Chitotriosidase, interleukin-1 beta and tumor necrosis factor alpha levels in mild preeclampsia
Chitotriosidase, interleukin-1 beta and tumor necrosis factor alpha levels in mild preeclampsia
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DOI：
10.1007/s00404-011-2157-6
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发表时间：
2012-06-01
影响因子：
2.6
通讯作者：
Baser, Iskender
中科院分区：
文献类型：
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作者：
Alanbay, Ibrahim;Coksuer, Hakan;Baser, Iskender
壳三糖苷酶(Chitotriosidase，CHT)是一种激活的巨噬细胞标志。肿瘤坏死因子α(TNF-α)和白介素1β(IL-1β)主要由巨噬细胞产生。为探讨轻度子痫前期患者血清CHT活性与肿瘤坏死因子-α、白介素1-β水平的关系，对32例正常妊娠妇女和32例正常妊娠妇女及32例轻度子痫前期患者血清CHT活性与肿瘤坏死因子-α、白介素1β水平的关系进行了研究。在研究开始时，所有研究参与者的年龄和胎龄都是匹配的。用荧光法测定血清CHT活性，用酶联免疫吸附试验测定血清肿瘤坏死因子-α和白介素1-β水平。两组的平均年龄、孕周、产次和孕周相似(>；0.05)。先兆子痫组的血清CHT活性显著高于对照组(P<0.05)。轻度子痫前期患者血清中肿瘤坏死因子-α和白介素1-β水平与对照组相似(>；0.05)。在PE组，CHT活性与TNF-α和IL-1β无相关性，轻度子痫前期患者CHT活性较高。这一结果提示活化的巨噬细胞在子痫前期的发病机制中起一定作用。这一建议需要在未来对更大人群的研究中得到证实。
Chitotriosidase (ChT) is an activated macrophage marker. Tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta) are mainly produced macrophages. The aim of the present study was to evaluate the relationship between serum ChT activity, levels of TNF-alpha and IL-1 beta in patients with mild preeclampsia and normal pregnancy.An overall 64 cases, 32 healthy pregnant control women (control group) and 32 women with mild preeclamptic patients (study group), were enrolled in this study. At the beginning of the study, all study participants were matched for age and gestational age. Serum ChT activity was measured by fluorometer; TNF-alpha and IL-1 beta levels were measured by enzyme-linked immunosorbent assay.The mean age, gestational week, parity and gravida were similar in the two groups ( > 0.05). Serum ChT activity was significantly higher in the preeclampsia group compared to the control group ( < 0.05). Levels of TNF-alpha and IL-1 beta in patients with mild preeclampsia were similar compared to the control group ( > 0.05). In the PE group, serum ChT activity was not correlated with TNF-alpha and IL-1 beta.Mild preeclampsia is found associated with higher ChT activity. This result suggests that activated macrophages play a role in the pathogenesis of preeclampsia. This suggestion needs to be confirmed in future studies with larger populations.