饮酒与脂肪肝，祸不单行为肝癌的风险

StephenW

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Alcohol Consumption and Fatty Liver—A Double Whammy for Liver Cancer Risk
by Kristine Novak

High to intermediate levels of ethanol consumption increase the risk for liver cancer in patients with fatty liver disease, researchers report in the April issue of Clinical Gastroenterology and Hepatology.

Nonalcoholic fatty liver disease is a common cause of chronic liver disease associated with obesity, dyslipidemia, pituitary dysfunction, hypertension, sleep apnea, and type 2 diabetes. Patients with nonalcoholic steatohepatitis are at higher risk of developing hepatocellular carcinoma (HCC).

Nonalcoholic and alcoholic fatty liver diseases can be differentiated based on degree of patients’ alcohol consumption. However, it is not clear how ethanol consumption affects the risk of HCC in patients with either form of fatty liver disease.

Yusuke Kawamura et al performed a retrospective study to determine the incidence and risk factors for HCC in 9959 patients in Japan with fatty liver disease, diagnosed by ultrasound and the FIB-4 index, with varying levels of ethanol consumption.

Ethanol intake in relationship to the odds for HCC in patients with fatty liver disease.

Ethanol intake in relationship to the odds for HCC in patients with fatty liver disease.

Patients were assigned to 4 categories based on reported level of ethanol consumption: <20 g/day (n = 6671), 20–39 g/day (n = 753), 40–69 g/day (n = 1589), and ≥70 g/day (n = 946). One standard drink contains 10 grams of alcohol—equivalent to one ordinary beer, a small glass of wine (100 mL), or 30 mL of spirits.

Forty-nine patients developed HCC during the follow-up period (mean, 5.4 years).

The annual incidence rate of HCC was 0.05% in patients with fatty liver disease and daily ethanol consumption <20 g/day. Increasing levels of ethanol consumption were associated with increased annual incidence rates of HCC: 0.06% for patients with 20–39 g/day ethanol consumption (hazard ratio, 1.54), 0.16% for patients with 40–69 g/day ethanol consumption (hazard ratio, 3.49), and 0.22% for patients with ≥70 g/day ethanol consumption (hazard ratio, 10.58), compared with patients with ethanol consumption <20 g/day.

Multivariate analysis showed that ethanol consumption ≥40 g/day was an independent risk factor for HCC.

Ethanol consumption strongly promoted hepatocarcinogenesis in patients with fatty liver disease who had abnormal liver function and advanced fibrosis, which the authors say was not surprising. However, ethanol intake also increased risk for HCC in patients with fatty liver disease yet normal liver function and nonadvanced fibrosis.

High levels of high-density lipoprotein cholesterol and triglyceride were also risk factors for HCC. The authors propose that fatty liver disease therefore promotes hepatocarcinogenesis with or without excessive ethanol consumption, but that ethanol consumption has a synergic effect with features of fatty liver. A previous study reported a synergistic effect of obesity and alcohol consumption on hepatocarcinogenesis in patients who tested positive for the hepatitis B virus antigen.

The authors point out that this was a retrospective study with a higher proportion of men than women (there were no women in the groups that consumed the greatest amounts of alcohol). Also, the study did not compare the incidence of HCC with that of the general Japanese population.

However, based on their findings, Kawamura et al recommend careful monitoring and follow-up of elderly patients with fatty liver disease and high serum levels of aspartate aminotransferase and low albumin levels, thrombocytopenia, diabetes, and a history of high or even intermediate ethanol consumption (≥40 g/day).

Kawamura et al also evaluated the usefulness for predicting hepatocarcinogenesis in patients with fatty liver disease with varying levels or absence of ethanol consumption.

Kristine Novak | March 22, 2016 at 7:14 am | Categories: Cancer, Liver/Biliary | URL: http://wp.me/p4B9rV-1Ah   

StephenW

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饮酒与脂肪肝，祸不单行为肝癌的风险
由克里斯汀·诺瓦克

高乙醇消费的中间水平的提高患者的脂肪肝患者肝脏患癌症的风险，研究人员在临床胃肠病学和肝病的4月问题报告。

非酒精性脂肪肝疾病是与肥胖，血脂异常，垂体功能障碍，高血压，睡眠呼吸暂停，和2型糖尿病有关的慢性肝病的常见原因。患者酒精性脂肪性肝炎是在开发肝细胞癌（HCC）的风险较高。

非酒精性和酒精性脂肪肝疾病可根据患者的饮酒程度有所区别。然而，乙醇消耗量如何影响HCC的患者的脂肪肝疾病的任一种形式的风险，目前尚不清楚。

川村雄介等人进行的一项回顾性研究，以确定发生率及危险因素在肝癌患者9959在日本脂肪肝，超声和FIB-4指数确诊，用乙醇的消费水平不同。

酒精摄入的患者的脂肪肝发病关系的可能性肝癌。

酒精摄入的患者的脂肪肝发病关系的可能性肝癌。

患者被分配到基于乙醇消费逐级上报4类：<20克/天（N = 6671），20-39克/天（N = 753），40-69克/天（N = 1589），和≥70克/天（N = 946）。一个标准的饮料含10克酒精，相当于一普通啤酒，一小杯葡萄酒（100毫升），或灵30毫升。

49例在随访期间（平均5.4岁）开发的肝癌。

HCC的年发病率在脂肪肝患者的疾病和日常消耗乙醇<20克/天为0.05％。患者20-39克/天乙醇消耗0.06％（危险比1.54），患者的40-69克/天乙醇消耗0.16％（危险：乙醇消费增加水平与HCC的年发病率升高有关比，3.49），和患者的≥70克/天乙醇消耗（风险比，10.58）0.22％，与患者用乙醇消耗<20克/天相比。

多因素分析表明，乙醇消费≥40克/天是HCC的独立危险因素。

乙醇消耗脂肪肝患者的疾病谁曾出现肝功能异常和肝纤维化，作者说的是并不奇怪有力地促进肝癌的​​发生。然而，酒精摄入也是脂肪肝患者的疾病，但肝功能正常和nonadvanced纤维化的风险增加肝癌。

高密度脂蛋白胆固醇和甘油三酯的水平高也为肝癌的危险因素。作者认为，脂肪肝疾病，因此促进肝癌的​​发生有或没有过多的酒精消费量，但乙醇消耗与脂肪肝的功能的协同效应。先前的研究报告，谁的乙肝病毒抗原检测阳性患者肝癌肥胖和饮酒的协同效应。

作者指出，这是一项回顾性研究与男性比女性比例较高（有在消费量最大的酒精的群体没有女性）。此外，这项研究并没有与一般的日本人群的比较肝细胞癌的发生率。

然而，根据他们的调查结果，河村等人建议仔细监测和随访老年患者的脂肪肝患者，谷草转氨酶和低白蛋白水平，血小板减少症，糖尿病的高血清水平，高位甚至中间乙醇消费的历史（≥40克/天）。

河村等人还评价了实用性为脂肪肝患者的病不同程度与否乙醇消费量的预测肝癌。

克里斯汀·诺瓦克| 2016年3月22日在上午7时14 |类别：肝癌，肝/胆道|网址：http://wp.me/p4B9rV-1Ah