Hepatitis C and pregnancy.

2013Oct
World J. Gastroenterol.
World J Gastroenterol 2013 Oct;19(40):6714-20

Acute hepatitis C is a rare event in pregnancy. The most common scenario is chronic hepatitis C virus (HCV) infection in pregnancy. During pregnancy in women with chronic HCV infection a significant reduction in mean alanine aminotransferase levels has been reported, with a rebound during the postpartum period. In few cases exacerbation of chronic hepatitis C has been reported in pregnancy. A cofactor that might play a role in the reduction of liver damage is the release of endogenous interferon from the placenta. Observations regarding serum HCV-RNA concentration have been variable. In some women HCV-RNA levels rise toward the end of pregnancy. In general, pregnancy does not have a negative effect on HCV infection. Conversely, chronic hepatitis does not appear to have an adverse effect on the course of pregnancy, or the birth weight of the newborn infant. The role of spontaneous abortion is approximately the same as in the general population. The overall rate of mother-to-child transmission for HCV is 3%-5% if the mother is known to be anti-HCV positive. Co-infection with human immunodeficiency virus (HIV) increases the rate of mother-to-child transmission up to 19.4%. Numerous risk factors for vertical transmission have been studied. In general, high viral load defined as at least 2.5 × 10(6) viral RNA copies/mL, HIV co-infection, and invasive procedures are the most important factors. Both interferon and ribavirin are contraindicated during pregnancy. Viral clearance prior to pregnancy increases the likelihood that a woman remains non-viremic in pregnancy with a consequent reduced risk of vertical transmission.

Similar Publications

2013Oct
World J. Gastroenterol.
World J Gastroenterol 2013 Oct;19(40):6714-20

Acute hepatitis C is a rare event in pregnancy. The most common scenario is chronic hepatitis C virus (HCV) infection in pregnancy. During pregnancy in women with chronic HCV infection a significant reduction in mean alanine aminotransferase levels has been reported, with a rebound during the postpartum period. In few cases exacerbation of chronic hepatitis C has been reported in pregnancy. A cofactor that might play a role in the reduction of liver damage is the release of endogenous interferon from the placenta. Observations regarding serum HCV-RNA concentration have been variable. In some women HCV-RNA levels rise toward the end of pregnancy. In general, pregnancy does not have a negative effect on HCV infection. Conversely, chronic hepatitis does not appear to have an adverse effect on the course of pregnancy, or the birth weight of the newborn infant. The role of spontaneous abortion is approximately the same as in the general population. The overall rate of mother-to-child transmission for HCV is 3%-5% if the mother is known to be anti-HCV positive. Co-infection with human immunodeficiency virus (HIV) increases the rate of mother-to-child transmission up to 19.4%. Numerous risk factors for vertical transmission have been studied. In general, high viral load defined as at least 2.5 × 10(6) viral RNA copies/mL, HIV co-infection, and invasive procedures are the most important factors. Both interferon and ribavirin are contraindicated during pregnancy. Viral clearance prior to pregnancy increases the likelihood that a woman remains non-viremic in pregnancy with a consequent reduced risk of vertical transmission.

2006Oct
Obstet Gynecol Surv
Obstet Gynecol Surv 2006 Oct;61(10):666-72

Hepatitis C is the most common chronic bloodborne infection in the United States. The diagnosis of vertical transmission is reliably established by a positive serum hepatitis C virus (HCV) RNA on 2 occasions 3 to 4 months apart after the infant is at least 2 months old and/or by the detection of anti-HCV antibodies after the infant is 18 months old. Vertical transmission in HCV RNA-negative pregnant women is approximately 1% to 3% versus approximately 4% to 6% in HCV RNA-positive women. From the standpoint of vertical transmission, no critical HCV RNA titer has been established. Coinfection with HIV has been shown to increase the risk of vertical transmission of HCV, but highly active antiretroviral therapy may decrease the risk significantly. In HIV-negative women, route of delivery does not influence vertical transmission. In HCV/HIV-coinfected women, decisions regarding mode of delivery should be based on HIV status. There is no association between vertical transmission of HCV and gestational age at delivery or the presence of chorioamnionitis. The use of a scalp electrode has been associated with vertical transmission and this practice is discouraged. Data are conflicting regarding duration of ruptured membranes and the risk of vertical transmission of hepatitis C. When the duration of membrane rupture exceeds 6 hours, the risk may be increased. There is no evidence demonstrating an increased risk of HCV transmission in HIV-negative women who breast feed. In HCV/HIV-coinfected women, breast feeding is discouraged in women who have consistent access to safe infant formula.
Obstetricians & Gynecologists, Family Physicians.
After completion of this article, the reader should be able to recall that vertical transmission of hepatitis C (HCV) does occur, state that coinfection with HIV increases the transmission rate, and summarize that there is no association between gestational age or presence of chorioamnionitis and no evidence that a cesarean delivery prevents transmission.

Globally, hepatitis C virus (HCV) infection affects approximately 130 million people and 3 million new infections occur annually. HCV is also recognized as an important cause of chronic liver disease in children. The absence of proofreading properties of the HCV RNA polymerase leads to a highly error prone replication process, allowing HCV to escape host immune response. The adaptive nature of HCV evolution dictates the outcome of the disease in many ways. Here, we investigated the molecular evolution of HCV in three unrelated children who acquired chronic HCV infection as a result of mother-to-child transmission, two of whom were also coinfected with HIV-1. The persistence of discrete HCV variants and their population structure were assessed using median joining network and Bayesian approaches. While patterns of viral evolution clearly differed between subjects, immune system dysfunction related to HIV coinfection or persistent HCV seronegativity stand as potential mechanisms to explain the lack of molecular evolution observed in these three cases. In contrast, treatment of HCV infection with PegIFN, which did not lead to sustained virologic responses in all 3 cases, was not associated with commensurate variations in the complexity of the variant spectrum. Finally, the differences in the degree of divergence suggest that the mode of transmission of the virus was not the main factor driving viral evolution.

1997Dec
Eur. J. Obstet. Gynecol. Reprod. Biol.
Eur J Obstet Gynecol Reprod Biol 1997 Dec;75(2):177-82

In this study, we sought to determine (1) the prevalence of hepatitis C virus (HCV) RNA, or its antibodies, in a healthy parturient Egyptian population and (2) the risk of mother-to-infant transmission in this population.
The serum of 499 pregnant Egyptian women was tested for anti-HCV with ELISA-3 and for HCV RNA by polymerase chain reaction (PCR). Neonatal cord blood and infant blood were similarly tested for anti-HCV and HCV RNA.
Recombinant immunoblot assay (RIBA) detected anti-HCV in 65/499 (13%) women; of these, 20/65 (31%) were PCR-positive. The total number of babies born was 499. Of the original group, 97 mothers and infants (HCV-negative) were lost to follow up and were excluded. Sixty-five anti-HCV-positive infants were born vaginally to the 65 anti-HCV-positive mothers, of which twenty (31%) corresponding mothers and babies were also positive for HCV RNA. Of these twenty babies, three died of hepatocellular disease by six months of age; sixteen developed chronic liver disease; the remaining nine remained asymptomatic but were serologically and PCR-positive. The mother-to-infant transmission rate was significantly increased (5%; P < 0.0001). Of the seropositive children, 45/65 (69%; P < 0.0001) seroreverted by eighteen months of age.
There is a high prevalence of anti-HCV in healthy pregnant Egyptian women and vertical transmission is a major risk for chronic HCV carriers.

2001Sep
Am. J. Gastroenterol.
Am J Gastroenterol 2001 Sep;96(9):2751-4

The risk of hepatitis C virus (HCV) infection in the newborn is estimated to be around 5%, but becomes very high in the case of coinfection with HIV. One of the main factors associated with the vertical transmission of HCV is the viral load. Our objective was to investigate the behavior of HCV viral load during pregnancy in relation to HIV coinfection, liver enzymes, and vertical transmission.
Three thousand seven hundred forty-eight women seen consecutively in their first trimester of pregnancy were screened for HCV infection. Sixty-five were found to be anti-HCV+/HCV RNA+ and were followed up with clinical and serological assessment (i.e., transaminases and quantitative polymerase chain reaction [PCR] for viral load) in their second and third trimesters and 6 months after delivery. All were anti-HIV and hepatitis B surface antigen negative. HCV RNA was 12.0+/-19.9 x 10(6) copies/ml in the first trimester and 10.9+/-13.3 x 10(6) in the second, but increased to 19.5+/-25.1 x 10(6) in the third trimester. Six months after delivery the viral load returned to the baseline levels; the changes in viral load did not reach any statistical significance, however. Transaminases tended toward a reduction from the baseline during the second and third trimesters, and then an increase in both AST and ALT was recorded 6 months after delivery. However, when the group whose AST/ALT were found abnormal at the first test was considered, no significant changes were recorded during the follow-up. The overall rate of vertical transmission was 4.6
With HCV+ mothers monitoring transaminases during pregnancy is unnecessary, and testing liver enzymes at the beginning of pregnancy is sufficient. Qualitative PCR should be done once during the pregnancy, but any staging of the liver disease should be taken after delivery. Quantitative PCR testing is expensive and pointless. Any decision for elective cesarean section in HCV RNA+ mothers should be confirmed by other studies.