Fatty liver disease: Definition, Causes, Manifestations, Treatment

Fatty liver disease: Definition, Causes, Manifestations, Treatment
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Hepatic steatosis is a relatively common metabolic disease. The term steatosis refers to an increased state of fat accumulation. The latter is very often associated with alcohol. However, the latter is not the only cause of liver steatosis. The accumulation of fat results in impaired function of this important organ.


Hepatic steatosis or fatty liver disease. It is classified as a metabolic disease. From a broader perspective, liver diseases are among the top ten causes of death in the European Union. The main group of diseases are hepatitis, steatosis, the most serious diseases include cirrhosis and the most serious is liver cancer.

A link can be found between these diseases. With steatosis of the liver is a process in which fatty tissue is deposited to an excessive degree in its area. Alcohol, and hence alcoholism, is not the only cause of its occurrence.

TIP: Read the article Do you know how alcoholism affects health?

What is steatosis?

The term steatosis includes the process in which fat is deposited in an increased proportion, in the form of tiny drops. It can accumulate inside the cells, i.e. intracellularly, but also around them, i.e. extracellularly. Steatosis (fatty change) can be macroscopic and microscopic.

  • macroscopic, when the affected organ is coated with fat, it is yellow to orange, for increased blood supply
  • microscopic if the fat droplets are free or even membrane-coated inside the cells
    • small droplet macroscopic steatosis means more small fat droplets in one cell
    • large droplet macroscopic (macrovesicular) steatosis means one large fat droplet that fills the cell and displaces its nucleus

The increased rate of fat storage is not only risky for the liver. It can affect other organs as well. For example, kidneys, heart muscle, blood vessels, but also the gallbladder, spleen or skin (such as skin tumours). When fat metabolism is disturbed, fat accumulates in the liver cell, resulting in fatty dystrophy and impaired liver cell function.

Hepatic calcification occurs due to the involvement of the original liver tissue. There is an accumulation of fatty particles in this tissue and, consequently, impaired function. It occurs when there is an excessive influx of fats and fatty acids into the liver, a disturbance in the release of fats from the liver into the bloodstream, or directly when the level of fat in the liver increases.

Steatosis is initially reversible, which means that it can be reversed and the liver will not be permanently damaged. However, with persistent exposure to negative factors, irreversible changes, i.e. irreversible damage, occur. This leads to inflammation and fibrosis of the liver tissue. Fibrotically altered tissue is referred to as cirrhosis.

And this in turn is a risk for liver cancer.

The overall issue of steatosis is complex. However, for simplicity, I will state that steatosis arises as a consequence of alcoholic liver damage, and the second group is non-alcoholic steatosis. The distinction of importance to the layman is mainly in the causes that divide these two groups.


Thus, fatty liver is the excessive deposition of fatty tissue in the liver. The fat negatively affects the surrounding tissue and consequently interferes with its function. The liver is an important organ and has several irreplaceable roles in the body.

It is impossible to survive without it.

Liver dysfunction affects the whole body, and there is no substitute mechanism for liver dysfunction. It is required in the processing of nutrients and has an irreplaceable metabolic and detoxifying function. It also serves as a reservoir of glycogen, protein and fat. During embryonic development, it serves for blood formation. A very important function is the production and secretion of bile, which is used in the digestion of fats.

The most common causes of steatosis are excessive intake of fatty foods and therefore fatty acids, obesity, but also sudden weight loss and starvation.

Alcoholism follows, but risk factors also include diabetes, high cholesterol, medications and an overall poor lifestyle.

Non-alcoholic steatosis of the liver

It is a common disease and it is obvious from the name that alcohol is not the cause. Nonalcoholic steatosis of the liver (NASP) is also abbreviated NAFLD, which is from the English nonalcoholic fatty liver. Its prevalence is reported to range from 16-23% of the adult population.

A serious complication of hepatic steatosis is non-alcoholic steatohepatitis (NASH), which in about 25% leads to cirrhosis of the liver.

Up to 40% of people with cirrhosis die from liver failure or hepatocellular carcinoma.

Table: risk factors for the development of hepatic steatosis

Risk factor Description
Obesity steatosis is present in all obese, even in obese children
Diabetes in type II diabetes, hepatic steatosis is present in approximately one-third of cases
Fatty abnormalities hypertriacylglycerolaemia,  Hypercholesterolaemia
Ethnicity and race more common in Hispanics

The most common causes of hepatic steatosis:

  • metabolic syndrome, and thus obesity
  • medicines (corticosteroids)
  • complete parenteral nutrition (nutrient supply outside the digestive tract)
  • high calorie diet
  • short bowel syndrome
  • Hypertriglyceridemia
  • low HDL cholesterol
  • hypertension
  • hyperglycaemia
  • insulin resistance

If steatosis continues, it is not prevented from developing, it will develop into non-alcoholic steatohepatitis (NASH), which is an inflammatory process. NASH is a high risk for cirrhosis, occurring in 20-30% of cases. A complication of cirrhosis is liver failure.

Some risk factors that influence the conversion of steatosis to steatohepatitis:

  • Hepatitis C
  • diabetes
  • certain medications (amiodarone, estrogens, corticosteroids)
  • fasting
  • rapid weight loss
  • parenteral nutrition
  • resection of the small intestine
  • gastroplasty
  • lipodystrophy
  • hydrocarbons

In favor of the development of an inflammatory response to steatosis, the so-called 2-hit theory is put forward, whereby the first hit causes the liver itself to get fatty. Behind it may be hidden the most common causes mentioned above (Diabetes mellitus type II, medications).

The risk is if there is another pathological process going on in parallel, an example of which is one of the risk factors mentioned above. This second hit is a trigger for inflammatory changes in the sense of non-alcoholic steatohepatitis.

Alcohol damage to the liver

Alcohol is an available drug. It has a negative effect on the body, but also on the psyche. Alcoholic liver damage is just one serious complication that alcoholism causes. For more information, see the article on the disease of alcoholism.

Steatosis develops quite quickly at the expense of alcohol. Already 10 days of drinking hard alcohol is a risk of its development. It is reported that 300-600 milliliters of 86% alcohol, during these days is the threshold for liver damage. If this damaging action is stopped, the resulting impairment is reversible.

However, if a person continues to drink alcohol, he or she exposes himself or herself to permanent damage. In these cases, acute alcoholic hepatitis may also develop. Prolonged drinking tends towards cirrhosis. Other risk factors and the genetic makeup of the individual are also necessary for its occurrence.

Risk factors behind alcoholic liver injury:

  • lifelong drinking of alcohol
  • drinking alcohol outside of dietary intake
  • highly concentrated alcoholic beverages, i.e. spirits
  • drinking different alcoholic beverages, i.e. mixing
  • women are more susceptible
  • malnutrition, starvation
  • drinking alcohol for viral hepatitis B and C
  • genetic predisposition

There is information circulating among people that even drinking a small amount of alcohol every day is not harmful. However, this statement is not universal. Each person should consider his or her individual disposition and any risks involved (primary disease, medication, genetic make-up).

Various literatures provide approximate values for safe and risky drinking levels.

Table: safe and risky levels of daily drinking

Safe daily dose
Men Women
less than 20 g of alcohol per day less than 10 g of alcohol per day
  • 60 - 100 ml of distillate
  • 200 - 300 of wine
  • 500 - 700 ml of beer
  • 30 - 50 ml of distillate
  • 100 - 150 ml of wine
  • 250 - 350 ml of beer
Risk for cirrhosis
more than 40 - 60 grams of alcohol per day more than 20 grams of alcohol per day


Non-alcoholic steatosis of the liver usually proceeds in the initial stages without visible symptoms and in a hidden manner. This is also why it is quite dangerous. If so, only non-specific symptoms occur.

Non-specific symptoms of hepatic steatosis include:

  • weakness
  • fatigue, malaise
  • inactivity
  • pain in the upper abdomen, especially in the right lower abdomen and mostly of a pressing nature
  • enlarged and sensitive liver
  • flatulence
  • sensation of being full
  • dyspeptic discomfort (upset stomach, feeling like vomiting, pain in the upper part, flatulence, lack of appetite)

According to how the disease manifests itself clinically, it is also classified as:

  • non-alcoholic steatosis without manifestations, not characterized by progression
  • chronic non-alcoholic steatohepatitis (NASH), progresses slowly, covers the majority of cases and also largely ends in cirrhosis
  • subacute NASH, which can end in death, however, this form is rare, occurring mainly in cases of starvation, reducing diets, after bowel surgery

The alcoholic form has more severe manifestations. When in her case, fatigue, malaise, nausea, flatulence are typical, a person also has disorders of defecation. Vomiting, jaundice, or icterus, disorder of consciousness, which are a manifestation of the failure of liver function, are associated.

The most serious condition occurs in so-called Reye's syndrome after a child ingests, for example, aspirin, which is accompanied by liver failure, disturbances of consciousness, brain damage, and sometimes this condition can end in death or long-term coma without medical intervention.

Complications of acute alcoholic hepatitis include:

  • ascites, or swelling of the abdomen
  • bleeding from oesophageal varices
  • bleeding conditions, for disorders of haemocoagulation
  • portal hypertension due to enlargement of the liver
  • liver failure
  • renal failure
  • hepatorenal syndrome (hepato- meaning of the liver, renal - meaning of the kidney)
  • hepatic encephalopathy
  • acute pancreatitis
  • disturbance of the internal environment
  • frequent infectious diseases


Symptoms of steatosis are many times non-specific, and this disease runs hidden for a long time. Therefore, the diagnosis of the disease can be accidental. As, for example, a secondary finding during the examination of other ailments. But also as a result of a preventive examination.

Ultrasonography, or medical ultrasound, or simply sonography, is used as the main examination method. Investigations such as X-rays, CT scans and MRIs are performed for abdominal problems, but may not provide the more detailed information needed to make an overall assessment of the diagnosis.

However, it is important to determine the extent of liver damage and the provoking cause. Such as hepatitis. When serologic blood testing and antibodies for Hepatitis C and B are performed. 

Other laboratory testing includes evaluation of iron (hemochromatosis), copper (Wilson's disease), type II diabetes mellitus. Of course, information on alcoholism or family history is also important. Liver function tests (AST/ALT, GMT) are used to determine liver function.

Liver biopsy is the collection of a sample of the liver for histological and morphological examination. The biopsy will identify fatty, inflammatory, fibrotic or necrotic tissue. The biopsy also serves as an indicator of treatment efficacy. Of course, treatment and elimination of the provoking cause is an important factor for success.


The course of hepatic steatosis is not specific. Of course, it depends on the provoking cause. However, if the course is chronic, in most cases the liver steatosis proceeds asymptomatically, i.e. covertly.

Later, mainly non-specific discomfort may be experienced.

A person may complain of flatulence, a sensation of discomfort in the upper abdomen. Discomfort is described as a vague sensation that is not unequivocal pain, i.e. a sensation of discomfort. Muscle weakness, fatigue, malaise and also more rapid exhaustion are associated with exertion.

The pain is mostly dull and occurs in the upper abdomen, especially in the right lower abdomen. This already indicates an enlargement of the liver, which the doctor can palpate on examination by palpation.

In obese patients may not be felt in the case of steatosis.

If there is acute impairment in the case of alcohol it is necessary that the supply of alcohol is stopped. As short-term consumption will not cause permanent damage. The acute and rapid progression of this disease in children is after ingestion of aspirin or other drug containing acetylsalicylic acid, when there is a risk of acute liver failure, and this condition has a designation as Reye syndrome.

The risk is the transition of steatosis to cirrhosis, which is subsequently a risk factor for the development of hepatocellular carcinoma. This is mainly due to continued drinking of high doses of hard alcohol. For long-term causes, the problem is the untreated underlying disease, but also, for example, an unchanged lifestyle.

Information about cirrhosis in a separate article among the diseases.

How it is treated: Fatty liver disease

How to treat fatty liver? Medication, diet. No alcohol, protect the liver

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Interesting resources

  • "Nonalcoholic Fatty Liver Disease & NASH". National Institute of Diabetes and Digestive and Kidney Diseases. November 2016. 
  • Singh, S; Osna, NA; Kharbanda, KK (28 September 2017). "Treatment options for alcoholic and non-alcoholic fatty liver disease: A review". World Journal of Gastroenterology23 (36): 6549–6570. 
  • Antunes, C; Azadfard, M; Gupta, M (January 2019). "Fatty Liver". 
  • Basra, Sarpreet (2011). "Definition, epidemiology and magnitude of alcoholic hepatitis". World Journal of Hepatology3 (5): 108–113. 
  • Iser, D; Ryan, M (July 2013). "Fatty liver disease—a practical guide for GPs". Australian Family Physician42 (7): 444–7. 
  • Chalasani, Naga; Younossi, Zobair; Lavine, Joel E.; Charlton, Michael; Cusi, Kenneth; Rinella, Mary; Harrison, Stephen A.; Brunt, Elizabeth M.; Sanyal, Arun J. (January 2018). "The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases". Hepatology67 (1): 328–357.
  • Singh, Siddharth; Allen, Alina M.; Wang, Zhen; Prokop, Larry J.; Murad, Mohammad H.; Loomba, Rohit (April 2015). "Fibrosis Progression in Nonalcoholic Fatty Liver vs Nonalcoholic Steatohepatitis: A Systematic Review and Meta-analysis of Paired-Biopsy Studies". Clinical Gastroenterology and Hepatology13 (4): 643–654.e9.
  • Younossi, Zobair; Anstee, Quentin M.; Marietti, Milena; Hardy, Timothy; Henry, Linda; Eslam, Mohammed; George, Jacob; Bugianesi, Elisabetta (20 September 2017). "Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention". Nature Reviews Gastroenterology & Hepatology15 (1): 11–20. 
  • Qian Y, Fan JG (May 2005). "Obesity, fatty liver and liver cancer". Hepatobiliary & Pancreatic Diseases International4 (2): 173–7. 
  • Bellentani, Stefano (January 2017). "The epidemiology of non-alcoholic fatty liver disease". Liver International37: 81–84.