunity in pregnant women with chronic HBV infection

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