Total antioxidant status and coronary artery calcification in type 1 diabetes.
OBJECTIVE
Type 1 diabetes is associated with a high risk of coronary heart disease (CHD), despite the absence of dyslipidemia. Oxidative modification may render LDLs more atherogenic. We aimed to assess antioxidant status in type 1 diabetes and its association with coronary artery calcification (CAC).


METHODS
Total antioxidant status (TAS) of serum was measured using the Trolox equivalent antioxidant capacity assay in 48 type 1 diabetic and 25 nondiabetic subjects. The presence of CAC was assessed in the diabetic subjects using electron beam computed tomography.


RESULTS
TAS was reduced in type 1 diabetic subjects compared with nondiabetic subjects (Mann-Whitney U test, P < 0.0001). There were associations between TAS and HbA(1c) (r = -0.43; P = 0.0026) and duration of diabetes (r = -0.35; P = 0.0157). Significant CAC was considered present if the Agatston score was >10. The diabetic subjects with significant CAC were older (P < 0.0001); had longer duration of diabetes (P = 0.0002); were more likely to have high blood pressure (P = 0.040); had higher total cholesterol concentration (P = 0.039), serum creatinine concentration (P = 0.003), and urinary albumin-to-creatinine ratio (P = 0.022); and had lower serum TAS (P = 0.018) compared with those without significant calcification. In logistic regression with CAC as the dependent variable, TAS was entered as a predictor, and the effects on its predictive value of adding other explanatory variables in bivariate analyses were assessed. The power of TAS to predict CAC was independent of many of the traditional CHD risk factors. Whereas TAS as a predictor was no longer statistically significant when age or duration of diabetes were entered into the model, the odds ratio for a TAS concentration above the median value predicting significant CAC only increased from 0.19 to 0.26 and 0.32, respectively.


CONCLUSIONS
TAS is reduced in type 1 diabetes and is associated with the presence of CAC.
Valabhji
J
J
Department of Endocrinology and Metabolic Medicine, Imperial College School of Medicine, St Mary's Hospital, Norfolk Place, London W2 1PG, United Kingdom. j.valabhji@ic.ac.uk
McColl
A J
AJ
Richmond
W
W
Schachter
M
M
Rubens
M B
MB
Elkeles
R S
RS
D000328:Adult; D000419:Albuminuria; D000975:Antioxidants / Q000032:analysis*; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D002114:Calcinosis / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D008076:Cholesterol, HDL / Q000097:blood; D002839:Chromans; D003327:Coronary Disease / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D003925:Diabetic Angiopathies / Q000097:blood / Q000503:physiopathology; D003930:Diabetic Retinopathy / Q000453:epidemiology; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D012907:Smoking
D000975:Antioxidants; D001786:Blood Glucose; D008076:Cholesterol, HDL; D002839:Chromans; D008055:Lipids; C010643:6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid