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葡萄胎中血清蛋白分布:一项免疫组织化学研究

Serum protein distribution in hydatidiform mole. An immunohistochemical study.

作者信息

Massi G, Coli A, De Carolis S

出版信息

Arch Pathol Lab Med. 1987 Aug;111(8):723-5.

PMID:3307688
Abstract

In normal placentas during the first trimester of pregnancy, the syncytiotrophoblast appeared to be immunoreactive to alpha-antitrypsin (alpha 1-AT), alpha 1-antichymotrypsin, albumin, IgG, and transferrin. The underlying cytotrophoblast was negative for these same serum proteins. In the hydatidiform mole, these findings were profoundly different. The syncytiotrophoblast lost its immunoreactivity to albumin, IgG, transferrin, and, less frequently, to alpha 1-AT. Furthermore, the underlying cytotrophoblast became immunoreactive to albumin, alpha 1-AT, IgG, transferrin, ferritin, orosomucoid, and, sometimes, to alpha 1-antichymotrypsin. This altered immunohistochemical pattern suggested a notable change in the pinocytotic activity of the trophoblast in the placenta during molar degeneration. The absence of pinocytosis in the syncytiotrophoblast for several proteins can be explained by the partial loss of specific membrane receptors. The contemporaneous appearance of numerous serum proteins in the cytotrophoblast could indicate an activation, not only proliferative, but also functional, in the germinative cytotrophoblast. Diagnostically, this histochemical finding in the hydatidiform mole, which was quite different from that seen in normal placentas during the first trimester of pregnancy, could provide additional evidence concerning trophoblastic abnormalities in the chorionic villi during molar degeneration.

摘要

在妊娠头三个月的正常胎盘中,合体滋养层细胞对α-抗胰蛋白酶(α1-AT)、α1-抗糜蛋白酶、白蛋白、IgG和转铁蛋白呈免疫反应阳性。其下方的细胞滋养层细胞对这些相同的血清蛋白呈阴性。在葡萄胎中,这些发现有很大不同。合体滋养层细胞对白蛋白、IgG、转铁蛋白以及较少见的α1-AT失去免疫反应性。此外,其下方的细胞滋养层细胞对白蛋白、α1-AT、IgG、转铁蛋白、铁蛋白、类粘蛋白,有时还对α1-抗糜蛋白酶呈免疫反应阳性。这种免疫组化模式的改变提示在葡萄胎变性过程中胎盘滋养层细胞的胞饮活性发生了显著变化。合体滋养层细胞对几种蛋白质缺乏胞饮作用可通过特异性膜受体的部分丧失来解释。细胞滋养层细胞中同时出现多种血清蛋白可能表明在生发细胞滋养层细胞中不仅有增殖激活,还有功能激活。在诊断方面,葡萄胎中的这种组织化学发现与妊娠头三个月正常胎盘的情况有很大不同,可为葡萄胎变性期间绒毛膜绒毛滋养层异常提供额外证据。

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