Evaluation of Cystatin C and Intercellular adhesion molecule –1 as markers of preclinical coronary artery disease in normoalbuminuric early type 2 diabetes individuals

Main Article Content

Nisha Jha (M.D)
Poornima A Manjrekar (M.D, Ph.D.)
Anupama Hegde (M.D)
Rukmini M S (M.D)
Yalla Durgarao (MSc, Ph.D.)

Abstract

Introduction: The presence of sub-chronic inflammation characterized by elevated intercellular adhesion molecule 1 (ICAM-1) and other cytokines has been quite evident in diabetes-associated coronary artery diseases. Cystatin-c, primarily developed as an early renal dysfunction marker, is found to be associated with insulin resistance and inflammation independent of renal function. The present study was designed to evaluate Cystatin-c and ICAM-1 as markers of pre-clinical coronary artery disease in normoalbuminuric early type 2 diabetes mellitus individuals.


Materials and Methods: Post-screening, study participants of both genders aged 35-55 years were divided into group 1 (31 healthy controls) and group 2 (31 normoalbuminuric early diabetes cases with a diabetes duration of 2-7 years). Fasting plasma glucose (hexokinase method), HbA1c (high-performance liquid chromatography) and random urine microalbumin (immuno-turbidometry) were estimated. Serum ICAM-1 and Cystatin-c levels were quantified by ELISA. Data analysis was performed using SPSS version 20.


Results: The average age of diabetes and control groups was found to be 49.68±4.60 and 45.23±5.73 years respectively. The mean diabetes duration was found to be 5.58±1.50 years. Compared to controls, diabetes group showed elevated ICAM 1 (630.26±266.062 vs 856.58±233.36 ng/mL, p=0.001) and cystatin-c (1118.26±262.980 vs 1229.10±457.74 ng/mL, p=0.383)


levels. Correlation of ICAM 1 with cystatin-c in both diabetes (r = 0.009, p = 0.96) and control (r = - 0.07, p = 0.68) groups was insignificant.


Conclusion: The significant increase in ICAM-1 levels over Cystatin-c in normoalbuminuric early diabetes individuals discriminates its superior role in assessing preclinical endothelial dysfunction and inflammation.

Article Details

Section
Articles