Evidence for an association between the aetiology of cirrhosis and pattern of hepatocellular carcinoma development
Evidence for an association between the aetiology of cirrhosis and pattern of hepatocellular carcinoma development
复制标题
DOI：
10.1136/gut.48.1.110
复制
发表时间：
2001-01-01
期刊：
影响因子：
24.5
通讯作者：
Alberti, A
中科院分区：
文献类型：
--
作者：
Benvegnù, L;Noventa, F;Alberti, A
背景-肝硬化患者有发生肝细胞癌（HCC）的显著风险，HCC可能发展为明确的结节性病变或更具侵袭性的浸润性肿瘤。目的-前瞻性比较与肝硬化患者中结节性或浸润性HCC相关的风险因素。患者和方法-我们研究了370例肝硬化患者，前瞻性地定期进行肝脏超声（US）检查，平均74.6（SD 32.4）个月，以确定HCC发展的发病率和模式。根据肿瘤的模式，使用单变量和多变量analysis.Results-Sixty 1（16.5%）的患者发展HCC：HCC被归类为结节性49（80.3%）和浸润性12（19.7%）根据美国和计算机断层扫描（CT）成像。结节性HCC的5年和10年累积概率分别为8.1%（95%置信区间（CI）5.2%-11%）和25.2%（15.0-35.4%），浸润性HCC的5年和10年累积概率分别为2.1%（0.5-3.7%）和6.9%（2.1-11.7%）。浸润性HCC患者比结节性HCC患者年轻（59.5 v66.2岁，95%CI 55.2-63.8和64.1-68.3岁; p=0.014）。多变量分析显示，结节性肝癌的发生与年龄较大有关（p=0.0002;相对风险（RR）3.1; 95% CI 1.6-5.2），持续时间较长（p=0.09; RR 2.6; 95%CI 1.8-3.4）和肝硬化晚期（p=0.002; RR 2.5; 95%CI 1.3-4.5），但与肝病病因无关。相反，浸润性肝癌的发生似乎与年龄、病程或分期无关，而与B型肝炎病毒感染有关（p=0.07; RR 3.96; 95% CI 1.1-5.2）和B型肝炎/丙型肝炎病毒合并感染（p=0.0007; RR 16.9; 95%CI 3.8-36.7）.结论-在肝硬化中，我们发现了两种具有不同危险因素的HCC发展模式。结节性肝癌与增生过程本身相关，不依赖于病因学因素，可能依赖于再生结节内的增殖活性，而浸润性肝癌与B型肝炎病毒感染有关，可能反映更直接的病毒诱导的致癌作用。
Background-Patients with liver cirrhosis are at significant risk of hepatocellular carcinoma (HCC) that may develop as well defined nodular lesions or as more aggressive infiltrating tumours.Aim-To compare prospectively risk factors associated with nodular or infiltrating HCC in cirrhotic patients.Patients and methods-We studied 370 patients with cirrhosis, followed prospectively by periodic ultrasound (US) of the liver, for a mean period of 74.6 (SD 32.4) months to define the incidence and patterns of HCC development. Patients who developed HCC were compared according to tumour pattern using univariate and multivariate analysis.Results-Sixty one (16.5%) patients developed HCC: HCC was classified as nodular in 49 (80.3%) and infiltrating in 12 (19.7%) according to US and computerised tomography (CT) imaging. The five and 10 year cumulative probabilities were 8.1% (95% confidence interval (CI) 5.2%-11%) and 25.2% (15.0-35.4%) for nodular HCC and 2.1% (0.5-3.7%) and 6.9% (2.1-11.7%) for infiltrating HCC. Patients with infiltrating HCC were younger than those with nodular HCC (59.5 v 66.2 years, 95% CI 55.2-63.8 and 64.1-68.3 years; p=0.014). Using multivariate analysis, development of nodular HCC was associated with older age (p=0.0002; relative risk (RR) 3.1; 95% CI 1.6-5.2), longer duration (p=0.09; RR 2.6; 95% CI 1.8-3.4), and more advanced stage (p=0.002; RR 2.5; 95% CI 1.3-4.5) of cirrhosis but not with the aetiology of liver disease. In contrast, development of infiltrating HCC appeared to be unrelated to age or disease duration or stage, while it was associated with hepatitis B virus infection (p=0.07; RR 3.96; 95% CI 1.1-5.2) and with hepatitis B/hepatitis C virus coinfection (p=0.0007; RR 16.9; 95% CI 3.8-36.7).Conclusions-In liver cirrhosis, we identified two patterns of HCC developing with distinct risk factors. Nodular HCC was related to the cirrhotic process per se independent of aetiological factors and may depend on the proliferative activity within regenerative nodules, while the infiltrating form of HCC was linked to hepatitis B virus infection and may reflect more direct virus induced carcinogenesis.