A 28-year-old pregnant woman (G1P0 at 24 weeks’ gestation) was referred to our hospital due to ultrasonographic findings of foetal heart defects in September 2011. The pregnancy was uneventful. All prenatal serological tests, including hepatitis B virus (HBV) markers and cytomegalovirus IgM, were normal or negative. There was no known harmful exposure before or during pregnancy. She was not taking any medications. She was previously healthy, lived with her husband, and worked in a primary school. The family history was unremarkable. Her 32-year-old husband was perinatally infected with HBV. His serologic testing has been positive for hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and antibody against hepatitis B core antigen. In December 2005, he started antiviral therapy with ADV (orally 10 mg/day) because of persistently abnormal liver functions and high HBV DNA level (1.1–9.6 × 106 copies/ml). Because of primary drug resistance (data not shown), he was switched to lamivudine (LAM) monotherapy in May 2007 and later to combined therapy with lamivudine and ADV in December 2007. His liver function test turned normal and his HBV DNA level was <500 copies/ml in March 2008. Since June 2008, He has been on ADV monotherapy (orally 10 mg/day) with HBV DNA persistently undetected and normal liver functions. Since the administration of ADV, his renal function tests have always been normal.
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Published online: September 04, 2014
© 2014 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Inc. All rights reserved.