Asthma and atopic dermatitis are both regarded as atopic diseases. Being born too early is associated with increased risk of asthma, but some studies have indicated that the opposite might be true for atopic dermatitis. We explored in more detail the associations between preterm birth, asthma, and atopic dermatitis.
We analyzed data from Norwegian registries with prospectively collected data. All live births in Norway from 1967 through 2001 were followed through 2005 by linking the Medical Birth Registry of Norway to the National Insurance Scheme and to Statistics Norway. Only severe asthma and atopic dermatitis were registered in the National Insurance Scheme.
Of a total of 1,760,821 children, we identified 9,349 cases (0.5%) with severe asthma and 6,930 cases (0.4%) with severe atopic dermatitis. Compared with children born at term (37-41 wk gestation), preterm birth was associated with increased odds for severe asthma (odds ratio (OR) 1.7 (95% confidence interval (CI): 1.6-1.8) for 32-36 wk gestation and OR 3.6 (95% CI: 3.1-4.2) for 23-31 wk) and decreased odds for severe atopic dermatitis (OR 0.9 (95% CI: 0.8-1.0) for 32-36 wk gestation and OR 0.7 (95% CI: 0.5-1.0) for 23-31 wk). Adjustment for perinatal and socio-demographic factors weakened the association between gestational age and severe asthma, while slightly strengthening the association between gestational age and severe atopic dermatitis.
Preterm birth was associated with increased risk of severe asthma and decreased risk of severe atopic dermatitis.
To assess the effects of socioeconomic factors on the association between parity and long-term maternal mortality.
This was a population-based cohort study of mothers with births registered in the Medical Birth Registry of Norway during the period 1967-2009. We estimated age-specific (40-69 years) cardiovascular and noncardiovascular mortality ratios by number of births using Cox proportional hazard models. To assess effect modification by mothers' attained education, we stratified on low (less than 11 years) and high (11 years or greater) educational level. We further evaluated fathers' mortality by number of births using the same analytical approach.
Mothers with low education had higher mortality (cardiovascular: hazard ratio 2.62, 95% confidence interval [CI] 2.34-2.93, noncardiovascular: hazard ratio 1.67, 95% CI 1.62-1.73). Among mothers with low education, cardiovascular mortality increased linearly with each additional birth above one (P trend=.02). In contrast, among mothers with high education, cardiovascular mortality declined with added births (P trend=.045). For noncardiovascular mortality there was no association among mothers with low education, whereas mortality declined with increasing number of births among mothers with high education (P trend
Maternal asthma has been associated with adverse pregnancy outcomes. Little is known about the influence of other atopic diseases on pregnancy outcomes. We assessed how various maternal atopic diseases might affect preterm birth, stillbirth, and neonatal death.
By linking Norwegian national registries, we acquired information on maternal health, socio-demographic factors, pregnancy, birth, and neonatal outcome on all births in Norway from 1967 to 2003.
A total of 1?974?226 births were included. Of these, 1.8% had a record of maternal asthma, 3.4% of maternal atopic dermatitis, and 0.4% of maternal allergic rhinoconjunctivitis. Overall rates of preterm birth, stillbirth, and neonatal death were 6.0%, 0.6%, and 0.5%, respectively. After adjustments for possible confounders, maternal asthma was associated with increased risk of preterm birth (relative risk (RR), 1.15, [95% confidence interval (CI) 1.10, 1.21]). In contrast, maternal atopic dermatitis was associated with decreased risk of preterm birth (RR 0.90, [95% CI 0.86, 0.93]), stillbirth (RR 0.70, [95% CI 0.62, 0.79]), and neonatal death (RR 0.76, [95% CI 0.65, 0.90]). Similarly, maternal allergic rhinoconjunctivitis was associated with decreased risk of preterm birth (RR 0.84, [95% CI 0.76, 0.94]) and stillbirth (RR 0.40, [95% CI 0.25, 0.66]).
We confirmed the previously reported association of maternal asthma with increased risk for preterm birth. Unexpectedly, maternal atopic dermatitis and allergic rhinoconjunctivitis were associated with decreased risk of preterm birth and stillbirth. Mechanisms for these protective associations are unclear, and our findings require confirmation in further studies.
To assess the association of pre-eclampsia with later cardiovascular death in mothers according to their lifetime number of pregnancies, and particularly after only one child.
Prospective, population based cohort study.
Medical Birth Registry of Norway.
We followed 836,147 Norwegian women with a first singleton birth between 1967 and 2002 for cardiovascular mortality through linkage to the national Cause of Death Registry. About 23,000 women died by 2009, of whom 3891 died from cardiovascular causes. Associations between pre-eclampsia and cardiovascular death were assessed by hazard ratios, estimated by Cox regression analyses. Hazard ratios were adjusted for maternal education (three categories), maternal age at first birth, and year of first birth
The rate of cardiovascular mortality among women with preterm pre-eclampsia was 9.2% after having only one child, falling to 1.1% for those with two or more children. With term pre-eclampsia, the rates were 2.8% and 1.1%, respectively. Women with pre-eclampsia in their first pregnancy had higher rates of cardiovascular death than those who did not have the condition at first birth (adjusted hazard ratio 1.6 (95% confidence interval 1.4 to 2.0) after term pre-eclampsia; 3.7 (2.7 to 4.8) after preterm pre-eclampsia). Among women with only one lifetime pregnancy, the increase in risk of cardiovascular death was higher than for those with two or more children (3.4 (2.6 to 4.6) after term pre-eclampsia; 9.4 (6.5 to 13.7) after preterm pre-eclampsia). The risk of cardiovascular death was only moderately elevated among women with pre-eclamptic first pregnancies who went on to have additional children (1.5 (1.2 to 2.0) after term pre-eclampsia; 2.4 (1.5 to 3.9) after preterm pre-eclampsia). There was little evidence of additional risk after recurrent pre-eclampsia. All cause mortality for women with two or more lifetime births, who had pre-eclampsia in first pregnancy, was not elevated, even with preterm pre-eclampsia in first pregnancy (1.1 (0.87 to 1.14)).
Cardiovascular death in women with pre-eclampsia in their first pregnancy is concentrated mainly in women with no additional births. This association might be due to health problems that discourage or prevent further pregnancies rather than to pre-eclampsia itself. As a screening criterion for cardiovascular disease risk, pre-eclampsia is a strong predictor primarily among women with only one child-particularly with preterm pre-eclampsia.
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Although preterm delivery is a well-established risk factor for cerebral palsy (CP), preterm deliveries contribute only a minority of affected infants. There is little information on the relation of CP risk to gestational age in the term range, where most CP occurs.
To determine whether timing of birth in the term and postterm period is associated with risk of CP.
Population-based follow-up study using the Medical Birth Registry of Norway to identify 1,682,441 singleton children born in the years 1967-2001 with a gestational age of 37 through 44 weeks and no congenital anomalies. The cohort was followed up through 2005 by linkage to other national registries.
Absolute and relative risk of CP for children surviving to at least 4 years of age.
Of the cohort of term and postterm children, 1938 were registered with CP in the National Insurance Scheme. Infants born at 40 weeks had the lowest risk of CP, with a prevalence of 0.99/1000 (95% confidence interval [CI], 0.90-1.08). Risk for CP was higher with earlier or later delivery, with a prevalence at 37 weeks of 1.91/1000 (95% CI, 1.58-2.25) and a relative risk (RR) of 1.9 (95% CI, 1.6-2.4), a prevalence at 38 weeks of 1.25/1000 (95% CI, 1.07-1.42) and an RR of 1.3 (95% CI, 1.1-1.6), a prevalence at 42 weeks of 1.36/1000 (95% CI, 1.19-1.53) and an RR of 1.4 (95% CI, 1.2-1.6), and a prevalence after 42 weeks of 1.44 (95% CI, 1.15-1.72) and an RR of 1.4 (95% CI, 1.1-1.8). These associations were even stronger in a subset with gestational age based on ultrasound measurements: at 37 weeks the prevalence was 1.17/1000 (95% CI, 0.30-2.04) and the relative risk was 3.7 (95% CI, 1.5-9.1). At 42 weeks the prevalence was 0.85/1000 (95% CI, 0.33-1.38) and the relative risk was 2.4 (95% CI, 1.1-5.3). Adjustment for infant sex, maternal age, and various socioeconomic measures had little effect.
Compared with delivery at 40 weeks' gestation, delivery at 37 or 38 weeks or at 42 weeks or later was associated with an increased risk of CP.
Cleft lip defects are usually regarded as a single entity, with the assumption that an accompanying cleft palate represents the more severe form. The authors linked data from the Medical Birth Registry of Norway with medical records from two centralized centers to provide a population-based data set. They assessed the distribution of cleft lip only and cleft lip with cleft palate by covariate. Among 1.8 million Norwegian livebirths between 1967 and 1998, there were 1,572 cases of cleft lip with cleft palate and 1,122 cases with cleft lip only. Seventeen percent of those with cleft lip and palate had another defect compared with 9% of those with cleft lip only. For boys, the risk was greater for cleft lip and palate than for cleft lip only (odds ratio=2.4 vs. 1.8, p
We have previously reported a threefold risk of cleft palate only (CPO) among children homozygous for the less common allele A2 at the TaqI marker site of the transforming growth factor alpha gene (TGFA) (Jugessur et al. [2003a] Genet. Epidemiol. 24:230-239). Here we assess possible interaction between the child's TGFA TaqI A2A2 genotype and maternal cigarette smoking, alcohol consumption, use of multivitamins and folic acid. This was done by comparing the strength of genetic associations between strata of exposed and unexposed case-parent triads. We also looked for possible gene-gene interaction with the polymorphic variant C677T of the folic acid-metabolizing gene MTHFR. We analyzed a total of 88 complete CPO triads selected from a population-based study of orofacial clefts in Norway (May 1996-1998). No evidence of interaction was observed with either smoking or alcohol use. The risk associated with two copies of the A2 allele at TGFA TaqI was strong among children whose mothers did not use folic acid (relative risk=4.5, 95% confidence interval=1.3-15.7), and was only marginal among children whose mothers reported using folic acid (RR=1.4, 95% CI=0.2-12.7). Although the interaction between the child's genotypes at TGFA TaqI and MTHFR-C677T was not statistically significant, the effect of the TGFA TaqI A2A2 genotype appeared to be stronger among children with either one or two copies of the T-allele at C677T (RR=4.0, 95% CI=1.1-13.9) compared to children homozygous for the C-allele (RR=1.7, 95% CI=0.2-15.7). In conclusion, we find little evidence of interaction between the child's genotypes at TGFA TaqI and various exposures for cleft palate, with the possible exception of folic acid intake.
The purpose of MOthers and BAbies in Norway and Denmark cerebral palsy (MOBAND-CP) was to study CP aetiology in a prospective design.
MOBAND-CP is a cohort of more than 210 000 children, created as a collaboration between the world's two largest pregnancy cohorts-the Norwegian Mother and Child Cohort study (MoBa) and the Danish National Birth Cohort. MOBAND-CP includes maternal interview/questionnaire data collected during pregnancy and follow-up, plus linked information from national health registries.
Initial harmonisation of data from the 2 cohorts has created 140 variables for children and their mothers. In the MOBAND-CP cohort, 438 children with CP have been identified through record linkage with validated national registries, providing by far the largest such sample with prospectively collected detailed pregnancy data. Several studies investigating various hypotheses regarding CP aetiology are currently on-going.
Additional data can be harmonised as necessary to meet requirements of new projects. Biological specimens collected during pregnancy and at delivery are potentially available for assay, as are results from assays conducted on these specimens for other projects. The study size allows consideration of CP subtypes, which is rare in aetiological studies of CP. In addition, MOBAND-CP provides a platform within the context of a merged birth cohort of exceptional size that could, after appropriate permissions have been sought, be used for cohort and case-cohort studies of other relatively rare health conditions of infants and children.
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Early delivery and low birth weight are strong predictors of the urogenital anomalies cryptorchidism (undescended testis) and hypospadias. Understanding these associations may lead to important etiologic clues. Therefore, the authors revisited the prevailing hypotheses regarding fetal growth restriction as a risk factor for urogenital anomalies. They studied a population of 934,538 Danish boys born alive between January 1, 1980, and December 31, 2008. Cryptorchidism and hypospadias were associated with low weight-for-gestational-age, an indicator of fetal growth restriction, and furthermore the authors observed strong interaction with early delivery. Low birth weight in a singleton compared with the mean birth weight of all singleton brothers in the family or in a twin compared with the male co-twin was associated with higher risk of urogenital anomalies, suggesting an effect of relative fetal growth restriction within families. Contrary to previous reports, newborns' body dimensions assessed independently of birth weight were not associated with urogenital anomalies. The hypothesis that shared factors cause both fetal growth restriction and urogenital anomalies was supported by comparison of urogenital anomaly risks in singletons and twins and by patterns of cryptorchidism and hypospadias co-occurrence in individuals. These novel insights might also extend to other male reproductive conditions with prenatal etiology.
Preterm delivery may predict an increased risk of cardiovascular disease in mothers, providing opportunities for prevention. No study had examined whether gestation length within the term period predicts future CVD, and there are few data segregating spontaneous from medically indicated deliveries.
We used proportional hazards models to predict CVD death by gestation length, adjusted for age, education, and delivery year among 688,662 women with births from 1967 through 1998 in the Medical Birth Registry of Norway. Mothers were traced in the National Cause of Death Registry through 2009; there were 2324 CVD deaths.
Compared with women who delivered spontaneously at 39-41 weeks' gestation, women who spontaneously delivered earlier had higher risks of CVD death. Hazard ratios were 1.9 at 22-31 weeks, 2.2 at 32-34 weeks, 1.6 at 35-36 weeks, and 1.4 at 37-38 weeks. Risks were higher among women with medically indicated deliveries (hazard ratio, 4.8 at 22-31 weeks, 2.7 at 32-34 weeks, 4.3 at 35-36 weeks, and 1.6 at 37-38 weeks compared with spontaneous deliveries at 39-41 weeks). Neither spontaneous nor indicated delivery after 41 weeks was associated with CVD mortality. Risks were highest with recurrent preterm pregnancies, and for women who delivered only one child, especially if that delivery was preterm.
Women who deliver spontaneously before 37 weeks had a 2-fold increased risk of CVD mortality compared with women who had delivered after 38 weeks. Even women with spontaneous deliveries at early term (37-38 weeks) had a 41% elevated risk of CVD death compared with women delivering at 39-41 weeks.