Abstract
Type 2 diabetes mellitus results from a combination of insulin resistance and inadequate insulin secretion, which together lead to impaired glucose homeostasis, culminating in hyperglycemia. Nonenzymatic attachment of glucose to a protein is termed glycation. The glucose concentration in blood modulates the extent of glycation of proteins in the circulation; higher glucose increases glycation. Hemoglobin A1c (Hb A1c)2 forms when glucose attaches to the N-terminal valine of the β chain of Hb A. Erythrocyte lifespan is approximately 120 days, and Hb A1c thus reflects the mean blood glucose concentration over the preceding 8–12 weeks. As a marker of chronic glycemia, Hb A1c is used extensively in individuals with diabetes to predict complications and monitor therapy, with target values established for optimal treatment (1). More recently, the use of Hb A1c was advocated for screening and diagnosis of diabetes (1). Several different methods, including immunoassay, HPLC, affinity chromatography, capillary electrophoresis, and enzymatic assay, are used to measure Hb A1c. Importantly, assay standardization has resulted in equivalent values among methods (2). Like other analytes, Hb A1c is not perfect. The main limitation is that the Hb A1c concentration may be altered by factors other than glycemia (3). In particular, any condition that changes erythrocyte lifespan will change Hb A1c. Examples include severe thalassemia, hereditary spherocytosis, splenomegaly, autoimmune hemolytic anemia, and some hemoglobin variants. Conceptually, this problem could be eliminated if one could apply a factor to correct for erythrocyte age. However, it is extremely difficult to measure erythrocyte lifespan, thus precluding the use of this strategy. Chronic renal failure is a common complication of diabetes. Patients with chronic renal failure have lower Hb A1c due to shortened erythrocyte survival. In many of these patients, erythropoietin is used …
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