Impaired lipid metabolism resulting from uncontrolled hyperglycaemia has been implicated in cardiovascular complications in diabetes patients. The aim of this study was to examine the impact of glycaemic control on the lipid profile of diabetic patients. We also determined the ability of glycated haemoglobin (HbA(1c)) as an indirect marker of dyslipidaemia. A total of 1011 type 2 diabetic patients (males, 574; females, 437; mean age, 59.76 years) were included in this study. Venous blood samples were collected from all the subjects after at least 8 h fasting. The sera were analysed for HbA(1c), fasting blood glucose (FBG), total cholesterol, triglycerides (TG), high-density lipoprotein cholesterol (HDL) and low-density lipoprotein cholesterol (LDL). The levels of HbA(1c), FBG and LDL did not differ significantly between males and females. Female patients showed significantly higher serum cholesterol and HDL but significantly lower TG levels as compared to males. There was a highly significant correlation between HbA(1c) and FBG. Both HbA(1c) and FBG exhibited direct correlations with cholesterol, TG and LDL and inverse correlation with HDL; the magnitude of significance for all these lipid parameters being greater with HbA(1c) than FBG. There was a linear relationship between HbA(1c) and dyslipidaemia. The levels of serum cholesterol and TG were significantly higher and of HDL significantly lower in patients with worse glycaemic control as compared to patients with good glycaemic control. The findings of this study clearly indicate that HbA(1c) is not only a useful biomarker of long-term glycaemic control but also a good predictor of lipid profile. Thus, monitoring of glycaemic control using HbA(1c) could have additional benefits of identifying diabetic patients who are at a greater risk of cardiovascular complications.

The biomarker potential of using various lipids fractions for predicting risk of acute myocardial infarction (AMI) is controversial. We therefore compared the lipid profiles, including serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol (HDL) and triglycerides (TG), in 67 AMI patients. Patients included 28 STEMI (ST-elevated myocardial infarction) patients, 39 NSTEMI (non-ST-elevated myocardial infarction) patients and 25 patients with chest pain. Control group included 54 age- and gender-matched normal subjects. We also studied the correlation between lipid profile and systemic inflammation in these subjects. There were significant decreases in TC, LDL and HDL levels in both STEMI and NSTEMI patients as compared to normal subjects; however, patients with chest pain did not show any significant change in these lipids. Serum TG levels did not differ significantly among the study groups. There were significant increases in serum high-sensitive C-reactive protein (hs-CRP) levels in STEMI and NSTEMI patients, as compared to control group. Serum hs-CRP showed significant inverse correlation with HDL; however, hs-CRP was not correlated with TC, LDL, and TG. In conclusion, our findings suggest that reduction in serum TC does not prevent the risk of AMI, whereas a decrease in serum HDL and increase in hs-CRP strongly predisposes the risky individuals to an AMI event. We emphasize the importance of HDL and CRP measurements for the assessment of a combined lipid-inflammation risk factor that could be a useful predictor of high risk individuals, as well as a prognostic marker in AMI patients.

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In cirrhotic patients, AFP has a poor screening and diagnostic value for HCC. Underlying viral etiology fails to influence the diagnostic accuracy of this test. An AFP level greater than 100 ng/ml has a high degree of specificity and may be used as a confirmatory test.