Narrative Review: Ketosis-Prone Type 2 Diabetes Mellitus

  1. Guillermo E. Umpierrez, MD;
  2. Dawn Smiley, MD; and
  3. Abbas E. Kitabchi, PhD, MD
  1. From Emory University School of Medicine, Atlanta, Georgia, and University of Tennessee Health Science Center, Memphis, Tennessee.

    Abstract

    Several investigators have reported that more than half of African-American persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immunologic features of type 2 diabetes during follow-up. These patients are usually obese, have a strong family history of diabetes, have a low prevalence of autoimmune markers, and lack a genetic association with HLA. Their initial presentation is acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a precipitating cause of metabolic decompensation. At presentation, they have markedly impaired insulin secretion and insulin action, but intensified diabetic management results in significant improvement in β-cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within a few months of follow-up. On discontinuation of insulin therapy, the period of near-normoglycemic remission may last for a few months to several years. The absence of autoimmune markers and the presence of measurable insulin secretion have proven useful in predicting near-normoglycemic remission and long-term insulin dependence in adult patients with a history of diabetic ketoacidosis. This clinical presentation is commonly reported in African and African-American persons but is also observed in Hispanic persons and those from other minority ethnic groups. The underlying mechanisms for β-cell dysfunction in ketosis-prone type 2 diabetes are not known; however, preliminary evidence suggests an increased susceptibility to glucose desensitization.

    Article and Author Information

    • Grant Support: In part by research grants from the American Diabetes Association (7-03-CR-35) (Dr. Umpierrez) and National Institutes of Health (R03 DK073190-01 and MO1-RR00039 [Dr. Umpierrez] and RR00211 [Drs. Kitabchi and Umpierrez]).

    • Potential Financial Conflicts of Interest: Grants received: A.E. Kitabchi (Lilly, Novo, Takeda, Aventis, Abbott).

    • Requests for Single Reprints: Guillermo E. Umpierrez, MD, Emory University School of Medicine, 49 Jesse Hill Jr. Drive, Atlanta, GA 30303; e-mail, geumpie{at}emory.edu.

    • Current Author Addresses: Drs. Umpierrez and Smiley: Emory University School of Medicine, 49 Jesse Hill Jr. Drive, Atlanta, GA 30303.

    • Dr. Kitabchi: University of Tennessee Health Science Center, Room 334D, 956 Court Avenue, Memphis, TN 38163.

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