Vago T, Clerici M, Norbiato G
Department of Endocrinology, Luigi Sacco Hospital, Milan, Italy.
Baillieres Clin Endocrinol Metab. 1994 Oct;8(4):789-802. doi: 10.1016/s0950-351x(05)80301-5.
Data reported in the literature show in the majority of cases an increased basal cortisol level in HIV-positive patients compared with controls, although the plasma concentration of cortisol in HIV-positive patients is generally within the physiological range. It is well known that pharmacological doses of glucocorticoids are immunosuppressive, but little is known about the effects of physiological concentrations of cortisol on the immune system. If a dialogue really exists between the HPA axis and the immune system, immune responses should be modulated by physiological concentrations of cortisol, as well as pathological levels of cortisol (high as in Cushing's syndrome or low as in Addison's disease), which are known to be associated with impaired immune system responses. We suggest that in HIV-positive patients, a chronic increase in the basal endogenous cortisol levels may provoke an imbalance in cytokine production, with a decrease in the production of type 1 and an increase in that of type 2. The type 1 to type 2 shift might be synergic with the increased cortisol levels in enhancing viral replication and apoptotic phenomena, and finally in causing the progression of HIV infection.
文献报道的数据显示，在大多数情况下，与对照组相比，HIV阳性患者的基础皮质醇水平升高，尽管HIV阳性患者的血浆皮质醇浓度通常在生理范围内。众所周知，药理剂量的糖皮质激素具有免疫抑制作用，但关于生理浓度的皮质醇对免疫系统的影响知之甚少。如果下丘脑-垂体-肾上腺（HPA）轴与免疫系统之间确实存在对话，那么免疫反应应该受到生理浓度皮质醇以及皮质醇病理水平（如库欣综合征中的高水平或艾迪生病中的低水平）的调节，已知这些与免疫系统反应受损有关。我们认为，在HIV阳性患者中，基础内源性皮质醇水平的慢性升高可能会引发细胞因子产生的失衡，导致1型细胞因子产生减少而2型细胞因子产生增加。1型向2型的转变可能与皮质醇水平升高协同作用，增强病毒复制和凋亡现象，最终导致HIV感染的进展。
