乙型肝炎病毒相关性肝细胞癌患者代偿性肝硬化状态可能与肿瘤大小呈负相关

Yanna Liu, X. Qian, Congying Wu, Weidong Pan, Jingmin Zhao, Xiangmei Chen, F. Lu
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摘要

肝硬化是肝细胞癌(HCC)发展的一个众所周知的危险因素。然而,这一观点最近受到了挑战。本研究旨在探讨肝硬化与乙型肝炎病毒(HBV)相关HCC的潜在关联。在这项研究中,回顾性研究了两个独立的多中心临床队列,包括1431例慢性HBV感染的HCC患者。第一组包括334例接受根治性切除和肝硬化的HCC患者,他们已被病理诊断。第二组包括1087例HCC患者,他们根据临床证据被诊断为存在肝硬化。每个队列的患者根据肝硬化的存在和肝硬化的严重程度进一步分为不同的亚组。在两个队列中,肝硬化患者的肿瘤大小均小于无肝硬化患者(P < 0.05),大肿瘤(定义为肿瘤直径> 5 cm)的比例相对较低(P < 0.05)。与代偿性肝硬化和非肝硬化患者相比,失代偿性肝硬化患者的血管侵犯和/或肝外转移率最高(53.0%比24.8%比26.9%,P < 0.001)。在第一个队列中,球蛋白(比值比[OR] = 1.096, P = 0.001)和血管侵犯(OR = 4.013, P = 0.013)是肝癌肿瘤大小>5 cm的独立危险预测因素,而肝硬化阶段Laennec 4B/C是保护因素(OR = 0.372, P = 0.002)。在第二组中也观察到类似的结果。综上所述,本研究提示HCC代偿性肝硬化患者肿瘤倾向于较小,而重度肝硬化则有利于肿瘤血管的侵袭和转移。
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The status of compensated cirrhosis might be negatively associated with the tumor size in patients with hepatitis B virus-related hepatocellular carcinoma
Liver cirrhosis has been a well-known risk factor for the development of hepatocellular carcinoma (HCC). However, this view has recently been challenged. This study aimed to investigate the potential association of cirrhosis with hepatitis B virus (HBV)-related HCC. In this study, two independent multicenter clinical cohorts that included 1,431 HCC patients with chronic HBV infection were retrospectively studied. The first cohort consisted of 334 HCC patients undergoing curative resection and cirrhosis, who have been pathologically diagnosed. The second cohort consisted of 1,087 HCC patients, who have been diagnosed for the presence of cirrhosis based on clinical evidence. Patients of each cohort were further divided into different subgroups according to the presence of cirrhosis and the severity of the cirrhosis. In both cohorts, patients with cirrhosis had smaller tumor size compared to those without cirrhosis (P < 0.05) and a relatively lower proportion of large tumor, defined as tumor size > 5 cm in diameter (P < 0.05). Patients with decompensated cirrhosis had the highest rate of vascular invasion and/or extrahepatic metastases compared with compensated cirrhosis and non-cirrhosis (53.0% vs. 24.8% vs. 26.9%, P < 0.001). In the first cohort, globulin (odds ratio [OR] = 1.096, P = 0.001) and vascular invasion (OR = 4.013, P = 0.013) were independent risk predictors of HCC tumor size >5 cm, while cirrhosis stage Laennec 4B/C was a protective factor (OR = 0.372, P = 0.002). Similar results were observed in the second cohort. In conclusion, this study implied that HCC patients with compensated cirrhosis tend to harbor smaller tumor, but severe cirrhosis favors tumor vascular invasion and metastasis.
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