Maeda T, Ashie T, Kikuiri K, Ishiyama N, Takakura M
Rinsho Ketsueki. 1989 Jul;30(7):1032-6.
A 32-year-old female was diagnosed as having Ph1-positive chronic myelocytic leukemia (CML) on March 6, 1985. She was intermittently treated with busulfan or 6-mercaptopurine. Her regimen was changed on February 27, 1987 to interferon-alpha (HLBI, Sumitomo) because of leukocytosis (46,200/microliters) with basophilia (45%) and splenomegaly refractory to conventional therapy. She was admitted to our hospital on November 27, 1987 because of blastic crisis. Cytogenetic analysis on peripheral cells was repeated six times during the treatment with HLBI. The sixth analysis was done on bone marrow cells as well. Nineteen to 22 metaphases were analyzed by the trypsin G-banding method after short-term culture. Cytogenetic analysis of peripheral cells revealed 46, XX, Ph1 in 9% of metaphases and 47, XX, Ph1, +8, i(17q) in 91% on March 2, 1987, and 47, XX, Ph1, +8, i(17q) in 95.2% of metaphases and 48, XX, Ph1, +8, i(17q), +19 in 4.8% on December 11, 1987. Karyotypes of bone marrow cells on December 11, 1987 were 48, XX, Ph1, +8, +8, 4(17q) in 73.7% of metaphases and 47, XX, Ph1, +8, i(17q) in 26.3%. It was speculated that abnormal clones might have developed in other sites than bone marrow.
一名32岁女性于1985年3月6日被诊断为Ph1阳性慢性粒细胞白血病(CML)。她曾间断接受白消安或6-巯基嘌呤治疗。由于白细胞增多(46,200/微升)伴嗜碱性粒细胞增多(45%)且脾脏肿大对传统治疗无效,其治疗方案于1987年2月27日改为α-干扰素(HLBI,住友制药)。1987年11月27日,她因急变期入住我院。在使用HLBI治疗期间,对外周血细胞进行了6次细胞遗传学分析。第6次分析也对骨髓细胞进行了。短期培养后,用胰蛋白酶G显带法分析了19至22个中期细胞。外周血细胞的细胞遗传学分析显示,1987年3月2日,9%的中期细胞为46, XX, Ph1,91%为47, XX, Ph1, +8, i(17q);1987年12月11日,95.2%的中期细胞为47, XX, Ph1, +8, i(17q),4.8%为48, XX, Ph1, +8, i(17q), +19。1987年12月11日骨髓细胞的核型为,73.7%的中期细胞为48, XX, Ph1, +8, +8, 4(17q),26.3%为47, XX, Ph1, +8, i(17q)。推测异常克隆可能在骨髓以外的其他部位形成。