The authors congratulate Eguchi et al. Citation[1] for their comprehensive review on novel findings related to the pathobiology of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), such as angiogenesis and fibrosis, the inflammasome complex, incretins and modulation of dietary lipids Citation[1]. It is worth looking at some current interventions.
The therapeutic approach of the patient with NAFLD should be multifactorial. The authors found after a 54-week multifactorial intervention (diet plus drugs, mainly hypolipidemic) in a randomized study with 186 NAFLD patients that 67% of participants 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) Citation[2]. The Assessing The Treatment Effect in Metabolic Syndrome Without Perceptible diabeTes (ATTEMPT) study included 1123 metabolic syndrome patients, while 326 had NAFLD Citation[3]. The intervention was also multifactorial (based on atorvastatin) and the follow-up was 42 months. NAFLD was substantially resolved by the end of the first year and also cardiovascular disease (CVD) risk practically vanished Citation[3].
In secondary CVD prevention, a post hoc analysis of the Greek Atorvastatin and Coronary Heart Disease Evaluation (GREACE) trial Citation[4] showed that atorvastatin was associated with a significant reduction in CVD events in patients with established CVD. This benefit was attributed to various factors, including the improvement of NAFLD, an independent CVD risk factor Citation[4]. In a recent preliminary report Citation[5], the authors have shown that rosuvastatin (10 mg/day) treatment in patients with NASH can completely resolve the laboratory and the histological findings of the disease (necroinflammation, ballooning and fibrosis) after a year of treatment; biochemical improvement was evident at 3 months. Given that diet alone has no effect on liver fibrosis and the speed of liver pathology improvement, the authors suggest that these effects of statins are mostly of pleiotropic nature. They probably address at least some of the mechanisms mentioned by Eguchi et al. Citation[1].
Declaration of interest
The authors state no conflict of interest and have received no payment in preparation of this manuscript.
Bibliography
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- Athyros VG, Mikhailidis DP, Didangelos TP, et al. Effect of multifactorial treatment on non-alcoholic fatty liver disease in metabolic syndrome: a randomised study. Curr Med Res Opin 2006;22:873-83
- Athyros VG, Giouleme O, Ganotakis ES, et al. Safety and impact on cardiovascular events of long-term multifactorial treatment in patients with metabolic syndrome and abnormal liver function tests: a post hoc analysis of the randomised ATTEMPT study. Arch Med Sci 2011;7:796-805
- Athyros VG, Tziomalos K, Gossios TD, GREACE Study Collaborative Group. Safety and efficacy of long-term statin treatment for cardiovascular events in patients with coronary heart disease and abnormal liver tests in the Greek Atorvastatin and Coronary Heart Disease Evaluation (GREACE) Study: a post-hoc analysis. Lancet 2010;376:1916-22
- Kargiotis K, Katsiki N, Athyros VG, et al. Effect of rosuvastatin on non-alcoholic steatohepatitis in patients with metabolic syndrome and hypercholesterolaemia. A preliminary report. Curr Vasc Pharmacol 2013; In press