ARTICOLI ORIGINALI   

Minerva Endocrinologica 2014 June;39(2):119-26

Copyright © 2014 EDIZIONI MINERVA MEDICA

lingua: Inglese

Association of hematological parameters with insulin resistance in type 1 diabetes

Bulum T. ¹, Kolarić B. ^{2, 3}, Duvnjak L. ¹, Vrhovac R. ⁴ ✉

¹ Vuk Vrhovac Clinic for Diabetes Endocrinology and Metabolic Diseases, University Hospital Merkur, School of Medicine University of Zagreb, Croatia; ² School of Medicine, University of Rijeka, Croatia; ³ Zagreb County Institute of Public Health, Zagreb, Croatia; ⁴ Department of Hematology, University Hospital Centre Zagreb School of Medicine, University of Zagreb, Croatia

AIM: Previous studies reported independent associations of hematological parameters with insulin resistance. The aim of this study was to explore the associations of hematological parameters, including red blood cell count (RBC), hemoglobin (Hgb), white blood cell count (WBC), and platelets with insulin resistance in type 1 diabetes.
METHODS: Study included 353 patients with type 1 diabetes. None showed signs of acute or chronic inflammatory, renal and cardiovascular diseases. Insulin sensitivity was measured with estimated glucose disposal rate (eGDR) calculated with the equation: eGDR=24.31-(12.22xWHR)-(3.29xAHT)-(0.57xHbA1c). The units were mg.kg-1min-1; WHR=waist to hip ratio; AHT=hypertension.
RESULTS: RBC, Hgb, and WBC significantly correlated with insulin resistance measured by eGDR (r=-0.12, -0.21, and -0.14, respectively, all P≤0.01), and its components disorders, most notably WHR (r=0.38, 0.44, and 0.16, respectively, all P≤0.001). In a multiple logistic regression analysis after adjustment for age, sex, duration of diabetes and BMI, the presence of insulin resistance was independently associated with WBC count (odds ratio=1.28, P<0.01). The risk of insulin resistance increases by a factor of 4.41 for those in the 4th quartile of WBC, compared to those in 1st quartile.
CONCLUSION: The significant independent association of WBC with the presence of insulin resistance suggests a role of subclinical inflammation in its pathogenesis.