Douer D, Eisenstein Z
Institute of Hematology, Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Eur J Haematol. 1988 Jan;40(1):91-4. doi: 10.1111/j.1600-0609.1988.tb00803.x.
The mechanism for agranulocytosis induced by antithyroid drugs is not established. The few available studies have proposed an immune-mediated process against mature granulocytes. We investigated the effect of methimazole and propylthiouracil and serum from a patient with methimazole-induced agranulocytosis on marrow myeloid colony growth. In the presence of normal serum or patient's recovery serum, antithyroid drugs had no effect on the growth of CFU-GM colonies from normal or patient's marrow. However, the patient's serum obtained during agranulocytosis inhibited the in vitro myeloid colony growth from both autologous and allogeneic bone marrow. These results are compatible with an immune-mediated mechanism for methimazole-induced agranulocytosis rather than a direct toxic effect of the drug on abnormally sensitive cells.
抗甲状腺药物所致粒细胞缺乏症的机制尚未明确。现有的少量研究提出了一种针对成熟粒细胞的免疫介导过程。我们研究了甲巯咪唑、丙硫氧嘧啶以及来自一名甲巯咪唑所致粒细胞缺乏症患者的血清对骨髓髓系集落生长的影响。在正常血清或患者恢复血清存在的情况下,抗甲状腺药物对正常或患者骨髓中CFU-GM集落的生长没有影响。然而,在粒细胞缺乏症期间获取的患者血清抑制了自体和异体骨髓的体外髓系集落生长。这些结果与甲巯咪唑所致粒细胞缺乏症的免疫介导机制相符,而非该药物对异常敏感细胞的直接毒性作用。