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目的探讨高原地区急性脑梗死(acute cerebral ischemic,ACI)与雄激素(androgen)水平的关系。方法采用放射免疫法检测高原地区(海拔2260m以上)男性ACI患者和对照组各60例血清睾酮、雌二醇(E2)、促红细胞生成素(EPO)、肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)和IL-6的水平。比色法检测甘油三脂(TG)、胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、载脂蛋白-A1(Apo-A1)和载脂蛋白-B(Apo-B)等含量。结果与对照组相比,高原地区男性ACI患者血清睾酮水平明显下降(P<0.01),血清E2水平无明显变化;ACI患者TG、LDL和Apo-B的含量增高,TC、HDL和Apo-A1含量无明显变化。病例组TNF-α、1L-1β和1L-6的水平明显高于对照组,EPO水平与对照组相比无统计学意义。相关性分析显示,男性ACI患者睾酮水平下降与TG、LDL、Apo-B、TNF-α、IL-1β和IL-6的水平间呈负相关,与E2、TC、HDL、Apo-A1和EPO相关不显著。结论低睾酮水平与高原男性ACI相关。雄激素水平的降低可能通过影响脂质代谢和参与炎症反应环节促进高原地区老年男性ACI的发生。
Objective To investigate the relationship between acute cerebral ischemic (ACI) and androgen levels in the plateau area. Methods Serum testosterone, estradiol (E2), erythropoietin (EPO) and tumor necrosis factor-α (TNF-α) were detected by radioimmunoassay in 60 ACU patients and 60 ACM patients in the plateau area , Interleukin-1β (IL-1β) and IL-6. Colorimetric method was used to detect triglyceride (TG), cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein (HDL), apolipoprotein-A1 -B) and other content. Results Compared with the control group, the level of serum testosterone was significantly decreased in ACI patients (P <0.01) and the level of serum E2 was not significantly changed in patients with ACI; the levels of TG, LDL and Apo-B were increased in ACI patients; the levels of TC, HDL and Apo-A1 No significant change in content. The levels of TNF-α, 1L-1β and 1L-6 in the case group were significantly higher than those in the control group, and the levels of EPO were not significantly different from those in the control group. Correlation analysis showed that there was a negative correlation between the level of testosterone and the levels of TG, LDL, Apo-B, TNF-α, IL-1β and IL-6 in male patients with ACI The correlation is not significant. Conclusions Low testosterone levels are associated with ACI in high altitude men. The decrease of androgen levels may promote the occurrence of ACI in elderly men in the plateau by affecting lipid metabolism and participating in the inflammatory response.