冠心病合并抑郁症患者血清adropin、血小板活化因子、胶质纤维酸性蛋白水平变化及意义

Changes of serum adropin, platelet activating factor and glial fibrillary acidic protein levels in patients with coronary heart disease complicating depression and their significance

  • 摘要:
      目的  探讨冠心病(CHD)合并抑郁症患者血清adropin、血小板活化因子(PAF)、胶质纤维酸性蛋白(GFAP)水平的变化及相关性。
      方法  选取163例CHD患者作为研究对象,根据汉密尔顿抑郁量表(HAMD)评分将其分为抑郁症组(HAMD评分≥18分)98例(轻度抑郁47例、中度抑郁31例、中度抑郁20例)和非抑郁症组(HAMD评分 < 18分)65例。采用酶联免疫吸附法(ELISA)检测患者血清adropin、PAF、GFAP水平,采用Pearson相关分析法分析CHD合并抑郁症患者血清adropin与PAF、GFAP水平的相关性;采用Logistic回归分析探讨CHD患者发生抑郁症的影响因素。
      结果  抑郁症组患者空腹血糖、PAF、GFAP水平高于非抑郁症组,血清adropin水平低于非抑郁症组,差异有统计学意义(P < 0.05);抑郁症组中,轻度、中度、重度抑郁患者的血清adropin水平逐渐降低,PAF、GFAP水平逐渐升高,差异有统计学意义(P < 0.05);Pearson相关分析显示,CHD合并抑郁症患者血清adropin水平与PAF、GFAP水平均呈负相关(r=-0.665、-0.643,P < 0.001);多因素Logistic回归分析显示,血清adropin < 49.36 pg/mL、PAF≥124.47 pg/mL、GFAP≥12.79 ng/mL是CHD患者并发抑郁症的独立危险因素(P < 0.05)。
      结论  随着抑郁程度的加重,CHD患者血清adropin水平降低,PAF、GFAP水平升高。血清adropin水平与PAF、GFAP水平均呈负相关,三者均是CHD患者并发抑郁症的独立影响因素。

     

    Abstract:
      Objective  To investigate the changes and correlations of serum adropin, platelet activating factor (PAF) and glial fibrillary acidic protein (GFAP) in patients with coronary heart disease (CHD) and depression.
      Methods  A total of 163 patients with CHD were selected as objects, the patients were divided into depression group (98 cases including 47 cases of mild depression, 31 cases of moderate depression and 20 cases of moderate depression, HAMD scored ≥ 18) and non-depression group (65 cases, HAMD scored < 18) according to Hamilton Depression Scale (HAMD) score. The levels of serum adropin, PAF and GFAP were detected by enzyme-linked immunosorbent assay (ELISA). Pearson method was used to analyze the correlations between serum adropin and PAF, GFAP levels in CHD patients with depression. Logistic regression analysis was used to analyze the influencing factors of depression in CHD patients.
      Results  The levels of fasting blood glucose, PAF and GFAP in the depression group were higher than those in non-depression group, while the level of serum adropin was lower than that in the non-depressive group (P < 0.05). In the depression group, serum adropin levels in mild, moderate and severe depression patients gradually decreased, while PAF and GFAP levels gradually increased (P < 0.05). Pearson correlation analysis showed that serum adropin level was negatively correlated with PAF and GFAP levels in CHD patients with depression (r=-0.665, -0.643, P < 0.001); multivariate Logistic regression analysis showed that serum adropin level < 49.36 pg/mL, PAF level ≥ 124.47 pg/mL, GFAP level ≥ 12.79 ng/mL were the independent influencing factors of depression in CHD patients (P < 0.05).
      Conclusion  With the aggravation of depression in patients with CHD, serum adropin level is decreased and levels of PAF and GFAP are increased. Serum adropin level is negatively correlated with PAF and GFAP levels, and all of them are independent influencing factors of depression in CHD patients.

     

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