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Abstract

Click to add/remove this article to your list of 'My Favorites' Leukocyte Differential and Coronary Artery Disease (CAD) in Type 1 Diabetes (T1D)

Year: 2009

Abstract Number: 1004-P

Authors: RACHEL G. MILLER, TREVOR J. ORCHARD

Institutions: Pittsburgh, PA

Results: White blood cell count has long been implicated in the pathogenesis of CAD though its role has not been fully elucidated. Here we compare the association between types of leukocytes and CAD in T1D. We also examined modification of the association by BMI, glomerular filtration rate (GFR), and both pro- (ie.C-reactive protein (CRP) and tumor necrosis factor α (TNFα)) and anti-inflammatory markers (total adiponectin (TA)). Data are from the 18-yr follow-up visit of the Pittsburgh Epidemiology of Diabetes Complications Study (EDC) of childhood-onset T1D (n=290, mean age=45.0, T1D duration=36.8 yrs). Participants were classified as having CAD (n=76, 26.2%) if a confirmed event (myocardial infarction, revascularization/blockage≥50%, ischemic ECG, or physician-diagnosed angina) occurred at any time prior to the 18-yr exam. Separate logistic regression models were built to assess the cross-sectional association between each type of leukocyte and CAD. Traditional risk factors were available for covariate adjustment. Leukocyte-BMI, -GFR, and -inflammatory marker interaction terms were assessed and stratified models were also examined. Odds ratios are per tertile. Total leukocyte (OR=1.44 p=0.03) and monocyte (OR=1.56 p=0.004) count were univariately associated with CAD prevalence but not after covariate adjustment. Neutrophil count was univariately associated with CAD (OR=1.64 p=0.004) and remained so after adjustment (OR=1.65 p=0.03). No other leukocytes were associated with CAD status. Interactions were found between neutrophils and BMI, GFR, and TA, with respect to CAD; ie. neutrophil count was only associated with CAD in those with BMI <25 OR=2.87, p=0.02 (v. OR=1.01 p=0.96 in BMI≥25), high TA ≥22.6 μg/ml OR=1.88, p=0.07 (v. OR=1.04 p=0.91 in low TA), and low GFR <90 mL/min/1.73 m2 OR=2.05, p=0.03 (v. OR=1.21 p=0.59 in high GFR). No interactions were found between neutrophils and the pro-inflammatory markers CRP and TNFα. These results suggest that neutrophils drive the CAD-leukocyte association in this T1D cohort and that the relationship may be modified by other measures of inflammation, kidney function, and BMI. Prospective analyses are needed to further examine the nature of the association.

Category: Epidemiology