Research Article KE and EE Genotypes of ICAM-1 Gene K469E Polymorphism Is Associated with Severe Preeclampsia Ehsan Tabatabai, 1,2 Saeedeh Salimi, 1,2 Milad Mohammadoo-khorasani, 1,2 Minoo Yaghmaei, 3 Mojgan Mokhtari, 3 Farzaneh Farajian Mashhadi, 1,4 and Anoosh Naghavi 1,5 1 Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan, Iran 2 Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran 3 Department of Obstetrics and Gynecology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran 4 Department of Pharmacology, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran 5 Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran Correspondence should be addressed to Saeedeh Salimi; sasalimi@yahoo.com Received 17 June 2013; Revised 18 October 2013; Accepted 2 December 2013; Published 30 January 2014 Academic Editor: Esperanza Ortega Copyright © 2014 Ehsan Tabatabai et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Preeclampsia (PE) is one of the most important complications of pregnancy that is associated with significant mortality and morbidity in mother and fetus. Since the etiologic factors in its development are still unclear, we aimed to examine the intercellular adhesion molecule-1 (ICAM-1) gene K469E polymorphism in preeclamptic and control healthy women. Materials and Methods. Genetic polymorphism was analyzed in 192 PE and 186 healthy control women. PCR-RFLP method was used to identify K469E polymorphism. Results. e frequency of KK, KE, and EE genotypes of ICAM-1 gene was not different between PE patients and healthy pregnant women. Whereas, the frequency of KE and EE genotypes was significantly higher in severe PE than mild PE women and control group, and the risk of severe PE was 2.4-fold higher in subjects with KE genotype (OR, 2.4 [95% CI, 1 to 5.9];  = 0.03) and 3.3-fold higher in subjects with EE genotype (OR, 3.3 [95% CI, 1.2 to 9];  = 0.015) compared to individuals with KK genotype. Conclusion. We concluded that KE and EE genotypes of K469E polymorphism could increase risk of severe PE. 1. Introduction Preeclampsia (PE) is a pregnancy syndrome that can affect virtually every organ system with a prevalence that varies from 5% to 10% [1]. It is clinically characterized by new onset of proteinuria and hypertension aſter 20 weeks of gestation and associated with significant mortality and morbidity in mothers and fetuses [2]. e pathophysiological mecha- nisms proposed for it are complex and include placental ischemia, inflammatory pathway, oxidative stress, the renin- angiotensin system, activation of thrombosis, and genetic factors [3]. A common clinical sign of PE is endothelial dys- function; however, the specific factors initiating endothelial dysfunction in PE are not clear. Although the etiology of PE has not been elucidated, family studies have suggested that genetic factors play an important role in its etiology [4]. Intercellular adhesion molecule-1 (ICAM-1) is involved in the pathogenetic mechanisms responsible for immune- mediated diseases including disorders of female reproductive system such as endometriosis, ovarian stimulation syndrome, and preeclampsia [5–7]. ICAM-1 is a transmembrane gly- coprotein and expressed in endothelial cells and leukocytes in the immune system [8, 9]. It plays an important role in cell-to-cell interactions and participates in inflammatory processes by facilitating leukocyte endothelial transmigration at site of inflammation [10]. e ICAM-1 gene is located in 19p13.2 and its polymorphisms have been suggested to have functional activity [11, 12]. e ICAM-1 gene has two single- base polymorphisms which are common genetic variations associated with diseases: Glycine or Arginine at codon 241 of exon 4 (G241R) and Lysine or Glutamine at codon 469 of exon 6 (K469E) [13]. Hindawi Publishing Corporation Disease Markers Volume 2014, Article ID 124941, 5 pages http://dx.doi.org/10.1155/2014/124941