Fatty Liver (Steatosis Hepatis)

In steatosis hepatis – colloquially called fatty liver – (synonyms: Fatty liver; Hepar adiposum; Steatosis; Steatosis hepatis; ICD-10 K76.0: Fatty liver [fatty degeneration], not elsewhere classified, including nonalcoholic fatty liver)) is a mild to moderate increase in size of the liver due to deposition of triglycerides (neutral fats) in the hepatocytes (liver cells). Fatty liver is said to occur when more than 50% of the hepatocytes are affected by hepatocellular fatty degeneration or when the percentage by weight of fat in the liver exceeds 10% of the total weight. Two forms of steatosis (fatty liver) are distinguished:

• Macrovesicular type (macrovesicular steatosis) – in this case, large fat droplets in the liver cells are noticeable; the most common form of fatty liver; it usually occurs alcohol abuse (alcohol dependence), diabetes mellitus (diabetes) or obesity (overweight); in developing countries, fatty liver often occurs in children due to protein malnutrition
• Microvesicular type (microvesicular steatosis) – here small fat droplets are found in the liver cells; occurs rarely, then rather in pregnancy

Another distinction is based on the cause of steatosis hepatis:

• Nonalcoholic fatty liver (NAFL; NAFLE; NAFLD, “nonalcoholic fatty liver disease”; ICD-10 K76.0); steatosis of the liver with a fat content of more than 5-10% of the liver weight or macrosteatosis of the hepatocytes (liver cells) with the same extent. There is no increased alcohol consumption (women: ≤ 10 g/d, men: ≤ 20 g/d).
• Alcoholic fatty liver (AFL; ALD; ICD-10 K70.0).
• Secondary hepatic steatosis (secondary steatosis/fatty liver), i.e., as an accompanying phenomenon of other diseases – see “Causes” for more details
• Metabolic syndrome
• Cryptogenic forms of steatosis hepatis, i.e. causes of the disease are unexplained

When inflammation is detectable in addition to steatosis hepatis, the disease is referred to as fatty liver hepatitis (K75.8 Other specified inflammatory liver diseases, including nonalcoholic steatohepatitis (NASH; ICD-10 K75.8)). Explanation of terms and abbreviations

Peak incidence: the maximum incidence of nonalcoholic fatty liver is between the ages of 35 and 45. The prevalence (disease incidence) for nonalcoholic fatty liver disease (NAFLD) is 20-40% of the adult population (in developed countries). 75% of overweight people and up to 80% of type 2 diabetics have fatty liver. The highest prevalence is in those > 60 years of age.In men, fatty liver content increases steadily between ages 20-50 years; in women, the increase does not begin until age 40 years and then continues until age 65 years.The prevalence of NAFLD in children and adolescents in the general population is lower than in adults, at 3-11%. However, more recent figures show an ominous increase: 1 in 5 participants in the British “Children of the 90s” study already had fatty liver by the age of 20. There is a positive correlation between NAFLD and various metabolic parameters (body mass index, abdominal circumference, triglycerides). Overweight and obese adolescents from puberty onwards are at increased risk for the presence of NAFLD. The prevalence for alcoholic fatty liver disease (ALD) is 5-10% of the population (Western Europe). Course and prognosis: Therapy depends on the underlying disease and also consists of avoiding the triggers of hepatocellular fatty degeneration. Steatosis hepatis is usually chronic, but can also occur acutely and then lead to the picture of acute liver failure (ALV).Therapy for non-alcoholic fatty liver (NAFLD) includes weight normalization, exercise, and if diabetes mellitus is present, optimal diabetes mellitus therapy. Furthermore, permanent medication must be checked for hepatotoxic (liver-damaging) drugs. These must then be discontinued or replaced immediately. In addition, alcohol restriction (< 20/d) applies. In alcoholic fatty liver (ALD), the only effective measure is alcohol abstinence. If therapy is started in time, the prognosis is good. In advanced stages of cirrhosis, complications from hepatic insufficiency (liver failure) and portal hypertension (portal hypertension; portal vein hypertension) are to be expected. Simple fatty liver is not associated with excess mortality. However, patients with NASH have increased all-cause mortality compared with healthy controls. Among these, cardiovascular causes of death rank first. Between 5-20% of fatty liver patients develop non-alcoholic steatohepatitis (NASH) during the course of their disease, in approximately 10-20% this progresses to higher grade fibrosis, and in approximately 2-5% of cases cirrhosis (connective tissue remodeling of the liver with functional impairment) develops within 10 years. NAFLD and mild alcoholic fatty liver disease (ALD) are reversible in most cases with adequate therapy (the most important measure is weight reduction). Comorbidities (concomitant diseases): nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus are mutually associated in terms of incidence and prognosis.Even in children, it is already associated with prediabetes (23.4%) or type 2 diabetes mellitus (6.2%).