Details

Autor(en) / Beteiligte

• MAUVAIS-JARVIS, Franck
• SOBNGWI, Eugène
• PORCHER, Raphaël
• RIVELINE, Jean-Pierre
• KEVORKIAN, Jean-Philippe
• VAISSE, Christian
• CHARPENTIER, Guillaume
• GUILLAUSSEAU, Pierre-Jean
• VEXIAU, Patrick
• GAUTIER, Jean-Francois

Titel

Ketosis-prone type 2 diabetes in patients of Sub-Saharan African origin: Clinical pathophysiology and natural history of β-cell dysfunction and insulin resistance

Ist Teil von

• Diabetes (New York, N.Y.), 2004-03, Vol.53 (3), p.645-653

Ort / Verlag

Alexandria, VA: American Diabetes Association

Erscheinungsjahr

2004

Quelle

MEDLINE

Beschreibungen/Notizen

• 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 beta-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 approximately 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 beta-cell dysfunction and insulin resistance reflecting a propensity to glucose toxicity.