RT Journal Article
SR Electronic
T1 Ketosis-Prone Type 2 Diabetes in Patients of Sub-Saharan African Origin
JF Diabetes
JO Diabetes
FD American Diabetes Association
SP 645
OP 653
DO 10.2337/diabetes.53.3.645
VO 53
IS 3
A1 Mauvais-Jarvis, Franck
A1 Sobngwi, Eugène
A1 Porcher, Raphaël
A1 Riveline, Jean-Pierre
A1 Kevorkian, Jean-Philippe
A1 Vaisse, Christian
A1 Charpentier, Guillaume
A1 Guillausseau, Pierre-Jean
A1 Vexiau, Patrick
A1 Gautier, Jean-François
YR 2004
UL http://diabetes.diabetesjournals.org/content/53/3/645.abstract
AB Nonautoimmune ketosis-prone diabetic syndromes are increasingly frequent in nonwhite populations. We have characterized a cohort of patients of sub-Saharan African origin who had ketosis-prone type 2 diabetes (n = 111), type 1 diabetes (n = 21), and type 2 diabetes (n = 88) and were admitted to a hospital for management of uncontrolled diabetes. We compared epidemiological, clinical, and metabolic features at diabetes onset and measured insulin secretion (glucagon-stimulated C-peptide) and insulin action (short intravenous insulin tolerance test) during a 10-year follow-up. Ketosis-prone type 2 diabetes shows a strong male predominance, stronger family history, higher age and BMI, and more severe metabolic decompensation than type 1 diabetes. In ketosis-prone type 2 diabetes, discontinuation of insulin therapy with development of remission of insulin dependence is achieved in 76% of patients (non–insulin dependent), whereas only 24% of patients remain insulin dependent. During evolution, ketosis-prone type 2 diabetes exhibit specific β-cell dysfunction features that distinguish it from type 1 and type 2 diabetes. The clinical course of non–insulin-dependent ketosis-prone type 2 diabetes is characterized by ketotic relapses followed or not by a new remission. Progressive hyperglycemia precedes and is a strong risk factor for ketotic relapses (hazard ratio 38). The probability for non–insulin-dependent ketosis-prone type 2 diabetes to relapse is 90% within 10 years, of whom ∼50% will become definitively insulin dependent. Insulin sensitivity is decreased in equal proportion in both ketosis-prone type 2 diabetes and type 2 diabetes, but improves significantly in non–insulin-dependent ketosis-prone type 2 diabetes, only after correction of hyperglycemia. In conclusion, ketosis-prone type 2 diabetes can be distinguished from type 1 diabetes and classical type 2 diabetes by specific features of clinical pathophysiology and also by the natural history of β-cell dysfunction and insulin resistance reflecting a propensity to glucose toxicity.