Fettleber

Fettleber, or hepatic steatosis, is fat accumulation in liver cells. It is commonly defined as fat present in at least 5% of hepatocytes. Fettleber is the hallmark of fatty liver disease and is divided into alcoholic fatty liver disease (AFLD) and non-alcoholic fatty liver disease (NAFLD). NAFLD can progress to non-alcoholic steatohepatitis (NASH), which includes inflammation and liver injury and may lead to fibrosis.

NAFLD is linked to metabolic risk factors such as obesity, insulin resistance, type 2 diabetes, dyslipidemia, and metabolic syndrome. AFLD results from sustained alcohol use. Other contributors include certain medications, rapid weight loss, malnutrition, viral hepatitis, and autoimmune conditions. NAFLD is among the most common chronic liver diseases in many regions and is rising with obesity rates.

Pathophysiology involves an imbalance between lipid uptake, synthesis, oxidation, and export, resulting in triglyceride accumulation in hepatocytes. In NAFLD, progression from simple steatosis to NASH increases the risk of fibrosis, cirrhosis, and liver cancer. Alcohol accelerates hepatocyte injury and fibrotic progression.

Most people with Fettleber are asymptomatic. When symptoms occur, they may include fatigue or discomfort in the upper right abdomen. Diagnosis relies on imaging (ultrasound, CT, MRI) showing increased liver fat, supported by abnormal liver enzymes and the exclusion of other causes. In uncertain cases or to stage fibrosis, liver biopsy may be used.

Management focuses on risk factor modification. Weight loss through diet and exercise (roughly 7–10% of body weight) improves steatosis. Diets emphasizing vegetables, fruits, and healthy fats (such as the Mediterranean pattern) are recommended. Abstinence from alcohol is essential for AFLD and advised in NAFLD. There is no universally approved drug for NAFLD/NASH; some therapies show promise in research and treatment is tailored to comorbidities.