阿托伐他汀联合N-乙酰半胱氨酸治疗糖皮质激素抵抗型免疫性血小板减少症的效果

Effect of atorvastatin combined with N-acetylcysteine on glucocorticoid resistant immune thrombocytopenia

目的探讨阿托伐他汀和N-乙酰半胱氨酸治疗糖皮质激素抵抗型免疫性血小板减少症(ITP)患者的效果。方法选取2017年10月至2019年2月兴化市人民医院血液科根据国际工作组(IWG)确诊为糖皮质激素耐药或抵抗ITP患者21例(抵抗组),同时选取与之相对应糖皮质激素敏感型ITP患者21例作为对照(敏感组)。采用流式细胞术检测以上各组患者骨髓内皮细胞(BMEPCs)变化、血小板计数变化、肝功能变化。结果糖皮质激素耐药或抵抗ITP患者经过治疗后总体反应率明显升高,血小板数量明显升高,肝功能未见明显异常,敏感组、抵抗组治疗前、抵抗组治疗后BMEPCs比例分别为0.12%±0.04%、0.02%±0.003%、0.13%±0.05%。敏感组与抵抗组治疗前比较及抵抗组治疗前后比较,差异均有统计学意义(P均<0.05)。结论骨髓内皮祖细胞数量减低在激素无效型ITP发病机制中起到重要作用,阿托伐他汀联合N-乙酰半胱氨酸在糖皮质激素抵抗患者治疗过程中明显有效,为糖皮质激素抵抗型ITP患者提供新的治疗方法。

Objective To investigate the effect of atorvastatin and N-acetyl-L-cysteine on patients with glucocorticosteroid-resistant ITP.Methods From October 2017 to December 2019,21 patients diagnosed with glucocorticosteroid-resistant ITP in our department according to the International Working Group IWG were selected as the resistant group.Meanwhile,the 21 patients with glucocorticoid sensitive ITP were selected as the sensitive group.Using flow cytometry to detect the above groups of patients with bone marrow endothelial cells(BMEPCs),platelet count change,liver function changes.Results After treatment,the overall response rate of patients with glucocorticosteroid-resistant ITP was significantly increased,the number of BMEPCs was significantly increased,and there was no significant abnormality in liver function.The proportion of BMEPCs in the sensitive group,the resistant group before and after treatment was 0.12%±0.04%,0.02%±0.003%,and 0.13%±0.05%,respectively.There were significant differences between the two groups before treatment,and between the resistant group before and after treatment(P<0.05).Conclusions The decrease in the number of bone marrow endothelial progenitor cells plays an important role in the pathogenesis of glucocorticosteroid-resistant ITP.Atorvastatin combined with N-acetyl-L-cysteine is significantly effective on patients with glucocorticosteroid resistance,providing a new treatment method for patients with glucocorticosteroid-resistant ITP.