PNPLA3 I148M (rs738409) genetic variant and age at onset of at-risk alcohol consumption are independent risk factors for alcoholic cirrhosis.
PNPLA3 I148M (rs738409) genetic variant and age at onset of at-risk alcohol consumption are independent risk factors for alcoholic cirrhosis.
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DOI：
10.1111/liv.12310
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发表时间：
2014-04
期刊：
影响因子：
--
通讯作者：
Ginanni Corradini S
中科院分区：
文献类型：
--
作者：
Burza MA;Molinaro A;Attilia ML;Rotondo C;Attilia F;Ceccanti M;Ferri F;Maldarelli F;Maffongelli A;De Santis A;Attili AF;Romeo S;Ginanni Corradini S
环境和遗传因素有助于酒精性肝硬化的发病。特别是，暴露于肝脏应激源的年龄已被证明是丙型肝炎患者纤维化进展的重要因素。然而，没有确切的数据表明年龄在开始危险饮酒时的作用。此外，马铃薯糖样磷脂酶结构域蛋白3（PNPLA 3）I148 M（rs738409）变异体与酒精性肝硬化相关，但仅在横断面研究中。本研究的目的是探讨高危饮酒开始时的年龄和PNPLA 3 I148 M变异对酒精性肝硬化发病率的作用。共有384名高危饮酒者进行了回顾性研究。检测了饮酒风险、PNPLA 3 I148 M变异和肝硬化发病率之间的关系。与年轻人（<24岁）相比，年龄较大（≥ 24岁）的酒精性肝硬化发病率较高（P值< 0.001）。此外，PNPLA 3 148 M等位基因携带者显示肝硬化的发病率增加（P值< 0.001）。发病年龄和PNPLA 3 148 M等位基因是肝硬化发生的独立危险因素（H.R. (95% C.I.）：2.76（2.18-3.50），P值< 0.001; 1.53（1.07-2.19），P值= 0.021）。148 M等位基因与年轻个体中肝硬化风险增加两倍相关，与开始危险酒精消费的年龄相比（H.R. (95% CI）：3.03（1.53-6.00）vs. 1.61（1.09-2.38）。酒精性肝硬化的发病年龄与酒精性肝硬化的发病率独立相关。
Environmental and genetic factors contribute to alcoholic cirrhosis onset. In particular, age at exposure to liver stressors has been shown to be important in progression to fibrosis in hepatitis C individuals. However, no definite data on the role of age at onset of at-risk alcohol consumption are available. Moreover, patatin-like phospholipase domain-containing protein 3 (PNPLA3) I148M (rs738409) variant has been associated with alcoholic cirrhosis, but only in cross-sectional studies. The aim of this study was to investigate the role of age at onset of at-risk alcohol consumption and PNPLA3 I148M variant on alcoholic cirrhosis incidence. A total of 384 at-risk alcohol drinkers were retrospectively examined. The association among age at onset of at-risk alcohol consumption, PNPLA3 I148M variant and cirrhosis incidence was tested. A higher incidence of alcoholic cirrhosis was observed in individuals with an older (≥24 years) compared with a younger (<24) age at onset of at-risk alcohol consumption (P-value < 0.001). Moreover, PNPLA3 148M allele carriers showed an increased incidence of cirrhosis (P-value < 0.001). Both age at onset of at-risk alcohol consumption and PNPLA3 148M allele were independent risk factors for developing cirrhosis (H.R. (95% C.I.): 2.76 (2.18–3.50), P-value < 0.001; 1.53(1.07–2.19), P-value = 0.021 respectively). The 148M allele was associated with a two-fold increased risk of cirrhosis in individuals with a younger compared with an older age at onset of at-risk alcohol consumption (H.R. (95% C.I.): 3.03(1.53–6.00) vs. 1.61(1.09–2.38). Age at onset of at-risk alcohol consumption and PNPLA3 I148M genetic variant are independently associated with alcoholic cirrhosis incidence.
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