Prenatal Exposure to Preeclampsia and Long-Term Ophthalmic Morbidity of the Offspring.
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ABSTRACT:
SUBMITTER: Kedar Sade E
PROVIDER: S-EPMC7287970 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Obesity is a leading cause of morbidity world-wide. Maternal obesity is associated with adverse perinatal outcomes. Furthermore, Obesity has been associated with increased susceptibility to infections. The purpose of this study was to evaluate long-term pediatric infectious morbidity of children born to obese mothers. This population-based cohort analysis compared deliveries of obese (maternal pre-pregnancy BMI ≥ 30 kg/m2) and non-obese patients at a single tertiary medical center. Hospitalizations of the offspring up to the age of 18 years involving infectious morbidities were evaluated according to a predefined set of ICD-9 codes. A Kaplan-Meier survival curve was used to compare cumulative hospitalization incidence between the groups and Cox proportional hazards model was used to control for possible confounders. 249,840 deliveries were included. Of them, 3399 were children of obese mothers. Hospitalizations involving infectious morbidity were significantly more common in children born to obese mothers compared with non-obese patients (12.5% vs. 11.0%, p < 0.01). The Kaplan-Meier survival curve demonstrated a significantly higher cumulative incidence of infectious-related hospitalizations in the obese group (log rank p = 0.03). Using the Cox regression model, maternal obesity was found to be an independent risk factor for long-term infectious morbidity of the offspring (adjusted HR = 1.125, 95% CI 1.021-1.238, p = 0.017).
| S-EPMC6780342 | biostudies-literature
Project description:Preeclampsia is a dangerous hypertensive disorder of pregnancy with known links to negative child health outcomes. Here, we review epidemiological and basic neuroscience work from the past several decades linking prenatal preeclampsia to altered neurodevelopment. This work demonstrates increased rates of neuropsychiatric disorders [e.g., increased autism spectrum disorder, attention deficit hyperactivity disorder (ADHD)] in children of preeclamptic pregnancies, as well as increased rates of cognitive impairments [e.g., decreased intelligence quotient (IQ), academic performance] and neurological disease (e.g., stroke and epilepsy). We also review findings from multiple animal models of preeclampsia. Manipulation of key clinical preeclampsia processes in these models (e.g., placental hypoxia, immune dysfunction, angiogenesis, oxidative stress) causes various disruptions in offspring, including ones in white matter/glia, glucocorticoid receptors, neuroimmune outcomes, cerebrovascular structure, and cognition/behavior. This animal work implicates potentially high-yield targets that may be leveraged in the future for clinical application.
| S-EPMC7170230 | biostudies-literature
Project description:Background: Chorioamnionitis during labor exposes the fetus to an intrauterine state that may alter the future immune response and may expose the offspring to future susceptibility to infectious disease. We evaluated the long-term pediatric infectious morbidity of children born at term to mothers who have chorioamnionitis during labor. Methods: This was a population-based cohort analysis including only term singleton deliveries at a regional tertiary hospital between the years 1991 and 2021. Offspring to mothers with and without a diagnosis of chorioamnionitis during labor were compared. Offspring hospitalizations up to the age of 18 years involving infectious morbidity were evaluated using the Kaplan-Meier survival curve and a Cox regression model to control possible confounders. Results: A total of 331,598 deliveries were included, 988 (0.3%) of which were of mothers diagnosed with chorioamnionitis during labor. All infectious morbidity rates included in the analysis were comparable between groups. The Kaplan-Meier survival curves were similar for both groups (log-rank = 0.881) and the multivariable analysis ascertained that chorioamnionitis during labor was not a risk factor for offspring's long-term infectious morbidity (HR 0.929, 95%CI 0.818-1.054, p = 0.254). Conclusions: In our cohort, term chorioamnionitis during labor was not associated with a higher risk of pediatric hospitalization due to infections. The infectious/inflammatory state during labor did not expose nor increase the susceptibility of the term offspring to future infectious morbidity.
| S-EPMC10856245 | biostudies-literature
Project description:The aim of this study was to evaluate perinatal outcome and long-term offspring gastrointestinal morbidity of women with celiac disease. Perinatal outcomes, as well as long-term gastrointestinal morbidity of offspring of mothers with and without celiac disease were assessed. The study groups were followed until 18 years of age for gastrointestinal-related morbidity. For perinatal outcomes, generalized estimation equation (GEE) models were used. A Kaplan-Meier survival curve was used to compare cumulative incidence of long-term gastrointestinal morbidity, and Cox proportional hazards models were constructed to control for confounders. During the study period, 243,682 deliveries met the inclusion criteria, of which 212 (0.08%) were to mothers with celiac disease. Using GEE models, maternal celiac disease was noted as an independent risk factor for low birth weight and cesarean delivery. Offspring born to mothers with celiac disease had higher rates of gastrointestinal related morbidity (Kaplan-Meier log rank test P < 0.001). Using a Cox proportional hazards model, being born to a mother with celiac disease was found to be an independent risk factor for long-term gastrointestinal morbidity of the offspring. Pregnancy of women with celiac disease is independently associated with adverse perinatal outcome as well as higher risk for long-term gastrointestinal morbidity of offspring.
| S-EPMC6912641 | biostudies-literature
Project description:Although prenatal tobacco exposure (PTE) is associated with several adverse offspring mental health outcomes, mechanisms remain unclear. We test whether associations between PTE and offspring psychopathology are explained by birthweight, one of the earliest-occurring outcomes of PTE. The analysis focuses on 238 offspring from a family study of depression with (1) collected prenatal histories and (2) at least one clinical interview in adulthood to assess psychiatric problems. Exposure was categorized by maternal smoking of ≥10 cigarettes daily/nearly daily; diagnostic outcomes were confirmed by clinicians using the best-estimate procedure, blind to exposure. After adjusting for potential confounders, PTE was associated with 0.7lb(9%) lower birthweight (p=0.0002), increased rates of disruptive behavior disorders [males: OR=2.66(1.15,6.16), and (trend) substance use disorders [females: OR=2.23(0.98,5.09)], and decreased rates of mood disorders (males: OR=0.42(0.17,0.98)]. Birthweight was not independently associated with diagnoses and did not mediate the association between exposure and psychopathology. Maternal smoking has long-term adverse consequences for offspring. Although birthweight cannot be manipulated, smoking is a modifiable risk factor. Thus, cessation efforts focused on pregnant women may not only improve maternal wellbeing, but also mitigate adverse proximal (e.g., birthweight) and long-term (psychopathology) outcomes in offspring.
| S-EPMC5438886 | biostudies-literature
Project description:To evaluate the perinatal outcome of women with tuberculosis and to assess a possible association between maternal tuberculosis and long-term infectious morbidity of the offspring. Perinatal outcome and long-term infectious morbidity of offspring of mothers with and without tuberculosis were assessed. The study groups were followed until 18 years of age tracking infectious-related morbidity and infectious-related hospitalizations and then compared. For perinatal outcome, generalized estimation equation models were used. A Kaplan-Meier survival curve was used to compare cumulative incidence of long-term infectious morbidity. A Cox proportional hazards model was conducted to control for confounders. During the study period, 243,682 deliveries were included, of which 46 (0.018%) occurred in women with tuberculosis. Maternal tuberculosis was found to be independently associated with placental abruption, cesarean deliveries, and very low birth weight. However, offspring born to mothers with tuberculosis did not demonstrate higher rates of infectious-related morbidity. Maternal tuberculosis was not noted as an independent risk factor for long-term infectious morbidity of the offspring. In our study, maternal tuberculosis was found to be independently associated with adverse perinatal outcomes. However, higher risk for long-term infectious morbidity of the offspring was not demonstrated. Careful surveillance of these women is required.
| S-EPMC7565561 | biostudies-literature
Project description:ImportanceFew studies have investigated the association of long-term ambient ozone exposures with respiratory morbidity among individuals with a heavy smoking history.ObjectiveTo investigate the association of historical ozone exposure with risk of chronic obstructive pulmonary disease (COPD), computed tomography (CT) scan measures of respiratory disease, patient-reported outcomes, disease severity, and exacerbations in smokers with or at risk for COPD.Design, setting, and participantsThis multicenter cross-sectional study, conducted from November 1, 2010, to July 31, 2018, obtained data from the Air Pollution Study, an ancillary study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). Data analyzed were from participants enrolled at 7 (New York City, New York; Baltimore, Maryland; Los Angeles, California; Ann Arbor, Michigan; San Francisco, California; Salt Lake City, Utah; and Winston-Salem, North Carolina) of the 12 SPIROMICS clinical sites. Included participants had historical ozone exposure data (n = 1874), were either current or former smokers (≥20 pack-years), were with or without COPD, and were aged 40 to 80 years at baseline. Healthy persons with a smoking history of 1 or more pack-years were excluded from the present analysis.ExposuresThe 10-year mean historical ambient ozone concentration at participants' residences estimated by cohort-specific spatiotemporal modeling.Main outcomes and measuresSpirometry-confirmed COPD, chronic bronchitis diagnosis, CT scan measures (emphysema, air trapping, and airway wall thickness), 6-minute walk test, modified Medical Research Council (mMRC) Dyspnea Scale, COPD Assessment Test (CAT), St. George's Respiratory Questionnaire (SGRQ), postbronchodilator forced expiratory volume in the first second of expiration (FEV1) % predicted, and self-report of exacerbations in the 12 months before SPIROMICS enrollment, adjusted for demographics, smoking, and job exposure.ResultsA total of 1874 SPIROMICS participants were analyzed (mean [SD] age, 64.5 [8.8] years; 1479 [78.9%] white; and 1013 [54.1%] male). In adjusted analysis, a 5-ppb (parts per billion) increase in ozone concentration was associated with a greater percentage of emphysema (β = 0.94; 95% CI, 0.25-1.64; P = .007) and percentage of air trapping (β = 1.60; 95% CI, 0.16-3.04; P = .03); worse scores for the mMRC Dyspnea Scale (β = 0.10; 95% CI, 0.03-0.17; P = .008), CAT (β = 0.65; 95% CI, 0.05-1.26; P = .04), and SGRQ (β = 1.47; 95% CI, 0.01-2.93; P = .048); lower FEV1% predicted value (β = -2.50; 95% CI, -4.42 to -0.59; P = .01); and higher odds of any exacerbation (odds ratio [OR], 1.37; 95% CI, 1.12-1.66; P = .002) and severe exacerbation (OR, 1.37; 95% CI, 1.07-1.76; P = .01). No association was found between historical ozone exposure and chronic bronchitis, COPD, airway wall thickness, or 6-minute walk test result.Conclusions and relevanceThis study found that long-term historical ozone exposure was associated with reduced lung function, greater emphysema and air trapping on CT scan, worse patient-reported outcomes, and increased respiratory exacerbations for individuals with a history of heavy smoking. The association between ozone exposure and adverse respiratory outcomes suggests the need for continued reevaluation of ambient pollution standards that are designed to protect the most vulnerable members of the US population.
| S-EPMC6902160 | biostudies-literature
Project description:Atrazine and its metabolites are present at high concentrations in many water supplies in agro-intensive areas. Because residents in these areas drink water from sources fed from these contaminated supplies, we investigated the long-term immunotoxicity of combined prenatal and neonatal (perinatal) exposure to atrazine via drinking water, on the immune system in mice. At 6 months of age, upon immunization with heat-killed Streptococcus pneumoniae, the serum IgG antibody response against the T independent antigen phosphorylcholine was significantly higher in male, but not female, atrazine-exposed mice as compared with that in untreated controls. No alterations were present in all offspring in the serum antibody response against the T-dependent antigen pneumococcal surface protein A (PspA). ELISpot analysis showed only a small, insignificant reduction in PspA-specific IgG producing splenocytes in atrazine-treated male offspring. Interestingly, upon ex vivo stimulation with anti-CD3 and anti-CD28 antibodies, significant decreases in interleukin (IL)-2, tumor necrosis factor-α, interferon-γ, and IL-17A and a decreasing trend in IL-10 were observed in splenocytes from atrazine-exposed male, but not female mice. Analysis of thymic and splenic cell populations showed no effects of atrazine exposure in either sex. This is the first time that long-term changes in the immune response were observed after a perinatal exposure to atrazine and it demonstrates that these early life exposures can result in permanent changes to the immune system as well as a male bias in these effects.
| S-EPMC6432865 | biostudies-literature
Project description:BackgroundMaternal exposure to major stressors during pregnancy has been found to increase the risk of neurodevelopmental, cognitive and psychiatric disorders in the offspring. However, the association between prenatal exposure to earthquake and the risk of adult schizophrenia has yet to be examined.AimsTo explore the potential long-term effects of prenatal exposure to maternal stress on the risk of schizophrenia in adulthood, using the Great Tangshan Earthquake in 1976 as a natural experiment.MethodWe obtained data from the Second China National Sample Survey on Disability, and analysed 94 410 Chinese individuals born between 1975 and 1979. We obtained difference-in-differences estimates of the earthquake effects on schizophrenia by exploiting temporal variation in the timing of earthquake exposure across four birth cohorts born between 1975 and 1979, along with geographical variation in earthquake severity at the prefecture level. Schizophrenia was ascertained by psychiatrists using the ICD-10 classification. Earthquake severity was measured by seismic intensity.ResultsEarthquake cohort who experienced prenatal exposure to felt earthquake had higher risk of schizophrenia (odds ratio, 3.38; 95% CI 1.43-8.00) compared with the unexposed reference cohort. After specifying the timing of exposure by the trimester of pregnancy, prenatal exposure to felt earthquake during the first trimester of pregnancy increased the risk of adulthood schizophrenia significantly (odds ratio, 7.45; 95% CI 2.83-19.59).ConclusionsPrenatal (particularly early pregnancy) exposure to maternal stress after a major disaster substantially affects the mental health of Chinese adults.
| S-EPMC7557601 | biostudies-literature
Project description:Toll-like receptor 2 (TLR2), which recognizes several lipopeptides and transduces inflammatory signaling, promotes the pathogenesis of diet-induced dyslipidemia and obesity. TLR2-deficient mice were shown to have improved insulin sensitivity and reduced diet-induced metabolic syndrome. Previous studies demonstrated that prenatal lipopolysaccharide (LPS) exposure causes dyslipidemia accompanied by increased body weight and insulin resistance in offspring. To determine whether TLRs are involved in this complex abnormal phenotype, we analyzed TLR2 and TLR4 expression levels in adipose tissues from offspring with prenatal LPS-exposure (offspring-pLPS) and compared these levels to those of control offspring with prenatal saline-exposure (offspring-pSaline). TLR2 expression was specifically upregulated in the adipose tissue of offspring-pLPS mice. However, unexpectedly, TLR2-deficient offspring-pLPS mice not only presented with an abnormal phenotype comparable to that of wild-type offspring-pLPS mice but also exhibited significantly more severe hyperlipidemia. Our further analyses revealed a dramatic upregulation of TLR4 expression and overactivation of the TLR4/Myd88 signaling pathway in TLR2-deficient offspring-pLPS adipose tissue. Our finding suggests a compensatory genetic interaction between TLR2 and TLR4 in the context of prenatal inflammatory stimulation, and this interaction likely contributes to the prenatal inflammation-induced hyperlipidemia and lipid overload-induced obesity, thus providing a potential mechanism for the fetal origin of adult metabolic diseases.
| S-EPMC6713936 | biostudies-literature