Pisciotta V
Drugs. 1978 Feb;15(2):132-43. doi: 10.2165/00003495-197815020-00003.
An unexpected precipitous fall in peripheral leucocyte count may occur during treatment of certain sensitised individuals with drugs usually well tolerated by most people. Three basic mechanisms for drug sensitivity have been found. One is characterised by sudden destruction of large numbers of leucocytes in peripheral blood by antibodies elicited in response to drug sensitivity. A prototype for this type of reaction is aminopyrine. A second mechanism involves the production of a lupus-like syndrome followed by leucopenia in response to sensitisation to drugs such as procainamide. A third type involves development of agranulocytosis following a latent period during which a sensitive patient is treated with large amounts of chlorpromazine. This type of reaction is associated with production of bone marrow insufficiency in a patient who is believed to have a limited proliferative potential of bone marrow cells, which limit compensatory bone marrow response during treatment with a drug (e.g. chlorpromazine) that has limited bone marrow toxicity.
在用大多数人通常耐受性良好的药物治疗某些敏感个体时,可能会出现外周白细胞计数意外急剧下降的情况。已发现药物敏感性的三种基本机制。一种机制的特征是,由于药物敏感性引发的抗体导致外周血中大量白细胞突然被破坏。这种反应类型的一个典型例子是氨基比林。第二种机制涉及产生狼疮样综合征,随后因对普鲁卡因胺等药物敏感而出现白细胞减少。第三种类型是在敏感患者接受大量氯丙嗪治疗的潜伏期后发生粒细胞缺乏症。这种反应类型与骨髓细胞增殖潜力有限的患者骨髓功能不全有关,这限制了在用具有有限骨髓毒性的药物(如氯丙嗪)治疗期间骨髓的代偿反应。