Tyrosine Kinase Inhibitor Induced Pulmonary Artery Hypertension: Reversible with Ponatinib?
Serkan Gokaslan *
Department of Cardiology, Faculty of Medicine, Afyon Kocatepe University, Afyonkarahisar, Turkey
Ersel Onrat
Department of Cardiology, Faculty of Medicine, Afyon Kocatepe University, Afyonkarahisar, Turkey
Cigdem Özer Gokaslan
Department of Radiology, Faculty of Medicine, Afyon Kocatepe University, Afyonkarahisar, Turkey.
Ibrahim Etem Dural
Department of Cardiology, Faculty of Medicine, Afyon Kocatepe University, Afyonkarahisar, Turkey
*Author to whom correspondence should be addressed.
Abstract
Pulmonary arterial hypertension (PAH) is a disease associated with progressive and comprehensive vascular remodeling of small pulmonary arteries. The prognosis of Chronic myelogenous leukemia (CML) has been improved by tyrosine kinase inhibitors (TKIs), which inhibit BCR/ABL kinase pathway. Most of the TKIs induced PAH is limited almost exclusively to dasatinib until now. There was only one report about, PAH was caused by the novel TKI ponatinib. We present a 73 years old-female patient with chronic myeloid leukemia, who had PAH after approximately 72 months with prior exposure to dasatinib. Dasatinib was replaced by nilotinib in this patient. Nilotinib was used 11 months for CML treatment, but no recovery was seen with also this TKI. Finally, ponatinib therapy was started for CML. Signs and symptoms of PAH improved with institution of ponatinib therapy. Therefore we report that the patient with dasatinib induced PAH did not recover after institution of nilotinib as a TKI instead of dasatinib but improved with ponatinib treatment using for CML.
Keywords: Chronic myelogenous leukemia (CML), Tyrosine kinase inhibitors (TKIs), Pulmonary arterial hypertension (PAH)