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首页> 外文期刊>World Journal of Gastroenterology >Serum omentin and vaspin levels in cirrhotic patients with and without portal vein thrombosis
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Serum omentin and vaspin levels in cirrhotic patients with and without portal vein thrombosis

机译:肝硬化合并门静脉血栓和不合并门静脉血栓的患者的血清网膜蛋白和vaspin水平

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AIM To investigate serum omentin and vaspin levels in cirrhotic patients; and to assess the relationship of these levels with hemostatic parameters, metabolic abnormalities, cirrhosis severity and etiology. METHODS Fifty-one cirrhotic patients (17 with portal vein thrombosis) were analyzed. Serum omentin and vaspin levels were measured with commercially available direct enzyme-linked immunosorbent assays (ELISAs). To assess platelet activity, the following tests were performed using a MULTIPLATE?PLATELET FUNCTION ANALYZER: (1) an ADP-induced platelet activation test; (2) a cyclooxygenase dependent aggregation test (ASPI test); (3) a von Willebrand factor and glycoprotein Ib-dependent aggregation (using ristocetin) test (RISTO test); and (4) a test for thrombin receptor-activating peptide-6 induced activation of the thrombin receptor, which is sensitive to IIb/IIIa receptor antagonists. RESULTS Omentin, but not vaspin, serum concentrations were significantly decreased in patients with portal vein thrombosis (PVT) ( P = 0.01). Prothrombin levels were significantly increased in patients with PVT ( P = 0.01). The thrombin receptor activating peptide (TRAP) test results were significantly lower in the PVT group ( P = 0.03). No significant differences in adipokines serum levels were found regarding the etiology or severity of liver cirrhosis assessed according to the Child-Pugh or Model of End-Stage Liver Disease (MELD) scores. There was a significant increase in the TRAP ( P = 0.03), ASPI ( P = 0.001) and RISTO high-test ( P = 0.02) results in patients with lower MELD scores. Serum omentin and vaspin levels were significantly down-regulated in patients without insulin resistance ( P = 0.03, P = 0.02, respectively). A positive relationship between omentin and vaspin levels were found both when all of the patients were analyzed ( r = 0.41, P = 0.01) and among those with PVT ( r = 0.94, P < 0.001). CONCLUSION Serum omentin levels are increased in patients without PVT. Cirrhosis origin and grade do not affect omentin and vaspin levels. The analyzed adipokines do not influence platelet activity.
机译:目的探讨肝硬化患者血清omentin和vaspin水平。并评估这些水平与止血参数,代谢异常,肝硬化严重程度和病因的关系。方法对51例肝硬化患者(17例门静脉血栓形成)进行分析。用可商购的直接酶联免疫吸附测定法(ELISAs)测量血清网膜蛋白和vaspin水平。为了评估血小板活性,使用MULTIPLATE ?血小板功能分析仪进行了以下测试:(1)ADP诱导的血小板活化测试; (2)依赖于环氧合酶的聚集试验(ASPI试验); (3)von Willebrand因子和糖蛋白Ib依赖性聚集(使用瑞斯托霉素)测试(RISTO测试); (4)凝血酶受体活化肽-6诱导凝血酶受体活化的测试,该试剂对IIb / IIIa受体拮抗剂敏感。结果门静脉血栓形成(PVT)患者的血清中的网膜素(但不是vaspin)显着降低(P = 0.01)。 PVT患者的凝血酶原水平显着升高(P = 0.01)。在PVT组中,凝血酶受体激活肽(TRAP)的测试结果明显较低(P = 0.03)。根据Child-Pugh或终末期肝病模型(MELD)评分评估的肝硬化的病因或严重程度,脂肪因子血清水平无明显差异。 MELD评分较低的患者的TRAP(P = 0.03),ASPI(P = 0.001)和RISTO高检(P = 0.02)显着增加。没有胰岛素抵抗的患者的血清omentin和vaspin水平显着下调(分别为P = 0.03,P = 0.02)。分析所有患者(r = 0.41,P = 0.01)和患有PVT的患者(r = 0.94,P <0.001)时,omentin和vaspin水平之间呈正相关。结论无PVT的患者血清omentin水平升高。肝硬化的起源和等级不影响omentin和vaspin水平。分析的脂肪因子不影响血小板活性。

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