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胎儿贫血中的造血细胞因子水平及体外集落形成试验

Hematopoietic cytokine levels and in vitro colony formation assay in fetal anemia.

作者信息

Yamada H, Kato E H, Furuta I, Hoshi N, Koizumi K, Sawada K, Fujimoto S

机构信息

Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Sapporo, Japan.

出版信息

Semin Thromb Hemost. 1998;24(5):485-90. doi: 10.1055/s-2007-996044.

Abstract

Fetal anemia causes hydrops fetalis and fetal ascites/hydrothorax, and in severe cases the prognosis is poor. Little other than alloimmunity and viral infections are known as mechanisms causing fetal anemia. The aim of this study was to elucidate any pathogenesis in fetal anemia due to otherwise idiopathic etiology. The levels of three hematopoietic cytokines, IL-3, erythropoietin (EPO), and granulocyte colony-stimulating factor (G-CSF) were measured in blood samples obtained by cordocentesis from six fetuses with anemia (Hb <10.0 g/dl) and 34 fetuses without anemia. Cordocentesis was performed prior to the onset of labor or uterine contractions in all pregnant women. The concentration of IL-3 in fetuses with anemia [M+/-(SD), 8.3 (10.1) pg/ml] was significantly lower than that in fetuses without anemia [59.9 (71.0) pg/ml]. EPO and G-CSF levels were not different between the two groups. In addition, through in vitro colony formation assay, using blood stem cells from two fetuses with severe anemia and three fetuses without anemia, it was found that colony forming unit-erythroid, burst forming unit-erythroid and granulocyte macrophage-colony forming unit were significantly suppressed in blood stem cells from the two fetuses with severe anemia. Thus, the malfunction of differentiation and proliferation of blood stem cells and the decrease of hematopoietic cytokine levels in the fetal circulation may be responsible for the occurrence of fetal anemia.

摘要

胎儿贫血会导致胎儿水肿以及胎儿腹水/胸腔积液,严重时预后较差。除了同种免疫和病毒感染外,几乎没有其他已知的导致胎儿贫血的机制。本研究的目的是阐明特发性病因导致的胎儿贫血的发病机制。通过脐血穿刺从6例贫血胎儿(血红蛋白<10.0 g/dl)和34例非贫血胎儿获取血样,检测三种造血细胞因子白细胞介素-3(IL-3)、促红细胞生成素(EPO)和粒细胞集落刺激因子(G-CSF)的水平。所有孕妇均在临产前或子宫收缩前进行脐血穿刺。贫血胎儿的IL-3浓度[中位数±标准差,8.3(10.1)pg/ml]显著低于非贫血胎儿[59.9(71.0)pg/ml]。两组之间EPO和G-CSF水平无差异。此外,通过体外集落形成试验,使用来自2例重度贫血胎儿和3例非贫血胎儿的血液干细胞,发现2例重度贫血胎儿的血液干细胞中红系集落形成单位、红系爆式集落形成单位和粒巨噬细胞集落形成单位均受到显著抑制。因此,胎儿循环中血液干细胞分化和增殖功能异常以及造血细胞因子水平降低可能是胎儿贫血发生的原因。

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