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Prenatal exposure to prednisone in humans and animals retards intrauterine growth
Insights
Prednisone use during pregnancy significantly lowers infant birth weight, increasing the rate of "light for dates" newborns. This corticosteroid effect was confirmed in mice, independent of maternal health.
Area of Science:
- Reproductive medicine
- Neonatal health
- Pharmacology
Background:
- Prednisone is sometimes used for infertility and pregnancy maintenance.
- Potential impacts of maternal corticosteroid use on fetal development are not fully understood.
Purpose of the Study:
- To investigate the effect of prednisone treatment on infant birth weight and incidence of low birth weight.
- To determine if corticosteroid exposure itself, or maternal condition, is responsible for observed birth weight changes.
Main Methods:
- Human study: analyzed birth weights of infants born to mothers treated with prednisone for infertility/pregnancy maintenance versus controls.
- Mouse study: compared birth weights of offspring exposed to corticosteroids in utero versus control groups.
Main Results:
- Human infants exposed to prednisone had significantly lower birth weights and a higher percentage of "light for dates" (<= 2500g) newborns.
- Mouse experiments confirmed that corticosteroid exposure, not maternal disease, caused the reduction in birth weight.
Conclusions:
- Prednisone treatment during pregnancy is associated with reduced infant birth weight.
- Corticosteroid exposure is a direct cause of decreased fetal growth, leading to low birth weight infants.
Abstract:
Prednisone treatment for infertility and subsequent pregnancy maintenance in humans resulted in a significant decrease in the birth weight of full-term infants and a marked increase in the percentage of newborn infants weighing 2500 grams or less, that is, "light for dates" in comparison to control offspring. A parallel experiment with mice indicated that the reduction of birth weight was caused by exposure to corticosteroids rather than to maternal disease or malfunction.