Association of placental weight with cerebral palsy: population-based cohort study in Norway.

OBJECTIVE: To study the risk of cerebral palsy (CP) associated with placental weight, and also with placental weight/birthweight ratio and placental weight/birth length ratio. DESIGN: Population-based cohort study. SETTING: Perinatal data in the Medical Birth Registry of Norway were linked with clinical data in the CP Register of Norway. POPULATION: A total of 533 743 singleton liveborn children in Norway during 1999-2008. Of these, 779 children were diagnosed with CP. METHODS: Placental weight, placental weight/birthweight ratio, and placental weight/birth length ratio were grouped into gestational age-specific quartiles. Odds ratios (OR) with 95% confidence intervals (95% CI) for CP were calculated for children with exposure variables in the lowest or in the highest quartile, using the second to third quartile as the reference. MAIN OUTCOME MEASURES: CP and CP subtypes. RESULTS: Overall, children with low placental weight had increased risk for CP (OR 1.5, 95% CI 1.2-1.7). Low placental weight/birthweight ratio (OR 1.2, 95% CI 1.0-1.4) and low placental weight/birth length ratio (OR 1.5, 95% CI 1.2-1.8) were also associated with increased risk for CP. In children born at term, low placental weight was associated with a twofold increase in risk for spastic bilateral CP (including both quadriplegia and diplegia) (OR 2.1, 95% CI 1.5-2.9). In children born preterm, high placental ratios were associated with increased risk for spastic quadriplegia. CONCLUSIONS: Our results suggest that placental dysfunction may be involved in causal pathways leading to the more severe subtypes of CP. TWEETABLE ABSTRACT: Low placental weight increases the risk for cerebral palsy, especially for the spastic bilateral subtype.

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

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.