Mannose-binding lectin genotypes and pre-eclampsia: A case-control study

被引:25
|
作者
van de Geijn, Fleur E. [1 ,2 ]
Dolhain, Radboud J. E. M. [1 ]
van Rijs, Wouter [2 ]
Hazes, Johanna M. W. [1 ]
de Groot, Christianne J. M. [3 ,4 ]
机构
[1] Univ Med Ctr Rotterdam, Erasmus MC, Dept Rheumatol, Rotterdam, Netherlands
[2] Univ Med Ctr Rotterdam, Erasmus MC, Dept Immunol, Rotterdam, Netherlands
[3] Univ Med Ctr Rotterdam, Erasmus MC, Dept Obstet & Gynaecol, Rotterdam, Netherlands
[4] Med Ctr Haaglanden, Dept Obstet & Gynaecol, The Hague, Netherlands
关键词
mannose-binding lectin; polymorphisms; pre-eclampsia;
D O I
10.1016/j.humimm.2007.10.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Both immunological and placenta[ factors are involved in the pathogenesis of pre-eclampsia. The complement factor mannose-binding lectin (MBL) is associated with adverse pregnancy outcomes and has been suggested to play a rote in abnormal placentation. We investigated whether MBL genotypes are associated with the systemic maternal syndrome pre-eclampsia. MBL2 gene polymorphisms were determined in a case-control study including 157 women with pre-eclampsia (case subjects) and 157 women with uncomplicated pregnancies (control subjects). Considering MBL polymorphisms, case and control subjects were categorized in groups of high (A), intermediate (B), and Low (C) MBL production. No association was found between MBL genotypes and pre-eclampsia; adjusted odds ratios and 95% confidence intervals (95% CI) for group B were 0.97 (95% CI = 0.46-2.07) and for group C were 1.44 (95% CI = 0.52-3.94). A trend was found between MBL genotype groups B and C and severe pre-eclampsia or eclampsia. MBL genotypes were not found to be associated with pre-eclampsia; however low-MBL production genotypes might be considered as disease modifier. This suggests that MBL may play a role in modulating placental inflammation by facilitating clearance of apoptotic cells and cell debris. (c) 2007 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. ALL rights reserved.
引用
收藏
页码:888 / 893
页数:6
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