H Narbonne1, E Renacco, V Pradel, H Portugal, B Vialettes. 1. Service de Nutrition, Maladies Métaboliques, Endocrinologie, Hôpital de Sainte Marguerite, 270 Bd de Sainte Marguerite B.P. 29, 13274 Marseille Cedex 9, France. hnarbonne@mail.ap-hop-hm.fr
Abstract
OBJECTIVE: To determine if fructosamine can be used as a surrogate for HbA(1c) to monitor whether therapeutic goals in diabetes mellitus are achieved when HbA(1c) cannot be used for this purpose (hemoglobinopathies, anemia...). MATERIAL AND METHODS: Blood samples of 76 diabetic patients and 30 healthy subjects characterized by the absence of any risk of interference in the interpretations of HbA(1c) and fructosamine were studied in order to, first, deduce from the correlation a prediction of HbA(1c) from the fructosamine values, second, to evaluate the predictive value of such predicted HbA(1c) in the determination of poor metabolic control as defined by UKPDS and DCCT studies. RESULTS: The correlation between predicted HbA(1c) and actual fructosamine was fair (r=0.88) in diabetic patients but not in control subjects (r=0.01). It was therefore only possible to estimate HbA(1c) from fructosamine in diabetic patients. Nevertheless, the range of positive and negative predictive values of estimated HbA(1c) to detect a poor metabolic control defined by two thresholds of HbA(1c) (7%, 7.5%) was 91-93% and 86-87%, respectively. Then, even in this highly selected population, the risk of misclassification was around 10% when fructosamine was used to estimate HbA(1c). These results were unchanged when fructosamine was corrected by plasma protein level. CONCLUSIONS: This study shows the limitations to use fructosamine in place of HbA(1c) to evaluate the efficacy of antidiabetic treatments, even in a selected population.
OBJECTIVE: To determine if fructosamine can be used as a surrogate for HbA(1c) to monitor whether therapeutic goals in diabetes mellitus are achieved when HbA(1c) cannot be used for this purpose (hemoglobinopathies, anemia...). MATERIAL AND METHODS: Blood samples of 76 diabeticpatients and 30 healthy subjects characterized by the absence of any risk of interference in the interpretations of HbA(1c) and fructosamine were studied in order to, first, deduce from the correlation a prediction of HbA(1c) from the fructosamine values, second, to evaluate the predictive value of such predicted HbA(1c) in the determination of poor metabolic control as defined by UKPDS and DCCT studies. RESULTS: The correlation between predicted HbA(1c) and actual fructosamine was fair (r=0.88) in diabeticpatients but not in control subjects (r=0.01). It was therefore only possible to estimate HbA(1c) from fructosamine in diabeticpatients. Nevertheless, the range of positive and negative predictive values of estimated HbA(1c) to detect a poor metabolic control defined by two thresholds of HbA(1c) (7%, 7.5%) was 91-93% and 86-87%, respectively. Then, even in this highly selected population, the risk of misclassification was around 10% when fructosamine was used to estimate HbA(1c). These results were unchanged when fructosamine was corrected by plasma protein level. CONCLUSIONS: This study shows the limitations to use fructosamine in place of HbA(1c) to evaluate the efficacy of antidiabetic treatments, even in a selected population.
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