Author(s) Chichareon P.; Modolo R.; Kogame N.; Takahashi K.; Wykrzykowska J. et al.
Source Journal of the American College of Cardiology; Oct 2019; vol. 74 (no. 13)
DOI 10.1016/j.jacc.2019.08.754
Background: Diabetes has been well recognized as a strong predictor of adverse outcomes after percutaneous coronary intervention (PCI), but studies in the era of drug-eluting stents and potent P2Y12 inhibitors have shown conflicting results. We assessed ischemic and bleeding outcomes after contemporary PCI according to diabetic status.

Method(s): We studied 15,957 patients in the GLOBAL LEADERS study with known baseline diabetic status. The primary endpoint was all-cause death or new Q-wave myocardial infarction at 2 years. The secondary safety endpoint was major bleeding defined as Bleeding Academic Research Consortium (BARC) type 3 or 5.

Result(s): A quarter of the study cohort had diabetes (4,038 of 15,957), and these patients had a significantly higher risk for the primary endpoint at 2 years compared with those without diabetes (adjusted hazard ratio [HR]: 1.36; 95% confidence interval [CI]: 1.14 to 1.61). The difference was driven by a significantly higher risk for all-cause mortality at 2 years in patients with diabetes (adjusted HR: 1.44; 95% CI: 1.18 to 1.75). The risk for BARC type 3 or 5 bleeding was comparable between the 2 groups (adjusted HR: 1.18; 95% CI: 0.92 to 1.50). The antiplatelet strategy (experimental vs. reference strategy) had no significant effect on the rates of the primary endpoint and secondary safety endpoint at 2 years in patients with and without diabetes.

​Conclusion(s): Patients with diabetes had a higher risk for ischemic events after PCI than those without diabetes, while bleeding risk was comparable. The outcomes of patients with diabetes following PCI were not affected by the 2 different antiplatelet strategies. Categories: CORONARY: Pharmacology/PharmacotherapyCopyright © 2019

• Available in full text at Journal of the American College of Cardiology from Unpaywall

Author(s) Ramtoola S.; Nyeland M.E.; Ploug U.J.; Kragh N.; Zimmermann E. et al.
Source Primary Care Diabetes; 2019
Aims: This retrospective, longitudinal study characterised 2430 adults (mean age 40.8 +/- 16.1 years) with newly diagnosed type 1 diabetes (T1D) over the first 5 years of insulin treatment.

Method(s): Data from 1 year pre- and up to 5 years post-insulin initiation were extracted from the UK Clinical Practice Research Datalink (1990-2013). Baseline HbA1c, BMI and Charlson comorbidity index (CCI) score were compared with data at 1, 2, 3 and 5 years. Result(s): Mean HbA1c decreased significantly from baseline 95 +/- 32.8 mmol/mol (10.8 +/- 3.0%) to 61 +/- 21.9 mmol/mol (7.7 +/- 2.0%) at 1 year, remaining significantly lower at 2, 3 and 5 years (p < 0.0001). One year after initiating insulin, only 6.3% of patients had HbA1c<48 mmol/mol (<6.5%). There was no further improvement in HbA1c after 1 year. Mean BMI increased significantly from baseline 25.3 +/- 5.5 kg/m2 to 27.2 +/- 5.8 kg/m2 at 1 year; p < 0.0001), remaining significantly higher thereafter, with over two-thirds having overweight/obesity by year 5. Mean CCI score increased significantly (1.32, baseline; 1.46, year 1; 1.75, year 5). CCI patterns were similar within BMI and HbA1c strata.

​Conclusion(s): More intensive support to reach and maintain glycaemic targets soon post-diagnosis, while avoiding weight gain, and prevention and optimal management of comorbidities are warranted.Copyright © 2019 The Authors

• Available in full text at Primary care diabetes from Unpaywall

​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