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Search: WFRF:(Fernández de la Cruz Lorena) > Maternal polycystic...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005472naa a2200577 4500
001oai:DiVA.org:oru-79502
003SwePub
008200129s2020 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:143609274
009oai:gup.ub.gu.se/279319
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-795022 URI
0247 a https://doi.org/10.1017/S00332917190004242 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1436092742 URI
0247 a https://gup.ub.gu.se/publication/2793192 URI
040 a (SwePub)orud (SwePub)kid (SwePub)gu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Cesta, Carolyn E.u Karolinska Institutet4 aut
2451 0a Maternal polycystic ovary syndrome and risk of neuropsychiatric disorders in offspring :b prenatal androgen exposure or genetic confounding?
264 1b Cambridge University Press,c 2020
338 a print2 rdacarrier
520 a BACKGROUND: Maternal polycystic ovary syndrome (PCOS) has been proposed as a model for investigating the role of prenatal androgen exposure in the development of neuropsychiatric disorders. However, women with PCOS are at higher risk of developing psychiatric conditions and previous studies are likely confounded by genetic influences.METHODS: A Swedish nationwide register-based cohort study was conducted to disentangle the influence of prenatal androgen exposure from familial confounding in the association between maternal PCOS and offspring attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and Tourette's disorder and chronic tic disorders (TD/CTD). PCOS-exposed offspring (n = 21 280) were compared with unrelated PCOS-unexposed offspring (n = 200 816) and PCOS-unexposed cousins (n = 17 295). Associations were estimated with stratified Cox regression models.RESULTS: PCOS-exposed offspring had increased risk of being diagnosed with ADHD, ASD, and TD/CTD compared with unrelated PCOS-unexposed offspring. Associations were stronger in girls for ADHD and ASD but not TD/CTD [ADHD: adjusted hazard ratio (aHR) = 1.61 (95% confidence interval (CI) 1.31-1.99), ASD: aHR = 2.02 (95% CI 1.45-2.82)] than boys [ADHD: aHR = 1.37 (95% CI 1.19-1.57), ASD: aHR = 1.46 (95% CI 1.21-1.76)]. For ADHD and ASD, aHRs for girls were stronger when compared with PCOS-unexposed cousins, but slightly attenuated for boys.CONCLUSIONS: Estimates were similar when accounting for familial confounding (i.e. genetics and environmental factors shared by cousins) and stronger in girls for ADHD and ASD, potentially indicating a differential influence of prenatal androgen exposure v. genetic factors. These results strengthen evidence for a potential causal influence of prenatal androgen exposure on the development of male-predominant neuropsychiatric disorders in female offspring of women with PCOS.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Hälsovetenskapx Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi0 (SwePub)303022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Health Sciencesx Public Health, Global Health, Social Medicine and Epidemiology0 (SwePub)303022 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Psykiatri0 (SwePub)302152 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Psychiatry0 (SwePub)302152 hsv//eng
653 a Androgens
653 a epidemiology
653 a familial confounding
653 a neuropsychiatric disorders
653 a polycystic ovary syndrome
7001 a Öberg, Anna S.u Karolinska Institutet4 aut
7001 a Ibrahimson, Abrahamu Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden4 aut
7001 a Yusuf, Ikramu Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden4 aut
7001 a Larsson, Henrik,d 1975-u Karolinska Institutet,Örebro universitet,Institutionen för medicinska vetenskaper,Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden4 aut0 (Swepub:oru)hiln
7001 a Almqvist, Catarinau Karolinska Institutet4 aut
7001 a D'Onofrio, Brian M.u Karolinska Institutet4 aut
7001 a Bulik, Cynthia M.u Karolinska Institutet4 aut
7001 a Fernández de la Cruz, Lorenau Karolinska Institutet4 aut
7001 a Mataix-Cols, Davidu Karolinska Institutet4 aut
7001 a Landén, Mikael,d 1966u Gothenburg University,Göteborgs universitet,Karolinska Institutet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xlandt
7001 a Rosenqvist, Mina A.u Karolinska Institutet4 aut
7102 a Karolinska Institutetb Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden4 org
7730 t Psychological Medicined : Cambridge University Pressg 50:4, s. 616-624q 50:4<616-624x 0033-2917x 1469-8978
8564 u https://doi.org/10.1017/S0033291719000424y Fulltext
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-79502
8564 8u https://doi.org/10.1017/S0033291719000424
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:143609274
8564 8u https://gup.ub.gu.se/publication/279319

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