Clinical approaches to non-alcoholic fatty liver disease

Abstract

Non-alcoholic fatty liver disease (NAFLD) ranges from simple steatosis to nonalcoholic steatohepatitis (NASH), leading to fibrosis and potentially cirrhosis, and it is one of the most common causes of liver disease worldwide. NAFLD is associated with other medical conditions such as metabolic syndrome, obesity, cardiovascular disease and diabetes. NASH can only be diagnosed through liver biopsy, but noninvasive techniques have been developed to identify patients who are most likely to have NASH or fibrosis, reducing the need for liver biopsy and risk to patients. Disease progression varies between individuals and is linked to a number of risk factors. Mechanisms involved in the pathogenesis are associated with diet and lifestyle, influx of free fatty acids to the liver from adipose tissue due to insulin resistance, hepatic oxidative stress, cytokines production, reduced very low-density lipoprotein secretion and intestinal microbiome. Weight loss through improved diet and increased physical activity has been the cornerstone therapy of NAFLD. Recent therapies such as pioglitazone and vitamin E have been shown to be beneficial. Omega 3 polyunsaturated fatty acids and statins may offer additional benefits. Bariatric surgery should be considered in morbidly obese patients. More research is needed to assess the impact of these treatments on a long-term basis. The objective of this article is to briefly review the diagnosis, management and treatment of this disease in order to aid clinicians in managing these patients.

Analytical, anthropometric and dietary factors associated with the development of fibrosis in patients with nonalcoholic fatty liver disease

“…It is important to highlight that patients with normal transaminases and hepatic steatosis (ultrasound) may also have NASH and liver fibrosis (18,19). Recent studies reported that there is no optimal level of ALT to predict NASH and advanced fibrosis (20,21).…”

Supplementation With 2:1 Ratio of N-6:n-3 Polyunsaturated Fatty Acid Improves Liver Steatosis and Serum Cytokine Levels in Young Obese Balinese Women: A Randomized Clinical Trial

“…If NAFLD is neither identified in its early stages nor managed appropriately, the disease will naturally progress to the severe NASH stage, which entails inflammation, fibrosis, and cirrhosis [3]. Non-invasive US imaging is an appropriate first-line method for the early detection of asymptomatic NAFLD [40].…”

“…Non-invasive US imaging is an appropriate first-line method for the early detection of asymptomatic NAFLD [40]. Schwenger et al [3] recommended that an improvement in diet and increase in physical activity should be the first choice to treat NAFLD, followed by the management of insulin resistance, oxidative stress, and obesity-associated morbidity.…”

“…NAFLD occurs as two entities, i.e, non-alcoholic fatty liver (NAFL) and succeeded by non-alcoholic steatohepatitis (NASH) in the later stage. NAFL is defined as hepatic steatosis without inflammation, whereas NASH is steatosis accompanied by inflammation [3]. NAFLD is the most common liver disorder and is the leading cause of hepatocyte injury and fibrosis.…”

“…This accumulation of fat, particularly intrahepatic triglycerides (TGs), occurs due to several mechanisms, i.e, increased influx of free fatty acids into the liver, increased fat synthesis, decreased TG export through very low-density lipoprotein (VLDL), and reduced β-oxidation [1][2][3]. Fat accumulation indicates that hepatic fatty acid uptake from the plasma and de novo fatty acid synthesis occur at a faster rate than do β-oxidation and export [3]. NAFLD occurs as two entities, i.e, non-alcoholic fatty liver (NAFL) and succeeded by non-alcoholic steatohepatitis (NASH) in the later stage.…”