Increased plasma malondialdehyde and fructosamine in iron deficiency anemia: Effect of treatment

Glycation and lipid peroxidation are spontaneous reactions that are believed to play a key role in the pathogenesis of many clinical disorders. Glycation of proteins is enhanced by elevated glucose concentrations. However, increased glycated hemoglobin levels have been documented in iron deficiency anemic patients without any history of diabetes. Collective evidences reveal that lipid peroxidation can modulate protein glycation. This study was undertaken to unravel the possible association of malondialdehyde and fructosamine in iron deficient anemic patients and to observe the possible alteration in malondialdehyde and fructosamine levels in these patients after one month supplementation with iron. Twenty non-diabetic anemic patients and 16 age-matched healthy subjects were enrolled for this study. Plasma lipid peroxides, fasting glucose, fructosamine, iron, ferritin and hemoglobin were analyzed in both the groups. Partial correlation analysis was performed to predict the independent association of malondialdehyde and fasting glucose on fructosamine. In anemic patients, while fructosamine and malondialdehyde levels were found to be significantly increased, hemoglobin, iron and ferritin levels decreased significantly when compared to before treatment. Fructosamine was found to have a significant positive correlation with malondialdehyde even after nullifying the effect of glucose. After one month supplementation with iron, both fructosamine and malondialdehyde levels decreased significantly when compared to before treatment. There was a significant increase in iron, ferritin and hemoglobin levels in anemic patients after one month of treatment. In conclusion, an increased level of fructosamine and malondialdehyde was found in anemic patients. These data suggest that fructosamine levels are closely associated with malondialdehyde concentrations in iron deficient anemic patients. (C) 2007 Elsevier Masson SAS. All rights reserved.