Schweiger F J, Kelton J G, Messner H, Klein M, Berger S, McIlroy W J, Falk J, Keating A
Department of Medicine, Toronto Western Hospital, Canada.
Acta Haematol. 1988;80(1):54-8. doi: 10.1159/000205599.
Phenytoin and carbamazepine are rarely associated with serious hematologic side effects but can include impairment of either humoral or cell-mediated immunity. We describe a patient who developed severe granulocytopenia while taking phenytoin. The phenytoin was replaced by carbamazepine and the patient subsequently developed erythroid hypoplasia, neutropenia and persistent thrombocytopenia. In vitro studies demonstrated a phenytoin-dependent antigranulocyte antibody directly implicating phenytoin in the leukopenia. An extremely high titre of platelet-associated IgG was found which was independent of the presence of carbamazepine. Autoantibodies directed against the patient's red cells, granulocytes and lymphocytes were also demonstrated. In vitro marrow culture studies failed to detect cellular or humoral inhibitors and were suggestive of a stem cell defect. These studies indicate that anticonvulsant therapy can result in sustained humoral abnormalities as well as in nonimmune mediated marrow suppression.
苯妥英钠和卡马西平很少引起严重的血液学副作用，但可能包括体液免疫或细胞介导免疫的损害。我们描述了一名在服用苯妥英钠时发生严重粒细胞减少的患者。将苯妥英钠换成卡马西平后，该患者随后出现红细胞发育不全、中性粒细胞减少和持续性血小板减少。体外研究表明存在一种苯妥英钠依赖性抗粒细胞抗体，直接表明苯妥英钠与白细胞减少有关。发现了极高滴度的血小板相关IgG，其与卡马西平的存在无关。还证实了针对患者红细胞、粒细胞和淋巴细胞的自身抗体。体外骨髓培养研究未能检测到细胞或体液抑制剂，提示存在干细胞缺陷。这些研究表明，抗惊厥治疗可导致持续的体液异常以及非免疫介导的骨髓抑制。
