肝细胞癌与 Resolvin D1 的关系

Z. Erdin, Özlem Gül, Bilal Ergül, Rıdvan Erdin, Harın Erdal, Üçler Kısa, Dilek Oğuz
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摘要

目的:肝癌是第二大常见癌症死因,而肝细胞癌(HCC)是最常见的肝原发性肿瘤。肝细胞癌的发生基于肝硬化肝脏的炎症。我们的研究旨在确定参与分解的脂质介质 Resolvin D1 的减少与肝癌发生之间的关系。研究方法研究对象包括 2018 年 3 月至 2019 年 6 月期间在本诊所随访的 30 名 HCC 患者、30 名肝硬化患者和 30 名健康受试者。从机构数据库中记录患者的常规实验室检查结果。比较了研究组的瑞舒文 D1 和其他参数。 结果研究发现,各组患者的 Resolvin D1 水平均有显著差异,具体排名如下:HCC 组(1.71±1.46 ng/ml)< 肝硬化组(3.63±2.92 ng/ml)< 健康对照组(6.24±3.18 ng/ml)。此外,Resolvin D1水平与甲胎蛋白(AFP)水平和肿瘤分期呈负相关。结论有助于化解过程的脂质介质减少会导致参与肝细胞癌发展的促炎细胞因子增加。Resolvin D1 的减少可作为一种生物标志物,通过引发慢性炎症和肝癌的发生,帮助诊断肝硬化患者向 HCC 的进展。
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The relationship between hepatocellular carcinoma and Resolvin D1
Aims: Liver cancer is the second most common cause of cancer death, and hepatocellular carcinoma (HCC) is the most common hepatic primary tumor. Hepatocellular carcinoma develops based on inflammation in the cirrhotic liver. The aim of our study was to determine the relationship between the decrease in Resolvin D1, the lipid mediator involved in the resolution, and hepatocarcinogenesis. Methods: Thirty patients with HCC, thirty patients with cirrhosis, and thirty healthy subjects followed in our clinic between March 2018 and June 2019 were included in the study. Routine laboratory test results of the patients were recorded from the institutional database. Resolvin D1 and other parameters of the study groups were compared. Results: The Resolvin D1 levels were found to be significantly different from each other group, with the ranking as follows: the HCC group (1.71 ± 1.46 ng/ml)< the cirrhotic group (3.63 ± 2.92 ng/ml)< the healthy control group (6.24 ± 3.18 ng/ml). Moreover, Resolvin D1 levels were negatively correlated with ?-fetoprotein (AFP) level and tumor stage. Conclusion: Reduced lipid mediators that aid in the resolution process cause an increase in pro-inflammatory cytokines involved in the development of hepatocellular carcinoma. A decrease in Resolvin D1 may serve as a biomarker contributing to the diagnosis of progression to HCC in cirrhotic patients by triggering chronic inflammation and hepatocarcinogenesis.
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