A great deal of research has established that the HbA1c level is a crucial test for use in the assessment of a diabetic patient's degree of glycemic control. The table shows the reduction in risk of diabetic complications per 1% decrease in HbA1c observed in major studies, emphasizing the robustness of this association across many differing patient groups.

Although HbA1c may be lowered by rapid erythrocyte turnover and is altered in certain hemoglobinopathies, it provides an excellent tool for assessing overall glycemic status. However, several caveats to the acceptance of HbA1c as an absolute guide to the level of control of a given patient have been recently recognized. Data presented at the June 2000 American Diabetes Association Scientific Sessions addressed this issue.^[1]

In the UKPDS, the relationship between glycated hemoglobin values and fasting plasma glucose (FGP) showed a wide confidence interval, with a HbA1c of 7% corresponding to a FPG of 149 mg/dL, with a 95% confidence interval of 83 to 212 mg/dL. In the DCCT, patients whose HbA1c was higher than expected relative to their glucose levels had a higher rate of developing retinopathy and nephropathy, suggesting that either protein glycation rates may vary for a given degree of glycemia and may contribute to differing rates of development of complications or that patients with higher HbA1c for a given mean glucose may have unrecognized glycemic variability.

Of interest, in patients with diabetes, the prandial glucose level is more strongly correlated with HbA1c than is the fasting glucose level.^[2] Population studies provide strong evidence that the 2-hour postchallenge glucose level is more strongly related to mortality than the fasting level.^[3] The risk of microvascular end points also increases with postload glycemia levels.^[4] The potential adverse effects of postprandial hyperglycemia include increased glomerular filtration rate and renal plasma flow, increased retinal blood flow, impaired endothelial vasodilation, increased procoagulative processes, and increased oxidative stress.

Thus, although HbA1c is currently the principal tool for assessing glycemic status, one must continue to measure fasting and, particularly, postprandial glucose levels, in the determination of individual glycemic risk.

1. Bloomgarden ZT. American Diabetes Association 60th Scientific Sessions, 2000: glucose tolerance, diabetes and cancer, glycemic control, monitoring, and related topics. Diabetes Care. 2001;24:779-784.
2. Avignon A, Radauceanu A, Monnier L. Nonfasting plasma glucose is a better marker of diabetic control than fasting plasma glucose in type 2 diabetes. Diabetes Care. 1997;20:1822-1826.
3. The DECODE Study Group. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria. The DECODE study group. European Diabetes Epidemiology Group. Diabetes Epidemiology: Collaborative analysis Of Diagnostic criteria in Europe. Lancet. 1999;354:617-621.
4. Ohkubo Y, Kishikawa H, Araki E, et al. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: a randomized prospective 6-year study. Diabetes Res Clin Pract. 1995;28:103-117.