The effect of rituximab on anti-platelet autoantibody levels in patients with immune thrombocytopenia

The effect of rituximab on anti-platelet autoantibody levels in patients with immune thrombocytopenia
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DOI:
10.1111/bjh.14664
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发表时间:
2017-07-01
影响因子:
6.5
通讯作者:
Nazy, Ishac
Nazy, Ishac
中科院分区:
医学2区
文献类型:
--
作者:
Arnold, Donald M.;Vrbensky, John R.;Nazy, Ishac

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利妥昔单抗是一种有效的治疗方法,可使60%的免疫性血小板减少症(ITP)患者的血小板计数得到改善。利妥昔单抗耗尽B细胞;因此,对于对这种治疗取得临床反应的患者,预计血小板自身抗体水平将会降低。这项研究的目的是确定利妥昔单抗是否与血小板自身抗体水平的降低有关,并将自身抗体的丧失与治疗反应的实现相关联。我们进行了一项病例对照研究,嵌套在先前的标准治疗加辅助剂利妥昔单抗或安慰剂的随机对照试验中。我们用抗原捕获试验检测了血小板结合的抗糖蛋白(GP)IIbIIIa和抗GPIbIX。在55名可评估的患者中,25名(45%)基线时有可检测到的血小板自身抗体。与安慰剂相比,利妥昔单抗与抗GPIIbIIIa水平显著降低(P=0.02)有关,但与抗GPIbIX水平无关(P=0.51)。基线时自身抗体的存在或治疗后自身抗体的丧失与利妥昔单抗的反应无关。持续自身抗体的患者在治疗后未能实现血小板计数反应,这表明血小板自身抗体的持续存在可以作为疾病严重程度的标志。
Rituximab is an effective therapy resulting in a platelet count improvement in 60% of patients with immune thrombocytopenia (ITP). Rituximab depletes B cells; thus, a reduction in platelet autoantibody levels would be anticipated in patients who achieve a clinical response to this treatment. The objectives of this study were to determine whether rituximab was associated with a reduction in platelet autoantibody levels, and to correlate the loss of autoantibodies with the achievement of a treatment response. We performed a case-control study nested within a previous randomized controlled trial of standard therapy plus adjuvant rituximab or placebo. We measured platelet-bound anti-glycoprotein (GP) IIbIIIa and anti-GPIbIX using the antigen capture test. Of 55 evaluable patients, 25 (45%) had a detectable platelet autoantibody at baseline. Rituximab was associated with a significant reduction in anti-GPIIbIIIa levels (P = 0.02) but not anti-GPIbIX levels (P = 0.51) compared with placebo. Neither the presence of an autoantibody at baseline nor the loss of the autoantibody after treatment was associated with a response to rituximab. The subset of patients with persistent autoantibodies after treatment failed to achieve a platelet count response, suggesting that persistence of platelet autoantibodies can be a marker of disease severity.