Background: There are concerns about the effects of in utero exposure to antiretroviral drugs (ARVs) on the development of HIV-exposed but uninfected (HEU) children. The aim of this study was to evaluate whether in utero exposure to ARVs is associated with lower birth weight/height and reduced growth during the first 2 years of life.
Methods: This cohort study was conducted among HEU infants born between 1996 and 2010 in Tertiary children's hospital in Rio de Janeiro, Brazil. Weight was measured by mechanical scale, and height was measured by measuring board. Z-scores for weight-for-age (WAZ), length-for-age (LAZ) and weight-for-length were calculated. We modeled trajectories by mixed-effects models and adjusted for mother's age, CD4 cell count, viral load, year of birth and family income.
Results: A total of 588 HEU infants were included of whom 155 (26%) were not exposed to ARVs, 114 (19%) were exposed early (first trimester) and 319 (54%) later. WAZ were lower among infants exposed early compared with infants exposed later: adjusted differences were -0.52 (95% confidence interval [CI]: -0.99 to -0.04, P = 0.02) at birth and -0.22 (95% CI: -0.47 to 0.04, P = 0.10) during follow-up. LAZ were lower during follow-up: -0.35 (95% CI: -0.63 to -0.08, P = 0.01). There were no differences in weight-for-length scores. Z-scores of infants exposed late during pregnancy were similar to unexposed infants.
Conclusions: In HEU children, early exposure to ARVs was associated with lower WAZ at birth and lower LAZ up to 2 years of life. Growth of HEU children needs to be monitored closely.
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http://dx.doi.org/10.1097/INF.0000000000000926 | DOI Listing |
Introduction: Adverse exposures in utero might cause adaptations of cardiovascular and metabolic organ development, predisposing individuals to an adverse cardio-metabolic risk profile from childhood onwards. We hypothesized that adaptations in metabolic pathways underlie these associations and examined associations of metabolite profiles at birth with childhood cardio-metabolic risk factors.
Methods: The study included 763 mother-child pairs participating in an ongoing population-based prospective cohort study with an overall low disease risk.
Exp Physiol
January 2025
Robinson Research Institute, University of Adelaide, Adelaide, South Australia, Australia.
The mechanisms linking maternal asthma (MA) exposure in utero and subsequent risk of asthma in childhood are not fully understood. Pathological airway remodelling, including reticular basement membrane thickening, has been reported in infants and children who go on to develop asthma later in childhood. This suggests altered airway development before birth as a mechanism underlying increased risk of asthma in children exposed in utero to MA.
View Article and Find Full Text PDFEndocrinology
January 2025
Cardiopulmonary Immunotoxicology Branch, Public Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, NC.
Maternal exposure to ozone during implantation results in reduced fetal weight gain in rats. Offspring from ozone-exposed dams demonstrate sexually dimorphic risks to high-fat diet feeding in adolescence. To better understand the adolescent hepatic metabolic landscape following fetal growth restriction, RNA sequencing was performed to characterize the effects of ozone-induced fetal growth restriction on male and female offspring.
View Article and Find Full Text PDFLiver Int
February 2025
Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Background And Aims: Maternal obesity increases the risk of the paediatric form of metabolic dysfunction-associated steatotic liver disease (MASLD), affecting up to 30% of youth, but the developmental origins remain poorly understood.
Methods: Using a Japanese macaque model, we investigated the impact of maternal Western-style diet (mWSD) or chow diet followed by postweaning WSD (pwWSD) or chow diet focusing on bile acid (BA) homeostasis and hepatic fibrosis in livers from third-trimester fetuses and 3-year-old juvenile offspring.
Results: Juveniles exposed to mWSD had increased hepatic collagen I/III content and stellate cell activation in portal regions.
Environ Pollut
January 2025
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR; Arkansas Children's Nutrition Center, Little Rock, AR.
The placenta is crucial for fetal development, is affected by PFAS toxicity, and evidence is accumulating that gestational PFAS perturb the epigenetic activity of the placenta. Gestational PFAS exposure can adversely affect offspring, yet individual and cumulative impacts of PFAS on the placental epigenome remain underexplored. Here, we conducted an epigenome-wide association study (EWAS) to examine the relationships between placental PFAS levels and DNA methylation in a cohort of mother-infant dyads in Arkansas (N=151).
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