Relationship of prospective GHb to glycated serum proteins in incident diabetic retinopathy: implications of the glycation gap for mechanism of risk prediction.

When estimating long-term glycemic control, A1C is considered the gold standard (1–3), but patients with seemingly equivalent A1C differ in their risk for microvascular complications (4,5). Recently, the “glycation gap,” defined as the difference between the measured A1C and that which would be predicted from another measure of glycemic control, fructosamine, has been proposed as a means of identifying sources of variance in the apparent risk (6). Because hemoglobin is an intracellular protein and fructosamine reflects extracellular proteins, the glycation gap could result from differences between the ambient glucose concentrations or rates of glycation in the intracellular and extracellular compartments or interindividual differences in the turnover/metabolism of underlying proteins (6). In this study, we sought to determine whether there are differences in the relationship of GHb to fructosamine in diabetic subjects who do or do not develop retinopathy.