Department of Women's and Children's Health, Division of Reproductive and Perinatal Health Care, and the Department of Clinical Science and Education, Södersjukhuset (KI SÖS), Karolinska Institutet, Stockholm, and the Centre for Clinical Research, Dalarna, Falun, Sweden; and the Center for Evidence Based Practice, Faculty of Health Sciences, Bergen University College, and the Department of Clinical Science, Faculty of Medicine and Dentistry, University of Bergen, Bergen, Norway.
To investigate the association between advanced maternal age and adverse pregnancy outcomes and to compare the risks related to advanced maternal age with those related to smoking and being overweight or obese.
A population-based register study including all nulliparous women aged 25 years and older with singleton pregnancies at 22 weeks of gestation or greater who gave birth in Sweden and Norway from 1990 to 2010; 955,804 women were analyzed. In each national sample, adjusted odds ratios (ORs) of very preterm birth, moderately preterm birth, small for gestational age, low Apgar score, fetal death, and neonatal death in women aged 30-34 years (n=319,057), 35-39 years (n=94,789), and 40 years or older (n=15,413) were compared with those of women aged 25-29 years (n=526,545). In the Swedish sample, the number of additional cases of each outcome associated with maternal age 30 years or older, smoking, and overweight or obesity, respectively, was estimated in relation to a low-risk group of nonsmokers of normal weight and aged 25-29 years.
The adjusted OR of all outcomes increased by maternal age in a similar way in Sweden and Norway; and the risk of fetal death was increased even in the 30- to 34-year-old age group (Sweden n=826, adjusted OR 1.24, 95% confidence interval [CI] 1.13-1.37; Norway n=472, adjusted OR 1.26, 95% CI 1.12-1.41). Maternal age 30 years or older was associated with the same number of additional cases of fetal deaths (n=251) as overweight or obesity (n=251).
For the individual woman, the absolute risk for each of the outcomes was small, but for society, it may be significant as a result of the large number of women who give birth after the age of 30 years.
The aetiology of mental retardation (MR) was studied in a population-based series of Norwegian children derived from 30 037 children born between 1980 and 1985. The study included 178 children, 79 with severe MR (SMR) (IQ
We sought to evaluate the impact of later menarche on the risk of operative delivery.
We studied 38,069 eligible women (first labors at term with a singleton infant in a cephalic presentation) from the Norwegian Mothers and Child Cohort Study. The main exposures were the age at menarche and the duration of the interval between menarche and the first birth.
Poisson's regression with a robust variance estimator.
Operative delivery, defined as emergency cesarean or assisted vaginal delivery (ventouse extraction or forceps).
A 5 year increase in age at menarche was associated with a reduced risk of operative delivery (risk ratio [RR] 0.84, 95%CI 0.78, 0.89; p?
The aim of this study was to investigate birth rates and use of hormonal contraception in different age groups among women with epilepsy (WWE) in comparison to women without epilepsy.
Demographic data and medical information on more than 25,000 pregnant women (40,000 births), representing 95% of all pregnancies in Oppland County, Norway, were registered in the Oppland Perinatal Database in the period 1989-2011. Data were analyzed with respect to epilepsy diagnoses, and 176 women with a validated epilepsy diagnosis (303 pregnancies) were identified. Age-specific birth rates in these women were estimated and compared with age-specific birth rates in women without epilepsy in the same county.
In WWE over 25 years of age, birth rates were significantly lower than in those of the same age group without epilepsy. In women below 20 years of age, birth rates were similar in those with and without epilepsy. The use of hormonal contraceptives prior to pregnancy was lower among WWE under 25 years than in the corresponding age group without epilepsy.
Health professionals who counsel WWE who are of fertile age should be aware of the strongly reduced birth rates in WWE over 25 years of age, and the lower rates of use of contraceptives among young WWE.
Experiencing a stillbirth can be a potent stressor for psychological distress in the subsequent pregnancy and possibly after the subsequent birth. The impact on women's relationship with her partner in the subsequent pregnancy and postpartum remains uncertain. The objectives of the study were 1) To investigate the prevalence of anxiety and depression in the pregnancy following stillbirth and assess gestational age at stillbirth and inter-pregnancy interval as individual risk factors. 2) To assess the course of anxiety, depression and satisfaction with partner relationship up to 3 years after the birth of a live-born baby following stillbirth.
This study is based on data from the Norwegian Mother and Child Cohort Study, a population-based pregnancy cohort. The sample included 901 pregnant women: 174 pregnant after a stillbirth, 362 pregnant after a live birth and 365 previously nulliparous. Anxiety and depression were assessed by short-form subscales of the Hopkins Symptoms Checklist, and relationship satisfaction was assessed by the Relationship Satisfaction Scale. These outcomes were measured in the third trimester of pregnancy and 6, 18 and 36 months postpartum. Logistic regression models were applied to study the impact of previous stillbirth on depression and anxiety in the third trimester of the subsequent pregnancy and to investigate gestational age and inter-pregnancy interval as potential risk factors.
Women pregnant after stillbirth had a higher prevalence of anxiety (22.5%) and depression (19.7%) compared with women with a previous live birth (adjusted odds ratio (aOR) 5.47, 95% confidence interval (CI) 2.90-10.32 and aOR 1.91, 95% CI 1.11-3.27) and previously nulliparous women (aOR 4.97, 95% CI 2.68-9.24 and aOR 1.91, 95% CI 1.08-3.36). Gestational age at stillbirth (>?30 weeks) and inter-pregnancy interval?
Low Apgar score has been associated with higher risk for several neurological and psychiatric disorders, including cerebral palsy and intellectual disability. Studies of the association between Apgar score and autism spectrum disorder (ASD) have been inconsistent. We aimed to investigate (1) the association between low Apgar score at 5 min and risk for ASD, and (2) the modifying effects of gestational age and sex on this association in the largest multinational database of ASD. We included prospective data from 5.5 million individuals and over 33,000 cases of ASD from Norway, Sweden, Denmark and Western Australia who were born between 1984 and 2007. We calculated crude and adjusted risk ratios (RR) with 95% confidence intervals (95% CIs) for the associations between low Apgar score and ASD. All analyses for ASD were repeated for autistic disorder (AD). We used interaction terms and stratified analysis to investigate the effects of sex, gestational age, and birth weight on the association. In fully adjusted models, low Apgar scores (1-3) (RR, 1.42; 95% CI, 1.16-1.74), and intermediate Apgar scores (4-6) (RR, 1.50; 95% CI, 1.36-1.65) were associated with a higher RR of ASD than optimal Apgar score (7-10). The point estimates for low (RR, 1.88; 95% CI, 1.41-2.51) and intermediate Apgar score (RR, 1.54; 95% CI, 1.32-1.81) were larger for AD than for ASD. This study suggests that low Apgar score is associated with higher risk of ASD, and in particular AD. We did not observe any major modifying effects of gestational age and sex, although there seems to be substantial confounding by gestational age and birth weight on the observed association.
BACKGROUND: There is evidence that atopic disorders may begin in intra-uterine life; however, studies of birth characteristics and atopy show conflicting results. METHODS: We wanted to investigate the association of birth weight and head circumference with serum total or specific IgE, allergic rhinitis or eczema while addressing the influence of demographic and geographical factors. In this historic prospective cohort study, data were collected from birth records for 1683 men and women born in 1947-1973, from six Nordic-Baltic populations participating in the European Community Respiratory Health Survey. Blood tests for the measurement of serum total and specific IgE were available for 1494 subjects. In multiple regression analyses, adjustments were made for birth length, gender, age, study centre, adult body mass index, level of education, parental and adult smoking. RESULTS There was no association of birth weight (n=1230) and head circumference (n=285) with serum total IgE, specific IgE antibodies, allergic rhinitis or eczema. There were neither significant interactions by gender or age, nor heterogeneity between the study centres in the analyses of birth weight and adult atopy. CONCLUSION: Birth size was not associated with atopy among adults in this large Nordic-Baltic population study.
To assess the association of Apgar score 5 minutes after birth with cerebral palsy in both normal weight and low birthweight children, and also the association with the cerebral palsy subdiagnoses of quadriplegia, diplegia, and hemiplegia.
Population based cohort study.
The Medical Birth Registry of Norway was used to identify all babies born between 1986 and 1995. These data were linked to the Norwegian Registry of Cerebral Palsy in Children born 1986-95, which was established on the basis of discharge diagnoses at all paediatric departments in Norway.
All singletons without malformations born in Norway during 1986-95 and who survived the first year of life (n=543?064).
Cerebral palsy diagnosed before the age of 5 years.
988 children (1.8 in 1000) were diagnosed with cerebral palsy before the age of 5 years. In total, 11% (39/369) of the children with Apgar score of less than 3 at birth were diagnosed with cerebral palsy, compared with only 0.1% (162/179?515) of the children with Apgar score of 10 (odds ratio (OR) 53, 95% CI 35 to 80 after adjustment for birth weight). In children with a birth weight of 2500 g or more, those with an Apgar score of less than 4 were much more likely to have cerebral palsy than those who had an Apgar score of more than 8 (OR 125, 95% confidence interval 91 to 170). The corresponding OR in children weighing less than 1500 g was 5 (95% CI 2 to 9). Among children with Apgar score of less than 4, 10-17% in all birthweight groups developed cerebral palsy. Low Apgar score was strongly associated with each of the three subgroups of spastic cerebral palsy, although the association was strongest for quadriplegia (adjusted OR 137 for Apgar score 8, 95% CI 77 to 244).
Low Apgar score was strongly associated with cerebral palsy. This association was high in children with normal birth weight and modest in children with low birth weight. The strength of the association differed between subgroups of spastic cerebral palsy. Given that Apgar score is a measure of vitality shortly after birth, our findings suggest that the causes of cerebral palsy are closely linked to factors that reduce infant vitality.
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.
Population-based cohort study.
Perinatal data in the Medical Birth Registry of Norway were linked with clinical data in the CP Register of Norway.
A total of 533 743 singleton liveborn children in Norway during 1999-2008. Of these, 779 children were diagnosed with CP.
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.
CP and CP subtypes.
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.
Our results suggest that placental dysfunction may be involved in causal pathways leading to the more severe subtypes of CP.
Low placental weight increases the risk for cerebral palsy, especially for the spastic bilateral subtype.
Three studies so far have investigated the effect of prenatal non-steroidal anti-inflammatory drug (NSAID) exposure on birth weight and gestational age. The aim in this study was to evaluate the association of prenatal ibuprofen with birth weight and gestational age at birth, using a sibling design in an attempt to adjust for the possibility of familial confounding.
Using data from the Norwegian Mother and Child Cohort Study (MoBa) and the Medical Birth Registry of Norway (MBRN), we identified 28 597 siblings, of whom 1080 were prenatally exposed to ibuprofen and 26 824 were not exposed to any NSAID. Random and fixed effects models with propensity score adjustment were used to evaluate the effects of ibuprofen exposure on birth weight and gestational age.
Ibuprofen exposure during the first trimester was associated with a decrease in birth weight of 79 grams (95% confidence interval -133 to -25 grams). In contrast, second and/or third trimester exposure, and duration of exposure had no impact on the effect estimates. We found no association between ibuprofen exposure and gestational age at birth.
Our results suggest that prenatal exposure to ibuprofen during the first trimester is associated with a slight decrease in birth weight. The association does not seem to be attributable to shared genetics and family environment, and could be explained by either exposure to ibuprofen, or to non-shared confounding between pregnancies.
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