Sex differences in stroke have been attributed to the neuroprotective effects of estrogen, yet most clinical trials of estrogen supplementation for stroke prevention have failed. The contribution of sex hormones to stroke outcome remains a subject of debate. Aromatization of testosterone to estradiol in neural tissue leads to sexual differentiation. Emerging data suggests aromatase activity increases in response to brain injury, and increased aromatase expression is seen in the ischemic penumbra in animal models. The objective of this study was to examine the levels of endogenous sex steroids after acute ischemic stroke and determine if levels of sex steroids were associated with acute stroke outcomes. Peripheral blood from ischemic stroke patients and controls was collected under an approved IRB within 24 h of symptom onset. 17β-estradiol, testosterone, and aromatase levels were measured in the serum of both men and women using ELISA. Hormone levels were compared in men vs. women in stroke and control groups and correlated with outcomes (NIHSS and change in the modified Rankin Scale (mRS), defined as the difference of premorbid and discharge mRS) using multivariate regression. We found no significant difference in estradiol levels 24 h after stroke in men (p = 0.86) or women (p = 0.10). In men, testosterone significantly decreased after stroke as compared with controls (1.83 ± 0.12 vs. 2.86 ± 0.65, p = 0.01). Aromatase levels were significantly increased in women after stroke as compared with controls (2.27 ± 0.22 vs. 0.97 ± 0.22, p = 0.002), but not in men (p = 0.84). Estradiol levels positively correlated with change in mRS in both women (r = 0.38, p = 0.02) and men (r = 0.3, p = 0.04). Estradiol levels correlated with functional outcomes (change in mRS) in both men and women, at least in the acute phase (24 h) of stroke. However, no significant difference in estradiol levels is seen 24 h post-stroke in men or women. Testosterone levels decrease at 24 h after stroke in men. As seen in animal models, aromatase levels increase after acute ischemic stroke, but this was only true for women. These indicate an active aromatization process in post-menopausal women after acute ischemic stroke.

中文翻译：

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绝经后妇女急性缺血性卒中后 P450 芳香化酶水平升高

中风的性别差异归因于雌激素的神经保护作用，但大多数补充雌激素预防中风的临床试验都失败了。性激素对中风结果的贡献仍然是一个争论的话题。睾酮在神经组织中芳香化为雌二醇导致性别分化。新出现的数据表明芳香酶活性随着脑损伤而增加，并且在动物模型的缺血半影区中可以看到芳香酶表达增加。本研究的目的是检查急性缺血性卒中后内源性性类固醇的水平，并确定性类固醇水平是否与急性卒中结局相关。缺血性中风患者和对照组的外周血在症状发作后 24 小时内在经批准的 IRB 下收集。17β-雌二醇，使用ELISA测量男性和女性血清中的睾酮和芳香酶水平。在中风组和对照组中比较男性与女性的激素水平，并使用多元回归与结果（NIHSS 和改良 Rankin 量表 (mRS) 的变化，定义为病前和出院 mRS 的差异）相关。我们发现男性（p = 0.86）或女性（p = 0.10）中风后 24 小时的雌二醇水平没有显着差异。在男性中，与对照组相比，中风后睾酮显着下降（1.83 ± 0.12 vs. 2.86 ± 0.65，p = 0.01）。与对照组相比，中风后女性的芳香酶水平显着增加（2.27 ± 0.22 vs. 0.97 ± 0.22，p = 0.002），但男性则没有（p = 0.84）。雌二醇水平与女性 (r = 0.38, p = 0.02) 和男性 (r = 0.3, p = 0.04)。雌二醇水平与男性和女性的功能结果（mRS 变化）相关，至少在中风的急性期（24 小时）。然而，在男性或女性中风后 24 小时，雌二醇水平没有显着差异。男性中风后 24 小时睾酮水平下降。正如在动物模型中所见，急性缺血性中风后芳香化酶水平会升高，但这仅适用于女性。这些表明急性缺血性中风后绝经后妇女的芳香化过程是活跃的。急性缺血性中风后芳香化酶水平会升高，但这仅适用于女性。这些表明急性缺血性中风后绝经后妇女的芳香化过程是活跃的。急性缺血性中风后芳香化酶水平会升高，但这仅适用于女性。这些表明急性缺血性中风后绝经后妇女的芳香化过程是活跃的。