Epidemiology, risk factors, and natural history of hepatocellular carcinoma
Epidemiology, risk factors, and natural history of hepatocellular carcinoma
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DOI：
10.1111/j.1749-6632.2002.tb04090.x
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发表时间：
2002-01-01
期刊：
影响因子：
--
通讯作者：
Castagnetta, LAM
中科院分区：
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作者：
Montalto, G;Cervello, M;Castagnetta, LAM
肝细胞癌的发病率在许多国家都在增加。估计每年新发病例超过50万例，年发病率占肝硬化患者的2.5%至7%。不同地理区域的发病率不同，发展中地区发病率较高；受影响的主要是男性，男女比例为2:3。异质的地理分布反映了主要病因和环境风险的流行病学影响，即乙型肝炎（HBV）和丙型肝炎（HCV）病毒。全球由HBV引起的肝细胞癌病例百分比为52.3%，在人群中HBsAg血清阳性率高的亚洲更高。然而，在一些东方国家开展的针对这种病毒的疫苗接种运动往往降低了肝细胞癌新发病例的发生率。由丙型肝炎病毒引起的肝细胞癌占25%，在日本、西班牙和意大利更为普遍，这些国家的肝细胞癌与丙型肝炎病毒抗体的相关性在50%至70%之间。在大多数情况下，肝细胞癌在肝硬化中发展，肝细胞的持续增殖是发展为肝细胞癌的关键因素，与病因无关。另一个较小的风险因素是食用安纳托毒素B1，这是非洲大多数肝细胞癌病例的原因，在那里食用受污染的食品是很常见的。其他已知的危险因素是一些遗传性疾病，如血色素沉着症、迟发性皮肤卟啉症、遗传性酪氨酸血症和α(1)抗胰蛋白酶缺乏症。肝细胞癌的自然史是异质性的，受结节大小、诊断时病灶的单发或多发、肿瘤的生长速度和肝硬化分期的影响。迄今为止的现有资料表明，肝硬化中肿瘤的生长是可变的，病变在达到2厘米之前无法检测到的时间在4到12个月之间。因此，建议肝硬化患者超声监测筛查的间隔时间为6个月。应该从筛查项目中受益的患者是那些如果被诊断为肝细胞癌将接受根治性治疗的患者。因此，理想的目标人群应限于Child-Pugh's A级肝硬化患者，且无明显合并症。
The incidence of hepatocellular carcinoma is increasing in many countries. The estimated number of new cases annually is over 500,000, and the yearly incidence comprises between 2.5 and 7% of patients with liver cirrhosis. The incidence varies between different geographic areas, being higher in developing areas; males are predominantly affected, with a 2:3 male/female ratio. The heterogeneous geographic distribution reflects the epidemiologic impact of the main etiologic factors and environmental risk, which are the hepatitis B (HBV) and hepatitis C (HCV) viruses. The percentage of cases of hepatocellular carcinoma attributable to HBV worldwide is 52.3% and is higher in Asia where the seroprevalence of HBsAg in the population is high. However, the vaccination campaign against this virus in some eastern countries has tended to lower the incidence of new cases of hepatocellular carcinoma. The percentage of cases of hepatocellular carcinoma attributable to HCV is 25%, and it is more prevalent in Japan, Spain, and Italy where the association between hepatocellular carcinoma and antibodies to HCV ranges between 50 and 70%. In most cases hepatocellular carcinoma develops in cirrhotic livers, where the persistent proliferation of liver cells represents the key factor of progression to hepatocellular carcinoma independent of the etiology. Another minor risk factor is anatoxin B1 consumption, which is responsible for most cases of hepatocellular carcinoma in Africa, where the consumption of contaminated foods is common. Other known risk factors are some hereditary diseases, such as hemochromatosis, porphyria cutanea tarda, hereditary tyrosinernia, and alpha(1) anti-trypsin deficiency. The natural history of hepatocellular carcinoma is heterogeneous and is influenced by nodule dimension, the mono- or plurifocality of lesions at diagnosis, the growth rate of the tumor, and the stage of the underlying cirrhosis. Available data to date suggest that tumor growth in a cirrhotic liver is variable and that the time in which a lesion in undetectable until it becomes 2 cm is between 4 and 12 months. Therefore, the suggested interval for surveillance screening with ultrasound in patients with liver cirrhosis has been set at 6 months. Patients who should benefit from screening programs are those who would be treated with curative therapy if diagnosed with hepatocellular carcinoma. Thus, the ideal target population should be limited to Child-Pugh's class A cirrhotic patients without significant comorbidity.