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Developmental origins of endometriosis: a Swedish cohort study

BACKGROUND: Endometriosis is a chronic condition affecting women of reproductive age and is associated with multiple health burdens. Yet, findings regarding its ‘developmental origins’ are inconsistent. We aimed to investigate the associations of birth characteristics with endometriosis. We also exp...

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Autores principales: Gao, Menghan, Allebeck, Peter, Mishra, Gita D, Koupil, Ilona
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6581098/
https://www.ncbi.nlm.nih.gov/pubmed/30661033
http://dx.doi.org/10.1136/jech-2018-211811
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author Gao, Menghan
Allebeck, Peter
Mishra, Gita D
Koupil, Ilona
author_facet Gao, Menghan
Allebeck, Peter
Mishra, Gita D
Koupil, Ilona
author_sort Gao, Menghan
collection PubMed
description BACKGROUND: Endometriosis is a chronic condition affecting women of reproductive age and is associated with multiple health burdens. Yet, findings regarding its ‘developmental origins’ are inconsistent. We aimed to investigate the associations of birth characteristics with endometriosis. We also explored potential mediation by adult social and reproductive factors. METHODS: This cohort study consisted of 3406 women born in Uppsala, Sweden, between 1933 and 1972. We used data from archived birth records and endometriosis diagnoses at ages 15–50 recorded in the national patient registers. Socioeconomic and reproductive characteristics were obtained from routine registers. HRs were estimated from Cox regression. RESULTS: During the follow-up, 111 women have been diagnosed with endometriosis, and most cases are external endometriosis (ie, outside the uterus, n=91). Lower standardised birth weight for gestational age was associated with increased rate of endometriosis (HR 1.35 per standard deviation decrease; 95% CI 1.08 to 1.67). This increased rate was also detected among women with fewer number of live births (HR 2.38; 95% CI 1.40 to 4.07 for one child vs ≥2 children; HR 6.09; 95% CI 3.88 to 9.57 for no child vs ≥2 children) and diagnosed infertility problem (HR 2.00; 95% CI 1.10 to 3.61) prior to endometriosis diagnosis. All the observed associations were stronger for external endometriosis. However, no evidence was found that number of births was the mediator of the inverse association between standardised birth weight and endometriosis. CONCLUSION: This study supports the developmental origins theory and suggests that exposure to growth restriction during the fetal period is associated with increased risk of endometriosis during reproductive years.
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spelling pubmed-65810982019-07-05 Developmental origins of endometriosis: a Swedish cohort study Gao, Menghan Allebeck, Peter Mishra, Gita D Koupil, Ilona J Epidemiol Community Health Research Report BACKGROUND: Endometriosis is a chronic condition affecting women of reproductive age and is associated with multiple health burdens. Yet, findings regarding its ‘developmental origins’ are inconsistent. We aimed to investigate the associations of birth characteristics with endometriosis. We also explored potential mediation by adult social and reproductive factors. METHODS: This cohort study consisted of 3406 women born in Uppsala, Sweden, between 1933 and 1972. We used data from archived birth records and endometriosis diagnoses at ages 15–50 recorded in the national patient registers. Socioeconomic and reproductive characteristics were obtained from routine registers. HRs were estimated from Cox regression. RESULTS: During the follow-up, 111 women have been diagnosed with endometriosis, and most cases are external endometriosis (ie, outside the uterus, n=91). Lower standardised birth weight for gestational age was associated with increased rate of endometriosis (HR 1.35 per standard deviation decrease; 95% CI 1.08 to 1.67). This increased rate was also detected among women with fewer number of live births (HR 2.38; 95% CI 1.40 to 4.07 for one child vs ≥2 children; HR 6.09; 95% CI 3.88 to 9.57 for no child vs ≥2 children) and diagnosed infertility problem (HR 2.00; 95% CI 1.10 to 3.61) prior to endometriosis diagnosis. All the observed associations were stronger for external endometriosis. However, no evidence was found that number of births was the mediator of the inverse association between standardised birth weight and endometriosis. CONCLUSION: This study supports the developmental origins theory and suggests that exposure to growth restriction during the fetal period is associated with increased risk of endometriosis during reproductive years. BMJ Publishing Group 2019-04 2019-01-19 /pmc/articles/PMC6581098/ /pubmed/30661033 http://dx.doi.org/10.1136/jech-2018-211811 Text en © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.
spellingShingle Research Report
Gao, Menghan
Allebeck, Peter
Mishra, Gita D
Koupil, Ilona
Developmental origins of endometriosis: a Swedish cohort study
title Developmental origins of endometriosis: a Swedish cohort study
title_full Developmental origins of endometriosis: a Swedish cohort study
title_fullStr Developmental origins of endometriosis: a Swedish cohort study
title_full_unstemmed Developmental origins of endometriosis: a Swedish cohort study
title_short Developmental origins of endometriosis: a Swedish cohort study
title_sort developmental origins of endometriosis: a swedish cohort study
topic Research Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6581098/
https://www.ncbi.nlm.nih.gov/pubmed/30661033
http://dx.doi.org/10.1136/jech-2018-211811
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