机构地区:[1]青岛大学医学院附属医院血液内科,山东青岛266003
出 处:《临床荟萃》2014年第2期155-158,共4页Clinical Focus
摘 要:目的 探讨初治多发性骨髓瘤(multiple myeloma,MM)患者不同方案治疗前、后内皮细胞功能的变化及其意义.方法 76例MM患者随机分成两组,36例MM患者采用长春地辛加表阿霉素加地塞米松(VAD)方案治疗,40例MM患者采用沙利度胺联合VAD(T-VAD)方案治疗,应用双抗体夹心酶联免疫法(ELISA)测定MM患者治疗前及2周期治疗后血浆内皮素1(ET-1)、凝血酶调节蛋白(TM)、组织因子(TF)、血管性血友病因子(vWF)水平以及应用发色底物法检测其血浆抗凝血酶(AT)、组织型纤溶酶原激活物(t-PA)及纤溶酶原激活物抑制物1(PAI-1)的活性水平.结果 两组不同方案治疗后MM患者血浆ET-1、TM、t-PA、PAI-1水平均较治疗前明显升高;治疗后血浆TF、AT水平有明显下降;治疗前、后比较差异有统计学意义(t=2.061~3.674,P〈0.05或〈0.01);VAD方案治疗前、后血浆vWF水平变化不明显,差异无统计学意义(t=1.873,P〉0.05);T-VAD组治疗后血浆vWF水平比治疗前明显升高,差异有统计学意义(t=2.648,P〈0.05).治疗后血浆ET-1、TM、TF、vWF、PAI-1水平T-VAD组比VAD组变化更明显,分别为(20.25±6.38) ng/L vs (14.12±5.16) ng/L(P〈0.01);(39.56±9.53) μg/L vs (33.91±9.42) μg/L(P〈0.05);(12.25±7.36) ng/L vs (15.85±5.28) ng/L(P〈0.05);(157.76±35.78)% vs (138.79±45.25)%(P〈0.05);(1.02±0.34) U/L vs (0.88±0.29) U/L(P〈0.05).结论 不同方案治疗MM患者均可导致内皮细胞损伤及纤溶异常,T-VAD治疗方案影响更显著;内皮细胞损伤及纤溶异常可能是MM患者治疗过程中易于发生血栓的主要原因.Objective To observe the influences of different treatments on endothelial cells in newly diagnosed patients with multiple myeloma(MM). Methods With the methods of random grouping,76 cases of MM were divided into two groups. Forty MM patients were treated with thalidomide plus VAD (T-VAD) regimen and 36 MM patients were given VAD regimen. The blood samples were taken from the vein at different times (before and after treatment by two cycles). The markers of endothelial cells, including serum levels of endothelin-1 (ET-1), thrombomodulin(TM), tissue factor(TF),yon- Willebrand factor(vWF),activities of antithrombin(AT),tissue type plasminogen activator(t- PA) as well as plasminogen activator inhibitor-1 (PAFI) were evaluated. Results The levels of plasma ET-1, TM, t- PA and PAI-1 in the patients with MM after treatment with VAD regimen or with T-VAD regimen were increased,but the levels of AT, TF were decreased. There were significant difference in the comparison with those before receiving different treatments ( t = 2. 061-3. 674, P 〈0.05, P 〈0.01). The vWF level in VAD group was not affected by treatment. The vWF level in T-VAD group was increased by treatment. The levels of ET-1, TM,TF,vWF, PAI-1 in patients with T-VAD group after treatment showed more dramatic changes than those in VAD group, (20.25± 6.38) ng/L vs (14.12±5.16) ng/L( P 〈0.01) ;(39.56±9.53) μg/L vs (33.91±9.42) μg/L( P 〈0.05) ;(12.25±7.36) ng/Lvs (15.85±5.28) ng/L(P〈0.05);(157.76±35.78)%vs (138.79±45.25)%(P〈0.05);(1.02±0.34) U/L vs (0.88 ± 0.29) U/L ( P 〈 0.05). Conclusion The treatment with VAD or T-VAD could both result in dysfunction of endothelial cell as well as dysfibrionlysis in have more significant effect. Dysfunction of endothelial thrombosis during treatment in MM patients. MM patients,of which the treatment with T-VAD would cell and dysfibrionlysis might be the material roles of thrombosis during treatment
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