目的 探讨伊马替尼辅助重组人干扰素α-2b治疗慢性髓性白血病（CML）患者的效果。方法 将2012年9月-2016年8月选择在汉中三二〇一医院血液科治疗的CML患者90例，随机分为各45例患者的实验组与对照组，对照组给予重组人干扰素α-2b治疗，实验组在对照组治疗的基础上给予伊马替尼辅助治疗，两组都治疗观察3个月。比较两组的遗传学疗效、血液学疗效，检测血清血管内皮生长因子（VEGF）和碱性成纤维细胞生长因子（bFGF）变化情况，并随访观察两组的生存状况。结果 治疗后实验组的完全细胞遗传学缓解（CCyR）率为88.9%，对照组为75.6%，实验组显著高于对照组（P<0.05）。治疗后实验组与对照组的总有效率分别为73.3%和51.1%，实验组显著高于对照组（P<0.05）。实验组与对照组治疗后的血清VEGF和bFGF含量与治疗前对比显著降低（P<0.05），治疗后实验组也比对照组显著降低（P<0.05）。随访至今，实验组的生存期和无病生存期都显著长于对照组（P<0.05）。结论 伊马替尼辅助重组人干扰素α-2b治疗CML能抑制血清VEGF和bFGF的表达，改善血液学和遗传学疗效，故而达到延长患者生存时间的目的。

Objective To investigate the effects of recombinant human interferon α-2b combined with imatinib in the treatment of patients with chronic myeloid leukemia(CML). Methods From September 2012 to August 2016, 90 patients with CML in our hospital department of hematology for treatment were selected as the research object, all the patients were divided into experimental group and control group with 45 patients in each group accorded randomly, the control group was treated with recombinant human interferon α-2b, the experimental group was treated with recombinant human interferon α-2b combined with imatinib, two groups were treated for 3 months. Results After treatment, the incidence of CCyR in the experimental group was 88.9%, so that was 75.6% in the control group, and the observation group was higher than that of the control group (P<0.05). After treatment, the total effective rates in the experimental group and the control group were 73.3% and 51.1%, respectively, and the experimental group was higher than that of the control group (P<0.05). The serum levels of VEGF and bFGF in the experimental group and the control group after treatment were significantly lower than those before treatment (P<0.05). After treatment, the experimental group were also significantly lower than that of the control group (P<0.05). After followed-up, the survival and disease-free survival times in the experimental group were significantly higher than those of the control group (P<0.05). Conclusion The recombinant human interferon α-2b combined with imatinib in the treatment of patients with chronic myeloid leukemia can inhibit the expression of serum VEGF and bFGF, improve the hematological and genetic efficacy, and prolong the survival time.