Gunawan Arief, Harrington Patrick, Garcia-Curto Natalia, McLornan Donal, Radia Deepti, Harrison Claire
Guy's and St Thomas' NHS Foundation Trust, London, UK.
King's College Hospital NHS Foundation Trust, London, UK.
Hemasphere. 2018 Jun 12;2(4):e56. doi: 10.1097/HS9.0000000000000056. eCollection 2018 Aug.
Deregulated Janus Kinase 2 (JAK2) activation is central to the pathogenesis of most myeloproliferative neoplasms (MPNs), of which essential thrombocythemia (ET) is the most common entity. Patients with ET are risk-stratified according to their risk of thrombo-hemorrhagic complications. High-risk patients are offered treatments to reduce their platelet count using cytoreductive therapy. The disease course is often long and therapy intolerance is not infrequent. Ruxolitinib, a Janus Kinase (JAK) 1/JAK2 inhibitor, has demonstrated efficacy in patients with both myelofibrosis (MF) and polycythemia vera and is well tolerated. Side effects include predictable cytopenias and an augmented risk of infections. Ruxolitinib has been investigated in a small group of ET patients who were refractory/intolerant to hydroxycarbamide (HC) and demonstrated improvements in both symptoms and splenomegaly. Of note, a proportion of treated patients (13.2%) also had a significant reduction in platelet counts. However, these results require further validation in comparison with conventional therapy. Recently, a randomized-controlled phase 2 study (MAJIC-ET) assessed the role of Ruxolitinib in patients refractory or intolerant to HC. This study revealed that Ruxolitinib demonstrated some clinical efficacy but was only superior in terms of symptom control. In clinical practice, some individuals with ET do exhaust all potential treatment options and there may well be a role for Ruxolitinib in such patients or those with a significant symptom burden. However, in the wider context the goal of therapy with the use of JAK inhibitor therapy in ET needs to be defined carefully and we explore this within this timely review article.
Janus激酶2(JAK2)的失调激活是大多数骨髓增殖性肿瘤(MPN)发病机制的核心,其中原发性血小板增多症(ET)是最常见的类型。ET患者根据其血栓出血并发症的风险进行风险分层。高危患者接受使用细胞减灭疗法降低血小板计数的治疗。该病病程通常较长,治疗不耐受情况并不少见。芦可替尼是一种Janus激酶(JAK)1/JAK2抑制剂,已在骨髓纤维化(MF)和真性红细胞增多症患者中显示出疗效,且耐受性良好。副作用包括可预测的血细胞减少和感染风险增加。芦可替尼已在一小群对羟基脲(HC)难治/不耐受的ET患者中进行了研究,并显示出症状和脾肿大均有改善。值得注意的是,一部分接受治疗的患者(13.2%)血小板计数也显著降低。然而,与传统疗法相比,这些结果需要进一步验证。最近,一项随机对照2期研究(MAJIC-ET)评估了芦可替尼在对HC难治或不耐受的患者中的作用。该研究表明,芦可替尼显示出一些临床疗效,但仅在症状控制方面更具优势。在临床实践中,一些ET患者确实用尽了所有潜在的治疗选择,芦可替尼在这类患者或症状负担较重的患者中可能会发挥作用。然而,在更广泛的背景下,ET中使用JAK抑制剂治疗的目标需要仔细界定,我们将在这篇及时的综述文章中探讨这一点。