Use of oral anti-diabetic agents in pregnancy: A pragmatic approach

Kalra, Bharti; Gupta, Yashdeep; Singla, Rajiv; Kalra, Sanjay

doi:10.4103/1947-2714.150081

Cited by 45 publications

(46 citation statements)

References 35 publications

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“…The supporting sign of this above thesis is the similarity between our postprandial plasma glucose response and non GLP-1 infused obese patients of Flint's study (which was higher than GLP-1 infused patients during postprandial period) [18]. Another supporting point of our thesis is recent evidence of success of metformin and glyburide in GDM management [19].…”

Section: Discussionsupporting

confidence: 72%

Plasma Urotensin II Concentration In Gestational Diabetes

Hurşitoğlu¹,

Ekiz²,

Mete³

et al. 2017

Archives of Clinical and Experimental Medicine

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Aim: Urotensin II (UII) and its system is implicated in the etiology of many diseases (including diabetes mellitus). We tried in this study to evaluate and compare UII levels in gestational diabetes mellitus (GDM). Methods: Thirty-six pregnant women (15 non-GDM patients consisted group 1 and 21 GDM patients consisted group 2) enrolled in this study. The 3rd group consisted of age matched 22 non pregnant healthy women. Plasma UII levels were determined at the beginning of the study. After 12 weeks of delivery, a second plasma UII was determined from group 1 and 2. Results: Gestational UII levels of both GDM and non-GDM patients were higher than non-pregnant healthy controls (p=0.0001 for both). Both gestational and postpartum UII levels of GDM patients were higher than non-GDM patients but had not reached statistical significance (P≥0.05). Plasma UII concentrations in non-GDM patients significantly decreased after delivery but not in GDM patients (p=0.036 and p≥0.05, respectively) Conclusions: The finding of elevated gestational plasma UII concentrations in GDM patients which did not decrease significantly after delivery (in compare to non-GDM patients) shows that plasma UII levels may have a role in the pathogenesis of GDM. Further detailed studies are needed in this field.

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Section: Discussionsupporting

confidence: 72%

Plasma Urotensin II Concentration In Gestational Diabetes

Hurşitoğlu¹,

Ekiz²,

Mete³

et al. 2017

Archives of Clinical and Experimental Medicine

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“…There is limited experience of sulfonylurea use in the first trimester; the data that exist suggest sulfonylureas are not teratogenic when used at conception or in the first trimester 22, 23, 29, although maternal HbA 1c was independently associated with congenital anomalies 30. Many studies group women who are on different oral agents together, however, so data for specific sulfonylureas, and in particular glibenclamide, are not available.…”

Section: Sulfonylurea Treatment In Pregnancy In Type 2 Diabetes and Gmentioning

confidence: 99%

Management of sulfonylurea‐treated monogenic diabetes in pregnancy: implications of placental glibenclamide transfer

et al. 2017

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The optimum treatment for HNF1A/HNF4A maturity‐onset diabetes of the young and ATP‐sensitive potassium (KATP) channel neonatal diabetes, outside pregnancy, is sulfonylureas, but there is little evidence regarding the most appropriate treatment during pregnancy. Glibenclamide has been widely used in the treatment of gestational diabetes, but recent data have established that glibenclamide crosses the placenta and increases risk of macrosomia and neonatal hypoglycaemia. This raises questions about its use in pregnancy. We review the available evidence and make recommendations for the management of monogenic diabetes in pregnancy. Due to the risk of stimulating increased insulin secretion in utero, we recommend that in women with HNF1A/ HNF4A maturity‐onset diabetes of the young, those with good glycaemic control who are on a sulfonylurea per conception either transfer to insulin before conception (at the risk of a short‐term deterioration of glycaemic control) or continue with sulfonylurea (glibenclamide) treatment in the first trimester and transfer to insulin in the second trimester. Early delivery is needed if the fetus inherits an HNF4A mutation from either parent because increased insulin secretion results in ~800‐g weight gain in utero, and prolonged severe neonatal hypoglycaemia can occur post‐delivery. If the fetus inherits a KATP neonatal diabetes mutation from their mother they have greatly reduced insulin secretion in utero that reduces fetal growth by ~900 g. Treating the mother with glibenclamide in the third trimester treats the affected fetus in utero, normalising fetal growth, but is not desirable, especially in the high doses used in this condition, if the fetus is unaffected. Prospective studies of pregnancy in monogenic diabetes are needed.

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“…[13][14][15][16][17][18][19] Several studies have shown fewer BMI changes among obese women with GDM treated with this drug. [20][21][22] The results of the present study identified that participants in both control and metformin groups showed no significant increase in BMI between gestational weeks 20 and 24-28. The combination of metformin with lifestyle changes represents a potentially effective and safe approach to obesity control.…”

Section: Discussionmentioning

confidence: 83%