Abstract
Clinically normal young adults with no well-known risk factors may present with metabolic syndrome, hypertension, atherogenic dyslipidemia and type-II diabetes. Age and sex are two non-modifiable risk factors for developing cardiovascular disturbances which may affect the levels of apolipoprotein B and apolipoprotein A-I.
The objective is to study serum apo B and A-I levels in association with the conventional lipid profile parameters in atherogenic dyslipidemia.
In this hospital-based prospective study, clinically normal males (n=172) and females (n=188), aged between 20-39 years, divided into two age groups: group-I (20-29 years) and group-II (30-39 years), subjected to overnight fasting had their lipid profile parameters (enzymatic colorimetric assay) along with the serum levels of apoB and apoA-I (immunoturbidimetry method) estimated. Subjects with body mass index (BMI) >30 were excluded from the study. Data was statistically analysed using Chi-square test and ROC curves.
ApoB levels showed continuous increase with age in both sexes with males having significantly raised (p<0.01) levels in both groups compared to females. ApoA-I levels declined with increasing age in both sexes and this decline was relatively earlier in males. Within each group females were having relatively raised (p<0.05) apoA-I levels than males. Moderate to strong correlations were observed between serum apoA-I and HDL-C concentrations (p<0.0001) and between serum apoB and LDL-C concentrations (p<0.0001), respectively.
ApoB may be a more sensitive measure of atherogenic dyslipidemia than LDL-C and a better index for assessing cardiovascular risk, whereas apoA-I did not add significantly to the estimation of future atherosclerotic vascular risk.
Keywords- ApoA-I, ApoB, Cardiovascular risk, Dyslipidemia, Lipid profile.
References
[1] Reddy KS, Rising burden of cardiovascular diseases in India. Cardiology Society of India 1998:63-72.
[2] Enas EA, Yusuf S, Sharma S, Coronary artery disease in South Indians: second meeting of the International Working Group, March 16, 1997, Anaheim, Carlifornia. Indian Heart Journal 1998;50:105-13.
[3] Enas EA, Yusuf S, Third Meeting on the International Working Group on Coronary Artery Disease in South Asians, March 29,1998, AtlantaGA, USA. Indian Heart Journal 1999;51:99-103.
[4] Ross R, Atherosclerosis- an inflammatory disease. New England Journal of Medicine 1999;340:115-126.
[5] Fuster V, Ross R, Topol EJ, eds, Atherosclerosis and coronary artery disease. Vol 1 and 2 Philadelphia: Lippincott Raven, 1996.
[6] Executive summary of third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA, 2001;285:2486-2497.
[7] A Onat, G Can, G Hergenc, M Yazici, A Karabulut and S Albayrak, Serum apolipoprotein B predicts dyslipidemia, metabolic syndrome and, in women, hypertension and diabetes, independent of markers of central obesity and inflammation, International Journal of Obesity 2007;31:1119-11125.
[8] R Sharma, B Singh, M Mahajan, R Kant, Age and Sex: important determinants in affecting the levels of serum apo B and A-I in Indian population. The Internet Journal of Cardiology 2006;4:1.
[9] Kannel WB, Castelli WP, Gordon T, Cholesterol in the prediction of atherosclerotic disease. New perspectives based on Framingham study. Annals of Internal Medicine 1979;90:85-91.
[10] Siedel J, Schiefer S, Rosseneu M, et al. Immunoturbidimetric Method for Routine Determinations of Apolipoproteins A-I, A-II and B in Normo and Hyperlipemic Sera compared with Immunonephelometry. Clinical Chemistry. 1988;34(9):1821-1825.
[11] Rifai N, King ME. Immunoturbidimetric Assays of Apolipoproteins A, AI, AII, and B in serum. Clinical chemistry. 1986;32:957-961.
[12] Naito HK. Reliability of Lipid, Lipoprotein and Apolipoprotein Measurements. Clinical Chemistry. 1988;34:B84-B94.
[13] Jungner I, Marcovina SM, Walldius G, Holme I, Kolar W and Steiner E, Apolipoprotein B and A-I value in 147576 Swedish males and females, standardized according to the world health organization- International Federation of Clinical First International Reference Materials. Clinical Chemistry 1998;44:1641-49.
[14] Valles V, Aguilar-Salinas CA, Gomez-Perez FJ, Rojas R, Franco A, Olaiz G et al., Apolipoprotein B and A-I distribution in Mexican Urban Adults: Results of a Nationwide survey. Metabolism 2002;51:560-68.
[15] Lamarche B, Tchernof A, Moorjani S, Cantin B, Dagenais GR, Lupien PJ et al., Small dense low density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from Quebec Cardiovascular study. Circulation 1997;95:69-75.
[16] Saman Miremadi, Allan Sniderman and Jiri Frohlich, Can Measurement of Serum Apolipoprotein replace the lipid profile monitoring of patients with lipoprotein disorders? Clinical Chemistry 2002;48:3484-88.
[17] Sweetnam PM, Bolton CH, Downs L, Durrington PN, Mackness MI, Elwood PC et al. Apolipoproteins AI, AII, and B, lipoprotein (a) and the risk of ischemic heart disease. Caerphilly study. European Journal of Clinical Investigations 2000;30:947-56.
[18] Fisher E et al., Apoprotein B 100 an atypical secretory protein, can be degraded by cytosolic pathway involving heat shock protein 70 and proteasomes. Journal of Biological Chemistry 1997;272:20427-20434.
[19] Connelly PW, Poapst M, Davingnon J, Lussier-Cacan S, Reeder B, Lessard R et al., Reference values of plasma apolipoproteins A-I and B, and association with nonlipid risk factors in the population of two Canadian provinces, Quebec and Saskatchewan. Canadian Heart Health Surveys Research Group. Canadian Journal of Cardiology 1999;40:586-92.
[20] Pfeffer MA, Sacks FM, Moye LA et al. Influence of baseline lipids on effectiveness of pravastatin in the cholesterol and recurrent events (CARE) Trial. American College of Cardiology 1993;33:125-130.
DOI: http://dx.doi.org/10.18535/jmscr/v4i6.55
