Beardsley G P, Cohen H J
Am J Hematol. 1978;4(3):255-9. doi: 10.1002/ajh.2830040307.
Pharmacologic doses of corticosteroids produce a profound, transient lymphocytopenia in man. We have studied the role of the spleen and possible induction of cytolytic factors in the generation of this effect. A 200 mg IV dose of hydrocortisone-21-hemisuccinate was administered to five normal subjects and five subjects whose spleens had been removed as a result of trauma. Sequential peripheral blood lymphocyte counts and subpopulations were then determined, and the effect of serum (obtained from the recipients at several time points after steroid administration) on autologous lymphocyte viability was assessed in vitro. The asplenic subjects experienced the same marked lymphocytopenia as normal individuals, and post-steroid serum was not cytotoxic to autologous lymphocytes. The in vitro results support the view that corticosteroid-induced lymphocytopenia is not the result of lymphocytolysis in man. If lymphocyte redistribution is the cause, as has been suggested, our in vivo results directly demonstrate that the spleen does not play a major role.
药理剂量的皮质类固醇可在人体中产生严重的、短暂的淋巴细胞减少。我们研究了脾脏的作用以及在产生这种效应过程中细胞溶解因子的可能诱导情况。给5名正常受试者和5名因外伤已切除脾脏的受试者静脉注射200mg氢化可的松21-半琥珀酸酯。然后测定外周血淋巴细胞计数及亚群的变化,并在体外评估血清(在给予类固醇后的几个时间点从受试者获取)对自体淋巴细胞活力的影响。无脾受试者与正常个体经历了相同程度的明显淋巴细胞减少,且类固醇给药后的血清对自体淋巴细胞无细胞毒性。体外实验结果支持这样的观点,即皮质类固醇诱导的淋巴细胞减少并非人体淋巴细胞溶解的结果。如果如所提出的那样,淋巴细胞重新分布是原因,那么我们的体内实验结果直接表明脾脏并不起主要作用。