Format

Send to

Choose Destination
Endocr Pract. 2007 Jul-Aug;13(4):350-4.

Influence of glycemic variables on hemoglobin A1c.

Author information

1
Division of Endocrinology, Mayo Clinic Rochester, Rochester, Minnesota 55905, USA.

Abstract

OBJECTIVE:

To assess the influences of a wide variety of glucose variables on hemoglobin A1c (A1C).

METHODS:

The Diabetes Control and Complications Trial database, restricted to volunteers whose 7-point daily capillary glucose profiles were complete in >or=80% of quarterly collections and who were in the study for >or=4 years, was used for analysis. Regression analyses were done to develop an equation for estimating A1C based on concurrent and prior mean blood glucose (MBG) values. The multivariate coefficient of determination (R2) was calculated for MBG, mean postprandial blood glucose, mean preprandial blood glucose, digestive glycemia, interdigestive glycemia, individual time points of the 7-point glucose profile, range of blood glucose, SD of blood glucose, M-value, and mean amplitude of glycemic excursions in relationship to A1C. By using regression analysis, the correlation between A1C and MBG within each study subject was determined.

RESULTS:

The most accurate prediction of A1C was obtained from the concurrent MBG. With use of univariate analysis, all glucose variables correlated significantly with concurrent A1C, the strongest correlation occurring with MBG. In multivariate analysis, the primary predictor of A1C was MBG; all other glucose variables added nothing to the models. Within-subject correlations between MBG and A1C showed considerable variation.

CONCLUSION:

A1C correlates best with MBG derived from 7-point-daily capillary glucose profiles. The influences of glucose measured at specific time points during the day or various measures of glucose variability on A1C are less than that of MBG. Within the limitations of the intermittent glucose determinations, wide variations in the relationship of MBG to A1C among and within patients with type 1 diabetes remain unexplained.

PMID:
17669710
DOI:
10.4158/EP.13.4.350
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Allen Press, Inc.
Loading ...
Support Center