Tsimberidou Apostolia M, Colburn Dawn E, Welch Mary Alma, Cortes Jorge E, Verstovsek Srdan, O'Brien Susan M, Albitar Maher, Kantarjian Hagop M, Giles Francis J
Department of Leukemia, The University of Texas, M.D. Anderson Cancer Center, 1400 Holcombe Boulevard, Houston, TX 77030, USA.
Cancer Chemother Pharmacol. 2003 Sep;52(3):229-34. doi: 10.1007/s00280-003-0651-7. Epub 2003 May 29.
The tyrosine kinase inhibitor imatinib mesylate inhibits the function of the Bcr-Abl oncoprotein associated with Philadelphia-positive chronic myelogenous leukemia (CML). Anagrelide suppresses megakaryocyte proliferation and differentiation. The objectives of this study were to investigate the feasibility and safety of imatinib mesylate and anagrelide combination therapy in patients with Ph-positive CML or chronic myeloproliferative disorders (MPD) with persistent thrombocythemia.
This study was a retrospective review of all available records of patients with chronic MPD presenting to the M.D. Anderson Cancer Center between October 1998 and May 2002, treated with imatinib mesylate combined with anagrelide.
Of 22 patients identified, 18 had Ph-positive CML (chronic phase, 16 patients; accelerated phase, 2 patients), 1 had agnogenic myeloid metaplasia (AMM), 2 had essential thrombocythemia (ET) and 1 had MPD transformed into refractory anemia with excess blasts (RAEB). The median age was 57 years (range 26-82 years). The median dose of imatinib mesylate administered was 400 mg (range 300-800 mg) and the median dose of anagrelide was 1.5 mg (range 0.5-4.0 mg). Imatinib mesylate and anagrelide combination therapy was feasible and tolerable. Of the 18 patients with Ph-positive CML, 15 in chronic phase and 1 in accelerated phase achieved a complete hematologic response (CHR), and 9 of the 18 achieved cytogenetic response (complete in 8 patients). No responses were noted in patients with AMM, ET or MPD transformed into RAEB.
The combination of imatinib mesylate and anagrelide was safe and was associated with an 89% CHR rate in patients with CML in chronic phase and persistent thrombocythemia.
酪氨酸激酶抑制剂甲磺酸伊马替尼可抑制与费城染色体阳性慢性髓性白血病（CML）相关的Bcr-Abl癌蛋白的功能。阿那格雷可抑制巨核细胞的增殖和分化。本研究的目的是探讨甲磺酸伊马替尼与阿那格雷联合治疗费城染色体阳性CML或伴有持续性血小板增多症的慢性骨髓增殖性疾病（MPD）患者的可行性和安全性。
本研究是对1998年10月至2002年5月期间在MD安德森癌症中心就诊、接受甲磺酸伊马替尼联合阿那格雷治疗的慢性MPD患者的所有可用记录进行的回顾性分析。
在确定的22例患者中，18例为费城染色体阳性CML（慢性期16例，加速期2例），1例为特发性骨髓化生（AMM），2例为原发性血小板增多症（ET），1例为MPD转化为伴有过多原始细胞的难治性贫血（RAEB）。中位年龄为57岁（范围26 - 82岁）。甲磺酸伊马替尼的中位给药剂量为400 mg（范围300 - 800 mg），阿那格雷的中位剂量为1.5 mg（范围0.5 - 4.0 mg）。甲磺酸伊马替尼与阿那格雷联合治疗是可行且可耐受的。在18例费城染色体阳性CML患者中，15例慢性期患者和1例加速期患者获得了完全血液学缓解（CHR），18例中有9例获得了细胞遗传学缓解（8例完全缓解）。AMM、ET或转化为RAEB的MPD患者未观察到缓解。
甲磺酸伊马替尼与阿那格雷联合用药安全，与慢性期CML伴持续性血小板增多症患者89%的CHR率相关。
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