Maternal antibodies against cytomegalovirus in pregnancy and the risk of fetal death and low birth weight

Eskild, Anne; Jenum, Pål A.; Bruu, Anne‐Lise

doi:10.1111/j.0001-6349.2005.00796.x

Cited by 11 publications

(10 citation statements)

References 28 publications

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“…Two‐sided P values lower than 0.05 were considered to be statistically significant. The number of cases and controls were based upon power calculations, assuming a first‐trimester CMV IgG seroprevalence of 70% among pregnant women in Norway 28 . Based upon these calculations, by including 1500 women in the case group and 1000 women in the control group our study had 80% power to detect a 5% higher proportion of women positive for CMV IgG antibodies in the case group, than in the control group (α = 0.05).…”

Section: Methodsmentioning

confidence: 99%

Cytomegalovirus antibody status at 17–18 weeks of gestation and pre‐eclampsia: a case–control study of pregnant women in Norway

Strand

Odland

Iversen

et al. 2012

BJOG

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Objective To assess the association between maternal cytomegalovirus (CMV) antibodies in mid-pregnancy and preeclampsia.Design Nested case-control study.Setting Pregnancies registered in the Norwegian Mother and Child Cohort Study (MoBa): a large population-based pregnancy cohort (1999)(2000)(2001)(2002)(2003)(2004)(2005)(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 preeclampsia.

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Section: Methodsmentioning

confidence: 99%

Cytomegalovirus antibody status at 17–18 weeks of gestation and pre‐eclampsia: a case–control study of pregnant women in Norway

Strand

Odland

Iversen

et al. 2012

BJOG

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“…Studies by Yow et al [11], as well as by GriYths and Baboonian [12], reported about fetal death and spontaneous abortion in women with CMV infection. Contrast studies by Moyo et al [13] and Eskild et al [14] could not Wnd a causal relationship. In this report we want to describe a case of fetal death caused by congenital CMV infection.…”

Section: Introductionmentioning

confidence: 67%

“…Therefore, an association between maternal CMV infection and fetal death was proposed. However, it has been postulated that these studies suVer from a limited number of cases with fetal deaths and that the estimated impact of CMV infection is uncertain [14]. Eskild et al [14] could not Wnd an impact of maternal CMV infection and the risk of fetal death in a study based on a source population of nearly 36,000 pregnant women.…”

Section: Discussionmentioning

confidence: 99%

“…However, it has been postulated that these studies suVer from a limited number of cases with fetal deaths and that the estimated impact of CMV infection is uncertain [14]. Eskild et al [14] could not Wnd an impact of maternal CMV infection and the risk of fetal death in a study based on a source population of nearly 36,000 pregnant women. In another study by Moyo et al [13] no increased prevalence of maternal or fetal CMV infection in over 100 cases compared to nearly 100 controls was seen.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Congenital cytomegalovirus infection in pregnancy: a case report of fetal death in a CMV-infected woman

Kost

Mylonas

Kästner

et al. 2007

Arch Gynecol Obstet

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Objectives The human cytomegalovirus (CMV) is universally distributed among human populations as one of the most common cause of congenital infection with an incidence of about 0.15-2.0% in developed countries. However, controversial data concerning intrauterine fetal death caused by CMV infection exist. Method A case report. Results In this case report we present a stillbirth in the 18th week of pregnancy, caused by a maternal serological and fetal histological congenital CMV infection. Conclusion Every attending physician and obstetrician should be aware of the possibility of a primary or even recurrent congenital CMV infection that could be a reason for sudden unknown congenital fetal death.

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“…These estimates represent the prevalence of infection and phenotypic outcomes at birth and beyond, not the incidence of infection and associated outcomes during the whole of gestation, particularly during the highly ontogenic first trimester. Unfortunately, the effect of CMV infection on early human embryogenesis is uncertain because human studies of early malformation and CMV infection are small, retrospective and temporally truncated [7,[12][13][14][15][16]. Nevertheless, mouse models clearly demonstrate that CMV disrupts early organ and tissue development [17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus-induced embryopathology: mouse submandibular salivary gland epithelial-mesenchymal ontogeny as a model

et al. 2006

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Background: Human studies suggest, and mouse models clearly demonstrate, that cytomegalovirus (CMV) is dysmorphic to early organ and tissue development. CMV has a particular tropism for embryonic salivary gland and other head mesenchyme. CMV has evolved to co-opt cell signaling networks so to optimize replication and survival, to the detriment of infected tissues. It has been postulated that mesenchymal infection is the critical step in disrupting organogenesis. If so, organogenesis dependent on epithelial-mesenchymal interactions would be particularly vulnerable. In this study, we chose to model the vulnerability by investigating the cell and molecular pathogenesis of CMV infected mouse embryonic submandibular salivary glands (SMGs).

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Maternal antibodies against cytomegalovirus in pregnancy and the risk of fetal death and low birth weight

Abstract: This study does not support a causal relation between CMV infection in pregnancy and fetal death or low birth weight.

Cited by 11 publications

References 28 publications

Cytomegalovirus antibody status at 17–18 weeks of gestation and pre‐eclampsia: a case–control study of pregnant women in Norway

Cytomegalovirus antibody status at 17–18 weeks of gestation and pre‐eclampsia: a case–control study of pregnant women in Norway

Congenital cytomegalovirus infection in pregnancy: a case report of fetal death in a CMV-infected woman

Cytomegalovirus-induced embryopathology: mouse submandibular salivary gland epithelial-mesenchymal ontogeny as a model

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