Reversible carfilzomib-induced pulmonary arterial hypertension: don't take your eyes off the ball!

Abstract

Extract

We read with interest the recent paper by Grynblat et al. [1] reporting the onset of proteasome inhibitor (PI)-induced pulmonary arterial hypertension (PAH) in 11 patients with multiple myeloma, median 6.5 (range 0.4–46.9) months after PI treatment initiation with carfilzomib or bortezomib. All patients had elevated natriuretic peptide levels at diagnosis, when measured. At follow-up after PAH diagnosis, five patients died, mostly due to right ventricular (RV) failure rather than myeloma. In survivors, following cessation of the first PI, pulmonary pressures normalised in three patients without PAH treatment, suggesting reversible drug-induced PAH; two patients required PAH therapies in addition to PI cessation. Grynblat et al. [1] also performed a meta-analysis and a systematic VIGIBASE analysis, showing a significantly stronger signal for carfilzomib (as compared to bortezomib) regarding both dyspnoea and pulmonary hypertension (PH).