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      Octreotide therapy and restricted fetal growth: pregnancy in familial hyperinsulinemic hypoglycemia

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          Abstract

          Summary

          Hypoglycemia during pregnancy can have serious health implications for both mother and fetus. Although not generally recommended in pregnancy, synthetic somatostatin analogues are used for the management of blood glucose levels in expectant hyperinsulinemic mothers. Recent reports suggest that octreotide treatment in pregnancy, as well as hypoglycemia in itself, may pose a risk of fetal growth restriction. During pregnancy, management of blood glucose levels in familial hyperinsulinemic hypoglycemia thus forms a medical dilemma. We report on pregnancy outcomes in a woman with symptomatic familial hyperinsulinemic hypoglycemia, type 3. During the patient’s first pregnancy with a viable fetus octreotide treatment was instituted in gestational age 23 weeks to prevent severe hypoglycemic incidences. Fetal growth velocity declined, and at 37 weeks of gestation, intrauterine growth retardation was evident. During the second pregnancy with a viable fetus, blood glucose levels were managed through dietary intervention alone. Thus, the patient was advised to take small but frequent meals high in fiber and low in carbohydrates. Throughout pregnancy, no incidences of severe hypoglycemia occurred and fetal growth velocity was normal. We conclude that octreotide treatment during pregnancy may pose a risk of fetal growth restriction and warrants careful consideration. In some cases of familial hyperinsulinemic hypoglycemia, blood glucose levels can be successfully managed through diet only, also during pregnancy.

          Learning points:
          • Gain-of-function mutations in GCK cause familial hyperinsulinemic hypoglycemia.

          • Hypoglycemia during pregnancy may have serious health implications for mother and fetus.

          • Pregnancy with hyperinsulinism represents a medical dilemma as hypoglycemia as well as octreotide treatment may pose a risk of fetal growth restriction.

          • In some cases of familial hyperinsulinemic hypoglycemia, blood glucose levels can be successfully managed through diet only.

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          Most cited references13

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          HbA1c levels are significantly lower in early and late pregnancy.

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            Glucokinase as pancreatic beta cell glucose sensor and diabetes gene.

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              Molecular mechanisms of congenital hyperinsulinism.

              Congenital hyperinsulinism (CHI) is a complex heterogeneous condition in which insulin secretion from pancreatic β-cells is unregulated and inappropriate for the level of blood glucose. The inappropriate insulin secretion drives glucose into the insulin-sensitive tissues, such as the muscle, liver and adipose tissue, leading to severe hyperinsulinaemic hypoglycaemia (HH). At a molecular level, genetic abnormalities in nine different genes (ABCC8, KCNJ11, GLUD1, GCK, HNF4A, HNF1A, SLC16A1, UCP2 and HADH) have been identified which cause CHI. Autosomal recessive and dominant mutations in ABCC8/KCNJ11 are the commonest cause of medically unresponsive CHI. Mutations in GLUD1 and HADH lead to leucine-induced HH, and these two genes encode the key enzymes glutamate dehydrogenase and short chain 3-hydroxyacyl-CoA dehydrogenase which play a key role in amino acid and fatty acid regulation of insulin secretion respectively. Genetic abnormalities in HNF4A and HNF1A lead to a dual phenotype of HH in the newborn period and maturity onset-diabetes later in life. This state of the art review provides an update on the molecular basis of CHI.

                Author and article information

                Journal
                Endocrinol Diabetes Metab Case Rep
                Endocrinol Diabetes Metab Case Rep
                EDM
                Endocrinology, Diabetes & Metabolism Case Reports
                Bioscientifica Ltd (Bristol )
                2052-0573
                15 February 2017
                2017
                : 2017
                : 16-0126
                Affiliations
                [1 ]Departments of Clinical Genetics
                [2 ]Departments of Obstetrics
                [3 ]Departments of Endocrinology , Odense University Hospital, Odense, Denmark
                [4 ]Department of Clinical Research , Faculty of Health, University of Southern Denmark, Odense, Denmark
                Author notes
                Correspondence should be addressed to M Geilswijk; Email: mariannegeilswijk@ 123456hotmail.com
                Article
                EDM160126
                10.1530/EDM-16-0126
                5404468
                1b2b0c42-0f60-46fb-a65d-f23829291e8e
                © 2017 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

                History
                : 28 November 2016
                : 13 January 2017
                Categories
                Error in Diagnosis/Pitfalls and Caveats

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