The Challenges of Treating Glucokinase MODY during Pregnancy: A Review of Maternal and Fetal Outcomes

Alena Kirzhner, Oren Barak, Edi Vaisbuch, Taiba Zornitzki and Tal Schiller
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Alena Kirzhner: Diabetes, Endocrinology and Metabolic Disease Institute, Kaplan Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Rehovot 9190401, Israel
Oren Barak: Department of Obstetrics and Gynecology, Kaplan Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Rehovot 9190401, Israel
Edi Vaisbuch: Department of Obstetrics and Gynecology, Kaplan Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Rehovot 9190401, Israel
Taiba Zornitzki: Diabetes, Endocrinology and Metabolic Disease Institute, Kaplan Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Rehovot 9190401, Israel
Tal Schiller: Diabetes, Endocrinology and Metabolic Disease Institute, Kaplan Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Rehovot 9190401, Israel

IJERPH, 2022, vol. 19, issue 10, 1-11

Abstract: Background: The optimal treatment strategy for the follow-up and management of women with glucokinase maturity-onset diabetes of the young (GCK−MODY)during pregnancy remains unknown. Data regarding maternal and fetal outcomes are lacking. Aim: This paper summarizes the existing literature regarding the maternal and fetal outcomes of women with glucokinase MODY to guide future treatment strategy. Methods: A literature search was conducted in Pubmed, Embace, and Cochrane library with citation follow-up using the terms: glucokinase, MODY, diabetes, pregnancy, gestation, and outcomes. We searched for articles with known fetal mutational status. Relevant outcomes included: birthweight, large for gestational age (LGA), small for gestational age (SGA), macrosomia, cesarean delivery (CD), shoulder dystocia, congenital anomalies, miscarriages, preterm births, and long-term outcomes. Results: Fourteen relevant manuscripts were identified describing maternal and fetal outcomes. The percentage of LGA and macrosomia in 102 glucokinase -unaffected offspring (GCK−) was significantly higher than in the glucokinase -affected offspring (GCK+) (44% vs. 10%, p < 0.001 and 22% vs. 2%, p < 0.001, respectively). Among the 173 GCK(+) offspring, only 5% were SGA, which can be expected according to the normal distribution. We observed higher rates of CD and shoulder dystocia in the GCK(−) offspring. Conclusions: GCK(−) offspring have significantly higher birthweights and more birth complications. The optimal treatment strategy to guide management should take into consideration multiple variables other than fetal mutational status.

Keywords: diabetes; glucokinase; MODY; MODY 2; pregnancy (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2022
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