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Cytomegalovirus antibody status at 17–18 weeks of gestation and pre‐eclampsia: a case–control study of pregnant women in Norway
Author(s) -
Strand KM,
Odland ML,
Iversen AC,
Nordbø SA,
Vik T,
Austgulen R
Publication year - 2012
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.2012.03420.x
Subject(s) - medicine , pregnancy , obstetrics , eclampsia , cytomegalovirus , odds ratio , human cytomegalovirus , gestation , gynecology , cohort , cohort study , norwegian , immunology , human immunodeficiency virus (hiv) , viral disease , biology , herpesviridae , virus , linguistics , genetics , philosophy
Please cite this paper as: Strand K, Odland M, Iversen A, Nordbø S, Vik T, Austgulen R. Cytomegalovirus antibody status at 17–18 weeks of gestation and pre‐eclampsia: a case–control study of pregnant women in Norway. BJOG 2012;119:1316–1323. Objective To assess the association between maternal cytomegalovirus (CMV) antibodies in mid‐pregnancy and pre‐eclampsia. Design Nested case–control study. Setting Pregnancies registered in the Norwegian Mother and Child Cohort Study (MoBa): a large population‐based pregnancy cohort (1999–2006). Sample A cohort of 1500 women with pre‐eclampsia and 1000 healthy pregnant women. Methods Plasma samples and pregnancy‐related information were provided by the MoBa. Antibody status (CMV IgG and CMV IgM) and levels (CMV IgG) at 17–18 weeks of gestation were determined by enzyme‐linked immunosorbent assay (ELISA). Main outcome measure A diagnosis of pre‐eclampsia, as defined in the Medical Birth Registry of Norway. Results There was no evidence of an effect of CMV IgG seropositivity on the likelihood of developing pre‐eclampsia, and CMV IgG antibody levels among women who were seropositive did not differ between groups. Adjusted for maternal age, parity and smoking, the odds ratio for pre‐eclampsia in women seropositive for CMV IgG was 0.89 (95% CI 0.74–1.05; P = 0.17). The proportions of women who were seropositive for IgM did not differ between women with pre‐eclampsia and women who were healthy ( P = 0.98). Among nulliparous women, the proportion of women who were seropositive for CMV IgG was slightly lower among women with pre‐eclampsia (53.5%) than among healthy women (59.8%) ( P = 0.03). Subgroup analyses were performed for women with early or late onset pre‐eclampsia, with preterm delivery and/or with neonates that were small for gestational age, but antibody status did not differ between pre‐eclampsia subtypes and controls. Conclusions The presence of maternal antibodies to CMV was not associated with pre‐eclampsia in our study. The results suggest that CMV infection is unlikely to be a major cause of pre‐eclampsia.