Background & Aims

Alcohol-related liver disease (ALD) causes chronic liver disease. We investigated how information on patients’ drinking history and amount, stage of liver disease, and demographic feature can be used to determine risk of disease progression.

Methods

We collected data from 2334 heavy drinkers (50 g/day or more) with persistently abnormal results from liver tests who had been admitted to a hepato-gastroenterology unit in France from January 1982 through December 1997; patients with a recorded duration of alcohol abuse were assigned to the development cohort (n=1599; 75% men) or the validation cohort (n=735; 75% men), based on presence of a liver biopsy. We collected data from both cohorts on patient history and disease stage at the time of hospitalization. For the development cohort, severity of the disease was scored by the METAVIR (due to the availability of liver histology reports); in the validation cohort only the presence of liver complications was assessed. We developed a model of ALD progression and occurrence of liver complications (hepatocellular carcinoma and/or liver decompensation) in association with exposure to alcohol, age at the onset of heavy drinking, amount of alcohol intake, sex and body mass index. The model was fitted to the development cohort and then evaluated in the validation cohort. We then tested the ability of the model to predict disease progression for any patient profile (baseline evaluation). Patients with a 5-y weighted risk of liver complications greater than 5% were considered at high risk for disease progression.

Results

Model results are given for the following patient profiles: men and women, 40 y old, who started drinking at an age of 25 y, drank 150 g/day, and had a body mass index of 22 kg/m² according to the disease severity at baseline evaluation. For men with baseline F0–F2 fibrosis, the model estimated the probabilities of normal liver, steatosis, or steatohepatitis at baseline to be 31.8%, 61.5% and 6.7%, respectively. The 5-y weighted risk of liver complications was 1.9%, ranging from 0.2% for men with normal liver at baseline evaluation to 10.3% for patients with steatohepatitis at baseline. For women with baseline F0–F2 fibrosis, probabilities of normal liver, steatosis, or steatohepatitis at baseline were 25.1%, 66.5% and 8.4%, respectively; the 5-y weighted risk of liver complications was 3.2%, ranging from 0.5% for women with normal liver at baseline to 14.7% for patients with steatohepatitis at baseline. Based on the model, men with F3–F4 fibrosis at baseline have a 24.5% 5-y weighted risk of complications (ranging from 20.2% to 34.5%) and women have a 30.1% 5-y weighted risk of complications (ranging from 24.7% to 41.0%).

Conclusions

We developed a Markov model that integrates data on level and duration of alcohol use to identify patients at high risk of liver disease progression. This model might be used to adapt patient care pathways.

中文翻译：

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一种识别肝病进展高危重度饮酒者的模型。

背景与目标

酒精相关性肝病 (ALD) 会导致慢性肝病。我们调查了有关患者饮酒史和饮酒量、肝病分期和人口统计学特征的信息如何用于确定疾病进展的风险。

方法

我们从 1982 年 1 月至 1997 年 12 月在法国肝胃肠病科住院的 2334 名酗酒者（50 克/天或更多）收集了数据，这些人的肝脏检查结果持续异常；基于肝活检的存在，记录了酗酒持续时间的患者被分配到发展队列（n=1599；75% 男性）或验证队列（n=735；75% 男性）。我们从两个队列中收集了住院时患者病史和疾病分期的数据。对于发展队列，疾病的严重程度由 METAVIR 评分（由于肝脏组织学报告的可用性）；在验证队列中，仅评估了肝脏并发症的存在。我们开发了一个 ALD 进展和肝脏并发症（肝细胞癌和/或肝功能失代偿）的发生模型，这些模型与酒精暴露、重度饮酒开始时的年龄、酒精摄入量、性别和体重指数有关。该模型适用于开发队列，然后在验证队列中进行评估。然后，我们测试了模型预测任何患者特征（基线评估）疾病进展的能力。肝脏并发症 5 年加权风险大于 5% 的患者被认为具有疾病进展的高风险。然后，我们测试了模型预测任何患者特征（基线评估）疾病进展的能力。肝脏并发症 5 年加权风险大于 5% 的患者被认为具有疾病进展的高风险。然后，我们测试了模型预测任何患者特征（基线评估）疾病进展的能力。肝脏并发症 5 年加权风险大于 5% 的患者被认为具有疾病进展的高风险。

结果

给出了以下患者概况的模型结果：男性和女性，40 岁，25 岁​​开始饮酒，每天饮酒 150 克，体重指数为 22 kg/m ²根据基线评估时的疾病严重程度。对于基线 F0-F2 纤维化的男性，该模型估计基线正常肝脏、脂肪变性或脂肪性肝炎的概率分别为 31.8%、61.5% 和 6.7%。肝脏并发症的 5 年加权风险为 1.9%，范围从基线评估时肝脏正常的男性的 0.2% 到基线时患有脂肪性肝炎的患者的 10.3%。对于基线 F0-F2 纤维化的女性，基线时正常肝脏、脂肪变性或脂肪性肝炎的概率分别为 25.1%、66.5% 和 8.4%；肝脏并发症的 5 年加权风险为 3.2%，范围从基线时肝脏正常的女性的 0.5% 到基线时患有脂肪性肝炎的患者的 14.7%。根据该模型，基线时患有 F3-F4 纤维化的男性有 24.5% 的 5 年并发症加权风险（范围为 20.

结论

我们开发了一个马尔可夫模型，该模型整合了酒精使用水平和持续时间的数据，以识别肝病进展风险高的患者。该模型可用于调整患者护理路径。