背景:相当比例的非酒精性脂肪性肝病(NAFLD)相关肝细胞癌(HCC)患者没有肝硬化。关于无肝硬化的NAFLD中HCC发展的发生率和预测因素的数据是有限的。我们进行了大规模的,无肝硬化记录的NAFLD患者的国家研究,以检查HCC发展的发病率和预测因素。
方法:这项回顾性研究包括751,603名NAFLD患者(54%为女性),无来自鉴定的OptumClinformatics®DataMart数据库的肝硬化。肝硬化患者,血小板<120,000/µL或FIB-4值>2.67被排除.
结果:平均年龄为53.7±15.0岁,45.9%为男性,39.5%有糖尿病,57.6%是白人,18.4%西班牙裔,8.2%的黑人和4.9%的亚洲人。平均血小板计数为264,000±72,000/微升,96.3%的患者FIB-4<1.30。超过1,686,607人年的随访,有76例肝癌事件,导致HCC发病率为0.05/1000人年。血小板≤150,000/µL的患者肝癌发病率较高,与那些血小板>150,000/微升(0.23/1000人年,vs.每1000人年0.04,p=0.02),但不在年龄的亚组分析中,性别,种族/民族或糖尿病。使用多变量Cox比例风险模型调整了多个混杂因素,血小板计数≤150,000/µL仍然是HCC发展的独立预测因子(校正HR5.80,95%CI1.67-20.1,p=0.006).
结论:在无肝硬化记录的NAFLD中,HCC发病率低于整体和多个亚组分析中的成本效益HCC监测阈值。血小板计数<150,000/µL可能是该人群中HCC发展的有用预测因子。
BACKGROUND: A substantial proportion of patients with nonalcoholic fatty liver disease (NAFLD)-related hepatocellular carcinoma (HCC) do not have cirrhosis. Data regarding the incidence and predictors of HCC development in NAFLD without cirrhosis are limited. We conducted a large, national
study of NAFLD patients without documented cirrhosis to examine the incidence and predictors for HCC development.
METHODS: This retrospective
study included 751,603 NAFLD patients (54% female) without documented cirrhosis derived from the deidentified Optum Clinformatics® Data Mart Database. Patients with cirrhosis, platelets < 120,000/µL or FIB-4 values > 2.67 were excluded.
RESULTS: The mean age was 53.7 ± 15.0 years, 45.9% were male, 39.5% had diabetes, 57.6% were White, 18.4% Hispanic, 8.2% Black and 4.9% were Asian. The mean platelet count was 264,000 ± 72,000/µL, and 96.3% of patients had a FIB-4 < 1.30. Over 1,686,607 person-years of follow-up, there were 76 incident cases of HCC, resulting in an HCC incidence rate of 0.05 per 1000 person-years. There was a higher HCC incidence rate among patients with platelets ≤ 150,000/µL, versus those with platelets > 150,000/µL (0.23 per 1000 person-years, vs. 0.04 per 1000 person-years, p = 0.02) but not in subgroup analyses for age, sex, race/ethnicity or diabetes. Using multivariable Cox proportional hazards model adjusted multiple confounders, platelet count ≤ 150,000/µL remained an independent predictor of HCC development (adjusted HR 5.80, 95% CI 1.67-20.1, p = 0.006).
CONCLUSIONS: HCC incidence in NAFLD without documented cirrhosis was below the threshold for cost-effective HCC surveillance in overall and multiple subgroup analyses. Platelet count < 150,000/µL may be a useful predictor of HCC development in this population.