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吕素娟, 朱焕玲, 李向龙等. 二代酪氨酸激酶抑制剂治疗慢性髓细胞白血病临床疗效分析[J]. 四川大学学报（医学版）, 2016, 47(2): 287-291.
引用本文: 吕素娟, 朱焕玲, 李向龙等. 二代酪氨酸激酶抑制剂治疗慢性髓细胞白血病临床疗效分析[J]. 四川大学学报（医学版）, 2016, 47(2): 287-291.
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LYU Su-juan, ZHU Huan-ling, LI Xiang-long. et alY。. Clinical Efficacy of Second-generation Tyrosine Kinase Inhibitor in Treating Chronic Myeloid Leukemia[J]. Journal of Sichuan University (Medical Sciences), 2016, 47(2): 287-291.
Citation: LYU Su-juan, ZHU Huan-ling, LI Xiang-long. et alY。. Clinical Efficacy of Second-generation Tyrosine Kinase Inhibitor in Treating Chronic Myeloid Leukemia[J]. Journal of Sichuan University (Medical Sciences), 2016, 47(2): 287-291.
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二代酪氨酸激酶抑制剂治疗慢性髓细胞白血病临床疗效分析

Clinical Efficacy of Second-generation Tyrosine Kinase Inhibitor in Treating Chronic Myeloid Leukemia

    摘要
  • 摘要: 目的 回顾性分析二代酪氨酸激酶抑制剂 (second-generation TKI)治疗慢性髓细胞白血病(CML)的临床疗效。方法 对近十年来在我院门诊接受二代酪氨酸激酶抑制剂治疗的97例CML患者的临床资料及随访结果进行回顾性分析。其中61例患者为慢性期，26例为加速期，10例为急变期。74例患者于伊马替尼（IM）耐药或不耐受后接受二代TKI治疗，其中57例患者接受尼洛替尼（NIL）治疗，17例患者接受达沙替尼（DAS）治疗；20例患者诊断后即接受二代TKI治疗，其中19例患者接受NIL治疗，1例患者接受DAS治疗；还有3例患者接受二代TKI合并造血干细胞移植（HSCT）及化疗等治疗。治疗期间定期监测患者血液学、细胞遗传学及分子生物学反应，评价治疗反应及疗效，采用Kaplan-Meier曲线进行生存分析。 结果 随访结束时总完全血液学缓解（CHR）率、主要细胞遗传学缓解（MCyR）率、完全细胞遗传学缓解（CCyR）率和主要分子生物学缓解（MMR）率分别为97.9%、63.9%、60.0%、44.3%，其中除CHR率外，MCyR、CCyR、MMR率慢性期患者均优于进展期（加速期+急变期）患者，差异有统计学意义（ P<0.05)。患者的1年、2年、3年和5年总生存（OS）率分别为（90.6±3.0）%、（80.1±4.5）%、(77.5±5.0)%和(64.6±9.3)%；1年、2年、3年和5年无事件生存（EFS）率分别为（81.1±4.0）%、（64.4±5.3）%、(56.4±6.0)%和(46.2±8.2)%；1年、2年、3年和5年无进展生存（PFS）率分别为（87.4±3.4）%、（73.2±4.9）%、(68.9±5.5)%和(57.4±8.7)%，其中慢性期患者总OS、EFS和PFS率均优于进展期患者，差异有统计学意义（P<0.05)。二代TKI一线治疗获得CHR、MCyR、CCyR、MMR率分别是100%、95%、95%、70%，二线治疗获得的则分别是97.3%、56.8%、48.6%、36.5%，其中除CHR率外，MCyR、CCyR、MMR率一线治疗均优于二线治疗，差异有统计学意义（ P<0.05)。结论 二代TKI治疗CML疗效及预后较好，且一线较二线治疗、慢性期较进展期更能使患者明显获益。

     

    Abstract: Objective To evaluate the efficacy of second-generation tyrosine kinase inhibitor (TKI) in treating chronic myeloid leukemia (CML). Methods A total of 97 patients with CML were enrolled. The patients were treated with TKI and monitored with complete blood count, cytogenetic and molecular indicators during the course of therapy. Survival analysis was performed to evaluate its clinical efficacy. Results The treatment achieved 97.9% complete hematologic response (CHR), 63.9% major cytogenetic response (MCyR), 60.0% complete cytogenetic response (CCyR) and 44.3% major molecular response (MMR) rates. Apart from CHR, better effects were shown in those indicators during chronic phase compared with progressive phase ( P＜0.05). The 1-year, 2-year, 3-year and 5-year overall survival (OS) rate was (90.6±3.0)%, (80.1±4.5)%, (77.5±5.0)% and (64.6±9.3)%, respectively, compared with an event-free survival (EFS) rate of (81.1±4.0)%, (64.4±5.3)%, (56.4±6.0)% and (46.2±8.2)%, respectively. The patients had a 1-year, 2-year, 3-year and 5-year progession-free survival (PFS) rate of (87.4±3.4)%, (73.2±4.9)%, (68.9±5.5)% and (57.4±8.7)%, respectively. A difference between chronic phase (better results) and progressive phase ( P＜0.05) was also found in survival indicators. The first-line TKI therapy had 100% CHR, 95% MCyR, 95% CCyR and 70% MMR, compared with 97.3% CHR, 56.8% MCyR, 48.6% CCyR and 36.5% MMR for the second-line TKI therapy. Apart from CHR, the first-line therapy produced better results than the seond-line therapy ( P＜0.05) . Conclusion CML patients in chronic phase and first-line use of TKI have better outcomes.

     

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