Time trends and geographic variations in the prevalence of hypospadias in China

BACKGROUND: Little is known about the main epidemiologic characteristics of hypospadias prevalence in China. We investigated the time trends and geographic variations in the prevalence of hypospadias in China from 1996 to 2008. METHODS: Data were retrieved from the hospital‐based birth defects monitoring system in China from 1996 to 2008. We used prevalence ratios (PRs) to describe the difference in prevalence of hypospadias between urban and rural areas, as well as among different regions. Poisson regression was used to explore the long time trend for the prevalence of hypospadias and its regional disparity. RESULTS: The prevalences of hypospadias for isolated anomalies, multiple anomalies, and overall cases were 7.64, 1.39, and 9.03 per 10,000 births, respectively. The national PRs (urban vs. rural) of hypospadias for overall and isolated cases were 1.25 (95% confidence interval [CI], 1.16–1.35) and 1.27 (95% CI, 1.17–1.38), respectively. The highest prevalence (12.10 per 10,000 births) was observed in the eastern region. A positive correlation was found between the prevalence of hypospadias and maternal age (p < 0.01). The average annual increase of 7.43% (95% CI, 5.52–9.38%) was observed in the overall prevalence of hypospadias in China; it was 5.28% (95% CI, 4.16–6.43%) in urban areas, 9.79% (95% CI, 7.72–11.90%) in rural areas, 9.08% (95% CI, 6.36–11.86%) in the eastern region, 4.76% (95% CI, 2.93–6.62%) in the central region, and 6.57% (95% CI, 4.44–8.74%) in the western region.CONCLUSION: The increasing trends and differences of hypospadias prevalence by urban‐rural classification and geographical location suggest that environmental exposure and maternal age might have a critical role in the development of hypospadias. Birth Defects Research (Part A), 2012. © 2011 Wiley Periodicals, Inc.     

Maternal obesity and morbid obesity: The risk for birth defects in the offspring

BACKGROUND : The objective of this study was to assess, in a large data set from Swedish Medical Health Registries, whether maternal obesity and maternal morbid obesity were associated with an increased risk for various structural birth defects. METHODS : The study population consisted of 1,049,582 infants born in Sweden from January 1, 1995, through December 31, 2007, with known maternal weight and height data. Women were grouped in six categories of body mass index (BMI) according to World Health Organization classification. Infants with congenital birth defects were identified from three sources: the Swedish Medical Birth Registry, the Register of Birth Defects, and the National Patient Register. Maternal age, parity, smoking, and year of birth were thought to be potential confounders and were included as covariates in the adjusted odds ratio analyses. RESULTS : Ten percent of the study population was obese. Morbid obesity (BMI ≥ 40) occurred in 0.7%. The prevalence of congenital malformations was 4.7%, and the prevalence of relatively severe malformations was 3.2%. Maternal prepregnancy morbid obesity was associated with neural tube defects OR 4.08 (95% CI 1.87–7.75), cardiac defects OR 1.49 (95% CI 1.24–1.80), and orofacial clefts OR 1.90 (95% CI 1.27–2.86). Maternal obesity (BMI ≥ 30) significantly increased the risk of hydrocephaly, anal atresia, hypospadias, cystic kidney, pes equinovarus, omphalocele, and diaphragmatic hernia. CONCLUSION : The risk for a morbidly obese pregnant woman to have an infant with a congenital birth defect is small, but for society the association is important in the light of the ongoing obesity epidemic. Birth Defects Research (Part A), 2010. © 2009 Wiley‐Liss, Inc.     

孕妇肥胖与死产关系的Meta分析

目的:探讨孕妇超重或肥胖与死产的关系。方法:采用RevMan4.2.10版本软件中的Meta分析,检索Pubmed文献数据库中1980年～2008年有关死产的孕妇超重或肥胖因素文献,并进行定量综合分析。结果:经检索、筛选后纳入的有关死产的孕妇超重或肥胖因素文献11篇;经异质性检验,采用固定效应模型、随机效应模型进行定量综合分析。综合结果表明孕妇超重、孕妇肥胖对死产的影响OR值分别为1.21(95%CI:1.05-1.40)、1.69(95%CI:1.51-1.90)。结论:孕妇因超重或肥胖的死产率明显高于正常体重孕妇。     

Evaluation of cord blood immunoglobulin E and its association with maternal factors in a group of Iranian newborns

Allergic disorders are among the most common diseases around the world especially in children. Many factors contribute to the pathogenesis of atopic disorders, but early events during the pregnancy are very important. The aim of this study was to evaluate the level of cord blood immunoglobulin E (CB-IgE) and its association with maternal in a group of Iranian newborns. In a cross-sectional study, 163 pregnant women randomly selected and information about pregnancy and atopy were taken by questionnaire. Blood samples of mothers and matched cord blood were collected and total serum IgE levels were measured by enzyme-linked immunosorbent assay (ELISA) method. To rolling out the possibility of contamination with maternal blood, total IgA was checked for all the cord blood samples. Sixteen percent of mothers had the history of atopic diseases and the mean IgE level was significantly higher in an atopic than nonatopic mothers (241 vs 102, P < 0.001). About 73.9% of cord blood samples, had high IgE level (>0.9 IU/mL). The level of cord blood IgE (CB-IgE) was not significantly different in male and female newborns (2.14 vs 2.15 IU/mL). There was no significant correlation between maternal factors such as age, pregnancy variables, allergens exposure, smoking, and maternal IgE with cord blood IgE. The results of this study showed that CB-IgE is high in a remarkable number of samples; independent of maternal or fetal factors. Further studies need to evaluate the reasons for the high level of IgE in cord blood in our area.     

Evaluation of preterm births and birth defects in liveborn infants of US military women who received smallpox vaccine

BACKGROUND: Women serving in the US military have some unique occupational exposures, including exposure to vaccinations that are rarely required in civilian professions. When vaccinations are inadvertently given during pregnancy, such exposures raise special concerns. These analyses address health outcomes, particularly preterm births and birth defects, among infants who appear to have been exposed to maternal smallpox vaccination in pregnancy. METHODS: This retrospective cohort study included 31,420 infants born to active‐duty military women during 2003–2004. We used Department of Defense databases to define maternal vaccination and infant health outcomes. Multivariable regression models were developed to describe associations between maternal smallpox vaccination and preterm births and birth defects in liveborn infants. RESULTS: There were 7,735 infants identified as born to women ever vaccinated against smallpox, and 672 infants born to women vaccinated in the first trimester of pregnancy. In multivariable modeling, maternal smallpox vaccination in pregnancy was not associated with preterm or extreme preterm delivery. Maternal smallpox vaccination in the first trimester of pregnancy was not significantly associated with overall birth defects (OR 1.40; 95% CI: 0.94, 2.07), or any of seven specific defects individually modeled. CONCLUSIONS: Results may be reassuring that smallpox vaccine, when inadvertently administered to pregnant women, is not associated with preterm delivery or birth defects in liveborn infants. Birth Defects Research (Part A) 2008. © 2008 Wiley‐Liss, Inc.     

Mendelian randomization supports causality between maternal hyperglycemia and epigenetic regulation of leptin gene in newborns

Leptin is an adipokine that acts in the central nervous system and regulates energy balance. Animal models and human observational studies have suggested that leptin surge in the perinatal period has a critical role in programming long-term risk of obesity. In utero exposure to maternal hyperglycemia has been associated with increased risk of obesity later in life. Epigenetic mechanisms are suspected to be involved in fetal programming of long term metabolic diseases. We investigated whether DNA methylation levels near LEP locus mediate the relation between maternal glycemia and neonatal leptin levels using the 2-step epigenetic Mendelian randomization approach. We used data and samples from up to 485 mother-child dyads from Gen3G, a large prospective population-based cohort. First, we built a genetic risk score to capture maternal glycemia based on 10 known glycemic genetic variants (GRS₁₀) and showed it was an adequate instrumental variable (β = 0.046 mmol/L of maternal fasting glucose per additional risk allele; SE = 0.007; P = 7.8 × 10⁻¹¹; N = 467). A higher GRS₁₀ was associated with lower methylation levels at cg12083122 located near LEP (β = −0.072 unit per additional risk allele; SE = 0.04; P = 0.05; N = 166). Direction and effect size of association between the instrumental variable GRS₁₀ and methylation at cg12083122 were consistent with the negative association we observed using measured maternal glycemia. Lower DNA methylation levels at cg12083122 were associated with higher cord blood leptin levels (β = −0.17 log of cord blood leptin per unit; SE = 0.07; P = 0.01; N = 170). Our study supports that maternal glycemia is part of causal pathways influencing offspring leptin epigenetic regulation.