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系统性红斑狼疮骨髓受累机制初步研究
引用本文:付蓉,上原灯纪子,巩路,邵宗鸿.系统性红斑狼疮骨髓受累机制初步研究[J].中华血液学杂志,2008,29(1):48-51.
作者姓名:付蓉  上原灯纪子  巩路  邵宗鸿
作者单位:1. 天津医科大学总医院血液肿瘤科,300052
2. 天津医科大学总医院感染免疫科,300052
基金项目:国家自然科学基金,天津市高等学校科研项目 
摘    要:目的 初步探讨系统性红斑狼疮(SLE)骨髓受累的可能机制.方法 对21例初治SEE患者骨髓标本21份,10例正常对照骨髓标本分别进行骨髓单个核细胞(BMMNC)Coombs试验并采用甲基纤维素法检测CFU-E、CFU-GM、BFU-E产率.结果 10份正常对照骨髓标本BMMNC-Coombs试验均为阴性,21例SLE患者,有12例(57.1%)阳性,其中17例合并血细胞减少者中有10例(58.2%)阳性;4例血细胞正常者中有2例(50.0%)阳性,SLE患者BMMNC-Coombs试验阳性率显著高于正常对照组(P<0.05).而SLE合并血细胞减少组与血细胞正常组相比,阳性率差异无统计学意义(P>0.05).BMMNC抗体类型与血细胞水平无显著相关性.SLE合并血细胞减少组的CFU-E、CFU-GM产率与正常对照组相比,差异无统计学意义(P>0.05).SLE血细胞正常组CFU-E、CFU-GM产率显著高于正常对照组(P<0.05).SLE患者中,合并血细胞减少组CFU-E、CFU-GM产率显著低于血细胞正常组(P<0.05).SEE患者无论是否合并血细胞减少其BFU-E产率均显著低于正常对照组(P值均<0.05).而SLE合并血细胞减少组与血细胞正常组患者相比,其BFU-E产率差异无统计学意义(P>0.05).结论 SLE患者BMMNC膜表面被覆自身抗体;造血祖细胞增殖、分化功能无明显异常,某些SLE患者可能通过造血祖细胞的代偿增殖维持正常的血细胞水平.

关 键 词:红斑狼疮  系统性  自身抗体  骨髓  集落形成单位测定

Study on the pathogenesis of blood cytopenia in patients with systemic lupus erythematosus
FU Rong,Uehara Toukiko,GONG Lu,SHAO Zong-hong.Study on the pathogenesis of blood cytopenia in patients with systemic lupus erythematosus[J].Chinese Journal of Hematology,2008,29(1):48-51.
Authors:FU Rong  Uehara Toukiko  GONG Lu  SHAO Zong-hong
Institution:Department of Hematology, Tianjin Medical University General Hospital, Tianjin 300052, China.
Abstract:OBJECTIVE: To explore the pathogenetic mechanism of cytopenia in the patients with systemic lupus erythematosus (SLE). METHODS: Twenty-one patients with SLE and 10 healthy controls were enrolled in this study. Bone marrow mononuclear cells (BMMNC) Coombs test was used to determine the autoantibodies and in vitro CFU-E, BFU-E and CFU-GM yields were used to determine the proliferation function of hematopoietic stem/progenitor cell (HSC). RESULTS: Positive results of BMMNC-Coombs test were observed in 12 patients with SLE (57.1%), among them, 10 with (58.2%) and 2 without blood cytopenia. The yields of CFU-GM (49 +/- 40), and CFU-E (49 +/- 35) in SLE patients without cytopenia were higher than that in normal controls, but lower than that in cytopenia SLE patients. The BFU-E yield in SLE patients (3 +/- 4) was significantly lower than that in normal controls (36 +/- 12). CONCLUSION: There were auto-antibodies on BMMNC in patients with SLE. The blood cytopenia in SLE patients maybe resulted from the destructions of bone marrow hematopoietic cells by the autoantibodies. The capacities of bone marrow HSC in SLE patients for proliferation compensation of hematopoietic cell destruction were not damaged.
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