Resegotti L, Pistone M A, Testa D, Charbonnier R, Toselli P, Vivalda S
Nouv Rev Fr Hematol (1978). 1985;27(1):19-22.
Bone marrow cells obtained from 15 patients treated with Ticlopidine (500 mg/day) for a month, and from 20 matched controls were cultured in agar. GM colonies and clusters were counted after 7 and 14 days of culture. CFU GM were slightly decreased in the patients treated by Ticlopidine. In 8 patients, in which the bone marrow was cultured on a second occasion 3 months latter, a slight increase in the inhibition of CFU GM was observed. It could be due to the mechanism of action of the drug (by an increased synthesis of PGE1) and not to a toxic side effect. The few cases of reversible agranulocytosis reported in the literature might be due to the inhibition of myelopoiesis in patients with medullary reserves already impaired.
从15名接受噻氯匹定(500毫克/天)治疗一个月的患者以及20名匹配的对照者身上获取骨髓细胞,在琼脂中进行培养。培养7天和14天后对粒细胞巨噬细胞集落(GM集落)和集簇进行计数。接受噻氯匹定治疗的患者中CFU-GM略有减少。在8名患者中,3个月后再次进行骨髓培养,观察到CFU-GM抑制作用略有增加。这可能是由于药物的作用机制(通过增加PGE1的合成),而不是毒性副作用。文献中报道的少数可逆性粒细胞缺乏症病例可能是由于骨髓储备已经受损的患者骨髓生成受到抑制所致。