Kew Michael C
Department of Medicine, Groote Schuur Hospital and University of Cape Town, Cape Town, and University of the Witwatersrand, Johannesburg, South Africa.
Ann Hepatol. 2015 May-Jun;14(3):299-303.
During recent years the incidence of obesity has increased significantly, and in some instances rapidly, in many resource-rich countries. Paralleling this increase has been an increase in the incidence of hepatocellular carcinoma. It has been estimated that as many as 90% of obese adults will develop the metabolic syndrome. The worldwide incidence of this syndrome in adults at this time ranges from 9 to 34%. Furthermore, obesity in childhood increases the risk of obesity in adulthood, and hence the development of the metabolic syndrome and hepatocellular carcinoma. Ten to 20% of patients with non-alcoholic fatty liver disease progress to non-alcoholic steatohepatitis, and 8.3% of the latter develop cirrhosis. Up to 50% of these patients with cirrhosis, and a significant proportion of those without cirrhosis, progress to hepatocellular carcinoma. Much remains to be learnt about the mechanisms by which obesity and the metabolic syndrome cause hepatocellular carcinoma, although insulin resistance, increased tissue necrosis factor activity, alterations in serum lipids, non-alcoholic fatty liver disease and non-alcoholic steatosis play important roles. There is also increasing evidence that gut microbiota play a role in the development of the metabolic syndrome and hence of hepatocellular carcinoma.
近年来，在许多资源丰富的国家，肥胖症的发病率显著上升，在某些情况下甚至迅速上升。与此同步的是，肝细胞癌的发病率也在上升。据估计，多达90%的肥胖成年人会患上代谢综合征。目前，该综合征在全球成年人中的发病率为9%至34%。此外，儿童肥胖会增加成年后肥胖的风险，进而增加代谢综合征和肝细胞癌的发病风险。10%至20%的非酒精性脂肪性肝病患者会进展为非酒精性脂肪性肝炎，其中8.3%会发展为肝硬化。这些肝硬化患者中高达50%以及相当一部分非肝硬化患者会进展为肝细胞癌。尽管胰岛素抵抗、组织坏死因子活性增加、血脂改变、非酒精性脂肪性肝病和非酒精性脂肪变性起着重要作用，但关于肥胖和代谢综合征导致肝细胞癌的机制仍有许多有待了解之处。越来越多的证据表明，肠道微生物群在代谢综合征的发展以及肝细胞癌的发生中起作用。
