From the Guidelines
The main causes of sudden steatosis (fatty liver) include metabolic disorders, such as insulin resistance and type 2 diabetes, as well as other cardiometabolic risk factors, as stated in the most recent study 1. The causes of sudden steatosis can be multifactorial, and it is essential to consider various factors, including:
- Metabolic disorders, such as insulin resistance and type 2 diabetes, which are major risk factors for developing nonalcoholic fatty liver disease (NAFLD) and its progression to nonalcoholic steatohepatitis (NASH) and cirrhosis 1
- Other cardiometabolic risk factors, such as obesity, atherogenic dyslipidemia, and hypertension, which are associated with insulin resistance and can contribute to the development of steatosis 1
- Certain medications, such as corticosteroids, amiodarone, tamoxifen, methotrexate, valproic acid, and tetracyclines, which can cause acute steatosis 1
- Rapid weight loss, particularly after bariatric surgery or extreme dieting, which can lead to sudden steatosis as fat is mobilized from adipose tissue and deposited in the liver 1
- Malnutrition, especially protein deficiency, which can disrupt normal liver metabolism and promote fat accumulation 1
- Certain genetic disorders affecting mitochondrial function or fatty acid metabolism, which can cause acute steatosis 1
- Viral infections, such as hepatitis C, which can trigger sudden fat accumulation in the liver 1 It is crucial to identify the underlying cause of sudden steatosis to provide appropriate management and prevent progression to more severe liver disease. The most recent study 1 emphasizes the importance of considering metabolic disorders and cardiometabolic risk factors in the diagnosis and management of NAFLD.
From the Research
Causes of Sudden Steatosis
- Hepatic steatosis can occur due to various factors, including nonalcoholic fatty liver disease (NAFLD), alcoholism, chemotherapy, and metabolic, toxic, and infectious causes 2
- A dietary excess of saturated fat contributes significantly to hepatocellular lipid accumulation, leading to hepatic steatosis 3
- Insulin resistance and increased oxidative stress are also important risk factors for nonalcoholic fatty liver disease (NAFLD) 4
- Obesity, type 2 diabetes, and alcohol intake are the main drivers of steatotic liver disease, which affects around 30% of the global population 5
Pathogenesis of Steatosis
- Elevated hepatocellular lipid levels mainly account for hepatic insulin resistance, which is probably mediated by partitioning of free fatty acids to the liver and by an imbalance of adipocytokines 3
- Free fatty acids and adipocytokines activate inflammatory pathways, including protein kinase C, the transcription factor nuclear factor kappaB, and c-Jun N-terminal kinase 1, which can accelerate the progression of hepatic steatosis to nonalcoholic steatohepatitis and cirrhosis 3
- The presence and progression of liver fibrosis led by hepatic inflammation is the main predictor of liver-related death across the entire spectrum of steatotic liver diseases 5
Patterns and Quantification of Steatosis
- Hepatic steatosis can present in various patterns, including diffuse, heterogenous, focal, multinodular, perilesional, perivascular, subcapsular, and lobar forms 2
- Proton-density fat fraction enabled easy and reproducible quantification of hepatic fat, and follow-up of patients with NAFLD can be performed for the assessment of treatment response using proton-density fat fraction as a biomarker 2
- Magnetic resonance (MR) elastography and functional evaluation with Gd-EOB-DTPA are becoming important for monitoring the progression of steatotic liver disease 2