The lack of utility of circulating biomarkers of inflammation and endothelial dysfunction for type 2 diabetes risk prediction among postmenopausal women: the Women’s Health Initiative Observational Study.
Arch Intern Med 2010;170:1557-65
Chao C, Song Y, Cook N, Tseng CH, Manson JE, Eaton C, Margolis KL, Rodriguez B, Phillips LS, Tinker LF, Liu S
The aim of this study was to determine the added predictive value of plasma inflammatory markers and endothelial dysfunction markers beyond the traditional diabetes risk factors in postmenopausal women of several ethnicities. The study population was derived from the prospective cohort of the Women’s Health Initiative Observation Study and included 1,584 incident type 2 diabetes cases and 2,198 matched controls aged 50 to 79 years who were free of reported diabetes and cardiovascular disease at baseline. Analyses revealed that plasma inflammatory markers (white blood cells, tumour necrosis factor receptor 2, interleukin-6 and high-sensitivity C-reactive protein levels) and endothelial dysfunction markers (E-selectin, soluble intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 levels) did not appear to improve the performance of risk stratification and prediction for type 2 diabetes. The addition of some novel biomarkers such as white blood cell count and levels of interleukin-6, high-sensitivity C-reactive protein and soluble intercellular adhesion molecule-1 significantly improved global model fit represented by the variable likelihood ratio x2 statistic. However, none of these biomarkers led to a meaningful improvement in model discrimination as assessed by the area under the receiver operating characteristic curve and the integrated discrimination improvement. Based on the evaluation of Bayesian information criteria, the best prediction model of novel plasma markers had a global model fit performance that was similar to the model incorporating only well-established traditional risk factors. Ethnic-specific analyses generated similar results. These findings support the notion that chronic inflammation and endothelial dysfunction are implicated in the pathophysiology of diabetes but they do not improve the risk stratification and prediction of type 2 diabetes in postmenopausal women.