Medizinische Klinik und Poliklinik, Klinikum rechts der Isar, Technische Universität München, Germany.
Dtsch Arztebl Int. 2010 Feb;107(7):114-21. doi: 10.3238/arztebl.2010.0114. Epub 2010 Feb 19.
The treatment options for bcr-abl positive chronic myelogenous leukemia (CML) include chemotherapy, immune therapy, allogeneic stem cell transplantation, and molecular therapy. The tyrosine kinase inhibitor imatinib was approved for the treatment of CML in 2002. Data from clinical trials allow a comparison of treatment options.
The literature on the treatment and monitoring of CML was selectively reviewed. A total of 94 original articles were analyzed, along with the recommendations of an international expert committee and the medical societies. This review is current as of November 2009.
In a clinical phase 3 trial of imatinib treatment for patients in the chronic phase of CML, the rates of progression-free and overall survival at 6 years were 93% and 88%, respectively. Thus, imatinib is clearly superior to interferon-alpha, hydroxyurea, and busulfan with respect to survival. Allogeneic stem-cell transplantation is only a fall back option because of transplantation-associated mortality. One in four patients in the chronic phase of CML has an inadequate cytogenetic response to imatinib and therefore requires a change of treatment. Most imatinib-resistant patients in the chronic phase of CML go into remission again after switching to one of the new tyrosine kinase inhibitors, dasatinib and nilotinib.
Imatinib is now the standard initial first-line treatment for CML in the chronic phase. Regular hematologic and cytogenetic monitoring during treatment is indispensable so that patients with an inadequate response can be identified.
治疗 bcr-abl 阳性慢性髓性白血病(CML)的选择包括化疗、免疫治疗、异基因造血干细胞移植和分子治疗。酪氨酸激酶抑制剂伊马替尼于 2002 年获准用于 CML 的治疗。临床试验数据允许对治疗选择进行比较。
对 CML 的治疗和监测文献进行了选择性回顾。共分析了 94 篇原始文章,以及国际专家委员会和医学协会的建议。本综述截至 2009 年 11 月仍为最新资料。
在伊马替尼治疗 CML 慢性期患者的一项临床 3 期试验中,6 年时无进展生存率和总生存率分别为 93%和 88%。因此,伊马替尼在生存方面明显优于干扰素-α、羟基脲和白消安。异基因造血干细胞移植仅作为移植相关死亡率的后备选择。在 CML 慢性期的四分之一患者中,伊马替尼的细胞遗传学反应不足,因此需要改变治疗方案。大多数 CML 慢性期的伊马替尼耐药患者在改用新型酪氨酸激酶抑制剂达沙替尼和尼罗替尼后再次缓解。
伊马替尼目前是 CML 慢性期的标准初始一线治疗。治疗期间定期进行血液学和细胞遗传学监测对于识别反应不足的患者是不可或缺的。