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


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.


CONCLUSIONS
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.
Department of Pediatrics, Division of Endocrinology, Emory University School of Medicine, 49 Jesse Hill Jr. Drive, Atlanta, GA 30303, USA.
Joey C
JC
Low
Eric I
EI
Felner
Andrew B
AB
Muir
Milton
M
Brown
Margalie
M
Dorcelet
Limin
L
Peng
Guillermo E
GE
Umpierrez
D000293:Adolescent; D001323:Autoantibodies / Q000097:blood; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000453:epidemiology* / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000453:epidemiology* / Q000276:immunology; D016883:Diabetic Ketoacidosis / Q000188:drug therapy / Q000453:epidemiology* / Q000276:immunology; D005260:Female; D005500:Follow-Up Studies; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D006943:Hyperglycemia / Q000453:epidemiology; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D008499:Medical Records / Q000706:statistics & numerical data; D009765:Obesity / Q000453:epidemiology*; D016036:Seroepidemiologic Studies
D001323:Autoantibodies; D007004:Hypoglycemic Agents; D007328:Insulin; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1