Afsar Cigdem U, Uzun Hafize, Yurdakul Selen, Muderrisoglu Cuneyt, Ergüney Mecdi, Demir Bulent, Aslan Aram, Aral Hale, Ozyazgan Sibel
Coronary Intensive Care Unit, Ministry of Health Istanbul Education and Research Hospital, Istanbul, Turkey.
Clin Invest Med. 2012 Aug 4;35(4):E206-15. doi: 10.25011/cim.v35i4.17149.
Fetuin-A is a multifunctional hepatic secretory protein that inhibits dystrophic vascular and valvular calcification. Our aim was to evaluate the relationship among fetuin-A levels, heart valve calcification and other biomarkers of inflammation in patients with acute coronary syndrome (ACS).
The associations among serum fetuin-A concentrations, mitral annular (MAC) and aortic valve calcification and other biomarkers of inflammation (hs-CRP, ferritin, fibrinogen, white blood cell count (WBC), erythrocyte sedimentation rate (ESR), albumin levels) were evaluated in ACS patients and healthy controls. The study included 95 patients (mean age 61.8 ± 12.10 years) and 81 healthy controls (mean age 48.33 ± 9.19 years).
Fetuin-A levels were significantly lower in patients with ACS than in healthy controls (0.76 ± 0.23 and 1.10 ± 0.45 g/L, respectively; p < 0.001). Fetuin-A was lower in patients with mitral annular calcification (p = 0.007) and aortic (p = 0.001) valve calcification. In patients with ACS, there was a negative correlation among serum urea (r = -0.377; p < 0.001) and creatinine (r = -0.232; p = 0.024) levels and fetuin-A, and a negative correlation among WBC (r = -0.156; p = 0,132), ESR (r = -0.214; p = 0.037), hs-CRP (r = -0.220; p = 0.032) levels and fetuin-A. A positive correlation was seen between albumin and fetuin-A (r = 0.362; p < 0.001). Multivariate logistic regression analysis revealed that fetuin-A was the variable that had a significant effect on ACS (p = 0.020 OR = .015; (95% CI)(0.000-0.520).
Fetuin-A levels decrease in patients with acute coronary syndromes, independent of heart valve calcification. Fetuin-A may therefore act as a negative acute phase protein after myocardial infarction.
胎球蛋白-A是一种多功能肝脏分泌蛋白，可抑制营养不良性血管和瓣膜钙化。我们的目的是评估急性冠状动脉综合征（ACS）患者中胎球蛋白-A水平、心脏瓣膜钙化与其他炎症生物标志物之间的关系。
在ACS患者和健康对照中评估血清胎球蛋白-A浓度、二尖瓣环（MAC）和主动脉瓣钙化与其他炎症生物标志物（高敏C反应蛋白、铁蛋白、纤维蛋白原、白细胞计数（WBC）、红细胞沉降率（ESR）、白蛋白水平）之间的关联。该研究纳入了95例患者（平均年龄61.8±12.10岁）和81例健康对照（平均年龄48.33±9.19岁）。
ACS患者的胎球蛋白-A水平显著低于健康对照（分别为0.76±0.23和1.10±0.45 g/L；p<0.001）。二尖瓣环钙化（p = 0.007）和主动脉瓣钙化（p = 0.001）患者的胎球蛋白-A水平较低。在ACS患者中，血清尿素（r = -0.377；p<0.001）和肌酐（r = -0.232；p = 0.024）水平与胎球蛋白-A呈负相关，白细胞（r = -0.156；p = 0.132）、红细胞沉降率（r = -0.214；p = 0.037）、高敏C反应蛋白（r = -0.220；p = 0.032）水平与胎球蛋白-A呈负相关。白蛋白与胎球蛋白-A呈正相关（r = 0.362；p<0.001）。多因素逻辑回归分析显示，胎球蛋白-A是对ACS有显著影响的变量（p = 0.020，OR = 0.015；（95%CI）（0.000 - 0.520））。
急性冠状动脉综合征患者的胎球蛋白-A水平降低，与心脏瓣膜钙化无关。因此，胎球蛋白-A可能在心肌梗死后作为一种负急性期蛋白发挥作用。
