SCHMIDT L H, SQUIRES W L
J Exp Med. 1951 Dec 1;94(6):501-20. doi: 10.1084/jem.94.6.501.
Studies have been made of the effects of cortisone on the course of primary and developed infections with P. cynomolgi in the rhesus monkey. This investigation has shown that repetitive admmistration of the hormone in daily doses of 10 mg. per kg. during the primary attack produced striking intensification of the peripheral blood infection during the postcrisis phases of the disease. Similar administration of 10 or 50 mg. per kg. doses of the hormone during the chronic or latent stages of the infection provoked recrudescences of remarkable severity. In both early and late infections the responses induced by cortisone treatment corresponded closely to the reactions to splenectomy. Collateral studies have shown that the doses of cortisone which produced the reactions described above also evoked a lymphopenia, marked reductions in the sizes of the axillary and inguinal lymph nodes and spleen, and striking histological changes in the latter organ. These changes involved severe regression or exhaustion of lymphoid elements in both splenic nodules and pulp with almost complete obliteration of proliferative activities involved in the production of macrophages from lymphocytes. Indications are that the resulting reduction in supply of macrophages, rather than inhibition of phagocytic activity per se, was responsible for the intensification of the disease produced by cortisone.
已经对可的松对恒河猴食蟹猴疟原虫原发性感染和已发展感染病程的影响进行了研究。这项调查表明,在原发性发作期间,每天每公斤重复给予10毫克激素,在疾病的危机后阶段会使外周血感染显著加剧。在感染的慢性或潜伏阶段,每公斤给予10或50毫克剂量的激素进行类似给药,会引发严重程度显著的复发。在早期和晚期感染中,可的松治疗引起的反应与脾切除后的反应密切对应。附带研究表明,产生上述反应的可的松剂量也会引起淋巴细胞减少、腋窝和腹股沟淋巴结及脾脏大小显著减小,以及后者器官出现明显的组织学变化。这些变化包括脾小结和脾髓中淋巴样成分的严重退化或耗竭,几乎完全消除了淋巴细胞产生巨噬细胞所涉及的增殖活动。有迹象表明,可的松导致疾病加剧的原因是巨噬细胞供应减少,而不是吞噬活性本身受到抑制。