Atamer Yildiz, Erden Ali Ceylan, Demir Bulent, Koçyigit Yuksel, Atamer Aytaç
Department of Biochemistry, School of Medicine, Dicle University, 21280 Diyarbakir, Turkey.
Acta Obstet Gynecol Scand. 2004 May;83(5):425-30. doi: 10.1111/j.0001-6349.2004.00276.x.
To clarify the role of leptin and androgens in the pathogenesis of preeclampsia, we wanted to assess role of maternal leptin in women with severe and mild preeclampsia and the effects of sex steroid hormones on leptin production.
The groups consisted of 40 healthy pregnant women (HPW) as well as 55 pregnant women with severe preeclampsia (SPE) and 41 pregnant women with mild preeclampsia (MPE). No significant differences were observed between the three groups regarding age, gestational age and body mass index (BMI). Plasma leptin, total testosterone (T), estradiol (E(2)), dehydroepiandrosterone sulfate (DHEAS) and androstenedione (A) levels were measured. Statistical analysis was achieved with one-way analysis of variance (anova) followed by post hoc multiple comparisons with the Tukey honestly significant difference (HSD) test by using SPSS for Windows statistical computer program, and the Pearson's coefficient of correlation was calculated.
The plasma level of leptin was significantly increased in the SPE and MPE groups (p < 0.001), whereas the plasma level of T was significantly increased only in the SPE group (p < 0.001). However, there was no significant difference in plasma levels of DHEAS among the three groups (p < 0.05). The plasma level of A was significantly decreased in the MPE group (p < 0.05). There was no significant difference in the plasma level of E(2) in the MPE and SPE groups (p < 0.05). There was a significant positive correlation between the plasma levels of leptin and E(2) in the MPE group (r = 0.41, p < 0.001).
We concluded that the elevated plasma levels of leptin and testosterone could contribute to the endothelial dysfunction involved in the pathogenesis of preeclampsia, and that estradiol might lead to an increase in the plasma levels of leptin.
为阐明瘦素和雄激素在子痫前期发病机制中的作用，我们想要评估母体瘦素在重度和轻度子痫前期女性中的作用以及性类固醇激素对瘦素产生的影响。
研究组包括40名健康孕妇（HPW）、55名重度子痫前期孕妇（SPE）和41名轻度子痫前期孕妇（MPE）。三组在年龄、孕周和体重指数（BMI）方面未观察到显著差异。检测血浆瘦素、总睾酮（T）、雌二醇（E₂）、硫酸脱氢表雄酮（DHEAS）和雄烯二酮（A）水平。使用Windows版SPSS统计计算机程序，通过单因素方差分析（anova）进行统计分析，随后采用Tukey真实显著差异（HSD）检验进行事后多重比较，并计算Pearson相关系数。
SPE组和MPE组的血浆瘦素水平显著升高（p < 0.001），而仅SPE组的血浆T水平显著升高（p < 0.001）。然而，三组之间的血浆DHEAS水平无显著差异（p < 0.05）。MPE组的血浆A水平显著降低（p < 0.05）。MPE组和SPE组的血浆E₂水平无显著差异（p < 0.05）。MPE组的血浆瘦素水平与E₂水平之间存在显著正相关（r = 0.41，p < 0.001）。
我们得出结论，血浆瘦素和睾酮水平升高可能导致子痫前期发病机制中涉及的内皮功能障碍，并且雌二醇可能导致血浆瘦素水平升高。
