Corrigan C J
Department of Allergy and Clinical Immunology, National Heart and Lung Institute, London, United Kingdom.
Am J Respir Crit Care Med. 1996 Aug;154(2 Pt 2):S53-5; discussion S55-7. doi: 10.1164/ajrccm/154.2_Pt_2.S53.
There is adequate evidence that clinical glucocorticoid resistance in asthma can be attributed at least partly to a relative resistance of T cells to inhibition by glucocorticoids. Although GR asthma defined according to the present criteria represents one end of a spectrum of clinical response, in clinical practice these patients would not be exposed for prolonged periods to dosages of glucocorticoids sufficient to inhibit their T cells in vivo. A more rational approach to the selection of alternative therapy for such patients might be possible when the mechanisms of this resistance are identified. In the meantime, there is some justification for assessing other drugs that inhibit T cells from patients with GR asthma at therapeutic concentrations for their efficacy and risk/benefit ratios in clinical practice.
有充分证据表明，哮喘中的临床糖皮质激素抵抗至少部分可归因于T细胞对糖皮质激素抑制作用的相对抵抗。尽管根据目前标准定义的糖皮质激素抵抗性哮喘代表了临床反应谱的一端，但在临床实践中，这些患者不会长时间暴露于足以在体内抑制其T细胞的糖皮质激素剂量下。当确定这种抵抗的机制时，可能会有一种更合理的方法来为这类患者选择替代疗法。与此同时，有理由评估其他能在治疗浓度下抑制糖皮质激素抵抗性哮喘患者T细胞的药物在临床实践中的疗效以及风险/效益比。
