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

Summary Both immunological and placental 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 role in abnormal placentation. We investigated whether MBL genotypes a...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Human immunology 2007-11, Vol.68 (11), p.888-893
Hauptverfasser: van de Geijn, Fleur E, Dolhain, Radboud J.E.M, van Rijs, Wouter, Hazes, Johanna M.W, de Groot, Christianne J.M
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Summary Both immunological and placental 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 role 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.
ISSN:0198-8859
1879-1166
DOI:10.1016/j.humimm.2007.10.002