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).

我们饶有兴趣地阅读了 Grynblat等人 [1] 最近的论文，该论文报道了 11 名多发性骨髓瘤患者蛋白酶体抑制剂 （PI） 诱导的肺动脉高压 （PAH） 的发作，中位时间为卡非佐米或硼替佐米 PI 治疗开始后 6.5 个月（范围 0.4-46.9）。测量时，所有患者在诊断时利钠肽水平均升高。在 PAH 诊断后的随访中，5 例患者死亡，主要死于右心室 （RV） 衰竭，而不是骨髓瘤。在幸存者中，在停止第一个 PI 后，3 例未接受 PAH 治疗的患者肺动脉压恢复正常，表明存在可逆的药物诱导的 PAH;2 例患者除了停止 PI 外，还需要 PAH 治疗。Grynblat等 [1] 还进行了一项荟萃分析和系统 VIGIBASE 分析，显示卡非佐米 （与硼替佐米相比） 在呼吸困难和肺动脉高压 （PH） 方面的信号明显更强。