Abstract:Objective: To study the changes and significance of apolipoprotein(apo)A1/apoB and lipoprotein(Lp)(a) in patients with hypercholesterolemia. Methods: 150 patients with hypercholesterolemia received from January 2017 to November 2017 were selected as the observation group, and 150 healthy were selected in our hospital for the same period as the control group. All personnel were collected from fasting venous blood at 2d after admission, the expression of low density lipoprotein cholesterol (LDL-C), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), triglyceride (TG), apoA1, apoB, apoA1/apoB, Lp(a) were detected, to analyze the changes and significance of apoA1/apoB and Lp(a) in patients with hypercholesterolemia. Results: The LDL-C, TC, HDL-C, apoA1, apoB, apoA1/apoB and Lp(a) in the observation group were(5.71±0.36)mmol/L,(6.83±0.47)mmol/L,(1.04±0.07)mmol/L,(1.07±0.18)g/L,(1.07±0.23)g/L、(1.06±0.32), (258.18±20.95)mg/L respectively, in the control group were(1.78±0.12)mmol/L,(3.62±0.29)mmol/L,(1.34±0.07)mmol/L,(0.38±0.22)g/L,(0.84±0.08)g/L,(1.67±0.32),(154.82±17.49)mg/L respectively, the differences has statistically significant(P<0.05); the Pearson correlation analysis showed that there was negatively correlated between apoA1/apoB and LDL-C and TC(r=-0.682, -0.679, P<0.05), there was a positive correlation between Lp(a) and LDL-C and TC(r=0.926, 0.909, P<0.05). Conclusion: There is obvious disorder of lipid metabolism in patients with hypercholesterolemia, and the decrease of apoA1/apoB and the increase of Lp (a) can reflect the disorder of lipid metabolism, this study also provides a new way for clinical treatment of hypercholesterolemia.
[1] 王亭.成人血脂异常的流行特征与影响因素[J].职业与健康,2015,31(7):1000~1005. [2] Lorenzo A, Silva JDLD, James CE, et al. Clinical, anthropometric and biochemical characteristics of patients with or without genetically confirmed familial hypercholesterolemia[J]. Arq Bras Cardiol, 2018, 110(2): 119~123. [3] Enkhmaa B, Anuurad E, Zhang W, et al. The roles of apo(a) size, phenotype, and dominance pattern in PCSK9-inhibition-induced reduction in Lp(a) with alirocumab[J].Lipid Res, 2017, 58(10): 2008~2016. [4] Badimon L, Padro T, Cubedo J. Protein changes in non-LDL-lipoproteins in familial hypercholesterolemia: implications in cardiovascular disease manifestation and outcome[J]. Curr Opin Lipidol, 2017, 28(5): 427~433. [5] Zhu Y, Wang X, Wang W, et al. Expression and influence of pentraxin-3, HbAlc and ApoA1/ApoB in serum of patients with acute myocardial infarction combined with diabetes mellitus type 2[J]. Exp Ther Med, 2018, 15(5): 4395~4399. [6] 汪峰,顾桂兰,王志勇,等.血清hs-CRP、LP(a)水平以及ApoB/ApoA1与冠心病相关性的分析[J].临床和实验医学杂志,2014,13(17):1478~1479. [7] Carroll MD, Mussolino ME, Wolz M, et al. Trends in apolipoprotein B, non-high-density lipoprotein and low-density lipoprotein for adults 60 years and older by use of lipid-lowering medications: united states, 2005 to 2006 through 2013 to 2014[J]. Circulation, 2018, 138(2): 208~210. [8] Cook NR, Mora S, Ridker PM. Lipoprotein(a) and cardiovascular risk prediction among women[J].Am Coll Cardiol, 2018, 72(3): 287~296. [9] Vuorio A, Watts GF, Kovanen PT. Depicting new pharmacological strategies for familial hypercholesterolaemia involving lipoprotein (a)[J]. Eur Heart, 2017, 38(48): 3555~3559.