Vol 4, No 1 (2013)
Case report
Published online: 2013-04-10
Reversible pulmonary arterial hypertension as a complication of dasatinib treatment, with effi cacious and safe continuation of chronic myeloid leukaemia therapy with nilotinib
Hematologia 2013;4(1):76-83.
Abstract
Tyrosine kinase inhibitors, such as dasatinib, are used in the treatment of chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) associated with the Philadelphia chromosome.
Recently however, dasatinib-related pulmonary arterial hypertension (PAH) has been described, which is a rarely arising side effect, and in most cases reversible after discontinuating the dasatnib therapy. A case study is presented of a 39-year-old woman in whom CML was diagnosed in 2005. Therapy had been started with hydroxyurea and continued for 4 months, followed by treatment with imatinib that continued on for 60 months. Due to resistance, imatinib was then
replaced by dasatinib. Following 3 years treatment, the patient presented with dyspnoea after performing physical effort, where lymphocyte-predominant pleural effusions together with pulmonary
artery hypertension were detected. When secondary causes of PAH had been excluded, a diagnosis of dasatinib-related PAH was made. The dasatinib was therefore discontinued and the patient received
nilotinib therapy for treating CML and sildenafi l therapy for the PAH. The latter treatment was however halted after 1.5 years, as by then the PAH symptoms had been resolved; this having been confi rmed after 4 weeks, where normal pulmonary artery pressure (PAP) was observed during rest and on exertion following heart catheterization. A major molecular response of the CML was thus achieved using the nilotinib treatment without increasing PAP.
Recently however, dasatinib-related pulmonary arterial hypertension (PAH) has been described, which is a rarely arising side effect, and in most cases reversible after discontinuating the dasatnib therapy. A case study is presented of a 39-year-old woman in whom CML was diagnosed in 2005. Therapy had been started with hydroxyurea and continued for 4 months, followed by treatment with imatinib that continued on for 60 months. Due to resistance, imatinib was then
replaced by dasatinib. Following 3 years treatment, the patient presented with dyspnoea after performing physical effort, where lymphocyte-predominant pleural effusions together with pulmonary
artery hypertension were detected. When secondary causes of PAH had been excluded, a diagnosis of dasatinib-related PAH was made. The dasatinib was therefore discontinued and the patient received
nilotinib therapy for treating CML and sildenafi l therapy for the PAH. The latter treatment was however halted after 1.5 years, as by then the PAH symptoms had been resolved; this having been confi rmed after 4 weeks, where normal pulmonary artery pressure (PAP) was observed during rest and on exertion following heart catheterization. A major molecular response of the CML was thus achieved using the nilotinib treatment without increasing PAP.
Keywords: pulmonary arterial hypertensionchronic myeloid leukemiadasatinibnilotinibtyrosine kinase inhibitorssildenafil