• Huiwen Tan, Chun Wang, and Yerong Yu.
• Division of Endocrinology and Metabolism, West China Hospital of Sichuan University, Chengdu.
• Medicine (Baltimore). 2019 Jun 1; 98 (25): e16076e16076.

RationaleIn recent years, there are more new insights into the clinical susceptibility, pathophysiological mechanism, and progression of classification and treatment of ketosis-prone diabetes mellitus (KPDM), which was once described as Idiopathic Type 1 Diabetes, Type 1B Diabetes or Flatbush Diabetes. ketosis-prone diabetes mellitus is still a heterogeneous syndrome reported in African-American or western Sub-Sahara-African, Hispanic descendant, and recently in Asian.Patient ConcernsAn obese 17-year-old student was admitted to a tertiary referral hospital (teaching hospital), presenting with thirst, polyuria fatigue, and a 9 kg weight loss in the preceding two weeks.DiagnosesPhysical examination showed body mass index (BMI) was 32.77 kg/m, arterial blood gas revealed a pH of 7.31. Serum glucose was 27.8 mmol/L with strong positive uric ketones (++++). Hemoglobin A1c (HbA1c) was 13.6%. The glucose disposal ratio (GDR) during the steady-state of euglycemic clamp test was 5.62 mg/kg/min and M value was 2.87 mg/kg/min during hyperglycemic clamp test. Those findings were sufficient to establish a diagnosis of ketosis-prone diabetes mellitus.InterventionsThis obese patient with KPDM received intensive insulin therapy and fluids infusion, and during the remainder of hospitalization his insulin requirement was approximately 1.5 U per kilogram of body weight per day. Blood glucose monitoring was rigorous until the diabetic ketoacidosis under control.OutcomesHe achieved the near-nomalglycemic remission uneventfully. At 12-month follow-up, his treatment was adjusted from insulin subcutaneous injection to oral hypoglycemic drugs.LessonThe present study of this obese adolescent with negative auto-antibodies but unprovoked diabetic ketoacidosis and partially preserved beta cell functional reserve after the acute of diabetic ketosis suggested that he has the phenotype of "A-β" KPDM. Further study of this syndrome will help illustrate the inadequacy of current classification and targeted therapies.

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