​Author(s): Shepherd M.; Brook A.J.; Chakera A.J.; Hattersley A.T.
Source: Diabetic Medicine; Oct 2017; vol. 34 (no. 10); p. 1332-1339
Publication Date: Oct 2017
Publication Type(s): Review
Available  at Diabetic medicine : a journal of the British Diabetic Association -  from Wiley Online Library Medicine and Nursing Collection 2018 - NHS
Abstract: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.Copyright © 2017 Diabetes UK
Database: EMBASE

Author(s): Shepherd M.; Brook A.J.; Chakera A.J.; Hattersley A.T.

Source: Diabetic Medicine; 2017

Available in full text at Diabetic Medicine -  from John Wiley and Sons

Abstract: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.Copyright © 2017 Diabetes UK.
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Database: EMBASE

Author(s): Ramtoola S.; Ploug U.J.; Kragh N.; Nyeland M.E.

Source: Diabetic Medicine; Mar 2017; vol. 34 ; p. 146

Publication Type(s): Journal: Conference Abstract

Available in full text at Diabetic Medicine -  from John Wiley and Sons

Abstract:Aims: To ascertain the body weight, body mass index (BMI) and comorbidities of adults with newly diagnosed Type 1 diabetes and assess the impact of initiating insulin therapy over the first 5 years after diagnosis. Methods: This was a non-interventional, retrospective, cohort study utilising data from the UK Clinical Practice Research Datalink database between 2001 and 2013. Included patients were aged 18-85 years, with a BMI of 11-50kg/m2 and a full medical history of >12 months prior to diagnosis. Glycated haemoglobin (HbA1c) and BMI levels were compared at baseline and 12, 24, 36 and 60 months after initiation of insulin therapy. Results: At baseline, patients had a mean +/- SD age of 40.8 +/- 16.1 years, HbA1c of 10.8 +/- 3.0%, and a BMI of 25.3 +/- 5.5kg/m2. Following initiation of insulin therapy, mean HbA1c declined from 10.8 +/- 3.0% to 7.7 +/- 2.0% at 12 months (p < 0.01), but subsequently increased to 8.1 +/- 2.0% at 24 months, remaining stable thereafter. Mean BMI consistently increased from 25.3 +/- 5.5 at baseline to 27.2 +/- 5.8, 27.4 +/- 5.7, 27.5 +/- 5.6, and 27.9 +/- 5.5kg/ m2 at 1, 2, 3 and 5 years, respectively. Conclusions: Whilst insulin therapy exerted an initial reduction in HbA1c at 12 months, mean HbA1c at 12 months was still above the National Institute for Health and Care Excellence (NICE) targets, and further deteriorated soon after. After beginning insulin therapy, patients with Type 1 diabetes were susceptible to longterm cumulative weight gain and increase in BMI. This study illustrates the need for greater emphasis on weight management in national Type 1 diabetes education programmes.
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Database: EMBASE