论文部分内容阅读
慢性粒细胞白血病(CML)和原发性血小板增多症(ET)皆为骨髓增生性疾病,如(Ph)缺如可否诊断为ET,意见不一。作者首次报道一例临床表型为血小板增多症,但细胞核型发现为Ph~+慢粒白血病变异体,跟沿用的探针杂交,信号弱,分子遗传学检查结果为一种罕见的BCR/ABL重排,而用沿袭的BCR/ABL探针则会导致假阴性。 病例 女,35岁,白细胞中度增高(25×10~9/L),血小板重度增高(100×10~9/L),LAP正常,而脾不肿大,染色体(Ph~+),羟基脲治疗8个月后,行去除T细胞异基因BMT,但一年后复发,继而接受供者淋巴细胞过继性免疫,获临床完全缓解,持续45个月。
Chronic myelocytic leukemia (CML) and essential thrombocythemia (ET) are all myeloproliferative diseases, and if there is a deficiency, the diagnosis of ET is not consistent. The author reported for the first time that one case of clinical phenotype was thrombocythemia, but the karyotype was found to be a variant of Ph~+ chronic myeloid leukemia, which was hybridized with the probes used. The signal was weak, and the result of molecular genetic examination was a rare BCR/ABL weight. Rows, while using the lineage of BCR/ABL probes, can lead to false negatives. Case female, 35 years old, with moderately elevated white blood cells (25 x 10-9/L), severely increased platelets (100 x 10-9/L), normal LAP, and no splenomegaly, chromosome (Ph~+), hydroxyl After 8 months of treatment with urea, allogeneic BMT was removed from the T cells, but relapsed after one year, followed by recipient donor lymphocyte adoptive immunization and complete clinical remission for 45 months.