1.
Steroid-Induced Diabetes Ketoacidosis in an Immune Thrombocytopenia Patient: A Case Report and Literature Review.
Alakkas, Z, Alzaedi, OA, Somannavar, SS, Alfaifi, A
The American journal of case reports. 2020;:e923372
Abstract
BACKGROUND Steroids are used as anti-inflammatory agents, administered for a variety of medical conditions, either as short- or long-term treatment. Steroid use is associated with many adverse effects, including hyperglycemia, but ketoacidosis is rare. CASE REPORT We present the case of a 53-year-old woman who developed diabetic ketoacidosis after administration of methylprednisolone during treatment of immune thrombocytopenic purpura. She did not have diabetes or a family history of diabetes. Steroid-induced hyperglycemia with insulin resistance, lipolysis, and ketogenesis occurred and were likely to have precipitated the ketoacidosis. Blood glucose, blood gases, and urine test results were diagnostic for ketoacidosis. CONCLUSIONS The risk of ketoacidosis and hyperglycemia should be considered in the course of steroid therapy, even without a diagnosis of diabetes, especially in patients who have risk factors for diabetes mellitus including obesity and long-term use of steroids, so that early identification of diabetic ketoacidosis can prevent further morbidity and mortality in chronic patients.
2.
Fulminant type 1 diabetes--an important subtype in East Asia.
Imagawa, A, Hanafusa, T
Diabetes/metabolism research and reviews. 2011;(8):959-64
Abstract
Fulminant type 1 diabetes is defined as a subtype of type 1 diabetes with a remarkably acute onset. A nationwide survey identified that this variant accounts for approximately 20% of acute-onset type 1 diabetic patients in Japan. Recent studies indicate that this is not a minor subtype in other East Asian countries. As genetic factors, we revealed association of HLA-DR-DQ, HLA-B and CTLA-4 to fulminant type 1 diabetes. As an environmental factor, viral infection would contribute to the development of this subtype. Cellular infiltration to islets was detected soon after the onset but not observed 1 month after the onset. Macrophages and T cells were the main components of the infiltrates. Enterovirus RNA and Toll-like receptor-3 expression, a signature of viral infection, was also observed. These findings suggest that viral infection in the susceptible individual might trigger anti-viral immune response and that pancreatic beta cells are rapidly destroyed through the accelerated immune reaction.