高血压病合并急性脑梗死患者血清游离脂肪酸的表达水平及临床意义
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摘要
目的探讨高血压合并急性脑梗死患者血清游离脂肪酸(FFA)含量变化及其临床意义。方法随机选取高血压合并急性脑梗死患者49例,采用酶终点法检测其发病后24 h内的血清FFA含量变化;随机选取单纯高血压病患者23例,并以同期在我院体检科体检的中老年健康人中随机选取30例作为平行对照。结果高血压合并急性脑梗死患者发病后24 h内的血清FFA表达水平为(0. 67±0. 29) mmol/L,与健康对照组(0. 36±0. 15) mmol/L和单纯高血压病患者(0. 53±0. 26) mmol/L比较,差异均具有统计学意义(P <0. 05)。通过ROC曲线分析,对于高血压合并急性脑梗死患者的诊断FFA的特异度和敏感度均高于血清总胆固醇(TC)和甘油三酯(TG)。结论高血压合并急性脑梗死患者血清FFA表达水平明显升高,血清FFA的水平与高血压和神经功能缺损有关。血清FFA作为一种诊断标志物,其诊断的敏感度高于传统的TG、TC指标的测定。血清FFA的测定可以作为预测高血压合并急性脑梗死的发生、发展的一种经济、简易且风险小的参考指标。
Objective: To investigate the clinical significance of changes in serum free fatty acid content in patients with hypertension complicated with acute cerebral infarction. Methods: Forty-nine patients with hypertension complicated with acute cerebral infarction were randomly selected,and 23 patients with hypertension alone were selected. Changes in serum FFA content within 24 hours after the onset were detected by enzyme endpoint method. In the experiment,30 healthy middle-aged and elderly people who had physical examination at the physical examination department of our hospital were randomly selected as parallel controls. Results: The serum FFA expression level( 0. 67 ± 0. 29) mmol/L in patients with hypertension complicated with acute cerebral infarction was significantly different from that of the healthy control group( 0. 36 ±0. 15) mmol/L within 24 hours after the onset of hypertension complicated with acute cerebral infarction( P < 0. 05). The serum FFA expression level( 0. 67 ± 0. 29) mmol/L in patients with hypertension complicated with acute cerebral infarction was higher than that in patients with hypertension alone( 0. 53 ± 0. 26) mmol/L,which had significant difference( P <0. 05). The specificity and sensitivity of FFA in patients with hypertension complicated with acute cerebral infarction were higher than that of TC and TG by ROC curve analysis. Conclusion: The serum FFA level of hypertensive patients with acute cerebral infarction is significantly increased,and the serum FFA level is related to hypertension and neurological function defects. As a diagnostic marker,the diagnostic sensitivity of serum FFA is higher than that of TG and TC. The determination of serum FFA can be used as an economic,simple and low risk index to predict the occurrence and development of hypertension complicated with acute cerebral infarction.
Objective: To investigate the clinical significance of changes in serum free fatty acid content in patients with hypertension complicated with acute cerebral infarction. Methods: Forty-nine patients with hypertension complicated with acute cerebral infarction were randomly selected,and 23 patients with hypertension alone were selected. Changes in serum FFA content within 24 hours after the onset were detected by enzyme endpoint method. In the experiment,30 healthy middle-aged and elderly people who had physical examination at the physical examination department of our hospital were randomly selected as parallel controls. Results: The serum FFA expression level( 0. 67 ± 0. 29) mmol/L in patients with hypertension complicated with acute cerebral infarction was significantly different from that of the healthy control group( 0. 36 ±0. 15) mmol/L within 24 hours after the onset of hypertension complicated with acute cerebral infarction( P < 0. 05). The serum FFA expression level( 0. 67 ± 0. 29) mmol/L in patients with hypertension complicated with acute cerebral infarction was higher than that in patients with hypertension alone( 0. 53 ± 0. 26) mmol/L,which had significant difference( P <0. 05). The specificity and sensitivity of FFA in patients with hypertension complicated with acute cerebral infarction were higher than that of TC and TG by ROC curve analysis. Conclusion: The serum FFA level of hypertensive patients with acute cerebral infarction is significantly increased,and the serum FFA level is related to hypertension and neurological function defects. As a diagnostic marker,the diagnostic sensitivity of serum FFA is higher than that of TG and TC. The determination of serum FFA can be used as an economic,simple and low risk index to predict the occurrence and development of hypertension complicated with acute cerebral infarction.
引文
[1]Summer R,Walsh K,Medoff BD.Obesity and pulmonary arterial hypertension:is adiponectin the molecular link between these conditions[J].Pulm Circ,2011,1(4):440-447.
[2]Jankov RP,Kantores C,Pan J,et al.Contribution of xanthine oxidase-derived superoxide to chronic hypoxic pulmonary hypertension in neonatal rats[J].Am J Physiol Lung Cell Mol Physiol,2008,294(2):233-245.
[3]Frommer KW,Schaffler A,Rehart S,Lehr A.Free fatty acids:potential proinflammatory mediators in rheumatic diseases[J].Annals of the Rheumatic Diseases,2015(74):303-310.
[4]Ayoub HM,Mc Donald MR,Sullivan JA,et al.Proteomic Profiles of Adipose and Liver Tissues from an Animal Model of Metabolic Syndrome Fed Purple Vegetables[J].Nutrients,2018;6(4):1-29.
[5]Liu J,Mazzone PJ,Cata JP,et al.Serum Free Fatty Acid Biomarkers of Lung Cancer[J].Chest,2014,146(3):670-679.
[6]Shangyu Hong,Wei Song,Peter-James H,et al.Phosphorylation of Beta-3 adrenergic receptor at serine 247 by ERK MAP kinase drives lipolysis in obese adipocytes[J].Mol Metab,2018,6:1-13.
[7]Burger CD,Foreman AJ,Miller DP,et al.Comparison of body habitus in patients with pulmonary arterial hypertension enrolled in the registry to evaluate early and long-term PAH disease management with normative values from the national health and nutrition examination survey[J].Mayo Clin Proc,2011,86(2):105-112.
[8]Weng M,Raher MJ,Leyton P,et al.Adiponectin decreases pulmonary arterial remodeling in murine models of pulmonary hypertension[J].Am J Respir Cell Mol Biol,2011,45(2):340-347.
[9]Eldor R,Norton L,Fourcaudot M,et al.Increased lipid availability for three days reduces whole body glucose uptake,impairs muscle mitochondrial function and initiates opposing effects on PGC-1αpromoter methylation in healthy subjects[J].PLo S One,2017,12(12):1-17.
[10]Ikeda T,Iwata K,Ochi H.Effect of insulin,proinsulin,and amylin on renin release from perfused rat kidney[J].Metabolism:clinical and experimental,2001,50(7):763-766.
[11]Wojcik B,Miklosz A,Zabielski P,et al.Effect of tachycardia on mRNA andf protein expression of the principal components of the lipolytic system in the rat's heart ventricles[J].J Physiol Pharmacol,2017:10.
[12]Zhang PY,Xu X,Li XC.Cardiovascular diseases:oxidative damage and antioxidant protection[J].European Review for Medical and Pharmacologocal Sciences,2014,18(20):3091-3096.
[2]Jankov RP,Kantores C,Pan J,et al.Contribution of xanthine oxidase-derived superoxide to chronic hypoxic pulmonary hypertension in neonatal rats[J].Am J Physiol Lung Cell Mol Physiol,2008,294(2):233-245.
[3]Frommer KW,Schaffler A,Rehart S,Lehr A.Free fatty acids:potential proinflammatory mediators in rheumatic diseases[J].Annals of the Rheumatic Diseases,2015(74):303-310.
[4]Ayoub HM,Mc Donald MR,Sullivan JA,et al.Proteomic Profiles of Adipose and Liver Tissues from an Animal Model of Metabolic Syndrome Fed Purple Vegetables[J].Nutrients,2018;6(4):1-29.
[5]Liu J,Mazzone PJ,Cata JP,et al.Serum Free Fatty Acid Biomarkers of Lung Cancer[J].Chest,2014,146(3):670-679.
[6]Shangyu Hong,Wei Song,Peter-James H,et al.Phosphorylation of Beta-3 adrenergic receptor at serine 247 by ERK MAP kinase drives lipolysis in obese adipocytes[J].Mol Metab,2018,6:1-13.
[7]Burger CD,Foreman AJ,Miller DP,et al.Comparison of body habitus in patients with pulmonary arterial hypertension enrolled in the registry to evaluate early and long-term PAH disease management with normative values from the national health and nutrition examination survey[J].Mayo Clin Proc,2011,86(2):105-112.
[8]Weng M,Raher MJ,Leyton P,et al.Adiponectin decreases pulmonary arterial remodeling in murine models of pulmonary hypertension[J].Am J Respir Cell Mol Biol,2011,45(2):340-347.
[9]Eldor R,Norton L,Fourcaudot M,et al.Increased lipid availability for three days reduces whole body glucose uptake,impairs muscle mitochondrial function and initiates opposing effects on PGC-1αpromoter methylation in healthy subjects[J].PLo S One,2017,12(12):1-17.
[10]Ikeda T,Iwata K,Ochi H.Effect of insulin,proinsulin,and amylin on renin release from perfused rat kidney[J].Metabolism:clinical and experimental,2001,50(7):763-766.
[11]Wojcik B,Miklosz A,Zabielski P,et al.Effect of tachycardia on mRNA andf protein expression of the principal components of the lipolytic system in the rat's heart ventricles[J].J Physiol Pharmacol,2017:10.
[12]Zhang PY,Xu X,Li XC.Cardiovascular diseases:oxidative damage and antioxidant protection[J].European Review for Medical and Pharmacologocal Sciences,2014,18(20):3091-3096.