COMMENTARY

Antiviral Therapy for HCV During Pregnancy to Prevent Transmission: 6 Reasons in Favor of a Controversial Concept

Digestive Disease Week (DDW) 2018

Nancy Reau, MD

Disclosures

July 23, 2018

Childhood HCV Is Increasing

Pediatric exposure to HCV is usually linked to MTCT. Although the MTCT of HCV is low, at a reported transmission rate between 5% and 15%, no known interventions exist to reduce the risk for MTCT. Specifically, elective cesarean delivery is not recommended to reduce the risk for MTCT of HCV, though minimizing invasive procedures such as scalp electrodes and amniocenteses should be avoided, as they could increase the risk for maternal blood exposure to the fetus. A recent study showed a correlation between MTCT of HCV and maternal viral load. In this study, women with a high viral load had MTCT rates as high as 17%.[6]

Rates of MTCT Transmission of HCV Are Nearly the Same as That of HBV

Although the treatment of HCV during pregnancy is not recommended by any expert panel, the rates of MTCT of HCV parallel the risk for MTCT of hepatitis B virus (HBV) in high-viremic mothers, despite active/passive immunization.[7] For pregnant patients with HBV, nucleoside or nucleotide therapy is recommended to disrupt MTCT of HBV, which one could argue sets a precedent for antiviral therapy to disrupt MTCT of HCV.[8]

Linkage to Care Is Harder Than It Looks

Although guidelines advocate for HCV therapy preconception, this option is not always available for women in this demographic (eg, younger patients, patients who have a history of addiction, underinsured patients). Many patients in this at-risk cohort have either no insurance, or insurance coverage that prohibits access to therapy because of fibrosis restrictions or mandatory drug testing with documented abstinence.

While postpartum treatment might be advocated for instead, access to care can then become an issue. Although pregnant women have insurance, maternal coverage typically ends shortly after delivery. Even if insurance coverage extends post-delivery, the same restrictions to therapy exist because of fibrosis, and drug testing also limits access.

Independent of access, women in this cohort are considered "easy to treat." Most women of childbearing age have had HCV for less than 5 years, have minimal fibrosis, and are treatment naive, factors that translate to a nearly 100% cure rate with 8-12 weeks of oral therapy. A pangenotypic, direct-acting antiviral therapeutic option could allow a simplistic algorithm wherein the same intervention (glecaprevir/pibrentasvir or sofosbuvir/velpatasvir) is applied to pregnant patients in the third trimester in whom active infection has been confirmed by HCV antibody with reflex to a positive HCV polymerase chain reaction test—similar to the current management of HBV during pregnancy.

I again would like to underscore that, while the concept of disrupting MTCT by administering antiviral therapy to pregnant HCV patients is an interesting concept, no current data or evidence-based studies support its use.

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