机构地区:[1]解放军海军总医院血液科,北京100048 [2]北京大学人民医院血液科北京大学血液病研究所,100044
出 处:《白血病.淋巴瘤》2016年第4期203-207,共5页Journal of Leukemia & Lymphoma
摘 要:目的探讨低剂量化疗联合酪氨酸激酶抑制剂(TKI)作为初诊费城染色体阳性急性淋巴细胞白血病(Ph+ALL)一线诱导治疗方案的可行性。方法回顾性分析61例初诊Ph+ALL患者接受不同诱导治疗方案的疗效与不良反应。结果全部患者初次诱导治疗的完全缓解(CR)率为73.8%(45/61),再次诱导CR率为86.7%(13/15),两程诱导治疗总的CR率为95.1%(58/61),治疗相关死亡1例(1.6%)。无论是否联用TKI,常规剂量组与低剂量组有效率差异无统计学意义[未联用组:65.5%(19/29)比60.0%(3/5),P=0.812;联用组:90.5%(19/21)比100.0%(6/6),P=0.432];低剂量化疗联合TKI的有效率与单用常规剂量化疗比较,差异亦无统计学意义(P=0.089)。无论化疗强度如何,联合TKI均能提高初次诱导治疗有效率(常规剂量组:P=0.041;低剂量组:P=0.087);联用TKI方案总有效率显著高于未联用TKI方案[92.6%(25/27)比64.7%(22/34),P=0.010]。对于未获CR患者,初次诱导时未联用TKI者再次诱导治疗联用TKI的有效率明显高于初次诱导曾联用TKI者[100.0%(8/8)比33.3%(1/3),P=0.011]。不同遗传学亚组问初次诱导治疗的有效率差异无统计学意义(均P〉0.05),联用TKI可在一定程度上提高有效率,但差异均无统计学意义(均P〉0.05)。全部患者初次诱导治疗的感染率为50.8%(31/61),出血发生率为4.9%(3/61)。常规剂量组总感染率[56.0%(28/50)]高于低剂量组[27.3%(3/11)],但差异无统计学意义(P=0.084),两组总出血发生率差异亦无统计学意义[6.0%(3/50)比0(0/11),P:0.405]。低剂量化疗联合TKI组的感染率低于常规剂量化疗联合TKI组[0(0/6)比71.4%(15/21),P=0.002],也低于单用常规剂量化疗组[0(0�Objective To explore the feasibility of low-dose chemotherapy (LDCT) combined with tyrosine kinase inhibitor (TKI) (LDCT+TKI regimen) as the first-line induction regimen for Philadelphia chromosome-positive acute lymphoblastie leukemia (Ph^-ALL). Methods The efficacies and adverse effects of various induction regimens in 61 newly diagnosed patients with Ph* ALL were retrospectively analyzed. Results The complete remission (CR) rate of the first induction therapy was 73.8 % (45/61) for all 61 cases, and that of the second induction therapy was 86.7 % (13/15) for non-remission (NR) patients after the first induction. The total CR rate for two-course induction was 95.1% (58/61). Treatment related mortality happened in one case (1.6 %) after the first induction therapy. The response rates between conventional-dose chemotherapy (CDCT)+TKI group and LDCT-+TKI group were not statistically different [without TKI, 65.5 % (19/29) vs 60.0 %(3/5), P = 0.812; with TKI, 90.5 % (19/21) vs 100.0 % (6/6), P = 0.432]. The response rate of LDCT+TK1 group was not statistically different from that of CDCT alone group (P = 0.089). The introduction of TKI to LDCT and CDCT could improve the response rate (CDCT+TKI group, P = 0.041; LDCT+TKI group, P = 0.087). The total response rate of the induction therapy with TKI was significantly higher than that without TKI [92.6 % (25/27) vs 64.7 % (22/34), P = 0.01]. The response rate of the TKI-based second induction therapy for non-CR eases after the first induction therapy without TKI was significantly higher than that after the first induction therapy with TKI [100.0 % (8/8) vs 33.3 % (1/3), P = 0.011]. There were no significant differences in the effieaeies of the first induction therapy between various genetic subgroups (all P 〉 0.05), and the introduction of TKI to the treatment of various genetic subgroups could improve the efficaeies to a certain extent without statistical significance
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