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日本慢性髓性白血病患者伊马替尼的停药。

Discontinuation of imatinib in Japanese patients with chronic myeloid leukemia.

机构信息

Department of Hematology, Nephrology, and Rheumatology, Akita University, Akita City, Akita, Japan.

出版信息

Haematologica. 2012 Jun;97(6):903-6. doi: 10.3324/haematol.2011.056853. Epub 2011 Dec 16.

Abstract

It was recently recognized that some chronic myeloid leukemia patients with a complete molecular response could sustain that response after discontinuation of imatinib. To characterize the clinical outcomes and profiles of chronic phase chronic myeloid leukemia patients who could discontinue imatinib, we conducted a nationwide survey in Japan. Among 3,242 imatinib-treated chronic myeloid leukemia patients, we identified 50 who had discontinued imatinib for at least six months; of these we analyzed 43. Molecular recurrence was detected in 19 patients, and a complete molecular response rate was estimated to be 47% following imatinib discontinuation. Based on multivariate regression analysis, imatinib dose intensity and prior interferon-α administration were independently predictive of molecular recurrence within 12 months. The depth of the molecular response should be a factor influencing long-term sustained complete molecular response after discontinuation of imatinib. Additionally, an immunological mechanism modified by interferon-α might control chronic myeloid leukemia stem cells.

摘要

最近发现,一些达到完全分子缓解的慢性髓性白血病患者在停止伊马替尼治疗后仍能维持缓解。为了明确能够停止伊马替尼治疗的慢性期慢性髓性白血病患者的临床结局和特征,我们在日本进行了一项全国性调查。在 3242 例接受伊马替尼治疗的慢性髓性白血病患者中,我们确定了 50 例至少停止伊马替尼治疗 6 个月的患者;我们对其中的 43 例进行了分析。19 例患者出现了分子学复发,停止伊马替尼治疗后完全分子学缓解率估计为 47%。基于多变量回归分析,伊马替尼剂量强度和既往干扰素-α治疗是 12 个月内分子复发的独立预测因素。分子反应的深度可能是影响伊马替尼停药后长期持续完全分子反应的一个因素。此外,干扰素-α修饰的免疫机制可能可以控制慢性髓性白血病干细胞。

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