Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China.
Clin Biochem. 2013 Nov;46(16-17):1694-700. doi: 10.1016/j.clinbiochem.2013.09.008. Epub 2013 Sep 21.
The practical application of elevated carbohydrate antigen 125 (CA125) to predict clinical outcome in chronic heart failure (CHF) is under debate. The mechanism for this CA125 elevation remains unknown. We hypothesize that mechanical stress on mesothelial cells initiates CA125 synthesis.
A total of 191 patients suffering from edema and/or dyspnea were enrolled. 109 patients were diagnosed as CHF, and 82 patients without CHF were assigned as control group. Echocardiography, CA125, N-terminal pro-brain natriuretic peptide (NT-proBNP), and other biochemical parameters were measured. All enrolled patients underwent heart function classification.
Patients with serous cavity effusion (SCE) demonstrated higher serum CA125 than patients without SCE (82.91 (61.90-103.92) vs. 44.98 (29.66-60.30) U/mL, P<0.001). In the absence of SCE, CA125 levels in CHF patients were slightly higher than non-CHF patients (52.37 (34.85-69.90) vs. 35.15 (23.81-46.49) U/mL, P=0.017). Additionally, compared with non-CHF patients, CHF patients had higher levels of high-sensitivity C-reactive protein (hsCRP) and lower superoxide dismutase (SOD). In all enrolled patients, CA125 levels were negatively correlated with SOD concentrations (r=-0.567, P<0.001), and positively correlated with hsCRP levels (r=0.608, P<0.001). Receiver operating characteristic curve analysis showed that CA125 was better in predicting SCE than NT-proBNP, while NT-proBNP was more suitable for predicting CHF than CA125. The in vitro study demonstrated that MUC16, the CA125 coding gene, was up-regulated by mechanical stretch on human mesothelial cell line (MeT-5A).
CA125 elevation in CHF was associated with SCE. Mechanical extension of mesothelial cells from SCE plays an important role in CA125 increase.
升高的糖链抗原 125（CA125）在慢性心力衰竭（CHF）中预测临床结局的实际应用存在争议。CA125 升高的机制尚不清楚。我们假设机械应力对间皮细胞会引发 CA125 的合成。
共纳入 191 例出现水肿和/或呼吸困难的患者。其中 109 例被诊断为 CHF，82 例无 CHF 的患者被分配为对照组。测量了超声心动图、CA125、N 末端脑利钠肽前体（NT-proBNP）和其他生化参数。所有入组患者均进行心功能分级。
有浆膜腔积液（SCE）的患者血清 CA125 高于无 SCE 的患者（82.91（61.90-103.92）vs. 44.98（29.66-60.30）U/ml，P<0.001）。在无 SCE 的情况下，CHF 患者的 CA125 水平略高于非 CHF 患者（52.37（34.85-69.90）vs. 35.15（23.81-46.49）U/ml，P=0.017）。此外，与非 CHF 患者相比，CHF 患者的高敏 C 反应蛋白（hsCRP）水平更高，超氧化物歧化酶（SOD）水平更低。在所有入组患者中，CA125 水平与 SOD 浓度呈负相关（r=-0.567，P<0.001），与 hsCRP 水平呈正相关（r=0.608，P<0.001）。受试者工作特征曲线分析表明，CA125 预测 SCE 优于 NT-proBNP，而 NT-proBNP 预测 CHF 优于 CA125。体外研究表明，人间皮细胞系（MeT-5A）上的机械拉伸使 CA125 编码基因 MUC16 上调。
CHF 中的 CA125 升高与 SCE 有关。SCE 中来自间皮细胞的机械伸展对 CA125 升高起重要作用。
