沙利度胺治疗急性白血病的疗效及对血管调控因子水平的影响

目的 观察沙利度胺联合化疗治疗急性白血病的临床疗效及其对血浆血管内皮生长因子(VEGF)、血管内皮生长因子受体(VEGFR)、碱性成纤维细胞生长因子(bFGF)水平的影响.方法 急性白血病患者36例,随机分为试验组及对照组各18例.每组均予以常规化疗方案标准剂量化疗,试验组同时口服沙利度胺100 mg/d.治疗前及治疗后8周分别采集外周血,双抗体夹心酶联免疫吸附法(ELISA)检测血浆VEGF、VEGFR、bFGF含量.以15位健康体检者为健康对照组.结果 试验组与对照组有效率分别为88.9%(16/18)和77.8%(14/18),差异有统计学意义(x2=4.103,P＜0.05).试验组与对照组治疗前血浆VEGF水平分别为(389.78±249.94)和(318.54±125.78)pg/ml,高于健康组的(132.91±26.66)pg/ml(t=3.141、3.024,均P＜0.01);治疗后分别为(211.74±36.72)和(288.02±31.77)pg/ml,高于健康组(t=2.413、2.324,均P＜0.05);试验组与对照组治疗前VEGF差异无统计学意义(t=1.384,P＞0.05),治疗后差异有统计学意义(t=2.793,P＜0.05).试验组与对照组治疗前血浆VEGFR水平分别为(2490.75±1695.9)和(2322.78±1105.87)pg/ml,高于健康组的(1134.98±378.45)pg/ml(t=2.914、2.783,均P＜0.01);治疗后分别为(1359.71±390.24)和(1753.89±337.04)pg/ml,与健康组相比差异有统计学意义(t=2.572、2.447,均P＜0.05);试验组与对照组治疗前VEGFR差异无统计学意义(t=1.276,P＞0.05),治疗后差异有统计学意义(t=2.486,P＜0.05).试验组与对照组治疗前血浆bFGF水平分别为(2.43±0.27)和(2.4l±0.33)ng/ml,高于健康组的(1.83±0.44)ng/ml(t=4.982、4.171,均P＜0.05);治疗后分别为(2.09±0.17)和(2.11±0.31)ng/ml,与健康组相比差异有统计学意义(t=3.01l、2.773,均P＜0.05);试验组与对照组治疗前及治疗后相比差异无统计学意义(t=0.953、1.282,均P＞0.05).结论 沙利度胺联合化疗可提高急性白血病患者的缓解率,有可能成为一种通过抗血管新生从而抑制白血病细胞生长及浸润的有效治疗方法.

Treatment effect and influence on the level of angiogenesis-associated factors in acute leukemia treated by thalidomide

Objective To observe on the clinical effect and the influence of the level of plasma vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor (VEGFR) and basic fibroblast growth factor (bFGF) in acute leukemia before and after treatment by thalidomide combined with chemotherapy. Methods Thirty-six cases of acute leukemia patients were randomly divided into experimental group and control group by 18 cases each. Each group was treated with conventional chemotherapy in the standard-dose, meanwhile in the experimental group additional thalidomide 100 mg/day were taken orally. Before treatment and 8 weeks after treatment, plasma were collected for the detection of VEGF, VEGFR and bFGF content by double antibody sandwich enzyme-linked immunosorbent assay (ELISA).Results The ratio of experimental group and control group, were 88.9 % (16/18), 77.8 % (14/18)respectively and the difference was statistically significant (x2 =4.103, P ＜0.05). The level of plasma VEGF (389.78+249.94 pg/ml, 318.54±125.78 pg/ml) of experimental group and control group before treatment was statistically significant (t = 3.141, t =3.024, P ＜0.01) compared with healthy group (132.91±26.66) pg/ml] respectively. The level of plasma VEGF of those groups after treatment (211.74+36.72) pg/ml, (288.02±31.77) pg/ml] was statistically significant (t =2.413, t =2.324, P ＜0.05) compared with healthy group respectively. The difference of the level of plasma VEGF of experimental group and control group before treatment was not statistically significant (t =1.384, P ＞0.05). The difference of the level of plasma VEGF of experimental group and control group after treatment was statistically significant(t =2.793,P ＜0.05). The level of plasma VEGFR (2490.75+1695.9) pg/ml, (2322.78+1105.87) pg/ml] of experimental group and control group before treatment was statistically significant (t =2.914, t =2.783, P ＜0.01) compared with healthy group (1134.98+378.45) pg/ml] respectively. The level of plasma VEGFR of those groups after treatment (1359.71± 390.24) pg/ml, (1753.89±337.04) pg/ml] was statistically significant(t =2.572, t =2.447, P ＜0.05) compared with healthy group respectively. The difference of the level of plasma VEGFR of experimental group and control group before treatment was not statistically significant (t =1.276, P ＞0.05). The difference of the level of plasma VEGFR of experimental group and control group after treatment was statistically significant (t = 2.486, P ＜0.05). The level of plasma bFGF (2.43±0.27) ng/ml, (2.41±0.33) ng/ml] of experimental group and control group before treatment was statistically significant(t =4.982, t =4.171, P ＜0.05) compared with healthy group (1.83±0.44) ng/ml respectively; the level of plasma bFGF of those groups after treatment (2.09±0.17) ng/ml,(2.11±0.31) ng/ml] was statistically significant (t =3.011, t =2.773, P ＜0.05) compared with healthy group respectively. The difference of the level of plasma bFGF of experimental group and control group before treatment was not statistically significant (t =0.953, P ＞0.05). The difference of the level of plasma bFGF of experimental group and control group after treatment was not statistically significant (t =1.282, P ＞0.05).Conclusion The remission rate could be improved by thalidomide combined with chemotherapy in acute leukemia, which could be an effective treatment by anti-angiogenesis and inhibiting the growth and infiltration of acute leukemia cells.