Hepatic Steatosis: Etiology, Patterns, and Quantification

Abstract

Hepatic steatosis can occur because of nonalcoholic fatty liver disease (NAFLD), alcoholism, chemotherapy, and metabolic, toxic, and infectious causes. Pediatric hepatic steatosis is also becoming more frequent and can have distinctive features. The most common pattern is diffuse form; however, it can present in heterogenous, focal, multinodular, perilesional, perivascular, subcapsular, and lobar forms. Focal steatosis and fat sparing can occur because of the presence of veins of Sappey, pancreaticoduodenal vein, and aberrant right and left gastric veins, which drain into the liver as third inflow. Hypersteatosis and multinodular forms can mimic metastasis in patients with cancer. Perilesional fat can be seen in insulinoma. Recent introduction of proton-density fat fraction enabled easy and reproducible quantification of hepatic fat. Follow up of patients with NAFLD can be performed for the assessment of treatment response using proton-density fat fraction as biomarker. Multiecho gradient-echo techniques also simultaneously calculate T2* maps, which is important to rule out coexisting hepatic iron overload. NAFLD can progress to steatohepatitis (nonalcoholic steatohepatitis), which can result in cirrhosis. Magnetic resonance (MR) elastography and functional evaluation with Gd-EOB-DTPA are becoming important for monitoring this process. Hepatocellular carcinoma can develop in patients with NAFLD, which is usually a large tumor with necrotic center. In the future, fatty acid maps obtained by MR imaging may allow more detailed analysis of steatosis. MR imaging is superior to ultrasonography and computed tomography for comprehensive evaluation of steatosis.