Athyros Vasilios G, Mikhailidis Dimitri P, Didangelos Triandafillos P, Giouleme Olga I, Liberopoulos Evangelos N, Karagiannis Asterios, Kakafika Anna I, Tziomalos Konstantinos, Burroughs Andrew K, Elisaf Moses S
Atherosclerosis and Metabolic Syndrome Units, Aristotelian University, Hippocration Hospital, Thessaloniki, Greece.
Curr Med Res Opin. 2006 May;22(5):873-83. doi: 10.1185/030079906X104696.
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome (MetS). There is no established treatment for NAFLD.
To evaluate a multifactorial intervention in the treatment of NAFLD.
A prospective, open-label, randomised study in non-diabetic patients (n = 186) with MetS (follow-up: 54 weeks). All patients had both biochemical and ultrasonographic evidence of NAFLD at baseline. Other causes of liver disease were excluded. Patients received lifestyle advice and treatment for hypertension (mainly inhibitors of the renin-angiotensin system), impaired fasting glucose (metformin), obesity (orlistat) and dyslipidaemia [randomly allocated to atorvastatin 20 mg/day (n = 63) or micronised fenofibrate 200 mg/day (n = 62) or both drugs (n = 61)]. Liver ultrasonography was assessed at baseline and at the end of the study.
At the end of treatment, 67% of patients on atorvastatin, 42% on fenofibrate and 70% on combination treatment no longer had biochemical plus ultrasonographic evidence of NAFLD (p < 0.05 vs. baseline for all comparisons). The percentage of patients who no longer had evidence of NAFLD was significantly higher (p < 0.009) in the atorvastatin and combination groups compared with the fenofibrate group. This effect was independently related to drug treatment, as well as to reductions in high-sensitivity C-reactive protein, waist circumference, body weight, triglycerides, low-density lipoprotein-cholesterol, total cholesterol, systolic blood pressure and glucose. Four patients discontinued treatment because of adverse effects.
Multifactorial intervention in MetS patients with both biochemical and ultrasonographic evidence of NAFLD offsets surrogate markers of NAFLD (i.e. elevated aminotransferase plus echogenic liver).
非酒精性脂肪性肝病（NAFLD）是代谢综合征（MetS）的肝脏表现形式。目前尚无针对NAFLD的确立治疗方法。
评估多因素干预对NAFLD的治疗效果。
对非糖尿病的MetS患者（n = 186）进行一项前瞻性、开放标签、随机研究（随访时间：54周）。所有患者在基线时均有NAFLD的生化和超声证据。排除其他肝病病因。患者接受生活方式建议以及针对高血压（主要是肾素 - 血管紧张素系统抑制剂）、空腹血糖受损（二甲双胍）、肥胖（奥利司他）和血脂异常[随机分配至阿托伐他汀20毫克/天（n = 63）或微粒化非诺贝特200毫克/天（n = 62）或两种药物联合使用（n = 61）]的治疗。在基线和研究结束时评估肝脏超声检查。
治疗结束时，接受阿托伐他汀治疗的患者中有67%、接受非诺贝特治疗的患者中有42%以及接受联合治疗的患者中有70%不再有NAFLD的生化和超声证据（与基线相比，所有比较的p < 0.05）。与非诺贝特组相比，阿托伐他汀组和联合治疗组中不再有NAFLD证据的患者百分比显著更高（p < 0.009）。这种效果与药物治疗以及高敏C反应蛋白、腰围、体重、甘油三酯、低密度脂蛋白胆固醇、总胆固醇、收缩压和血糖的降低独立相关。四名患者因不良反应停药。
对同时有NAFLD生化和超声证据的MetS患者进行多因素干预可抵消NAFLD的替代指标（即转氨酶升高加肝脏回声增强）。
