Do obese children with diabetic ketoacidosis have type 1 or type 2 diabetes?

• Type of Material: Article
• Authors: Joey C. Low, Emory University; Eric Ian Felner, Emory University; Andrew B. Muir, Emory University; Milton R Brown, Emory University; Margalie Dorcelet, Emory University; Limin Peng, Emory University; Guillermo Umpierrez, Emory University
• Language: English
• Date: 2012-04
• Publisher: Elsevier
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2011 Primary Care Diabetes Europe. Published by Elsevier Ltd. All rights reserved.
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.1016/j.pcd.2011.11.001
• Title of Journal or Parent Work: Primary Care Diabetes
• ISSN: 1751-9918
• Volume: 6
• Issue: 1
• Start Page: 61
• End Page: 65
• Grant/Funding Information: This work was partially supported by research grants from the National Institutes of Health UL1 RR025008 (Atlanta Clinical and Translational Science Institute), American Diabetes Association 7-03-CR-35 (GEU) and Emory Egleston Children’s Research Center Seed Grant (EIF).
• Keywords: Obese; Ketosis-prone diabetes; Diabetic ketoacidosis; Atypical diabetes; Hyperglycemic crises; Type 2 diabetes
• Research Categories: Health Sciences, Public Health

Abstract

Objective Many obese children with unprovoked diabetic ketoacidosis (DKA) display clinical features of type 2 diabetes during follow up. We describe the clinical presentation, autoimmune markers and the long-term course of obese and lean children with DKA. Research design and methods We reviewed the medical records on the initial acute hospitalization and outpatient follow-up care of 21 newly diagnosed obese and 20 lean children with unprovoked DKA at Emory University affiliated children’s hospitals between 1/2003 and 12/2006. Results Obese children with DKA were older and predominantly male, had acanthosis nigricans, and had lower prevalence of autoantibodies to islet cells and glutamic acid decarboxylase than lean children. Half of the obese, but none of the lean children with DKA achieve near-normoglycemia remission and discontinued insulin therapy during follow-up. Time to achieve remission was 2.2 ± 2.3 months. There were no differences on clinical presentation between obese children who achieved near-normoglycemia remission versus those who did not. The addition of metformin to insulin therapy shortly after resolution of DKA resulted in lower hemoglobin A1c (HbA1c) levels, higher rates of near-normoglycemia remission, and lower frequency of DKA recurrence. Near-normoglycemia remission, however, was of short duration and the majority of obese patients required reinstitution of insulin treatment within 15 months of follow-up. Conclusion In contrast to lean children with DKA, many obese children with unprovoked DKA display clinical and immunologic features of type 2 diabetes during follow-up. The addition of metformin to insulin therapy shortly after resolution of DKA improves glycemic control, facilitates achieving near-normoglycemia remission and prevents DKA recurrence in obese children with DKA.