Metabolic dysfunction associated steatotic liver disease

Changed by Daniel J Bell, 30 May 2022
Disclosures - updated 3 May 2022: Nothing to disclose

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Non-alcoholic fatty liver disease (NAFLD), also known as metabolic associated fatty liver disease(MAFLD), occurs when fat is deposited into hepatocytes without a known cause (such as with alcoholic fatty liver disease). The deposition of fat may lead to hepatic inflammation (hepatitis) and mayeven eventually lead to cirrhosis.

Terminology

Non-alcoholic fatty liver disease (NAFLD) is differentiateddivided by some into:

  • non-alcoholic fatty liver (NAFL)
    • signs of hepatic inflammation are absent
  • non-alcoholic steatohepatitis (NASH)
    • signs of hepatic inflammation are present

Epidemiology

NAFLDNon-alcoholic fatty liver disease has a prevalence of ~30% (range 10-46%) in the U.S. 2 and a prevalence worldwide of ~ 20% (range 6-35%) 3. NASHNon-alcoholic steatohepatitis has a prevalence of 3-5% 3. It is common in children, with a prevalence of 10% 5. It is more commonly seen at ages 40-60 ref. No gender predominance has been noted ref.

Clinical presentation

Often asymptomatic, although vague abdominal pain has been reported. HepatomegalyHepatomegaly has been reported in a minority of patients. Elevated liver enzymes (such as AST/ALT) may be present, especially with NASHnon-alcoholic steatohepatitis

Pathology

By definition, hepatic steatosis is present when 5% of the weight of the liver is intrahepatic fat 6

The pathogenesis of NAFLDnon-alcoholic fatty liver disease is not well understood, but it has been associated with dysmetabolic conditions:

Radiographic features

The role of imaging is to demonstrate fat deposition in the liver, determine if cirrhotic changes are present, and to exclude other possible diagnoses. For general features of fatty deposition in the liver, see diffuse hepatic steatosis.

Liver biopsy may be needed in indeterminate situations to establish the diagnosis.

Ultrasound
CT
  • diffuse hypoattenuation of the liver relative to the spleen
    • non-contrast liver attenuation of <40 HU is specific, but not sensitive for diffuse hepatic steatosis
MRI
  • IP/OP: drop in signal intensity in liver on the out-of-phase sequence, compatible with intracellular lipid deposition

Treatment and prognosis

No definitive treatment has been established for NAFLDnon-alcoholic fatty liver disease, but weight loss is thought to eliminate one of the factors contributing to the condition.

Patients who develop cirrhosis from NASHnon-alcoholic steatohepatitis are treated similarly to other patients with cirrhosis.

Differential diagnosis

See also

  • -<p><strong>Non-alcoholic fatty liver disease (NAFLD)</strong>, also known as <strong>metabolic associated fatty liver disease</strong> <strong>(MAFLD)</strong>, occurs when fat is deposited into hepatocytes without a known cause (such as with alcoholic fatty liver disease). The deposition of fat may lead to hepatic inflammation (hepatitis) and may eventually lead to <a href="/articles/cirrhosis">cirrhosis</a>.</p><h4>Terminology</h4><p>Non-alcoholic fatty liver disease (NAFLD) is differentiated by some into:</p><ul>
  • +<p><strong>Non-alcoholic fatty liver disease (NAFLD)</strong>, also known as <strong>metabolic associated fatty liver disease</strong>, occurs when fat is deposited into hepatocytes without a known cause (such as with <a href="/articles/alcoholic-fatty-liver-disease">alcoholic fatty liver disease</a>). The deposition of fat may lead to hepatic inflammation (hepatitis) and even eventually to <a href="/articles/cirrhosis">cirrhosis</a>.</p><h4>Terminology</h4><p>Non-alcoholic fatty liver disease (NAFLD) is divided by some into:</p><ul>
  • -</ul><h4>Epidemiology</h4><p>NAFLD has a prevalence of ~30% (range 10-46%) in the U.S. <sup>2</sup> and a prevalence worldwide of ~ 20% (range 6-35%) <sup>3</sup>. NASH has a prevalence of 3-5% <sup>3</sup>. It is common in children, with a prevalence of 10% <sup>5</sup>. It is more commonly seen at ages 40-60 <sup>ref</sup>. No gender predominance has been noted <sup>ref</sup>.</p><h4>Clinical presentation</h4><p>Often asymptomatic, although vague abdominal pain has been reported. Hepatomegaly has been reported in a minority of patients. Elevated liver enzymes (such as AST/ALT) may be present, especially with NASH. </p><h4>Pathology</h4><p>The pathogenesis of NAFLD is not well understood, but it has been associated with dysmetabolic conditions:</p><ul>
  • +</ul><h4>Epidemiology</h4><p>Non-alcoholic fatty liver disease has a prevalence of ~30% (range 10-46%) in the U.S. <sup>2</sup> and a prevalence worldwide of ~ 20% (range 6-35%) <sup>3</sup>. Non-alcoholic steatohepatitis has a prevalence of 3-5% <sup>3</sup>. It is common in children, with a prevalence of 10% <sup>5</sup>. It is more commonly seen at ages 40-60 <sup>ref</sup>. No gender predominance has been noted <sup>ref</sup>.</p><h4>Clinical presentation</h4><p>Often asymptomatic, although vague abdominal pain has been reported. <a href="/articles/hepatomegaly">Hepatomegaly</a> has been reported in a minority of patients. Elevated liver enzymes (such as AST/ALT) may be present, especially with non-alcoholic steatohepatitis. </p><h4>Pathology</h4><p>By definition, hepatic steatosis is present when 5% of the weight of the liver is intrahepatic fat <sup>6</sup>. </p><p>The pathogenesis of non-alcoholic fatty liver disease is not well understood, but it has been associated with dysmetabolic conditions:</p><ul>
  • -<li>dyslipidaemia</li>
  • -<li>hypothyroidism</li>
  • +<li><a href="/articles/dyslipidaemia">dyslipidaemia</a></li>
  • +<li><a href="/articles/hypothyroidism">hypothyroidism</a></li>
  • -</ul><h5>CT</h5><ul><li>diffuse hypoattenuation of the liver relative to the spleen<ul><li>non-contrast liver attenuation of &lt;40 HU is specific, but not sensitive for diffuse hepatic steatosis</li></ul>
  • +</ul><h5>CT</h5><ul><li>diffuse hypoattenuation of the liver relative to the spleen<ul><li>non-contrast liver attenuation of &lt;40 <a href="/articles/hounsfield-unit">HU</a> is specific, but not sensitive for diffuse hepatic steatosis</li></ul>
  • -<a href="/articles/in-phase-and-out-of-phase-sequences-1"><strong>IP/OP</strong></a>: drop in signal intensity in liver on the out-of-phase sequence, compatible with intracellular lipid deposition</li></ul><h4>Treatment and prognosis</h4><p>No definitive treatment has been established for NAFLD, but weight loss is thought to eliminate one of the factors contributing to the condition.</p><p>Patients who develop cirrhosis from NASH are treated similarly to other patients with cirrhosis.</p><h4>Differential diagnosis</h4><ul>
  • +<a href="/articles/in-phase-and-out-of-phase-sequences-1">IP/OP</a>: drop in signal intensity in liver on the out-of-phase sequence, compatible with intracellular lipid deposition</li></ul><h4>Treatment and prognosis</h4><p>No definitive treatment has been established for non-alcoholic fatty liver disease, but weight loss is thought to eliminate one of the factors contributing to the condition.</p><p>Patients who develop cirrhosis from non-alcoholic steatohepatitis are treated similarly to other patients with cirrhosis.</p><h4>Differential diagnosis</h4><ul>

References changed:

  • 6. Nassir F, Rector R, Hammoud G, Ibdah J. Pathogenesis and Prevention of Hepatic Steatosis. Gastroenterol Hepatol (N Y). 2015;11(3):167-75. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4836586">PMC4836586</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/27099587">Pubmed</a>

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Nonalcoholic steatohepatitis (NASH)

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NASH (liver disease)

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NAFLD (liver disease)

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Title was changed:
NAFL (liver disease)

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