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Pm25 and Fetal Growth Contrast Study Review Article

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Review

doi: ten.3389/fendo.2021.802423. eCollection 2021.

Pregnancy in Women With Monogenic Diabetes due to Pathogenic Variants of the Glucokinase Factor: Lessons and Challenges

Affiliations

  • PMID: 35069449
  • PMCID: PMC8766338
  • DOI: 10.3389/fendo.2021.802423

Complimentary PMC article

Review

Pregnancy in Women With Monogenic Diabetes due to Pathogenic Variants of the Glucokinase Cistron: Lessons and Challenges

José Timsit  et al. Front Endocrinol (Lausanne). .

Free PMC article

Abstruse

Heterozygous loss-of-role variants of the glucokinase (GCK) gene are responsible for a subtype of maturity-onset diabetes of the young (MODY). GCK-MODY is characterized past a mild hyperglycemia, mainly due to a higher blood glucose threshold for insulin secretion, and an upward-regulated glucose counterregulation. GCK-MODY patients are asymptomatic, are not exposed to diabetes long-term complications, and exercise not require handling. The diagnosis of GCK-MODY is made on the discovery of hyperglycemia by systematic screening, or past family screening. The situation is peculiar in GCK-MODY women during pregnancy for three reasons: 1. the degree of maternal hyperglycemia is sufficient to induce pregnancy agin outcomes, as in pregestational or gestational diabetes; 2. the probability that a fetus inherits the maternal mutation is 50% and; 3. fetal insulin secretion is a major stimulus of fetal growth. Consequently, when the fetus has not inherited the maternal mutation, maternal hyperglycemia will trigger increased fetal insulin secretion and growth, with a loftier risk of macrosomia. Past dissimilarity, when the fetus has inherited the maternal mutation, its insulin secretion is fix at the same threshold as the mother's, and no fetal growth excess will occur. Thus, handling of maternal hyperglycemia is necessary only in the former state of affairs, and will lead to a risk of fetal growth restriction in the latter. It has been recommended that the direction of diabetes in GCK-MODY pregnant women should be guided by cess of fetal growth by series ultrasounds, and institution of insulin therapy when the intestinal circumference is ≥ 75th percentile, considered every bit a surrogate for the fetal genotype. This strategy has not been validated in women with in GCK-MODY. Recently, the feasibility of non-invasive fetal genotyping has been demonstrated, that volition improve the care of these women. Several challenges persist, including the identification of women with GCK-MODY before or early in pregnancy, and the modalities of insulin therapy. Yet, retrospective observational studies have shown that fetal genotype, not maternal handling with insulin, is the main determinant of fetal growth and of the chance of macrosomia. Thus, further studies are needed to specify the management of GCK-MODY pregnant women during pregnancy.

Keywords: GCK-MODY; genotype; glucokinase; insulin therapy; macrosomia; non-invasive fetal genotyping; pregnancy.

Conflict of interest argument

The authors declare that the research was conducted in the absenteeism of whatsoever commercial or financial relationships that could exist construed as a potential conflict of interest.

Figures

Figure 1
Figure 1

Suggested algorithms to initiate insulin therapy in pregnant women with GCK-MODY. The left part of the effigy describes the approach based, as in "common" gestational diabetes, on maternal blood glucose (BG) values. The middle part illustrates current recommendations, based on the series measurement of fetal abdominal circumference (Ac) by ultrasounds (US), and initiation of insulin therapy when AC is ≥ 75thursday percentile (Pc), which suggests the absence of the maternal GCK mutation in the fetus and a run a risk of macrosomia. In the correct part, initiation of insulin therapy will exist based on the absenteeism of the maternal mutation (M) in the fetus, diagnosed by not-invasive prenatal testing. The bottom part of the effigy indicates the main pitfalls of each strategy. SGA, small for gestational age.

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Source: https://pubmed.ncbi.nlm.nih.gov/35069449/

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