J Hepatol. 2019 Sep 6. pii: S0168-8278(19)30516-1. doi: 10.1016/j.jhep.2019.08.023. [Epub ahead of print]
Risk of hepatitis B surface antigen seroreversion after corticosteroid in patients with previous hepatitis B virus exposure.
Wong GL1, Wong VW1, Yuen BW2, Tse YK2, Yip TC2, Luk HW3, Lui GC3, Chan HL4.
Author information
1
Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong Special Administrative Region; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong Special Administrative Region.
2
Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong Special Administrative Region; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region.
3
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region.
4
Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong Special Administrative Region; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong Special Administrative Region. Electronic address: [email protected].
Abstract
BACKGROUND AND AIMS:
Systemic corticosteroid may cause hepatitis B virus (HBV) reactivation, but the impact on patients with previous HBV exposure is poorly defined. We aimed to study the risk of hepatitis B surface antigen (HBsAg) seroreversion and hepatitis flare in patients with previous HBV exposure.
METHODS:
Patients who were negative for HBsAg and received corticosteroid in 2001-2010 were included. Patients who were positive for antibody to HBsAg (anti-HBs) and/or to hepatitis B core antigen (anti-HBc) was defined to have previous HBV exposure. The primary endpoint was HBsAg seroreversion; secondary endpoint was hepatitis flare (alanine aminotransferase >80U/L) at one year.
RESULTS:
12,997 patients fulfilled the inclusion criteria: anti-HBs positive only (n=10,561); anti-HBc positive only (n=970); anti-HBs & anti-HBc positive (n=830) and anti-HBs & anti-HBc both negative (n=636). HBsAg seroreversion occurred in 165 patients. Patients who were anti-HBc positive only had higher risk of HBsAg seroreversion (one-year incidence 1.8%) than those negative for both anti-HBs & anti-HBc (0%; p=0.014). Patients with previous HBV exposure had similarly low risk of liver failure than unexposed subjects (1.1% vs. 0.9%). Risk of hepatitis flare started to increase in those receiving corticosteroid of peak daily dose 20-40mg (aHR 2.19, p=0.048) or >40mg (aHR 2.11, p=0.015) prednisolone equivalents even for <7 days, which was also increased for 7-28 days and >28 days (aHR 2.02-3.85; p <0.001-0.012).
CONCLUSIONS:
HBsAg-negative patients who were anti-HBc alone positive had HBsAg seroreversion rate of 1.8 % after corticosteroid therapy. The rate of liver failure was low and similar in HBV exposed and unexposed individuals (1.1% vs. 0.9 %); there were no deaths or requirement of liver transplantation.
LAY SUMMARY:
It is important to know the hepatitis B virus (HBV) status before starting corticosteroid therapy. Patients with resolved HBV infection without detectable anti-HBs, i.e. negative for HBsAg and anti-HBs but positive for anti-HBc would have increased risk of HBsAg seroreversion after corticosteroid therapy. High peak daily dose of corticosteroid >40mg prednisolone equivalents is found to increase the risk for hepatitis flare, but not HBsAg seroreversion, in patients have previous hepatitis B virus exposure, regardless of duration. Interval monitoring of liver biochemistries would be essential for the early detection of hepatitis flare in patients with past hepatitis B virus infection.