ABSTRACT
Background and Objective: A major modifiable risk factor for atherosclerotic cardiovascular disease is abnormalities in lipid and lipoprotein metabolism which are frequently seen in HIV as well as its treatment. Apo-E is a protein that is important in plasma lipid homeostasis and its genetic alleles have been shown to contribute to lipid abnormalities. We examined for the effect of Apo-E gene polymorphisms on plasma lipid levels in PLHIV on protease inhibitor therapy. Methods: This was a cross-sectional study conducted among adult persons living with HIV. Lipid profile, Apo-B and Apo-A were measured in fasting plasma. Amplification and analysis of Apo-E genotypes were determined using the Seeplex Apo-E ACE genotyping kit. Differences in quantitative values were compared with non-parametric analysis methods. Results: Eighty-four persons were recruited into the study, 75% of whom were virally suppressed. The 3 homozygous genotypes had significantly different levels of low-density lipoprotein cholesterol (LDL-C), Apolipoprotein B (Apo-B) and Apolipoprotein A1 (Apo-A1). Persons with apo ε2/ε2 had higher LDL-C compared to those with apo ε3/ε3 (3.26 (3.61) mmol/L vs. 2.76 (1.28) mmol/L, p = 0.010). Those with apo ε4/ε4 had lower Apo-A1 compared to those with apo ε3/ε3 (0.84 (0.48) g/dL vs. 1.27 (0.70) g/dL, p =0.009). Compared with the same group, the heterozygous genotype, apo ε2/ε3 had lower triglyceride levels :1.33 (0.65) mmol/ L vs. 1.86 (1.11) mmol/L, p = 0.045. Conclusion: Polymorphisms in the Apo-E gene may have significant influences on plasma lipid and apolipoprotein levels in PLHIV on PI therapy. This may have implications for the assessment of risk for cardiovascular disease.
ABSTRACT
BACKGROUND: There is at present the dearth of information on the possible contribution of insulin resistance to scores obtained from mortality risk estimation in patients with type 2 diabetes mellitus (T2DM). AIM: This study determined the mortality risk scores in patients with T2DM and its relationship with insulin resistance. METHODS: Fasting plasma glucose, total cholesterol, high-density lipoprotein cholesterol (HDL), triglycerides, serum and urinary creatinine, glycated hemoglobin (HbA1c), serum insulin, and urinary albumin were determined in 111 T2DM patients. Thereafter, low-density lipoprotein cholesterol (LDL), quantitative insulin sensitivity check index (QUICKI), urinary albumin-to-creatinine ratio (UACR), and estimated glomerular filtration rate (eGFR) were calculated using the standard formula. Mortality risk was estimated using the validated Gargano mortality risk calculator with scores ≤0.67, 0.68-0.79, and ≥0.80 considered as low, intermediate, and high risks, respectively. RESULTS: Of the total patients, 5 (4.5%), 28 (25.2%), and 78 (70.3%) patients had high, intermediate, and low mortality risk, respectively. There was no difference in the median QUICKI values when the three groups were compared. However, there was a significant elevation in the median eGFR in patients with high mortality risk compared with patients with low and intermediate mortality risks. Also, the median mortality risk score of patients with low insulin sensitivity (QUICKI ≤0.3) was similar to that obtained in patients with normal insulin sensitivity (QUICKI ≥0.31). No significant correlation was found between QUICKI and mortality risk scores. CONCLUSION: Insulin sensitivity status does not have a direct effect on scores obtained from the Gargano mortality risk prediction model.
