The age-adjusted hospital admission rate for diabetic ketoacidosis (DKA) has remained high in African Americans since 1980 (1,6). In 2003, the age-adjusted DKA rate was 28.6 per 1000 blacks with diabetes compared to 21.4 per 1000 whites with diabetes (1). DKA appears to be a more aggressive disease in black males when compared with the whites. Mortality from DKA is about threefold higher in black males compared with whites. Cessation of insulin therapy is the major precipitating cause for DKA in African-American and Hispanic patients (7,8). In many cases, omission of insulin therapy was due to lack of resources in the economically disadvantaged patient (7).
Over the years, increasing number of patients from ethnic minority populations with type 2 diabetes, particularly African Americans and Hispanics have been noted to present with DKA (9-11). About 50% of such patients present with DKA as initial manifestation of
type 2 diabetes (9,10). Patients with this entity known as ketosis-prone type 2 diabetes, exhibit initial profound impairment in insulin secretion and action, which resolves with correction of DKA and hyperglycemia using insulin therapy. After a 10-year follow-up period, 40% of patients with ketosis-prone diabetes have remained well controlled without insulin (10). This finding is of significant therapeutic implication in ethnic minority patients with type 2 diabetes. The precise etiology of acute severe but transient p-cell failure is uncertain. Postulated mechanisms include glucotoxicity, lipotoxicity and genetic predisposition. A genetic association between glucose-6-phosphate dehydrogenase deficiency and ketosis-prone type 2 diabetes has been reported (11).
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