Ann Hematol DOI 10.1007/s00277-013-1936-5
LETTER TO THE EDITOR
Hepatitis B virus reactivation associated with ruxolitinib Chien-Heng Shen & Cih-En Hwang & Yi-Yang Chen & Chih-Cheng Chen
Received: 4 October 2013 / Accepted: 8 October 2013 # Springer-Verlag Berlin Heidelberg 2013
Dear Editor, Ruxolitinib, a potent inhibitor of Janus kinases (JAKs) 1 and 2, is an effective therapy for patients with myelofibrosis (MF) by reducing spleen size, ameliorating debilitating symptoms, and improving overall survival [1, 2]. The reported incidence of treatment-associated hepatotoxicity was low [1, 2]. Herein, we describe a patient who experienced hepatitis B virus (HBV) reactivation during extended treatment with ruxolitinib. A 72-year-old man with a 7-year long history of essential thrombocythemia (ET) presented with progressive debilitating constitutional symptoms and painful splenomegaly. He has been a known carrier of HBV for decades. Post-ET MF was confirmed, and treatment with ruxolitinib commenced at the dose of 40 mg per day shortly afterwards. He had an excellent response with complete resolution of symptoms and significant reduction of spleen size while reporting minimal clinical side effects. About 8 months after start of therapy, his serum levels of transaminases rose [alanine aminotransferase (ALT), 179 U/ L; aspartate aminotransferase (AST), 136 U/L]. This was initially considered as drug-related hepatotoxicity, and an approach of step-wise reduction of ruxolitinib dosage was taken to avoid cytokine rebound phenomenon. However, with ruxolitinib at the maintenance dose of 10 mg twice a day, the levels of ALT and AST kept rising (291 and 185 U/ L, respectively), which prompted us to discontinue the medication gradually (Fig. 1). The serum levels of both C.
LETTER TO THE EDITOR
Hepatitis B virus reactivation associated with ruxolitinib Chien-Heng Shen & Cih-En Hwang & Yi-Yang Chen & Chih-Cheng Chen
Received: 4 October 2013 / Accepted: 8 October 2013 # Springer-Verlag Berlin Heidelberg 2013
Dear Editor, Ruxolitinib, a potent inhibitor of Janus kinases (JAKs) 1 and 2, is an effective therapy for patients with myelofibrosis (MF) by reducing spleen size, ameliorating debilitating symptoms, and improving overall survival [1, 2]. The reported incidence of treatment-associated hepatotoxicity was low [1, 2]. Herein, we describe a patient who experienced hepatitis B virus (HBV) reactivation during extended treatment with ruxolitinib. A 72-year-old man with a 7-year long history of essential thrombocythemia (ET) presented with progressive debilitating constitutional symptoms and painful splenomegaly. He has been a known carrier of HBV for decades. Post-ET MF was confirmed, and treatment with ruxolitinib commenced at the dose of 40 mg per day shortly afterwards. He had an excellent response with complete resolution of symptoms and significant reduction of spleen size while reporting minimal clinical side effects. About 8 months after start of therapy, his serum levels of transaminases rose [alanine aminotransferase (ALT), 179 U/ L; aspartate aminotransferase (AST), 136 U/L]. This was initially considered as drug-related hepatotoxicity, and an approach of step-wise reduction of ruxolitinib dosage was taken to avoid cytokine rebound phenomenon. However, with ruxolitinib at the maintenance dose of 10 mg twice a day, the levels of ALT and AST kept rising (291 and 185 U/ L, respectively), which prompted us to discontinue the medication gradually (Fig. 1). The serum levels of both C.
