慢性粒细胞白血病急粒变与急淋变骨髓细胞形态学、免疫表型、细胞遗传学特征及预后差异分析

本研究旨在观察慢性粒细胞白血病（c池）急粒变及急淋变患者骨髓细胞形态学、免疫表型、细胞遗传学特征及预后差异，为分层诊治和预后判断提供实验学基础。回顾性分析西安交通大学医学院第一附属医院血液内科2009年1月-2014年1月期间收治的31例CML急变期临床资料，其中24例急粒变及7例急淋变，对患者外周血及骨髓原始细胞比例、嗜酸及嗜碱细胞百分比、免疫分型、细胞遗传学特征及预后进行差异分析。结果表明，CML急粒变患者外周血及骨髓原始细胞比例无明显差别，在外周血及骨髓中易见嗜酸及嗜碱细胞。慢性粒细胞白血病急淋变患者骨髓原始细胞比例高于外周血，且外周血及骨髓中嗜酸及嗜碱细胞少见。7例CML急淋变患者均为B系ALL，均表达CD10、CD19、CD34、nA—DR，淋系积分≥1．5分；2例同时伴髓系CD13及CD33表达，髓系积分均为1分。24例慢粒急粒变患者主要表达CD33、CD13、CD38、CD34、CD11b及HLA-DR，髓系积分≥2分，其中2例伴淋系积分别为0．5、1分。31例CML患者初诊时检测Ph染色体100％阳性，其中CML急粒变患者有3例同时检出其它染色体畸变。CML急粒变及急淋变患者总生存率无明显差异，但应用酪氨酸激酶抑制剂治疗者的总生存率高于未用酪氨酸激酶抑制剂治疗者。结论：CML急淋变患者外周血嗜酸及嗜碱细胞较CML急粒变患者少见，B系ALL多见，主要表达cD10及cD19；CML急粒变患者主要表达CD33、CD／3、CD38、CD34、CD11b及HLA-DR；慢粒急变期患者均可伴有其他系抗原表达，但一般积分小于2；CML急粒变患者常伴有Ph染色体以外的畸变；CML急粒及急淋变患者总生存率无明显差异，但应用酪氨酸激酶抑制剂治疗者总生存率优于未用酪氨酸激酶抑制剂者。

Differential Analysis of BM Cell Morphology,Immunophenotypic, Cytogenetic Characters and Prognosis between Myeloblasitic and Lymphoblastic Crisis of CML

This study was purposed to investigate the difference of morphology, immunophenotype, cytogenetic features and prognosis between myeloid blast crisis and lymphoid blast crisis of chronic myelogenous leukemia（CML）. A total of 31 patients with CML in blastic crisis in Department of Hematology, the First Affiliated Hospital of Xi＇an Jiaotong University school of Medicine from 2009 January to 2014 January were enrolled in this study. Out of 31 CML patients, 24 cases were patients with myeloid blast crisis and other 7 cases were patients with lymphoblastic crisis. The clinical data, blast cell percentage in peripheral blood and bone marrow, eosinophil and basophil percentage, immunophenotype, cytogenetic characteristics and prognosis were analyzed. The results indicated that there was no significant difference of blastic cell percentage in peripheral blood and bone marrow of CML with myeloid blast crisis, and the eosinophil and basophil cells could be easily detected. The ratio Of blastic cells in BM was higher than that in PB in lymphoid blastic crisis of CML, eosinophil and basophil cells were rare. 7 cases of CML with lymphoid blastic crisis were B ALL with CD10, CD19, CD34, HLA-DR expression, and 2 cases with CD13 and CD33 expression. The lym-phoid score was in all CML patients with lymphoid blastic crisis was greater than or equal to 1.5;and 2 patients with CD13 and CD33 expression, and with 1 myeloid score. 24 cases of myeloid blastic crisis of CML patients mainly expressed CD33, CD13, CD38, CD34, CDllb and HLA-DR, and their myeloid score greater than or equal to 2, among them the lymphoid scores of 2 patients were 0.5 and 1 score, respectively. All the 31 patients showed 100% Ph＋ chromosome, among them 3 cases also showed other new chromosome aberrations. There was no significant difference of overall survival rate between lymphoid and myeloid blastic crisis of CML, but the overall survival rate of patients treated with tyrosine kinase inhibitor （TKI） was higher than that in the patients without TKI treatment. It is concluded that eosinophil and basophil cells in paripheral blood of lymphoid blastic crisis were less than that of CML patients with myeloid blastic crisis. Lymphoid blastic crisis of CML patients occurred mostly in B ALL cases with expression of CD10 and CD19. Patients with myeloid blastic crisis of CML mainly expressed CD33, CD13, CD38, CD34, CDllb and HLA-DR, and could be accompanied by other lineage antigen expression, but the score was less than 2. New chromosome aberration is easily observed in myeloid blastic crisis of CML. There is no significant difference of overall survival rate of between CML patients with lymphoid and myeloid blastic crisis, but the overall survival rate of patients treated with TKI is higher than the patients without TKI treatment.