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1
المؤلفون: Mike Dolan Fliss, Mary E. Cox, Scott Proescholdbell, Anna E. Austin, Rebecca B. Naumann, Vito Di Bona
المصدر: American journal of public health. 111(9)
مصطلحات موضوعية: Adult, Pediatrics, medicine.medical_specialty, Young Adult, Pregnancy, medicine, North Carolina, Humans, Medical prescription, health care economics and organizations, Retrospective Studies, business.industry, Medicaid, Public Health, Environmental and Occupational Health, Infant, Newborn, Opioid use disorder, medicine.disease, Opioid-Related Disorders, United States, Buprenorphine, Analgesics, Opioid, Pregnancy Complications, Neonatal Opioid Withdrawal Syndrome, Prenatal Exposure Delayed Effects, Female, business, Neonatal Abstinence Syndrome
الوصف: Objectives. To estimate use of medication for opioid use disorder (MOUD) and prescription opioids in pregnancy among mothers of infants with neonatal opioid withdrawal syndrome (NOWS). Methods. We used linked 2016–2018 North Carolina birth certificate and newborn and maternal Medicaid claims data to identify infants with an NOWS diagnosis and maternal claims for MOUD and prescription opioids in pregnancy (n = 3395). Results. Among mothers of infants with NOWS, 38.6% had a claim for MOUD only, 14.3% had a claim for prescription opioids only, 8.1% had a claim for both MOUD and prescription opioids, and 39.1% did not have a claim for MOUD or prescription opioids in pregnancy. Non-Hispanic Black women were less likely to have a claim for MOUD than non-Hispanic White women. The percentage of infants born full term and normal birth weight was highest among women with MOUD or both MOUD and prescription opioid claims. Conclusions. In the 2016–2018 NC Medicaid population, 60% of mothers of infants with NOWS had MOUD or prescription opioid claims in pregnancy, underscoring the extent to which cases of NOWS may be a result of medically appropriate opioid use in pregnancy.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::16e26084bfd8bc1d20f7373abf22bf59Test
https://pubmed.ncbi.nlm.nih.gov/34383554Test -
2
المؤلفون: Keely Cheslack-Postava, Alan S. Brown
المصدر: Schizophrenia Research. 247:7-15
مصطلحات موضوعية: Psychosis, Offspring, Zika virus, Serology, 03 medical and health sciences, 0302 clinical medicine, Pregnancy, Risk Factors, medicine, Humans, Pregnancy Complications, Infectious, Biological Psychiatry, biology, Zika Virus Infection, business.industry, Confounding, COVID-19, Herpes Simplex, Zika Virus, medicine.disease, biology.organism_classification, 030227 psychiatry, Psychiatry and Mental health, Psychotic Disorders, Schizophrenia, Case-Control Studies, Prenatal Exposure Delayed Effects, Immunology, biology.protein, Female, Antibody, business, 030217 neurology & neurosurgery
الوصف: Epidemiologic studies have provided evidence that prenatal exposure to maternal infection is associated with an increased risk of developing schizophrenia in the offspring. Research over the past decade has added further to our understanding of the role of prenatal infection in schizophrenia risk. These investigations include several well-powered designs, and like some earlier studies, measured maternal antibodies to specific infectious agents in stored serum samples and large registers to identify clinically diagnosed infections during pregnancy. Convergent findings from antibody studies suggest that prenatal maternal infection with Toxoplasma gondii is associated with increased schizophrenia risk in the offspring, while associations with HSV-2 infection are likely attributable to confounding. Maternal influenza infection remains a viable candidate for schizophrenia, based on an early serological study, though there has been only one attempt to replicate this finding, with a differing methodology. A prior association between maternal serologically confirmed cytomegalovirus infections require further study. Clinically diagnosed maternal infection, particularly bacterial infection, also appears to be associated with increased risk of offspring schizophrenia, and heterogeneity in these findings is likely due to methodological differences between studies. Further clarification may be provided by future studies that address the timing, type, and clinical features of infections. Important insight may be gained by examining the long-term offspring outcomes in emerging epidemics such as Zika virus and COVID-19, and by investigating the interaction between exposure to prenatal infection and other risk or protective factors.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e45a89344f4eeeb7c949ba972a56f790Test
https://doi.org/10.1016/j.schres.2021.05.014Test -
3
المؤلفون: Charlotte Archuleta, Ashley Tian, Kartik Mody, Becky Micetic, Christine Wade
المصدر: American Journal of Perinatology. 39:1292-1298
مصطلحات موضوعية: Pediatrics, medicine.medical_specialty, Coronavirus disease 2019 (COVID-19), Inflammation, Third trimester, Fetus, Post-Acute COVID-19 Syndrome, Pregnancy, Seizures, medicine, Humans, Pregnancy Complications, Infectious, Prenatal exposure, SARS-CoV-2, Transmission (medicine), business.industry, Infant, Newborn, Pregnancy Outcome, COVID-19, Obstetrics and Gynecology, medicine.disease, Infectious Disease Transmission, Vertical, Prenatal Exposure Delayed Effects, Pediatrics, Perinatology and Child Health, Female, medicine.symptom, business, Ventriculomegaly
الوصف: The long-term effects of prenatal coronavirus disease 2019 (COVID-19) infection on the fetal brain are mostly unknown at this time; however, there is increasing evidence being published.Two cases of severe ventriculomegaly, neurological dysfunction, and seizures were found in neonates with prenatal exposure to COVID-19 infection during the first and third trimesters of pregnancy.Inflammation during the prenatal and neonatal periods may be associated with neurological disorders or injury. Despite the presumed lack of vertical transmission, post-COVID-19 syndrome and its associated inflammation may have an impact on the unborn fetus. Hyper-vigilance and dissemination of adverse findings are of significant importance as we navigate through this evolving pandemic and its effects.· Prenatal exposure to COVID-19 may affect the fetal brain.. · There is a possibility of neonatal neurological sequelae from maternal COVID-19.. · Does maternal COVID-19 infection cause infantile seizures?.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::16b456e7cb0d42c6ef4694f261ecf441Test
https://doi.org/10.1055/a-1704-1929Test -
4
المؤلفون: Bo Wah Leung, Daljit Singh Sahota, Tak Yeung Leung, Sakita Moungmaithong, Chi Chui Wang, Liona C. Poon
المصدر: The Journal of Maternal-Fetal & Neonatal Medicine. 35:8786-8793
مصطلحات موضوعية: Aspirin, Perinatal Exposure, business.industry, Anti-Inflammatory Agents, Non-Steroidal, Obstetrics and Gynecology, Ibuprofen, Embryo culture, Embryo, Embryo morphology, Rats, Andrology, Mice, Pregnancy, Prenatal Exposure Delayed Effects, Pediatrics, Perinatology and Child Health, medicine, Humans, Animals, Female, business, Prenatal exposure, Acetaminophen, medicine.drug
الوصف: Recent evidence from a meta-analysis indicates that maternal prenatal exposure, single or repeated, to non-steroidal anti-inflammatory drugs (NSAIDs) or non-opioid painkillers, is associated with increased risk of cerebral palsy and cognitive-behavioral disorders in offspring. One potential route of action is interference with the neurulation process and hence early brain development.To examine the effect of prenatal exposure to common NSAIDs and non-opioid drugs on neurulation using anMouse embryos from in-bred Institute of Cancer Research albino strain mice were exteriorized on embryonic day 7.5 and cultured for 48 h in either 1 mL heat-inactivated rat serum + 0.1% dimethyl sulfoxide ("Control") or 1 mL of rat serum supplemented with six increasing concentrations of laboratory-grade aspirin, paracetamol, and ibuprofen ("Experimental"). After culture, embryo morphological and developmental parameters were documented using standardized scoring systems at each dosage concentration. The assessed concentration in rat serum culture ranged from 1.23 to 13.57 mg/mL for aspirin and 0.06-4.93 mg/mL for paracetamol and ibuprofen. The equivalent respective human dosages were 600-6600 mg and 30-2400 mg.Between-group comparisons ("Control" vs "Experimental") and post-hoc pair-wise tests, adjusted for multiple comparisons, indicating no statistically significant effect on crown-rump length (This study has demonstrated that there are no safety concerns regarding high-dose aspirin, ibuprofen, and paracetamol on mice's embryonic development.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11c1f1d29a81ce007cdd02a4e9532d4fTest
https://doi.org/10.1080/14767058.2021.2005020Test -
5
المؤلفون: Bikash Medhi, Ashutosh Singh, Rahul Singh, Saurabh Sharma, Lokesh Saini, Amit Sharma, Rubal Singla, Ashish Jain, Manish Modi, Seema Bansal, Gitika Batra, Abhishek Mishra
المصدر: CNS & Neurological Disorders - Drug Targets. 21:399-408
مصطلحات موضوعية: Autism Spectrum Disorder, Cellular differentiation, Central nervous system, Gut flora, CREB, Pregnancy, medicine, Animals, Humans, gamma-Aminobutyric Acid, PI3K/AKT/mTOR pathway, Pharmacology, Valproic Acid, Behavior, Animal, biology, business.industry, General Neuroscience, medicine.disease, biology.organism_classification, Disease Models, Animal, medicine.anatomical_structure, Autism spectrum disorder, Prenatal Exposure Delayed Effects, Food Preservatives, biology.protein, Female, Enteric nervous system, Propionates, business, Neuroscience, medicine.drug
الوصف: Autism spectrum disorder (ASD) is a composite disorder of brain development with uncertain etiology and pathophysiology. Genetic factors are important in ASD causation, although environmental factors are also involved in ASD pathophysiology. Environmental factors might affect the genetic processes of brain development through the modulation of molecular pathways that might be involved with ASD. Valproic acid and propionic acid are the major environmental factors that serve as medicine and food preservative. VPA is used as an anti-epileptic medicine, but it has adverse effects on pregnant women and alters the developmental patterns of the embryo. It is a multi- targeting agent and affects 5-HT, GABA, etc. PPA is a secondary metabolite of gut microbiota that is commonly used as a food preservative. PPA plays a significant role in ASD causation by altering the several developmental molecular pathways like PTEN/Akt, mTOR/Gskβ, Cytokines activated pathways, etc., at the prenatal and neonatal stage. Moreover, ASD complexity might be increased by other important factors like vitamin A deficiency. Vitamin A is important for cortical brain development and neuronal cell differentiation. Additionally, several important genes such as RELN, Lhx2, CREB, IL-6, NMDA, BDNF, etc., are also altered in ASD and involved in brain development, central nervous system, and enteric nervous system. These genes affect neuronal differentiation, hyperactivity, oxidative stress, oxytocin, and GABA imbalance lead to improper behavior in autistic individuals. These genes are also studied in VPA and PPA ASD-like animal models. In this review, we explored the mechanical pathways that might be altered with VPA and PPA exposures at the embryonic developmental stage or neonatal developmental stage.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cc9df279a80ee27ebc25fbf2b412f922Test
https://doi.org/10.2174/1871527320666210806165430Test -
6
المؤلفون: Ted Reichborn-Kjennerud, Marcus R. Munafò, Ole A. Andreassen, Jeremy A. Labrecque, Luisa Zuccolo, Hannah M Sallis, Alexandra Havdahl, Eivind Ystrom, Elis Haan
المساهمون: Erasmus MC other, Epidemiology, Radiology & Nuclear Medicine
المصدر: Addiction
Addiction, 117(5), 1458-1471. Wiley-Blackwell Publishing Ltd
Haan, E, Sallis, H M, Zuccolo, L, Labrecque, J, Ystrom, E, Reichborn-Kjennerud, T, Andreassen, O A, Havdahl, K A & Munafo, M R 2021, ' Prenatal smoking, alcohol and caffeine exposure and maternal-reported attention deficit hyperactivity disorder symptoms in childhood : triangulation of evidence using negative control and polygenic risk score analyses ', Addiction . https://doi.org/10.1111/add.15746Testمصطلحات موضوعية: Longitudinal study, negative control, Offspring, Medicine (miscellaneous), smoking, Article, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, SDG 3 - Good Health and Well-being, Pregnancy, Risk Factors, Caffeine, GenR, Medicine, Attention deficit hyperactivity disorder, Humans, 030212 general & internal medicine, Longitudinal Studies, intrauterine effects, MoBa, caffeine, alcohol, business.industry, Confounding, Smoking, Odds ratio, ALSPAC, medicine.disease, 3. Good health, Psychiatry and Mental health, childhood ADHD, Attention Deficit Disorder with Hyperactivity, Prenatal Exposure Delayed Effects, polygenic risk score, Generation R, Female, business, 030217 neurology & neurosurgery, Demography, Cohort study
الوصف: Background and aims: Studies have indicated that maternal prenatal substance use may be associated with offspring attention deficit hyperactivity disorder (ADHD) via intrauterine effects. We measured associations between prenatal smoking, alcohol and caffeine consumption with childhood ADHD symptoms accounting for shared familial factors. Design: First, we used a negative control design comparing maternal and paternal substance use. Three models were used for negative control analyses: unadjusted (without confounders), adjusted (including confounders) and mutually adjusted (including confounders and partner's substance use). The results were meta-analysed across the cohorts. Secondly, we used polygenic risk scores (PRS) as proxies for exposures. Maternal PRS for smoking, alcohol and coffee consumption were regressed against ADHD symptoms. We triangulated the results across the two approaches to infer causality. Setting: We used data from three longitudinal pregnancy cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC) in the United Kingdom, Generation R study (GenR) in the Netherlands and Norwegian Mother, Father and Child Cohort study (MoBa) in Norway. Participants: Phenotype data available for children were: N ALSPAC = 5455–7751; N GENR = 1537–3119; N MOBA = 28 053–42 206. Genotype data available for mothers was: N ALSPAC = 7074; N MOBA = 14 583. Measurements: A measure of offspring ADHD symptoms at age 7–8 years was derived by dichotomizing scores from questionnaires and parental self-reported prenatal substance use was measured at the second pregnancy trimester. Findings: The pooled estimate for maternal prenatal substance use showed an association with total ADHD symptoms [odds ratio (OR) SMOKING = 1.11, 95% confidence interval (CI) = 1.00–1.23; OR ALCOHOL = 1.27, 95% CI = 1.08–1.49; OR CAFFEINE = 1.05, 95% CI = 1.00–1.11], while not for fathers (OR SMOKING = 1.03, 95% CI = 0.95–1.13; OR ALCOHOL = 0.83, 95% CI = 0.47–1.48; OR CAFFEINE = 1.02, 95% CI = 0.97–1.07). However, maternal associations did not persist in sensitivity analyses (substance use before pregnancy, adjustment for maternal ADHD symptoms in MoBa). The PRS analyses were inconclusive for an association in ALSPAC or MoBa. Conclusions: There appears to be no causal intrauterine effect of maternal prenatal substance use on offspring attention deficit hyperactivity disorder symptoms.
وصف الملف: application/pdf
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5d38cbb53ce09d0fb8381aa022932dffTest
http://www.scopus.com/inward/record.url?scp=85120466038&partnerID=8YFLogxKTest -
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المؤلفون: Siara Kate Rouzer, Marvin R. Diaz
المصدر: Neuropsychopharmacology. 47:2140-2149
مصطلحات موضوعية: Male, Agonist, medicine.medical_specialty, animal structures, Corticotropin-Releasing Hormone, medicine.drug_class, Anxiety, Inhibitory postsynaptic potential, Receptors, Corticotropin-Releasing Hormone, Amygdala, Rats, Sprague-Dawley, Basal (phylogenetics), Pregnancy, Internal medicine, medicine, Animals, Tonic (music), RNA, Messenger, Pharmacology, business.industry, Central Amygdaloid Nucleus, Rats, Psychiatry and Mental health, Endocrinology, medicine.anatomical_structure, Prenatal Exposure Delayed Effects, Prenatal alcohol exposure, Gestation, Female, medicine.symptom, business, Stress, Psychological
الوصف: Anxiety disorders are highly prevalent among individuals with a history of prenatal alcohol exposure (PAE), and adolescent rodents demonstrate anxiety-like behavior following moderate PAE on Gestational Day (G) 12. A likely systemic target of PAE is the stress peptide corticotrophin-releasing factor (CRF), as activation of CRF receptor 1 (CRFR1) in the medial nucleus of the central amygdala (CeM) is known to increase anxiety-like behavior in adults. To determine if CRF-CRFR1 interactions underly PAE-induced anxiety, functional changes in CRF system activity were investigated in adolescent male and female Sprague Dawley rats following G12 PAE. Compared to air-exposed controls, PAE increased basal spontaneous (s) inhibitory post-synaptic current (IPSC) frequency in the CeM of males, but not females. Furthermore, PAE blunted CRFR1-regulated miniature (m) IPSCs in a sex- and dose-specific manner, and only PAE males demonstrated tonic CRFR1 activity in the CeM. It was further determined that G12 PAE decreased CRFR1 mRNA in the CeM of males while increasing regional expression in females. Finally, infusion of a CRFR1 agonist into the CeM of adolescents produced a blunted expression of CRFR1-induced anxiety-like behavior exclusively in PAE males, mirroring the blunted physiology demonstrated by PAE males. Cumulatively, these data suggest that CRFR1 function within the CeM is age- and sex-specific, and PAE not only increases the expression of anxiety-like behavior, but may reduce the efficacy of treatment for PAE-induced anxiety through CRFR1-associated mechanisms. Therefore, future research will be necessary to develop targeted treatment of anxiety disorders in individuals with a history of PAE.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a67983d6fdbf133efa3e19011298ad62Test
https://doi.org/10.1038/s41386-022-01327-zTest -
8
المؤلفون: Gordon Taylor, Elis Haan, Marcus R. Munafò, Westmoreland Ke, Luisa Zuccolo, Laura Schellhas, Hannah M Sallis
المصدر: Haan, E, Westmoreland, K E, Schellhas, L, Sallis, H M, Taylor, G, Zuccolo, L & Munafò, M R 2022, ' Prenatal smoking, alcohol and caffeine exposure and offspring externalizing disorders : a systematic review and meta-analysis ', Addiction, vol. 117, no. 10, pp. 2602-2613 . https://doi.org/10.1111/add.15858Test
مصطلحات موضوعية: Conduct Disorder, ODD, Substance-Related Disorders, Offspring, Fetal alcohol syndrome, Medicine (miscellaneous), PsycINFO, alchol, smoking, systematic review, Pregnancy, Caffeine, Humans, ADHD, Medicine, caffeine, Ethanol, conduct disorder, business.industry, Smoking, medicine.disease, Newcastle–Ottawa scale, meta-analysis, Psychiatry and Mental health, Attention Deficit Disorder with Hyperactivity, Conduct disorder, Prenatal Exposure Delayed Effects, Meta-analysis, Autism, Female, business, Clinical psychology
الوصف: Background and aimsSeveral studies have indicated that there is an association between maternal prenatal substance use and offspring externalising disorders. However, it is uncertain whether this relationship is causal. Therefore, we updated a previously conducted systematic review to determine if the literature supports 1) a causal role of maternal prenatal substance use on offspring externalising disorders and 2) whether these associations differ across externalising disorders.MethodsWe searched Web of Science, Embase, PsycINFO and Medline databases. We included studies that examined smoking, alcohol or caffeine use during pregnancy as an exposure, and diagnosis of attention-deficit hyperactivity disorder (ADHD), conduct disorder (CD) and oppositional-defiant disorder (ODD) in offspring as an outcome. Studies on non-English language, fetal alcohol syndrome and comorbid autism spectrum disorders were excluded. Risk of bias assessment was conducted using Newcastle Ottawa Scale (NOS) and where possible meta-analysis was conducted for studies classed as low risk of bias.ResultsWe included 63 studies. All studies were narratively synthesised, and 7 studies were meta-analysed on smoking and ADHD. The majority of studies (46 studies) investigated the association between smoking and ADHD. Studies which accounted for genetic effects indicate that the association between smoking and ADHD is unlikely to be causal. Studies on alcohol exposure in all the outcomes reported inconsistent findings and no strong conclusions on causality can be made. Studies on caffeine exposure were mostly limited to ADHD and these studies do not support a causal effect.ConclusionsThere is no causal relationship between maternal smoking during pregnancy and attention-deficit hyperactivity (ADHD) in offspring. However, given that the majority of identified studies investigated the association between ADHD and smoking exposure, findings with alcohol and caffeine exposures and conduct disorder (CD) and oppositional-defiant disorder (ODD) need more research, especially using more genetically sensitive designs.
وصف الملف: application/pdf
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a99445faf5113ea19f2a6cbb399823ffTest
https://doi.org/10.1111/add.15858Test -
9
المصدر: Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. 7:231-238
مصطلحات موضوعية: Adult, Male, Offspring, Cognitive Neuroscience, Birth weight, Amygdala, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Pregnancy, medicine, Humans, Radiology, Nuclear Medicine and imaging, Longitudinal Studies, Young adult, Child, Biological Psychiatry, 030304 developmental biology, 0303 health sciences, Early embryonic stage, Depression, business.industry, Infant, Newborn, Beck Depression Inventory, Anatomy, medicine.disease, Magnetic Resonance Imaging, medicine.anatomical_structure, Prenatal stress, Prenatal Exposure Delayed Effects, Female, Neurology (clinical), business, 030217 neurology & neurosurgery
الوصف: Background Exposure to maternal stress in utero has long-term implications for the developing brain and has been linked with a higher risk of depression. The amygdala, which develops during the early embryonic stage and is critical for emotion processing, might be particularly sensitive. Methods Using data from a neuroimaging follow-up of the European Longitudinal Study of Pregnancy and Childhood prenatal birth cohort (n = 129, 47% men, 23–24 years old), we studied the impact of prenatal stress during the first and second halves of pregnancy on the volume of the amygdala and its nuclei in young adult offspring. We further evaluated the relationship between amygdala anatomy and offspring depressive symptomatology. Amygdala nuclei were parcellated using FreeSurfer’s automated segmentation pipeline. Depressive symptoms were measured via self-report using the Beck Depression Inventory. Results Exposure to stress during the first half of pregnancy was associated with smaller accessory basal (Cohen’s f2 = 0.27, false discovery rate [FDR]-corrected p [pFDR] = .03) and cortical (Cohen’s f2 = 0.29, pFDR = .03) nuclei volumes. This effect remained significant after correcting for sex, stress during the second half of pregnancy, maternal age at birth, birth weight, maternal education, and offspring’s age at magnetic resonance imaging. These two nuclei showed a quadratic relationship with Beck Depression Inventory scores in young adulthood, where both smaller and larger volumes were associated with more depressive symptoms (accessory basal nucleus: adj. R2 = 0.05, pFDR = .015; cortical nucleus: adj. R2 = 0.04, pFDR = .015). Conclusions We conclude that exposure to stress during the first half of pregnancy might have long-term implications for amygdala anatomy, which may in turn predict the experience of depressive symptoms in young adulthood.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::59aa5138115751a42f7efca076e1a676Test
https://doi.org/10.1016/j.bpsc.2021.07.009Test -
10
المؤلفون: Natalie C. Momen, Trine Munk-Olsen, Thalia K. Robakis, Veerle Bergink, Abraham Reichenberg, Xiaoqin Liu
المساهمون: Psychiatry
المصدر: Neuropsychopharmacology, 47(3), 759-766. Nature Publishing Group
Momen, N C, Robakis, T, Liu, X, Reichenberg, A, Bergink, V & Munk-Olsen, T 2022, ' In utero exposure to antipsychotic medication and psychiatric outcomes in the offspring ', Neuropsychopharmacology, vol. 47, no. 3, pp. 759-766 . https://doi.org/10.1038/s41386-021-01223-yTest
Neuropsychopharmacologyمصطلحات موضوعية: medicine.medical_specialty, PRESCRIPTION, SYMPTOMS, DOPAMINE SYSTEM, Offspring, medicine.medical_treatment, Article, Cohort Studies, Danish, SDG 3 - Good Health and Well-being, Pregnancy, SCHIZOPHRENIA, medicine, Humans, Child, Antipsychotic, Psychiatry, Proportional Hazards Models, RISK, Pharmacology, business.industry, Mental Disorders, Hazard ratio, BIPOLAR DISORDER, DEPRESSION, medicine.disease, ANTIDEPRESSANTS, Confidence interval, language.human_language, PREVALENCE, Discontinuation, Psychiatry and Mental health, In utero, Prenatal Exposure Delayed Effects, language, Female, business, PREGNANT-WOMEN, Antipsychotic Agents
الوصف: Information on neurodevelopmental effects of antenatal exposure to antipsychotics is limited to 10 studies, all examining children up to 5 years of age or less. The paper aimed to investigate the association between in utero exposure to antipsychotics and psychiatric outcomes in children using Danish nationwide registers. In total, 9011 liveborn singletons born 1998–2015 in Denmark whose mothers took antipsychotic medication before pregnancy were identified. Children whose mothers continued to take antipsychotics during pregnancy were compared with children of mothers who discontinued antipsychotics before pregnancy. As a negative control, paternal antipsychotic use in the same window was investigated. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards regression for the primary outcome of psychiatric disorders, as well for subcategories of psychiatric disorders. In total, 9.9% of children in the discontinuation group and 11.0% of children in the continuation group received a psychiatric disorder diagnosis during follow-up. The adjusted HR for psychiatric disorders among offspring in the continuation group compared to the discontinuation group was 1.10 (95% CI 0.93–1.30). For antipsychotic use in the fathers, the HR was 1.05 (95% CI 0.89–1.24). The study does not provide evidence of increased risk of psychiatric disorders among children of women who continue antipsychotic treatment during pregnancy. This was observed after accounting for the underlying risk conferred by maternal psychiatric disorders. This suggests women who need to continue antipsychotic medications during pregnancy can do so without adverse psychiatric outcomes for offspring.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d31c115b0a7e26d9d6ce7c6ac59d1548Test
https://pure.eur.nl/en/publications/b54db0ee-ed05-46ff-8ac0-1b9a9e699c2eTest