Fatty liver disease

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Fatty liver
Other namesHepatic steatosis
Wilson disease, primary sclerosing cholangitis[3]
TreatmentAvoiding alcohol, weight loss[3][1]
PrognosisGood if treated early[3]
FrequencyNAFLD: 30% (Western countries)[2]
ALD: >90% of heavy drinkers[4]

Fatty liver disease (FLD), also known as hepatic steatosis and steatotic liver disease (SLD), is a condition where excess fat builds up in the liver.[1] Often there are no or few symptoms.[1][2] Occasionally there may be tiredness or pain in the upper right side of the abdomen.[1] Complications may include cirrhosis, liver cancer, and esophageal varices.[1][3]

The main subtypes of fatty liver disease are

alcohol-associated liver disease (ALD), with the category "metabolic and alcohol associated liver disease" (metALD) describing an overlap of the two.[5]

The primary risks include alcohol, type 2 diabetes, and obesity.[1][3] Other risk factors include certain medications such as glucocorticoids, and hepatitis C.[1] It is unclear why some people with NAFLD develop simple fatty liver and others develop nonalcoholic steatohepatitis (NASH), which is associated with poorer outcomes.[1] Diagnosis is based on the medical history supported by blood tests, medical imaging, and occasionally liver biopsy.[1]

Treatment of NAFLD is generally by dietary changes and exercise to bring about weight loss.[1] In those who are severely affected, liver transplantation may be an option.[1] More than 90% of heavy drinkers develop fatty liver while about 25% develop the more severe alcoholic hepatitis.[4] NAFLD affects about 30% of people in Western countries and 10% of people in Asia.[2] NAFLD affects about 10% of children in the United States.[1] It occurs more often in older people and males.[3][6]

Classification

Fatty liver disease was classified into:

In 2023, a new nomenclature was chosen,[5][7] with the classifications including:

  • Metabolic dysfunction–associated steatotic liver disease (MASLD), including:
    • Metabolic dysfunction-associated steatohepatitis
      (MASH)
  • Metabolic and alcohol associated liver disease (metALD). Describes those with MASLD who consume greater amounts of alcohol per week but not enough to be categorized as ALD)
  • Alcohol-associated liver disease
    (ALD)
  • Specific aetiology SLD (including drug-induced, monogenic diseases and others)

Signs and symptoms

Often there are no or few symptoms.[1] Occasionally there may be tiredness or pain in the upper right side of the abdomen.[1]

Complications

Fatty liver can develop into hepatic fibrosis, cirrhosis or liver cancer.[8] For people affected by NAFLD, the 10-year survival rate was about 80%. The rate of progression of fibrosis is estimated to be one per 7 years in NASH and one per 14 years in NAFLD, with an increasing speed.[9][10] There is a strong relationship between these pathologies and metabolic illnesses (diabetes type II, metabolic syndrome). These pathologies can also affect non-obese people, who are then at a higher risk.[8]

Less than 10% of people with cirrhotic alcoholic FLD will develop hepatocellular carcinoma,[11] the most common type of primary liver cancer in adults, but up to 45% people with NASH without cirrhosis can develop hepatocellular carcinoma.[12]

The condition is also associated with other diseases that influence fat metabolism.[13]

Causes

Different stages of liver damage

Fatty liver (FL) is commonly associated with metabolic syndrome (diabetes, hypertension, obesity, and dyslipidemia), but can also be due to any one of many causes:[14][15]

Alcohol
Alcohol use disorder
is one of the causes of fatty liver due to production of toxic metabolites like aldehydes during metabolism of alcohol in the liver. This phenomenon most commonly occurs with chronic alcohol use disorder.
Metabolic
abetalipoproteinemia, glycogen storage diseases, Weber–Christian disease, acute fatty liver of pregnancy, lipodystrophy
Nutritional
bacterial overgrowth
Drugs and toxins
glucocorticoids, tamoxifen,[16] environmental hepatotoxins (e.g., phosphorus, mushroom poisoning
)
Other
celiac disease,[17] inflammatory bowel disease, HIV, hepatitis C (especially genotype 3), and alpha 1-antitrypsin deficiency[18]

Pathology

trichrome stain

The fatty change represents the

Reye's syndrome are examples of severe liver disease caused by microvesicular fatty change.[19] The diagnosis of steatosis is made when fat in the liver exceeds 5–10% by weight.[13][20][21]

Mechanism leading to hepatic steatosis

Defects in fatty acid metabolism are responsible for pathogenesis of FLD, which may be due to imbalance in energy consumption and its combustion, resulting in lipid storage, or can be a consequence of peripheral resistance to insulin, whereby the transport of fatty acids from adipose tissue to the liver is increased.[13][22] Impairment or inhibition of receptor molecules (

SREBP1
) that control the enzymes responsible for the oxidation and synthesis of fatty acids appears to contribute to fat accumulation. In addition, alcohol use disorder is known to damage mitochondria and other cellular structures, further impairing cellular energy mechanism. On the other hand, non-alcoholic FLD may begin as excess of unmetabolised energy in liver cells. Hepatic steatosis is considered reversible and to some extent nonprogressive if the underlying cause is reduced or removed.

Micrograph of inflamed fatty liver (steatohepatitis)

Severe fatty liver is sometimes accompanied by

Pathological lesions in both conditions are similar. However, the extent of inflammatory response varies widely and does not always correlate with degree of fat accumulation. Steatosis (retention of lipid) and onset of steatohepatitis may represent successive stages in FLD progression.[23]

Liver disease with extensive inflammation and a high degree of steatosis often progresses to more severe forms of the disease.

zone 3 around the terminal hepatic veins.[25]

The progression to cirrhosis may be influenced by the amount of fat and degree of steatohepatitis and by a variety of other sensitizing factors. In alcoholic FLD, the transition to cirrhosis related to continued alcohol consumption is well-documented, but the process involved in non-alcoholic FLD is less clear.

Diagnosis

Liver steatosis (fatty liver disease) as seen on CT
Ultrasound showing diffuse increased echogenicity of the liver
Flow chart for diagnosis[15]
Elevated liver enzyme
Serology to exclude viral hepatitis
Imaging study showing
fatty infiltrate
Alcohol intake
Less than two drinks per day‡More than two drinks per day‡
Nonalcoholic fatty liver disease likelyAlcoholic liver disease likely
‡ Criteria for nonalcoholic fatty liver disease:
consumption of ethanol less than 20 g/day for women and 30 g/day for men[26]

Most individuals are asymptomatic and are usually discovered incidentally because of abnormal liver function tests or hepatomegaly noted in unrelated medical conditions. Elevated liver enzymes are found in as many as 50% of patients with simple steatosis.[27]: 1794  The serum alanine transaminase (ALT) level usually is greater than the aspartate transaminase (AST) level in the nonalcoholic variant and the opposite in alcoholic FLD (AST:ALT more than 2:1). Simple blood tests may help to determine the magnitude of the disease by assessing the degree of liver fibrosis.[28] For example, AST-to-platelets ratio index (APRI score) and several other scores, calculated from the results of blood tests, can detect the degree of liver fibrosis and predict the future formation of liver cancer.[29]

Imaging studies are often obtained during the evaluation process.

computed tomography (CT), and fat appears bright in T1-weighted magnetic resonance images (MRIs). Magnetic resonance elastography, a variant of magnetic resonance imaging, is investigated as a non-invasive method to diagnose fibrosis progression.[32] Histological diagnosis by liver biopsy is the most accurate measure of fibrosis and liver fat progression as of 2018.[8] Conventional imaging methods, such as ultrasound, CT and MRI, are not specific enough to detect fatty liver disease unless fat occupies at least 30% of the liver volume.[33]

Treatment

Decreasing caloric intake by at least 30% or by approximately 750–1,000 kcal/day results in improvement in hepatic steatosis.

NAFLD or NASH, weight loss via a combination of diet and exercise was shown to improve or resolve the disease.[8] In more serious cases, medications that decrease insulin resistance, hyperlipidemia, and those that induce weight loss such as bariatric surgery as well as vitamin E have been shown to improve or resolve liver function.[8][15]

Bariatric surgery, while not recommended in 2017 as a treatment for FLD alone, has been shown to revert FLD, NAFLD, NASH and advanced steatohepatitis in over 90% of people who have undergone this surgery for the treatment of obesity.[8][34]

In the case of long-term total-parenteral-nutrition-induced fatty liver disease, choline has been shown to alleviate symptoms.[35][36][37] This may be due to a deficiency in the methionine cycle.[38]

Epidemiology

NAFLD affects about 30% of people in Western countries and 10% of people in Asia.[2] In the United States rates are around 35% with about 7% having the severe form NASH.

liver function tests in the United States.[14] Fatty liver is more prevalent in Hispanic people than white, with black people having the lowest prevalence.[10]

In the study

transient elastography found over 20% to have the fatty deposits on the liver, indicating non-alcoholic fatty liver disease; half of those were classified as severe. The scans also found that 2.4% had a degree of liver fibrosis, which can lead to cirrhosis.[41][42]

After the

lockdown of the COVID-19 pandemic, a study demonstrated that 48% of patients with liver steatosis gained weight, while 16% had a worsened steatosis grade. Weight gain was associated with poor adherence to the suggested diet, reduced levels of physical activity, and increased prevalence of homozygosity for the PNPLA3 rs738409 single nucleotide polymorphism.[43] PNPLA3 rs738409 is already a known risk factor for NAFLD.[44][45]

In animals

Fatty liver disease can occur in pets such as reptiles (particularly

gavage in geese or ducks to produce foie gras. Fatty liver can also be induced in ruminants such as sheep by a high-caloric diet.[49][50]

References

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  31. ^ Costantino A, Piagnani A, Caccia R, Sorge A, Maggioni M, Perbellini R, Donato F, D'Ambrosio R, Sed NPO, Valenti L, Prati D, Vecchi M, Lampertico P, Fraquelli M. Reproducibility and accuracy of a pocket-size ultrasound device in assessing liver steatosis. Dig Liver Dis. 2023 Nov 27:S1590-8658(23)01032-0. doi: 10.1016/j.dld.2023.11.014. Epub ahead of print. PMID 38016894.
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  42. ^ SPINK HEALTH (11 April 2019). "Nonalcoholic fatty liver disease found in large numbers of teenagers and young adults". EurekAlert! (Press release). American Association for the Advancement of Science. Retrieved 4 July 2023.
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  44. ^ Liu, Y.L.; Patman, G.L.; Leathart, J.B.; Piguet, A.C.; Burt, A.D.; Dufour, J.F.; Day, C.P.; Daly, A.K.; Reeves, H.L.; Anstee, Q.M. Carriage of the PNPLA3 rs738409 C >G polymorphism confers an increased risk of non-alcoholic fatty liver disease associated hepatocellular carcinoma. J. Hepatol. 2014, 61, 75–81.
  45. ^ Eslam, M.; Valenti, L.; Romeo, S. Genetics and epigenetics of NAFLD and NASH: Clinical impact. J. Hepatol. 2018, 68, 268–279.
  46. ^ Lock B (8 August 2017). "Hepatic Lipidosis (Fatty Liver Disease) in Reptiles". Vin.com. Retrieved 29 December 2020.
  47. ^ "Fatty Liver Disease in Birds". Animal House of Chicago. Retrieved 29 December 2020.
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External links
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