Obstetric comprehensive approach to pre-term birth and growth restriction and its relationship with chronic adult diseases
DOI:
https://doi.org/10.29193/RMU.36.1.9Keywords:
FETAL GROWTH RETARDATION, PREMATURE BIRTH, CHRONIC DISEASES, EPIGENOMICSAbstract
Preterm birth and growth restriction are obstetric syndromes which share etiopathogenic and pathophysiological mechanisms that often interact and feed from each other. Etiologically, they may be classified into inflammation, maternal stress, low socio-economic background and vulnerability of rights, endocrine disruptors, diet and microbiota alterations and vascular conditions, depending on specific conditions. These conditions, either in isolation or more often combined, create an unfavorable environment for the development of pregnancy, causing specific effects such as maternal immune response that may be mediated by infections, the activation of the hypothalamic-pituitary-adrenal (HPA) axis, drop in progesterone levels, dysbiosis, both intestinal and vaginal, and placental dysfunction caused by ageing. The unfavorable environment has an impact on the utero-feto-placental unit resulting in either preterm birth of growth restriction, depending on the predominance of the different responses. Regardless of the prevailing syndromic response, both preterm birth and growth restriction share the development of the thrifty pheno-genotype, essential for fetal survival. The cost of this epigenetic modulation is an increase in chronic adult diseases, which, conceptually, are transmissible diseases due to social vulnerability where these people live.
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(2) Lee A, Kozuki N, Cousens S, Stevens G, Blencowe H, Silveira M, et al. Estimates of burden and consequences of infants born small for gestational age in low and middle income countries with INTERGROWTH-21 st standard: analysis of CHERG datasets. BMJ 2017; 358:j3677.
(3) Drake A, Walker B. The intergenerational effects of fetal programming: non-genomic mechanisms for the inheritance of low birth weight and cardiovascular risk. J Endocrinol 2004; 180(1):1-16.
(4) Sykes L, MacIntyre D, Yap X, Teoh T, Bennett P. The Th1:th2 dichotomy of pregnancy and preterm labour. Mediators Inflamm 2012; 2012:967629.
(5) Hill A, Pallitto C, McCleary-Sills J, Garcia-Moreno C. A systematic review and meta-analysis of intimate partner violence during pregnancy and selected birth outcomes. Int J Gynaecol Obstet 2016; 133(3):269-76.
(6) Stanislawski M, Dabelea D, Wagner B, Sontag M, Lozupone C, Eggesbø M. Pre-pregnancy weight, gestational weight gain, and the gut microbiota of mothers and their infants. Microbiome 2017; 5(1):113.
(7) Ferguson K, McElrath T, Chen Y, Mukherjee B, Meeker J. Urinary phthalate metabolites and biomarkers of oxidative stress in pregnant women: a repeated measures analysis. Environ Health Perspect 2015; 123(3):210-6.
(8) Porter T, Kent S, Su W, Beck H, Gohlke J. Spatiotemporal association between birth outcomes and coke production and steel making facilities in Alabama, USA: a cross-sectional study. Environ Health 2014; 13:85.
(9) Burton G, Fowden A, Thornburg K. Placental origins of chronic disease. Physiol Rev 2016; 96(4):1509-65.
(10) Burton G, Jauniaux E. Pathophysiology of placental-derived fetal growth restriction. Am J Obstet Gynecol 2018; 218(2S):S745-61.
(11) Kajantie E. Fetal origins of stress-related adult disease. Ann N Y Acad Sci 2006; 1083:11-27.
(12) Hardy D, Janowski B, Corey D, Mendelson C. Progesterone receptor plays a major antiinflammatory role in human myometrial cells by antagonism of nuclear factor-kappaB activation of cyclooxygenase 2 expression. Mol Endocrinol 2006; 20(11):2724-33.
(13) Maršál K. Preeclampsia and intrauterine growth restriction: placental disorders still not fully understood. J Perinat Med 2017; 45(7):775-7.
(14) Vidal A, Benjamin Neelon S, Liu Y, Tuli A, Fuemmeler B, Hoyo C, et al. Maternal stress, preterm birth, and DNA methylation at imprint regulatory sequences in humans. Genet Epigenet 2014; 6:37-44.
(15) Radtke K, Ruf M, Gunter H, Dohrmann K, Schauer M, Meyer A, et al. Transgenerational impact of intimate partner violence on methylation in the promoter of the glucocorticoid receptor. Transl Psychiatry 2011; 1(7):e21.
(16) Tehranifar P, Wu H, Fan X, Flom J, Ferris J, Cho Y, et al. Early life socioeconomic factors and genomic DNA methylation in mid-life. Epigenetics 2013; 8(1):23-7.
(17) Liu Y, Murphy S, Murtha A, Fuemmeler B, Schildkraut J, Huang Z, et al. Depression in pregnancy, infant birth weight and DNA methylation of imprint regulatory elements. Epigenetics 2012; 7(7):735-46.
(18) Tobi E, Lumey L, Talens R, Kremer D, Putter H, Stein A, et al. DNA methylation differences after exposure to prenatal famine are common and timing- and sex-specific. Hum Mol Genet 2009; 18(21):4046-53.
(19) Krautkramer K, Dhillon R, Denu J, Carey H. Metabolic programming of the epigenome: host and gut microbial metabolite interactions with host chromatin. Transl Res 2017; 189:30-50.
(20) Burris H, Baccarelli A, Wright R, Wright R. Epigenetics: linking social and environmental exposures to preterm birth. Pediatr Res 2016; 79(1-2):136-40.
(21) Parets S, Conneely K, Kilaru V, Menon R, Smith A. DNA methylation provides insight into intergenerational risk for preterm birth in African Americans. Epigenetics 2015; 10(9):784-92.
(22) Montirosso R, Casini E, Provenzi L, Putnam S, Morandi F, Fedeli C, et al. A categorical approach to infants’ individual differences during the Still-Face paradigm. Infant Behav Dev 2015; 38:67-76.
(23) Banister C, Koestler D, Maccani M, Padbury J, Houseman E, Marsit C. Infant growth restriction is associated with distinct patterns of DNA methylation in human placentas. Epigenetics 2011; 6(7):920-7.
(24) Ding Y, Cui H. Integrated analysis of genome-wide DNA methylation and gene expression data provide a regulatory network in intrauterine growth restriction. Life Sci 2017; 179:60-5.
(25) Chen P, Chu A, Liao W, Rubbi L, Janzen C, Hsu F, et al. Prenatal growth patterns and birthweight are associated with differential dna methylation and gene expression of cardiometabolic risk genes in human placentas: a discovery-based approach. Reprod Sci 2018; 25(4):523-39.
(26) Barker D. The developmental origins of chronic adult disease. Acta Paediatr Suppl 2004; 93(446):26-33.
(27) Briozzo L, Coppola F, Gesuele J, Tomasso G. Restricción de crecimiento fetal, epigenética y transmisión trans generacional de las enfermedades crónicas y la pobreza. Horiz Med 2013; 13(4):45-53.
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Briozzo L, Viroga S. Obstetric comprehensive approach to pre-term birth and growth restriction and its relationship with chronic adult diseases. Rev. Méd. Urug. [Internet]. 2020 Feb. 17 [cited 2024 Dec. 4];36(1):85-92. Available from: https://revista.rmu.org.uy/index.php/rmu/article/view/504
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