Maternal and Infant Outcomes in GCK-MODY Complicated by Pregnancy
- PMID: 37011183
- DOI: 10.1210/clinem/dgad188
Maternal and Infant Outcomes in GCK-MODY Complicated by Pregnancy
Abstract
Context: Challenges exist in the management of Glucokinase-maturity-onset diabetes of the young (GCK-MODY), especially during pregnancy.
Objective: This work aimed to evaluate the prevalence of congenital anomaly in newborns from GCK-MODY mothers, and the relationship between fetus genotype and the risk of congenital malformation as well as other adverse pregnancy outcomes.
Methods: Electronic databases including PubMed, EMBASE, and Cochrane database last updated July 16, 2022, were searched. We included observational studies conducted in GCK-MODY complicated by pregnancy, and reporting at least one pregnancy outcome. We extracted data in duplicate, and the risk of bias was evaluated by the Newcastle-Ottawa Quality Assessment Scale (NOS). All statistical analysis was performed by Cochrane Review Manager.
Results: Eight studies were selected in the meta-analysis. Five were of high quality and 3 were of medium quality evaluated by NOS. A total of 257 GCK-MODY mothers and 499 offspring were enrolled. Among them, 370 offspring were divided into 2 groups: GCK-affected offspring (GCK+, n = 238) and GCK-unaffected offspring (GCK-, n = 132). The percentage of congenital malformations in GCK pregnant women's offspring was 2.4%. The risk of congenital malformations was similar between the GCK+ and GCK- group (odds ratio = 0.56; 95% CI, 0.07-4.51; I2 = 0%; P = .59). The risk of macrosomia/large for gestational age, neonatal hypoglycemia, and combined adverse neonatal outcome was significantly lower in offspring with the GCK mutation compared with non-GCK mutation carriers.
Conclusion: The percentage of congenital malformations was 2.4% in GCK-MODY pregnant women's offspring, and newborns with the GCK mutation have lower birth complication than non-GCK mutation carriers.
Keywords: GCK-MODY; congenital malformation; pregnancy outcome.
© The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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