Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2026
Ketosis-Prone Type 2 Diabetes Mellitus: 3 Decades of Clinical, Pathophysiologic, and Therapeutic Insights.
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Umpierrez Guillermo, Vellanki Priyathama, Oladejo Omolade
Аннотация
BACKGROUND: Over 3 decades ago, our group reported that newly diagnosed Black patients with diabetic ketoacidosis (DKA) are obese and that many of them can discontinue insulin after the acute episode, revealing a clinical course consistent with type 2 diabetes. This presentation is now recognized as ketosis-prone type 2 diabetes mellitus (KPDM).
METHODS: We review observational, prospective, and interventional studies that characterize the epidemiology, clinical features, pathophysiology, and management of KPDM. Patients typically present with severe hyperglycemia, metabolic acidosis, obesity, male predominance, and a strong family history of type 2 diabetes.
RESULTS: KPDM accounts for 20% to 50% of new-onset DKA in Black and Hispanic adults and has been reported globally. Acute management follows standard DKA protocols, but insulin requirements decline rapidly after the crisis, with ∼70% achieving near-normoglycemic remission. Pathophysiologic studies show reversible β-cell dysfunction and transient insulin resistance, resembling type 2 diabetes. Low prevalence of autoantibody positivity distinguishes KPDM from latent autoimmune diabetes. Pharmacologic therapy with metformin, dipeptidyl peptidase-4 inhibitors, or glucagon-like peptide-1 receptor agonists prolongs remission, preserves β-cell function, and reduces hyperglycemic relapse.
CONCLUSIONS: KPDM exemplifies diabetes heterogeneity and is a common presentation of DKA, particularly among obese Black and Hispanic adults. Early recognition and individualized therapy optimize β-cell recovery, prolong near-normoglycemic remission, and improve outcomes. Further research is needed to define optimal long-term management and prevention strategies to sustain remission and reduce diabetic complications.
METHODS: We review observational, prospective, and interventional studies that characterize the epidemiology, clinical features, pathophysiology, and management of KPDM. Patients typically present with severe hyperglycemia, metabolic acidosis, obesity, male predominance, and a strong family history of type 2 diabetes.
RESULTS: KPDM accounts for 20% to 50% of new-onset DKA in Black and Hispanic adults and has been reported globally. Acute management follows standard DKA protocols, but insulin requirements decline rapidly after the crisis, with ∼70% achieving near-normoglycemic remission. Pathophysiologic studies show reversible β-cell dysfunction and transient insulin resistance, resembling type 2 diabetes. Low prevalence of autoantibody positivity distinguishes KPDM from latent autoimmune diabetes. Pharmacologic therapy with metformin, dipeptidyl peptidase-4 inhibitors, or glucagon-like peptide-1 receptor agonists prolongs remission, preserves β-cell function, and reduces hyperglycemic relapse.
CONCLUSIONS: KPDM exemplifies diabetes heterogeneity and is a common presentation of DKA, particularly among obese Black and Hispanic adults. Early recognition and individualized therapy optimize β-cell recovery, prolong near-normoglycemic remission, and improve outcomes. Further research is needed to define optimal long-term management and prevention strategies to sustain remission and reduce diabetic complications.