Nonalcoholic Fatty Liver

Aka: Nonalcoholic Fatty Liver, Nonalcoholic Steatohepatitis, Idiopathic Fatty Liver, Steatosis, Steatohepatitis, Steatotic Liver Disease, Fatty Liver, NASH, Nonalcoholic Fatty Liver Disease, NAFLD, Metabolic Dysfunction Associated Steatotic Liver Disease, MASLD, MASLD and Increased Alcohol Intake, MetALD

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II. Definitions

  1. Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD)
    1. Previously known as Nonalcoholic Fatty Liver Disease (NAFLD)
    2. Spectrum of disorders of liver fat infiltration not due to Alcohol, medication or hereditary disorder
    3. Severity ranges from Steatosis to severe fibrosis (MASH or NASH)
    4. For brevity, this outline uses NAFLD/MASLD and NASH/MASH interchangeably (esp. when spelled out)
      1. Nonalcoholic Fatty Liver Disease is far shorter than the "new and improved" MASLD terms

III. Epidemiology

  1. Most common cause of liver disease in western countries
    1. MASLD Prevalence: 10-30% of U.S. population (17% in Framingham study)
    2. Nonalcoholic Steatohepatitis (NASH/MASH) accounts for up to one third of MASLD cases
      1. Occurs in up to 3-5% of the U.S. population
      2. Affects up to 66% of age >50 years with Obesity or Diabetes Mellitus
      3. Risk of Liver Fibrosis, Cirrhosis and Hepatocellular Carcinoma
  2. Frequent cause of mild Liver Function Test Abnormality
    1. Most common cause of mildly abnormal ALT and AST in U.S. (accounts for up to 51% of cases)
  3. Most common cause of cryptogenic Cirrhosis (U.S. adult)
    1. By 2030, projected U.S. Prevalence 100 Million cases, will become the top indication for Liver Transplant

IV. Pathophysiology

  1. Energy Intake more than metabolic needs leads to increased free Fatty Acids
    1. Adipose fat storage capacity exceeded drives Insulin Resistance, inflammation and free Fatty Acids
    2. Increased Carbohydrate intake increases lipogenesis, Triglyceride and VLDL increases
  2. Free Fatty Acids lead to lipotoxic agents (e.g. ceramides, diacylglycerols, lysophosphatidic acids)
    1. Results in hepatocyte stress and inflammation (via Oxidants, inflammasomes)
  3. Hepatocyte inflammation, given NASH genetic predispositions, progresses to further hepatic complications
    1. Cirrhosis
    2. Hepatocellular Carcinoma

V. Types

  1. Nonalcoholic Fatty Liver
    1. Definition: >5% hepatic Steatosis without inflammation
    2. Insulin Resistance is a major inciting factor of hepatic Steatosis
    3. Lipotoxicity from free Fatty Acids
  2. Nonalcoholic Steatohepatitis
    1. Definition: >5% hepatic Steatosis with Hepatic Injury and inflammation (and risk of Cirrhosis)
    2. Hepatocyte injury with cell ballooning and inflammation
    3. Inflammatory factors include Cytokines and oxidative stress
    4. Progresses to Hepatic Fibrosis and Cirrhosis, and increased risk of Hepatocellular Carcinoma

VI. Risk Factors: Adults

  1. Obesity
    1. NASH occurs in 30% of patients with Obesity
      1. NASH effects 66% of all obese patients (BMI>30) over age 50 years old
      2. NASH occurs in 90% of patients at BMI>39
    2. Consider screening Liver Biopsy before Bariatric Surgery
      1. Significant fibrosis present in up to 1 in 12 patients undergoing Bariatric Surgery
      2. Cirrhosis in up to 1 in 25 patients undergoing Bariatric Surgery
  2. Hyperglycemia (75% of NASH patients)
    1. Metabolic Syndrome
    2. Type II Diabetes Mellitus (33-70% will develop MASLD, 40% MASH and 15% significant fibrosis)
    3. Type I Diabetes Mellitus (<25% of patients have MASLD)
    4. Polycystic Ovary Syndrome
  3. Hyperlipidemia (especially Hypertriglyceridemia)
    1. More than half of those with Hyperlipidemia will develop MASLD
    2. High Triglyceride to HDL ratio is associated with up to 78% Prevalence of MASLD
  4. Rapid weight loss
    1. Starvation
    2. Gastric Bypass
  5. Genetic Associations
    1. Patatin-Like Phospholipase Domain-Containing Protein 3 (PNPLA3)
      1. Associated with 2 fold increased risk of MASLD/NAFLD with Hepatic Fibrosis
  6. Refeeding Syndrome
  7. Total Parenteral Nutrition
  8. Older age (Prevalence increases with age)
  9. Hispanic descent
  10. More common in women
  11. Obstructive Sleep Apnea
  12. Hypothyroidism
  13. HIV Infection
  14. Chemotherapeutic Agents
    1. Asparaginase
    2. Cisplatin
    3. Fluorouracil
    4. Irinotecan
    5. Methotrexate
    6. Tamoxifen
  15. Other Medications
    1. Amiodarone
    2. Diltiazem
    3. Antiretroviral Therapy (esp. Protease Inhibitors)
    4. Corticosteroids
    5. Cocaine
    6. Tetracyclines
    7. Valproic Acid
    8. NSAIDs
    9. Aspirin

VII. Risk Factors: Children

  1. Overall NAFLD risk: 1 in 13 children
  2. Obesity (1 in 3 children)
  3. Prediabetes or Type 2 Diabetes Mellitus (50% of children)
  4. Polycystic Ovarian Syndrome (teen biologic females)

VIII. Symptoms

  1. Asymptomatic in most cases
  2. Fatigue
  3. Malaise
  4. Right upper quadrant pain

IX. Signs

  1. Hepatomegaly (50%)

X. Differential Diagnosis

  1. See Liver Function Test Abnormality
  2. Comorbid second diagnosis (in addition to NASH) is found in 18% of cases
  3. Viral Hepatitis (Hepatitis B, Hepatitis C)
  4. Alcoholic Hepatitis
  5. Hepatotoxins (e.g. Methotrexate, Corticosteroids, TPN)
  6. Autoimmune Hepatitis
  7. Hereditary Hemochromatosis
  8. Wilson Disease
  9. Alpha-1-Antitrypsin Deficiency
  10. Rapid weight loss
  11. Celiac Disease
  12. Diabetes Mellitus
  13. Panhypopituitarism

XI. Labs: Liver specific (first-line)

  1. Precautions
    1. Routine NAFLD screening for those at risk is not recommended in U.S.
    2. Liver Function Tests and Hepatic Ultrasound have insufficient NAFLD Test Sensitivity for screening
  2. Liver Transaminases (ALT, AST)
    1. Normal in some cases
    2. Typically 2-3 fold increase in transaminases
      1. If over 1000 consider other cause
        1. Viral Hepatitis
        2. Hepatotoxin exposure
    3. AST/ALT ratio <0.8 (not true in late disease)
      1. If AST exceeds ALT, consider Alcoholic Hepatitis
  3. Alkaline Phosphatase may be increased up to 2 fold
  4. Gamma-Glutamyltransferase (GGT) increased in some cases
    1. If over 2 times normal consider Alcoholic Hepatitis
  5. Cirrhosis screening (includes Liver synthetic function)
    1. Serum Bilirubin
    2. Serum Albumin
    3. Prothrombin Time

XII. Labs: Secondary causes - common

  1. See Liver Function Test Abnormality
  2. Metabolic Syndrome and other causes of lipid abnormalities
    1. Hemoglobin A1C
    2. Fasting Glucose
    3. Lipid profile with Fasting Serum Triglycerides, LDL Cholesterol and HDL Cholesterol
    4. Thyroid Stimulating Hormone
  3. Viral Hepatitis
    1. Hepatitis B Surface Antigen (HBsAg)
    2. Hepatitis C Virus Antibody (xHCV)
  4. Hemochromatosis (Bronze Diabetes with Arthritis, Heart Failure, Family History)
    1. Serum Ferritin
    2. Serum Iron
    3. Transferrin Saturation
    4. Complete Blood Count
    5. Consider HemochromatosisGenetic Testing (HFE)

XIII. Labs: Secondary causes - uncommon (consider if other testing negative)

  1. Autoimmune Hepatitis (esp. women, history of Thyroid disease)
    1. Antinuclear Antibody
    2. Smooth Muscle Antibody
    3. Consider liver and Kidney microsomal antibodies
  2. Alpha-1-Antitrypsin Deficiency
    1. Alpha-1-Antitrypsin total level
    2. Alpha-1-Antitrypsin Phenotype
  3. Wilson Disease (consider in <40 years old, with liver disease or neuropsychiatric disorder, Family History)
    1. Ceruplasmin
    2. Consider 24 hour urinary Copper

XIV. Imaging

  1. Right upper quadrant Ultrasound (Preferred first-line)
    1. Finding
      1. Increased liver echoes (fatty infiltrates)
    2. Disadvantages
      1. Does not determine disease severity
      2. Fibrosis and Steatosis are indistinguishable on Ultrasound
    3. Efficacy
      1. Test Sensitivity: 82-89% (increases with greater fat infiltration)
      2. Test Specificity: 93%
        1. False Positive Rate in some studies as high as 15% (leading to an overdiagnosis of NAFLD)
        2. Rowe (2018) Lancet Gastroenterol Hepatol 3(1): 66-72 [PubMed]
  2. CT Abdomen (unenhanced)
    1. Precautions
      1. CT with contrast decreases the Test Specificity compared to unenhanced CT
    2. Advantages
      1. Better sensitivity than Ultrasound
      2. Better identification of other liver abnormalities
    3. Disadvantages
      1. CT-associated Radiation Exposure
      2. Higher cost than Ultrasound
    4. Efficacy
      1. Test Sensitivity: 88-95%
      2. Test Specificity: 90-99%
  3. MRI Abdomen with elastography
    1. Advantages
      1. Highest accuracy
    2. Disadvantages
      1. Expensive
    3. Efficacy: Steatosis
      1. Test Sensitivity: 96%
      2. Test Specificity: 93%
    4. Efficacy: Fibrosis
      1. Test Sensitivity: 94%
      2. Test Specificity: 73%

XV. Diagnosis: Noninvasive Tests for Advanced Fibrosis in NAFLD patients

  1. Lab findings (insufficient alone for NAFLD or NASH diagnosis)
    1. AST/ALT ratio (AAR)
      1. Score 0.8 or higher is suggestive of NAFLD with advanced fibrosis (Test Sensitivity: 74%, Test Specificity: 78%)
      2. Alternatively, Alcoholic Hepatitis also presents with AST > ALT
    2. AST/Platelet Count ratio index (APRI)
      1. AST/Platelet Count ratio index <0.3 to 0.5 excludes significant Liver Fibrosis or Cirrhosis
      2. AST/Platelet Count ratio index >1.5 rules in significant Liver Fibrosis or Cirrhosis
      3. Loaeza-del-Castillo (2008) Ann Hepatol 7(4):350-7 [PubMed]
  2. NAFLD Fibrosis Score (preferred)
    1. https://www.mdcalc.com/calc/3081/nafld-non-alcoholic-fatty-liver-disease-fibrosis-score
    2. Liver Fibrosis risk based on age, Hyperglycemia, BMI, Platelet Count, Serum Albumin, AST, ALT
    3. Score <-1.455 excludes advanced fibrosis while score >0.675 suggests advanced Liver Fibrosis (90% Test Sensitivity)
    4. Consider MR Elastography or Fibroscan for Fibrosis Score >-1.455
    5. Angulo (2007) Hepatology 45(4):846-54 [PubMed]
  3. Fibrosis Probability Score (FIB-4 Index, preferred)
    1. https://www.hepatitisc.uw.edu/page/clinical-calculators/fib-4
    2. Clinical score based on age, Platelet Count, AST and ALT
    3. Efficacy: Test Sensitivity: 85%, Test Specificity: 65% (high Negative Predictive Value, low Positive Predictive Value)
    4. Score <1.45 excludes advanced fibrosis while score >3.25 suggests advanced Liver Fibrosis
    5. Consider MR Elastography (or Fibroscan) for Fibrosis Probability Score >1.45
  4. Magnetic Resonance Elastography (MR Elastography)
    1. MR Elastography score > 3.62 kPa is suggestive of advanced fibrosis
    2. Preferred if BMI >36.65 kg/m2
  5. Vibration-Controlled Transient Elastography (Fibroscan)
    1. MR Elastography is preferred (more accurate, but less available)
    2. Imaging study with high sensitivity for even mild Liver Fibrosis
    3. May be limited by operator experience and morbidly obese
    4. Fibroscan > 9.9 kPa is suggestive of advanced fibrosis
    5. Myers (2012) Hepatology 55(1): 199-208 [PubMed]
  6. Alcoholic Liver Disease to NAFLD Index
    1. Used to distinguish Alcoholic Liver Disease from NAFLD (based on ALT, AST, MCV, height, weight, gender)
    2. https://www.mayoclinic.org/medical-professionals/model-end-stage-liver-disease/alcoholic-liver-disease-nonalcoholic-fatty-liver-disease-index
  7. BARD Score
    1. Score <2 has a strong Negative Predictive Value (90-97%) for NAFLD with fibrosis
  8. HAIR Score
    1. Severely obese (BMI >35 kg/m2) patient assessment for risk of Nonalcoholic Steatohepatitis (NASH)
    2. Assign one point each for Hypertension, elevated ALT, Insulin Resistance
    3. Score 2 or 3 predicts progressive liver injury
  9. NASHnext (NIS4 Algorithm)
    1. Proprietary test assigns composite score based on 4 markers (miR34a, a2M, YKL-40/CHI3L1 and Hemoglobin A1C)
    2. High risk NASH or advanced fibrosis predicted by score of 0.36 to 0.63 (moderate) or >0.63 (high risk)
    3. Only industry funded studies are available (needs further validation for significant clinical use)
    4. Hoffman and Chandler (2023) Am Fam Physician 108(4): 408-10 [PubMed]
  10. Other tests
    1. See MRI Abdomen with elastography above
    2. Enhanced Liver Fibrosis panel (Test Sensitivity and Test Specificity approach 100%)
    3. FibroTest or FibroSure (Test Sensitivity: 15%, Test Specificity: 98%)
    4. Fibrometer (Test Sensitivity: 79%, Test Specificity: 96%)

XVI. Diagnosis: Liver Biopsy

  1. Non-invasive tests listed above are preferred (see complications)
  2. Indications
    1. Liver Disease etiology is unclear (distinguish NASH from conditions listed below)
    2. Increased risk of NASH or advanced fibrosis
  3. Grades degree of fatty infiltration
    1. Hepatic Steatosis (fat accumulation in liver)
      1. Intracellular fat in >5% of hepatocytes
    2. Nonalcoholic Steatohepatitis (Steatosis AND liver cell injury and inflammation)
      1. Hepatocyte ballooning
      2. Mallory hyaline
      3. Perivenular inflammatory infiltrate (Lymphocytes, Neutrophils)
      4. Hepatocyte necrosis and apoptosis
      5. Hepatocyte fibrosis may be present
  4. Distinguishes NASH from other causes of liver injury and inflammation
    1. Autoimmune Hepatitis
    2. Alpha-1-Antitrypsin Deficiency
    3. Alpha-1-Antitrypsin
    4. Hemochromatosis
    5. Wilson Disease
  5. Complications of liver biopsy occur in >6% of patients
    1. Major Bleeding (4.5%)
    2. Death (1.6%)

XVII. Evaluation: Initial

  1. History and exam
    1. Consider comorbid history
      1. Premature COPD in Alpha-1 Antitrypsin Deficiency
      2. Obesity
        1. Calculate Body Mass Index (BMI)
        2. Measure Waist Circumference
    2. Consider differential diagnosis (see above)
      1. Alcoholic Hepatitis
        1. Ask about excessive Alcohol use
      2. Hepatoxic Medication
      3. Viral Hepatitis
    3. Consider Family History
      1. Hemochromatosis
      2. Wilson Disease
    4. Evaluate for likelihood of NASH
      1. Diabetes Mellitus or Metabolic Syndrome
      2. Body Mass Index
      3. Waist Circumference
  2. Labs
    1. Start with liver specific first-line labs and common secondary cause labs above
    2. Consider uncommon secondary cause labs as above (based on history, risk factors)
  3. Diagnostics
    1. Consider liver imaging (e.g. RUQ Ultrasound)

XVIII. Management: Approach

  1. Step 1: Initial
    1. Confirm likelihood of NASH as underlying cause
    2. Start with initial evaluation as above
      1. Confirm Liver Function Test Abnormality
      2. Consider RUQ Ultrasound
    3. Institute lifestyle change (e.g. weight loss, Healthy Diet, Exercise, hyperlidemia management)
      1. See Interventions below
  2. Step 2: Month 6 (following lifestyle change)
    1. Repeat Liver Function Tests
    2. If Abnormal Liver Function Testing
      1. Consider liver imaging (RUQ Ultrasound) if not already done
  3. Step 3: Evaluate with noninvasive tests for Liver Fibrosis (see above)
    1. Perform scoring
      1. NAFLD Fibrosis Score (abnormal >-1.455) or
      2. Fibrosis Probability Score or FIB-4 Index (abnormal >1.45)
    2. Obtain Elastography Imaging if either score is abnormal
      1. Magnetic Resonance Elastography (MR Elastography, preferred if BMI>36)
        1. MR Elastography score > 3.62 kPa is suggestive of advanced fibrosis
      2. Vibration-Controlled Transient Elastography (Fibroscan)
        1. Fibroscan > 9.9 kPa is suggestive of advanced fibrosis
  4. Step 4: Gastroenterology referral indications (for evaluation and often liver biopsy)
    1. Noninvasive tests and inmaging suggest fibrosis (see Step 3)
    2. Persistently elevated Liver Function Tests despite interventions
    3. Suspected secondary cause of Steatosis other than NASH (e.g. Hemochromatosis, Autoimmune Hepatitis)
  5. Step 5: Monitoring
    1. Repeat liver transaminases at least every 2 years for those with hepatic Steatosis on imaging

XIX. Management: Interventions

  1. See Prevention of Liver Disease Progression
  2. Weight Reduction
    1. Single most effective and important intervention
    2. Liver Function Tests improve or normalize with as little as 5-10% weight loss
      1. Hepatic Steatosis improves with 3-5% weight loss
      2. NAFLD histopathologic changes improve with 7-10% weight loss
    3. Fibrosis may not improve after weight loss
    4. Low to moderate fat intake and low Carbohydrate
      1. Avoid high fructose corn syrup (beverages, foods)
      2. Consider Mediterranean Diet
        1. Zeiber-Sagi (2017) Liver Int 37(7): 936-49 [PubMed]
    5. Physical Activity 150 to 200 minutes of moderate to vigorous Exercise
    6. Consider Obesity Medications (e.g. GLP1 Agonists such as Semaglutide)
    7. Consider Bariatric Surgery
      1. NASH resolved in 85% of 109 patients in one study
      2. However, fibrosis may worsen in up to 1 in 8 patients undergoing Bariatric Surgery
        1. Benefits may be outweighed if Cirrhosis or stage 3 fibrosis is present
      3. Lassailly (2015) Gastroenterology 149(2): 379-88 [PubMed]
  3. Avoid Hepatotoxins
    1. Restrict Alcohol intake (2 standard drinks/day for men, 1/day for women)
    2. Eliminate Hepatotoxins
  4. Maximize Glucose control
    1. Conditions
      1. Type II Diabetes Mellitus
      2. Metabolic Syndrome
    2. Medications: Glucophage (Metformin)
      1. Recommended in Type II Diabetes
      2. Previously recommended to reduce transaminases and Steatosis in non-diabetics
        1. However, subsequent studies find no associated improvement in liver histology
    3. Medications: GLP-1 Agonist or Incretin Mimetic (Liraglutide or Semaglutide)
      1. Appears to improve NASH and very effective in assisting weight loss in Obesity
      2. May also be considered in non-diabetic patients
    4. Medications: Glitazones
      1. Pioglitazone up to 30 mg orally daily
      2. Glitazones may be used if AST amd ALT <3x normal
      3. Monitor AST and ALT every 3 months
      4. Reduces transaminases, Steatosis in non-diabetics
        1. However, Glitazones also increase weight
        2. Not recommended in non-diabetics without biopsy proven NAFLD
  5. Lipid Reduction as needed with AntiHyperlipidemic
    1. AntiHyperlipidemic may be used if AST,ALT <3x normal
    2. Monitor AST and ALT every 3 months
    3. Statins (preferred) decrease transaminases, Steatosis
      1. Discontinue Statin if liver enzymes increase 2 fold at 3 months after starting medication
    4. Mixed results with Ursodeoxycholic Acid
  6. Control Hypertension
    1. Angiotensin Receptor Blockers
  7. Supplements that may offer benefit
    1. L-Carnitine
    2. Vitamin E 800 IU/day (variable efficacy, risk of Prostate Cancer, Hemorrhagic CVA)
    3. Avoid Milk Thistle (ineffective)
    4. Omega-3 Fatty Acids have not been found effective in NAFLD
    5. Vitamin D Supplementation has not been found effective
  8. Refractory Cases with Fibrosis (medications employed by liver specialists)
    1. Resmetirom (Rezdiffra)
  9. References
    1. Musso (2010) Hepatology 52(1): 79-104 [PubMed]

XX. Prognosis

  1. Nonalcoholic Fatty Liver (Hepatic Steatosis without inflammation)
    1. Rare progression to Cirrhosis
    2. However NAFLD overall is associated with increased cardiovascular mortality risk
  2. Nonalcoholic Steatohepatitis (5% of general population, up to 66% of age >50 years with Diabetes Mellitus, Obesity)
    1. Hepatocellular Carcinoma: 1-5% risk
    2. Cirrhosis risk: 20% overall
      1. Advanced fibrosis in 15-30% of cases
      2. Advanced fibrosis progresses to Cirrhosis in 12-35%

XXI. Complications

  1. Portal Hypertension
  2. Cirrhosis if associated with severe comorbid condition
    1. Morbid Obesity (BMI >30)
    2. Type II Diabetes Mellitus
    3. AST to ALT ratio >1
  3. Coronary Artery Disease
    1. Results in greatest morbidity
    2. Treat underlying Hyperlipidemia
  4. Diabetic Retinopathy
    1. Associated with increased Incidence in those with NAFLD and Diabetes Mellitus

XXII. References

  1. Angulo (2002) N Engl J Med 346:1221-31 [PubMed]
  2. Bayard (2006) Am Fam Physician 73:1961-68 [PubMed]
  3. Careyva (2016) Am Fam Physician 94(12): 980-6 [PubMed]
  4. Chalasani (2018) Hepatology 67(1): 328-57 [PubMed]
  5. Kumar (2000) Mayo Clin Proc 75:733-9 [PubMed]
  6. Musso (2017) JAMA Intern Med 177(5): 633-40 [PubMed]
  7. Oh (2017) Am Fam Physician 96(11): 709-15 [PubMed]
  8. Sanyal (2002) Gastroenterology 123:1705-25 [PubMed]
  9. Westfall (2020) Am Fam Physician 102(10): 603-12 [PubMed]
  10. Wilkins (2013) Am Fam Physician 88(1): 35-42 [PubMed]

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Related Studies

Ontology: Fatty Liver (C0015695)

Definition (MSHCZE) steatóza jater – nahromadění tuku v jaterních buňkách, časté při obezitě, alkoholismu, hyperlipoproteinemii, diabetu, těžké malnutrici; akutně u některých intoxikací, Reyově syndromu aj. Játra bývají zvětšená; s. je možné diagnostikovat morfologicky, je patrná i při sonografii (zvýšená echogenita při výraznějším postižení), bývají větš. změny jaterních testů vč. alkalické fosfatázy. Mikroskopicky se rozlišuje častější velkokapénková a malokapénková forma. (cit. Velký lékařský slovník online, 2013 http://lekarske.slovniky.cz/ )
Definition (MSH) Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.
Definition (CSP) yellow discoloration of the liver due to fatty degeneration of liver parenchymal cells.
Concepts Disease or Syndrome (T047)
MSH D005234
SnomedCT 197321007, 390002007, 5360002, 371330000
English Liver, Fatty, LIVER FATTY, LIVER FATTY CHANGE, LIVER FATTY DEGENERATION, LIVER FATTY INFILTRATION, LIVER FATTY METAMORPHOSIS, Fatty change of liver, Fatty infiltration of liver, Fatty changes in liver, Fatty Liver, fatty liver, fatty liver (diagnosis), Liver fatty change, Degeneration fatty liver, Liver fatty degeneration, Fatty liver infiltration, Infiltration fatty liver, Liver fatty infiltration, Liver fatty, Fatty liver metamorphosis, Liver fatty metamorphosis, Metamorphosis fatty liver, Hepatic lipidosis, Fatty liver, Fatty Liver [Disease/Finding], fatty livers, hepatic lipidosis, changes fatty liver, liver steatosis, fatty infiltration liver, change fatty liver, fatty liver metamorphosis, liver fatty change, liver fatty infiltration, hepatic steatosis, steatosis of liver, fatty liver infiltration, fatty change liver, Fatty change of liver (disorder), Fatty liver (disorder), Lipidosis of liver, degeneration; fatty, liver, degeneration; liver, fatty, fat; liver, fatty; degeneration liver, fatty; liver degeneration, infiltrate; liver, fatty, liver; degeneration, fatty, liver; fat, liver; infiltrate, fatty, hepatitic steatosis
French STEATOSE HEPATIQUE, Dégénérescence graisseuse du foie, Stéatose par infiltration, Infiltration graisseuse du foie, Stéatose avec métamorphose, Stéatose par infiltration graisseuse, Altération de la stéatose du foie, DEGENERESCENCE GRAISSEUSE DU FOIE, INFILTRATION GRAISSEUSE DU FOIE, METAMORPHOSE GRAISSEUSE DU FOIE, TRANSFORMATION GRAISSEUSE DU FOIE, Stéatose hépatique, Stéatose du foie
Spanish HIGADO GRASO, Hígado graso, Metamorfosis grasa de hígado, Transformación grasa de hígado, Infiltración grasa de hígado, Degeneración grasa del hígado, HIGADO, CAMBIO GRASO, HIGADO, INFILTRACION GRASA, HIGADO, METAMORFOSIS GRASA, hígado graso, lipidosis hepática, hígado graso (trastorno), Hígado Graso
German FETTLEBER, Leber, Verfettung, Infiltration, Fettleber, fettige Infiltration der Leber, Metamorphose, Fettleber, Leber, fettige Metamorphose, fettige Degeneration der Leber, fettige Metamorphose der Leber, Leber, fettige Degeneration, Leber, fettige Infiltration, LEBER FETTIGE DEGENERAT, LEBER FETTIGE INFILTRAT, LEBER FETTIGER UMBAU, LEBERSTEATOSE, Fettleber
Dutch leververvetting, leververvettingsverandering, vette lever infiltratie, leververvetting infiltratie, infiltratie van leververvetting, leververvettingsdegeneratie, leververvetting metamorfose, degeneratie vette lever, vette lever, vette lever metamorfose, metamorfose vette lever, degeneratie; lever, vettig, degeneratie; vettig, lever, infiltraat; lever, vettig, lever; degeneratie, vettig, lever; infiltraat, vettig, lever; vet, vet; lever, vettig; degeneratie lever, vettig; leverdegeneratie, Leversteatose, Leververvetting, Vetlever
Italian Infiltrazione grassa del fegato, Metamorfosi grassa del fegato, Trasformazione grassa del fegato, Degenerazione adiposa del fegato, Trasformazione adiposa del fegato, Infiltrazione lipidica epatica, Degenerazione grassa del fegato, Steatosi epatica
Portuguese Degenerescência gorda do fígado, Metamorfose de fígado gordo, Fígado gordo, Alteração gorda do fígado, Infiltração gorda do fígado, Metamorfose gorda do fígado, Infiltração de fígado gordo, Figado gordo, DEGENERESCENCIA GORDA DO FIGADO, GORDURA NO FIGADO, INFILTRACAO LIPIDICA NO FIGADO, METAMORFOSE LIPIDICA DO FIGADO, TRANSFORMACAO LIPIDICA DO FIGADO, Esteatose Hepática, Esteatohepatite, Fígado Gorduroso
Japanese 肝脂肪浸潤, 肝脂肪変性, ｶﾝｼﾎﾞｳﾍﾝｾｲ, ｶﾝｼﾎﾞｳｼﾝｼﾞｭﾝ, ｼﾎﾞｳｶﾝ, 脂肪肝
Swedish Fettlever
Finnish Rasvamaksa
Russian PECHENI ZHIROVAIA DISTROFIIA, ПЕЧЕНИ ЖИРОВАЯ ДИСТРОФИЯ
Czech Hepatální steatóza, Jaterní steatóza, Degenerativní jaterní steatóza, Steatóza jater, ztučnělá játra, ztučnění jater
Polish Stłuszczenie wątroby, Choroba stłuszczeniowa wątroby
Hungarian Zsíros májdegeneratio, máj zsíros átalkulása, Máj zsíros infiltrációja, Zsíros máj metamorphosis, Zsíros máj infiltratio, Máj zsíros elváltozása, Zsíros máj, Zsírmáj, degeneratio adiposa hepatis, Máj zsíros infiltratioja, Máj zsíros metamorphosisa
Norwegian Fettlever
Derived from the NIH UMLS (Unified Medical Language System)

Ontology: Fatty degeneration (C0152254)

Definition (NCI) A morphologic finding indicating intracytoplasmic fat accumulation in the liver parenchyma.
Concepts Pathologic Function (T046)
SnomedCT 190803000, 29185008
English fatty change, fatty degeneration, fatty metamorphosis, steatosis, changes fatty, Fatty Change, Lipoid degeneration, Fatty change, Fatty metamorphosis, Steatosis, Fatty degeneration, Fatty degeneration (morphologic abnormality)
Spanish acumulación grasa intraparenquimatosa, degeneración grasa (anomalía morfológica), degeneración grasa, degeneración lipoidea, esteatosis, metamorfosis grasa
Derived from the NIH UMLS (Unified Medical Language System)

Ontology: Non-alcoholic Fatty Liver Disease (C0400966)

Definition (NCI) A term referring to fatty replacement of the hepatic parenchyma which is not related to alcohol use.
Definition (MSH) Fatty liver finding without excessive ALCOHOL CONSUMPTION.
Concepts Disease or Syndrome (T047)
MSH D065626
ICD10 K76.0
SnomedCT 197315008, 371329005, 5360002
English NAFLD - Nonalcoholic fatty liver disease, nonalcoholic fatty liver, nonalcoholic fatty liver (diagnosis), NAFLD - Nonalcoholic Fatty Liver Disease, Nonalcoholic fatty liver disease (NAFLD), non-alcoholic fatty liver, Nonalcoholic fatty liver disease, Nonalcoholic fatty liver (disorder), Nonalcoholic fatty liver, Liver, Nonalcoholic Fatty, Non-alcoholic Fatty Liver Disease, Fatty Liver, Nonalcoholic, Nonalcoholic Fatty Livers, Fatty Livers, Nonalcoholic, Livers, Nonalcoholic Fatty, Nonalcoholic Fatty Liver, Nonalcoholic Fatty Liver Disease, Non alcoholic Fatty Liver Disease, NAFLD, Non-alcoholic fatty liver, Non-alcoholic fatty liver (disorder)
Spanish esteatohepatitis no alcohólica, Hígado graso no alcohólico, hígado graso no alcohólico, hígado graso no alcohólico (trastorno), esteatosis hepática no alcohólica (trastorno), esteatosis hepática no alcohólica, hígado graso de causa no alcohólica
Czech Nealkoholická jaterní steatóza
Dutch niet-alcoholische leververvetting
French Stéatose hépatique non éthylique
German nicht-alkoholische Fettleber
Hungarian Nem-alkoholos zsírmáj
Italian Steatosi epatica non alcolica
Japanese 非アルコール性脂肪肝, ﾋｱﾙｺｰﾙｾｲｼﾎﾞｳｶﾝ
Portuguese Fígado gordo não alcoólico
Derived from the NIH UMLS (Unified Medical Language System)

Ontology: Steatohepatitis (C2711227)

Definition (MSH) Inflammation of the liver related to lipid accumulation in fatty liver.
Definition (MSHCZE) Mikroskopický obraz steatózy jater se známkami zánětu v periportálních oblastech infiltrace a vznikem lipogranulomů. (cit. Velký lékařský slovník online, 2013 http://lekarske.slovniky.cz/ )
Concepts Disease or Syndrome (T047)
MSH D005234
SnomedCT 442191002, 197321007
Italian Steatosi epatica
Dutch steatose lever, lever; steatose, steatose; lever, hepatische steatose
German Steatosis der Leber, Steatosis hepatis
Portuguese Esteatose hepática, Estenose hepática
Japanese 脂肪肝, ｼﾎﾞｳｶﾝ
English Liver steatosis, hepatic steatosis, Hepatic steatosis, Steatosis hepatic, Steatohepatitis (disorder), Liver Steatosis, Steatohepatitis, Steatosis, Liver, Steatoses, Liver, Steatosis of Liver, Steatohepatitides, Visceral Steatosis, Liver Steatoses, Visceral Steatoses, Steatoses, Visceral, Steatosis, Visceral, Steatosis of liver, Steatosis of liver (disorder), liver; steatosis, steatosis; liver
Czech Jaterní steatóza, steatohepatitida, steatóza jater, jaterní steatóza
Spanish esteatohepatitis, esteatohepatitis (trastorno), esteatosis hepática (trastorno), esteatosis hepática, Esteatosis hepática
French Stéato-hépatite, Stéatose viscérale, Stéatohépatite, Stéatose hépatique
Hungarian Máj steatosis, Steatosis hepatis
Norwegian Leversteatose
Derived from the NIH UMLS (Unified Medical Language System)

Ontology: Nonalcoholic Steatohepatitis (C3241937)

Definition (NCI) Fatty replacement and damage to the hepatocytes not related to alcohol use. It may lead to cirrhosis and liver failure.
Concepts Disease or Syndrome (T047)
MSH D065626
ICD10 K75.81
SnomedCT 442685003
English nonalcoholic steatohepatitis (diagnosis), nonalcoholic steatohepatitis, Nonalcoholic steatohepatitis, NASH - Nonalcoholic steatohepatitis, Nonalcoholic steatohepatitis (disorder), NASH - Nonalcoholic Steatohepatitis, Nonalcoholic steatohepatitis (NASH), Non-alcoholic steatohepatitis, Nonalcoholic Steatohepatitides, Steatohepatitis, Nonalcoholic, Nonalcoholic Steatohepatitis, Steatohepatitides, Nonalcoholic
Spanish esteatohepatitis no alcohólica (trastorno), esteatohepatitis no alcohólica, esteatosis hepática no alcohólica (trastorno), esteatosis hepática no alcohólica, Esteatohepatitis no alcohólica
Czech Nealkoholická steatohepatitida
German nicht-alkoholische Fettleber
Hungarian Nem-alkoholos steatohepatitis
Italian Steatoepatite non alcolica
Japanese 非アルコール性脂肪性肝炎, ﾋｱﾙｺｰﾙｾｲｼﾎﾞｳｾｲｶﾝｴﾝ
Portuguese Esteatose hepática não alcoólica
Dutch niet-alcoholische steatohepatitis
French Stéatose hépatique non alcoolique
Derived from the NIH UMLS (Unified Medical Language System)

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