Case report demonstrates drug-induced pulmonary arterial hypertension in a leukaemia patient receiving ponatinib, indicating a potential adverse class effect across tyrosine kinase inhibitors.
Over 50 drugs, including anorexigens, abused substances and recently the tyrosine kinase inhibitor (TKI) dasatinib, have been temporally and/or mechanistically related to the development of pulmonary arterial hypertension (PAH) in humans (where the evidence base for causality is wide ranging) and in animal models [1–3]. The TKIs imatinib, dasatinib, nilotinib and bosutinib are available to treat chronic myelogenous leukaemia (CML) and acute lymphoblastic leukaemia. These drugs are associated with distinctive respiratory adverse effects (AEs), including pleural and/or pericardial effusion, PAH (an AE so far almost exclusively restricted to dasatinib) and pulmonary infiltrates [1, 4–6]. The novel TKI ponatinib is prescribed for the same indications as above, in patients whose haematological malignancy has become resistant to, or who develop intolerance to the earlier TKIs [7]. Here, we present a female CML patient with prior exposure to dasatinib who developed PAH 6 months into ponatinib therapy, an association that has not previously been reported. Signs and symptoms of PAH improved following drug discontinuation and institution of targeted anti-PAH therapy. A case of pulmonary hypertension associated with ponatinib therapy in a chronic myelogenous leukaemia patient <http://ow.ly/V8reI> We thank Jean-Christophe Eicher (Dept of Cardiology, CHU de Bourgogne, Dijon, France), who performed the right heart catheterisation, and Philip Bastable (UFR Médecine, Université de Bourgogne, Dijon, France) for his help.
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Quilot et al. (2016) studied this question.
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