Severe exacerbation of chronic hepatitis B viral infection due to Cushing's disease

Introduction: Exacerbation of chronic hepatitis B viral infection may be observed spontaneously or more common after iatrogenic immunosuppression either due to chemotherapy or due to chronic administration of immunosuppressive drugs such as corticosteroids. In the pre-HAART era, exacerbation of HBV infection was also observed in patients with deteriorating CD4 cells. However, acquired endogenous immunosuppression due to elevated cortisol excretion is rarely observed.

Case: We present a patient with severe exacerbation of HBV infection due to Cushing's disease. A 55 years-old woman presented to our outpatient department with moon face, buffalo hump, proximal muscle wasting of the limbs and striae. Endocrinological screening revealed significant hypercortisolism and a severe cholestatic liver disease with a maximum γ-GT of 5118U/l and only moderately increased ALT activities (maximum 258U/l). Serum bilirubin was elevated up to 3.3mg/dl. HBV viral load was 76 000 IU/l.

Percutaneous liver biopsy showed a chronic hepatitis with only a mild fibrosis (stage I) but active inflammation (grade 3). Oral entecavir therapy was initiated at a dose of 0.5mg per day. Bilirubin and ALT levels as well as viral load declined rapidly under therapy.

The patient was referred to bilateral adrenalectomy and readmitted to our clinic after surgery. Meanwhile transaminase levels as well as bilirubin normalized but γ-GT is still elevated.

Discussion: Whereas reactivation and exacerbation of chronic HBV infection is frequent in patients under iatrogenic immunosuppression, exacerbation due to intrinsic hypercortisolism has been reported only once in a patient that developed massive liver necrosis. To our knowledge our case is the first to present with a cholestatic course of exacerbated chronic HBV infection in the setting of Cushing's disease and the first to demonstrate that anti-viral therapy is effective even under ongoing endogeneous cortisol excess.