Retrospective Study
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 21, 2017; 23(27): 4942-4949
Published online Jul 21, 2017. doi: 10.3748/wjg.v23.i27.4942
Perinatal transmission in infants of mothers with chronic hepatitis B in California
Jennifer C Burgis, Darryl Kong, Catheryn Salibay, Jennifer Zipprich, Kathleen Harriman, Samuel So
Jennifer C Burgis, Department of Pediatrics, Stanford University, Palo Alto, CA 94304, United States
Darryl Kong, Catheryn Salibay, Jennifer Zipprich, Kathleen Harriman, California Department of Public Health, Immunization Branch, Richmond, CA 94804, United States
Samuel So, Asian Liver Center, Stanford University, Palo Alto, CA 94304, United States
Author contributions: Burgis JC, Kong D, Salibay C, Zipprich J, Harriman K and So S contributed equally to this work; Burgis JC, Kong D, Salibay C, Zipprich J, Harriman K and So S designed the research; Burgis JC, Kong D, Salibay C, Zipprich J and Harriman K performed the research; Kong D and Salibay C analyzed the data; Burgis JC, Kong D, Salibay C, Zipprich J, Harriman K and So S wrote the paper.
Institutional review board statement: This study was reviewed and approved by the California Health and Human Services Agency Committee for the Protection of Human Subjects and the Stanford University Human Subjects Research and Institutional Review Board.
Conflict-of-interest statement: There are no conflicts of interest to disclose.
Data sharing statement: Technical appendix, statistical code and dataset available upon request from author Jennifer Zipprich (jennifer.zipprich@cdph.ca.gov).
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Jennifer C Burgis, MD, Clinical Assistant Professor, Department of Pediatrics, Stanford University, 750 Welch Road, Suite 116, Palo Alto, CA 94304, United States. jburgis@stanford.edu
Telephone: +1- 650-7235070 Fax: +1- 650-4985608
Received: March 24, 2017
Peer-review started: March 29, 2017
First decision: April 25, 2017
Revised: May 11, 2017
Accepted: June 18, 2017
Article in press: June 19, 2017
Published online: July 21, 2017
Processing time: 120 Days and 0.7 Hours
Abstract
AIM

To evaluate maternal hepatitis B virus (HBV) DNA as risk for perinatal HBV infection among infants of HBV-infected women in California.

METHODS

Retrospective analysis among infants born to hepatitis B surface antigen (HBsAg)-positive mothers who received post vaccination serologic testing (PVST) between 2005 and 2011 in California. Demographic information was collected from the California Department of Public Health Perinatal Hepatitis B Program databaseand matched to birth certificate records. HBV DNA level and hepatitis B e antigen (HBeAg) status were obtained from three large commercial laboratories in California and provider records if available and matched to mother infant pairs. Univariate analysis compared infected and uninfected infants. Multivariate analysis was restricted to infected infants and controls with complete maternal HBV DNA results using a predefined high HBV DNA level of > 2 × 107 IU/mL, a 5:1 ratio of cases to controls and a two-sided confidence level of 95%.

RESULTS

A total of 17687 infants were born to HBsAg positive mothers in California between Jan 1 2005 and Dec 31, 2011. Among 11473 infants with PVST, only 125 (1.1%) were found to be HBV infected. Among these infected infants, lapses in Advisory Committee on Immunization Practices recommended post exposure prophylaxis (PEP) occurred in only 9 infants. However, PEP errors were not significantly different between infected and uninfected infants. Among the 347 uninfected and infected infants who had maternal HBeAg and HBV DNA level, case-control analysis found HBeAg positivity (70.4% vs 28.9%, OR = 46.76, 95%CI: 6.05-361.32, P < 0.001) and a maternal HBV DNA level ≥ 2 × 107 IU/mL (92.6% vs 18.5%, OR = 54.5, 95%CI: 12.22-247.55, P < 0.001) were associated with perinatal HBV infection. In multivariate logistic regression, maternal HBV DNA level ≥ 2 × 107 IU/mL was the only significant independent predictor of perinatal HBV infection.

CONCLUSION

In California, transmission is low and most infected infants receive appropriate PEP and vaccination. Maternal HBV DNA ≥ 2 × 107 IU/mL is associated with high risk of perinatal infection.

Keywords: Perinatal transmission; Hepatitis B virus DNA; Pregnancy; Hepatitis B; Vaccination; Post-vaccine serology testing

Core tip: Most infants born to hepatitis B surface antigen positive woman in California received appropriate post exposure prophylaxis and vaccination but a low postvaccination serologic testing rate represents a missed opportunity to identify chronically infected infants needing lifelong medical care. Overall the perinatal transmission rate in California is low at 1.1% and only high maternal hepatitis B virus (HBV) DNA level predicts risk for perinatal transmission. Maternal HBV DNA is a vital prenatal screen if targeted antiviral therapy for high-risk mothers becomes a strategy to reduce transmission.