HBV Reactivation in an HIV-Infected Patient

A Cautionary Tale

Rajesh T. Gandhi, MD


AIDS Clinical Care 

In This Article

Abstract and Introduction


Interaction between an inhaled corticosteroid and the patient's antiretroviral regimen apparently triggered the event.


Hepatitis B virus (HBV) infection can reactivate in patients who are receiving systemic corticosteroids. Receipt of inhaled or topical steroids, which result in lower systemic levels than oral steroids, is not typically thought of as a risk factor for HBV reactivation. However, a recent case report shows that we need to rethink this assumption.

An HIV-infected man with a history of prior HBV infection that was thought to have cleared (based on a negative HBV surface antigen [HBsAg] result and positive tests for antibodies against HBV surface antigen [anti-HBs] and HBV core antigen [anti-HBc]) was hospitalized with jaundice and elevated transaminase levels. At the time of admission, he was receiving inhaled fluticasone and triamcinolone for pulmonary disease. He was also receiving a boosted protease inhibitor (PI)-containing antiretroviral regimen (abacavir + boosted lopinavir + saquinavir), although he had been intermittently nonadherent. His CD4 count was 332 cells/mm3, and his HIV RNA level was >100,000 copies/mL.

On evaluation, repeat HBV testing was consistent with reactivation (positive HBsAg result, HBV DNA level >106 copies/mL). Sequencing revealed several mutations in the HBsAg gene. Although the patient had detectable anti-HBs, it did not bind effectively to the mutated HBsAg, suggesting immune escape. After initiation of tenofovir/FTC + boosted lopinavir + enfuvirtide, HBV DNA became undetectable and transaminase levels normalized.


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