Role of serum lipoprotein (a) in type 2 diabetes mellitus and its association with glycemic control

Abstract

Diabetes mellitus (DM) is an established risk factor for cardiovascular disease. At present global risk assessment, lipid profile is only the blood test routinely recommended most commonly. Increased lipoprotein (a) [Lp(a)] contributing factor to accelerated development of macrovascular complications in DM. However Lp(a) and hsCRP evaluation may have the potential to improve cardiovascular risk prediction when used in addition to traditional lipid profile. Hence the study was undertaken to estimate the serum lipoprotein (a), lipid profile, lipid ratios and hsCRP in diabetic patients and their association with glycemic control. Within the diabetic patients we examined Lp(a) levels among controlled and uncontrolled diabetic individuals. Materials and Methods: An observational study comprises of 150 participants. 75 were type 2 diabetic patients and 75 were healthy controls. Diabetic patients were further sub classified into good and poor glycemic control group depending on their HbA1c levels 7.5% as cut-off value. Fasting venous blood sample was collected and used for analysis of fasting glucose, lipoprotein (a), lipid profile, high sensitive C reactive protein (hsCRP) and glycosylated hemoglobin (HbA1c). Results: A significant increase (p Conclusion: The study helps in identification of at risk individuals for CAD beyond the routinely done lipid profile especially in insufficient resource situations. In our study we have higher levels of Lp(a), hsCRP and other atherogenic risk factors cluster more in diabetic patients compared to healthy controls. FBS, TG, hsCRP and TG/HDL are positively correlated with HbA1c. Thus Lp(a) and hsCRP evaluation may have the potential to improve cardiovascular risk prediction when used in addition to traditional lipid profile in diabetic patients. Poor glycemic control subjects have significantly higher hsCRP and TGs compared to good glycemic controls. There is no effect of glycemic control on Lp(a) levels, hence Lp(a) is independent ris