Lab result explainedLiverLast updated November 8, 2026

AST/ALT ratio (De Ritis ratio): what a ratio above 2, around 1 or below 1 means for your liver

AST/ALT ratio (De Ritis ratio) (AST/ALT) · Calculated from the comprehensive metabolic panel (CMP) or hepatic function panel · reported in A ratio with no units, calculated from AST and ALT in U/L

The AST/ALT ratio, also called the De Ritis ratio after the Italian physician who described it in 1957, is simply your aspartate aminotransferase (AST) result divided by your alanine aminotransferase (ALT) result, both in U/L. It is not a separate test but a pattern read from two enzymes that appear on every comprehensive metabolic panel. In most healthy adults, and in most people with mild liver disease, ALT is a little higher than AST, so the ratio is below 1, typically around 0.8.

The ratio earns its place because different liver diseases damage the liver in different ways. In alcohol-related liver disease, AST usually exceeds ALT, and a ratio above 2 is found in about 70 percent of patients; a ratio above 3 is almost specific for alcohol. In non-alcoholic (metabolic) fatty liver disease, viral hepatitis and most medication injuries, ALT rises more than AST and the ratio stays below 1. As any chronic liver disease progresses to cirrhosis, however, the ratio drifts above 1, which is why it is built into fibrosis calculators such as the NAFLD fibrosis score and the BARD score and why a rising ratio in someone with known fatty liver or hepatitis C is taken seriously.

The ratio only means something when at least one of the enzymes is actually raised. With both AST and ALT in the normal range, a ratio of 1.3 is noise, not cirrhosis. AST also comes from muscle, heart and red blood cells, so a hard workout, a muscle injury, hypothyroidism or a haemolysed sample can push the ratio above 1 or 2 with the liver entirely innocent. Reading it with GGT, platelets, bilirubin, albumin and creatine kinase is what turns a number into a diagnosis.

AST/ALT at a glance

  • What it is: AST divided by ALT, two enzymes released by damaged liver cells; the pattern hints at the cause and stage of liver disease.
  • Typical healthy value: below 1 (about 0.7–1.0), but only interpretable when AST or ALT is above normal (ALT upper limit roughly 29–33 U/L in men, 19–25 in women by ACG criteria; AST about 40).
  • Below 1 with raised enzymes: fatty liver disease, viral hepatitis, medication injury or early chronic liver disease.
  • 1 to 2 with raised enzymes: mixed picture; in fatty liver or hepatitis C a ratio above 1 raises concern for advanced fibrosis or cirrhosis.
  • Above 2 with raised enzymes (AST usually under 300 U/L and GGT high): alcohol-related liver disease; above 3 is highly suggestive. Also seen in muscle injury, heart attack, Wilson's disease and ischaemic liver injury.
  • Next step: check GGT, platelets, albumin, bilirubin, creatine kinase, TSH and viral hepatitis serology, calculate a FIB-4 score, and have an honest conversation about alcohol.

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What AST/ALT measures

AST and ALT are both enzymes that transfer amino groups during amino-acid metabolism and both leak into the blood when liver cells are injured. ALT is found mainly in the cytoplasm of liver cells and in only small amounts elsewhere, so it is the more liver-specific marker. AST exists in two forms, one in the cytoplasm and one inside mitochondria, and is also abundant in heart muscle, skeletal muscle, kidney, brain and red blood cells. ALT has a half-life of about 47 hours and AST of about 17, so after a one-off injury AST falls faster and the ratio drops as the days pass.

The alcohol pattern has three explanations. Alcohol is toxic to mitochondria, releasing the mitochondrial form of AST that other liver injuries largely spare. Heavy drinkers are often deficient in pyridoxal 5'-phosphate (active vitamin B6), a cofactor both enzymes need but ALT depends on more, so ALT production falls and the ratio rises; in one study, ALT activity in alcoholic hepatitis rose when B6 was given. And alcohol injures the zone of the liver lobule around the central vein, where AST is relatively concentrated. The result is a modest AST rise, rarely above 300 U/L, with a proportionally smaller ALT.

The cirrhosis pattern has a different mechanism. As liver cells are replaced by scar, the remaining tissue makes and releases less ALT, while AST, cleared more slowly by damaged sinusoidal cells and still released from mitochondria, holds up better. So the ratio rises from below 1 toward and past 1 as fatty liver or viral hepatitis advances. This is why the ratio contributes to the NAFLD fibrosis score and BARD score, and why the related FIB-4 score (age multiplied by AST, divided by platelet count multiplied by the square root of ALT) is now the recommended first-line test for fibrosis in anyone with fatty liver or metabolic risk factors.

Normal range for AST/ALT

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

GroupTypical range (A ratio with no units, calculated from AST and ALT in U/L)Notes
Healthy adults (both enzymes normal)About 0.7–1.0; often not meaningfulWhen AST and ALT are both within range, the ratio is not interpreted. Lean, older people and women often have AST slightly above ALT with no disease.
Reference values for the componentsALT roughly 7–55 U/L on many labs; AST 8–40 U/LThe American College of Gastroenterology suggests true healthy upper limits of 29–33 U/L for ALT in men and 19–25 in women. Labs differ.
Below 1 with raised enzymesALT higher than ASTTypical of metabolic (non-alcoholic) fatty liver disease, chronic hepatitis B or C, acute viral hepatitis, medication or supplement injury, coeliac disease and haemochromatosis in earlier stages.
1 to 2 with raised enzymesAST modestly higher than ALTMixed or non-specific. In known fatty liver or hepatitis C, a ratio above 1 raises the probability of advanced fibrosis or cirrhosis; in a chronic hepatitis C cohort a ratio of 1 or more had 100 percent specificity for cirrhosis.
Above 2 with raised enzymesAST more than double ALTAlcohol-related liver disease in about 70 percent of cases when AST is under 300 U/L and GGT is raised. Also muscle injury, heart attack, ischaemic hepatitis and cirrhosis of any cause.
Above 3AST more than triple ALTHighly suggestive of alcohol-related liver disease if muscle and heart sources are excluded; occurs in about 20 percent of alcoholic hepatitis.
Above 2.2 in acute liver failureWith alkaline phosphatase to bilirubin ratio below 4Strongly points to Wilson's disease as the cause of acute liver failure in young people; nearly 100 percent sensitive and specific in the validation study.
Fibrosis scores using the ratioBARD: AST/ALT of 0.8 or more scores 2 points; NAFLD fibrosis score and FIB-4 use AST and ALT separatelyFIB-4 below 1.3 (2.0 if over 65) makes advanced fibrosis unlikely; above 2.67 makes it likely and prompts elastography or specialist referral.

High AST/ALT ratio (above 1, and especially above 2)

A ratio above 1 means AST is higher than ALT. If both enzymes are normal this is unremarkable and is common in lean people, older adults and women. If either enzyme is raised, the ratio becomes informative. A ratio above 2, with AST typically between 100 and 300 U/L, a GGT several times normal and often a raised MCV, is the classic signature of alcohol-related liver disease; in the original study of this pattern, 70 percent of people with alcoholic hepatitis or cirrhosis had a ratio over 2 compared with 4 percent of those with viral hepatitis, and above 3 the pattern was almost exclusive to alcohol. An AST above 500 U/L is unusual in alcoholic hepatitis and should prompt a search for another cause, such as acetaminophen, a viral infection or a period of low blood pressure (ischaemic hepatitis).

A ratio that has crept above 1 in someone known to have fatty liver disease or chronic hepatitis B or C carries a different message: the liver may be scarring. In hepatitis C, a ratio of 1 or more identified cirrhosis with 100 percent specificity in one study, and in fatty liver a ratio of 0.8 or more is one of the three items of the BARD score, which has a 96 percent negative predictive value for advanced fibrosis when the total score is low. These patients usually go on to a FIB-4 calculation and, if that is indeterminate or high, to a FibroScan (transient elastography) or specialist review.

A high ratio is not always the liver. AST is plentiful in skeletal and heart muscle and in red cells, so rhabdomyolysis, a marathon or heavy weight training, inflammatory muscle disease, hypothyroidism, a recent heart attack and haemolysis all raise AST more than ALT. Creatine kinase sorts this out: a high CK with a high AST/ALT ratio and normal GGT means muscle, not liver. Wilson's disease, ischaemic hepatitis and some drugs (notably isoniazid and some statin myopathies) are the other named causes of a high ratio.

Common causes

  1. Alcohol-related liver disease

    Alcoholic hepatitis and alcohol-related cirrhosis produce a ratio above 2 in about 70 percent of cases, through mitochondrial AST release, vitamin B6 depletion lowering ALT, and pericentral injury. AST rarely exceeds 300 U/L; GGT, MCV and often carbohydrate-deficient transferrin are raised alongside.

  2. Cirrhosis from any cause

    As fatty liver, hepatitis B or C, autoimmune hepatitis or haemochromatosis progresses to cirrhosis, ALT production falls and the ratio rises above 1. In cirrhosis both enzymes may be only mildly raised or even normal, so a ratio above 1 with a low platelet count or low albumin is a stronger signal than the ratio alone.

  3. Muscle injury and strenuous exercise

    Rhabdomyolysis, crush injury, seizures, polymyositis, muscular dystrophy, statin myopathy and a hard or unaccustomed workout release AST (and some ALT) from skeletal muscle; AST can reach several times normal with a ratio of 2 to 3 for a few days. Creatine kinase is raised in proportion.

  4. Heart attack and heart failure

    Heart muscle contains abundant AST, which was once used to diagnose myocardial infarction; congestive hepatopathy from right heart failure also tends to raise AST more than ALT.

  5. Ischaemic hepatitis (shock liver)

    A period of very low blood pressure or oxygen causes a dramatic rise of both enzymes into the thousands, with AST initially above ALT; the pattern then reverses as AST clears faster, often within 2 to 3 days.

  6. Wilson's disease

    Copper accumulation damages mitochondria, so AST rises more than ALT. In acute liver failure in a young person, a ratio above 2.2 with an alkaline phosphatase to bilirubin ratio below 4 is almost diagnostic; low alkaline phosphatase and haemolysis complete the picture.

  7. Hypothyroidism and haemolysis

    Untreated hypothyroidism raises AST and creatine kinase from muscle; haemolysis, either in the body or in the sample tube, releases red-cell AST (and LDH) and can double the ratio without any liver problem.

  8. Medications and supplements

    Isoniazid, methotrexate, amiodarone and anabolic steroids can produce AST-predominant injury, and statins, fibrates and some herbal products cause muscle-derived AST rises. Many other drugs produce an ALT-predominant pattern instead.

  9. Macro-AST

    A rare benign condition in which AST binds to immunoglobulins and is cleared slowly, producing a persistently raised AST, a high ratio and a completely healthy liver; confirmed by polyethylene-glycol precipitation or electrophoresis.

Symptoms that can go with it

  • Often none; the ratio is usually discovered on routine blood tests
  • Fatigue, nausea, poor appetite and right upper abdominal discomfort with alcoholic hepatitis
  • Jaundice, fever and a tender enlarged liver in severe alcoholic hepatitis
  • Signs of cirrhosis: spider veins on the chest, red palms, swollen abdomen, leg swelling, easy bruising, confusion
  • Muscle pain, weakness and dark urine when the source is muscle rather than liver
  • Chest pain or breathlessness if the AST is coming from the heart

Low AST/ALT ratio (below 1)

A ratio below 1 means ALT is higher than AST. This is the normal state for most healthy adults and needs no interpretation when both enzymes are within range. When ALT is raised and the ratio is below 1, the pattern points to the liver cell injuries that spare mitochondria and preserve ALT production: metabolic dysfunction-associated (non-alcoholic) fatty liver disease, which is now the most common cause of raised ALT in the United States, chronic hepatitis B and C, acute viral hepatitis, medication or supplement injury, coeliac disease and the earlier stages of haemochromatosis and autoimmune hepatitis.

In fatty liver disease ALT is typically 1.5 to 3 times normal with AST lower, so the ratio sits around 0.5 to 0.9. A low ratio in this setting is relatively reassuring about fibrosis, because the ratio rises as scarring advances. It is not a guarantee: a substantial minority of people with advanced fibrosis from fatty liver have a ratio below 1, which is why guidelines now recommend calculating FIB-4 in everyone with fatty liver, type 2 diabetes or obesity rather than relying on the ratio or on ALT alone.

In acute viral hepatitis or acetaminophen injury, both enzymes may be in the thousands with ALT ahead of AST; the absolute levels and the bilirubin, INR and mental state determine how serious the situation is, not the ratio. A very low ratio (for example 0.3) has no special significance beyond ALT predominance.

Common causes

  1. Metabolic dysfunction-associated (non-alcoholic) fatty liver disease

    Fat accumulation and the inflammation it provokes release cytoplasmic ALT preferentially. Affects about a third of US adults and is the leading cause of a mildly raised ALT with a ratio below 1, usually alongside central obesity, raised triglycerides, low HDL and raised glucose or A1C.

  2. Chronic hepatitis B and C

    Viral infection of liver cells produces an ALT-predominant pattern through most of the disease course; a ratio climbing above 1 later signals cirrhosis.

  3. Acute viral hepatitis (A, B, E, EBV, CMV)

    Both enzymes rise steeply, often above 1,000 U/L, with ALT higher than AST; the ratio falls further over the first week as AST, with its shorter half-life, clears faster.

  4. Medication and supplement injury

    Acetaminophen, antibiotics (amoxicillin-clavulanate, nitrofurantoin), anti-seizure drugs, NSAIDs, statins (in the hepatic rather than muscle pattern), green tea extract, kava and bodybuilding supplements typically cause an ALT-predominant hepatocellular injury.

  5. Coeliac disease, haemochromatosis and autoimmune hepatitis

    Coeliac disease raises ALT mildly in up to 40 percent of untreated cases; iron overload and autoimmune hepatitis produce ALT-predominant patterns until fibrosis is advanced.

  6. Normal physiology

    Healthy adults, especially younger men and people with higher muscle mass, usually have ALT a little above AST. A ratio below 1 with both enzymes normal is simply normal.

Symptoms that can go with it

  • Usually none; fatty liver and chronic viral hepatitis are typically silent until advanced
  • Fatigue and vague right upper abdominal fullness
  • Features of metabolic syndrome: central weight gain, high blood pressure, raised blood sugar
  • Nausea, loss of appetite, dark urine, pale stools and jaundice in acute hepatitis
  • Itching, joint pains or rashes with some autoimmune and drug-induced causes

Read it alongside

  • AST and ALT absolute values — the ratio is meaningless unless at least one is raised; the degree of elevation (mild under 5 times, moderate 5–15, marked over 15) matters more than the ratio.
  • GGT — raised several-fold in alcohol-related disease and supports an alcohol explanation for a ratio above 2; normal GGT with a high ratio points to muscle or heart.
  • Creatine kinase (CK) — the single most useful test to prove that a high AST/ALT ratio is coming from muscle rather than liver.
  • Platelets — a count below 150,000 with a ratio above 1 raises the probability of cirrhosis substantially and is a component of FIB-4 and APRI.
  • Albumin, bilirubin and INR — measure how well the liver is actually working; they fall (albumin) or rise (bilirubin, INR) as cirrhosis decompensates and define the Child-Pugh and MELD scores.
  • MCV — a raised mean cell volume without anaemia is a supporting sign of heavy alcohol use.
  • Ferritin and transferrin saturation — identify haemochromatosis and are often raised as acute-phase reactants in fatty liver and alcohol.
  • Hepatitis B and C serology, TSH and coeliac antibodies — standard tests when the cause of raised enzymes is not obvious.

What usually happens next

  1. If both AST and ALT are within the normal range, the ratio does not need interpreting; if you have fatty liver, diabetes or obesity, ask for a FIB-4 score anyway, because enzymes can be normal in advanced fibrosis.
  2. If the ratio is above 2 with raised enzymes, expect direct questions about alcohol (an honest answer changes management), a GGT, MCV and sometimes carbohydrate-deficient transferrin or phosphatidylethanol, and a creatine kinase to exclude muscle as the source.
  3. If the ratio is above 1 in someone with known fatty liver or chronic hepatitis, expect a FIB-4 calculation; a value above 1.3 (2.0 if over 65) usually leads to transient elastography (FibroScan) or an enhanced liver fibrosis blood test, and above 2.67 to hepatology referral.
  4. If the ratio is below 1 with raised ALT, the usual work-up is a metabolic assessment (waist, glucose or A1C, lipids), hepatitis B and C serology, iron studies, coeliac antibodies, a medication and supplement review, and an ultrasound; FIB-4 is still calculated.
  5. Repeat the panel in 4 to 12 weeks after any change (stopping alcohol, a new medicine, weight loss) rather than acting on a single value; AST falls within days and ALT within weeks when the cause is removed.
  6. Ask what your ratio and enzymes were on earlier tests; a ratio that has risen from 0.7 to 1.3 over a few years in fatty liver is more informative than any single number.

Diet, lifestyle and natural levers with evidence

What can move AST/ALT once the cause is known. Nothing here replaces finding the cause.

Stop or sharply reduce alcohol

Strong evidence

Abstinence is the only intervention that reliably reverses the alcohol pattern. AST has a half-life of about 17 hours, so it falls within days of stopping; GGT normalises over 2 to 6 weeks and MCV over about 3 months. In alcoholic hepatitis, continued abstinence is the strongest predictor of survival, with 5-year survival roughly double that of people who keep drinking, and early alcohol-related cirrhosis can stabilise or partially regress. Even in fatty liver that is primarily metabolic, alcohol adds to the injury and any regular intake above about one drink a day worsens outcomes.

Stopping suddenly after heavy daily drinking can cause withdrawal seizures; people who drink heavily every day should stop with medical support.

Lose 7 to 10 percent of body weight if you have fatty liver

Strong evidence

In a 12-month trial of 293 people with biopsy-proven non-alcoholic steatohepatitis, those who lost 7 percent or more of body weight through diet and exercise had resolution of steatohepatitis in most cases, and at 10 percent or more loss 90 percent had resolution and 45 percent had regression of fibrosis; ALT fell in step with weight. Even 3 to 5 percent loss reduces liver fat and ALT. Weight loss lowers both enzymes, and because ALT falls proportionally more, the ratio may rise slightly as it normalises; that is expected.

Mediterranean-style eating with less fructose and refined carbohydrate

Moderate evidence

In a six-week randomised crossover trial, a Mediterranean diet reduced liver fat by 39 percent compared with 7 percent on a low-fat, high-carbohydrate diet, without weight loss, and improved insulin sensitivity. Larger trials and meta-analyses confirm lower ALT and liver fat with Mediterranean patterns, and sugar-sweetened drinks and high fructose intake are consistently linked to more liver fat. Guidelines from the American Association for the Study of Liver Diseases and European societies recommend this pattern as first-line dietary treatment for fatty liver.

Coffee, 2 to 3 cups a day

Moderate evidence

A meta-analysis of nine cohort studies found that two extra cups of coffee a day were associated with a 44 percent lower risk of cirrhosis, and other pooled analyses show lower ALT, less advanced fibrosis in fatty liver and hepatitis C, and lower liver cancer risk in regular drinkers. The effect appears for caffeinated and, more weakly, decaffeinated coffee, suggesting polyphenols as well as caffeine. No randomised trials exist, but the consistency across populations and diseases led liver societies to state that coffee is not harmful and probably protective.

Unfiltered coffee raises LDL cholesterol modestly; added sugar and syrups undo the benefit for fatty liver.

Regular aerobic and resistance exercise

Moderate evidence

A meta-analysis of randomised trials found exercise training reduced liver fat by about 20 to 30 percent and lowered ALT even when body weight did not change, with 150 to 250 minutes a week of moderate aerobic activity or three resistance sessions a week the doses studied. Benefits appear within 4 to 12 weeks. Exercise also improves insulin sensitivity, the main driver of fatty liver.

A very hard or unaccustomed session raises AST from muscle for 2 to 3 days and can push the ratio above 1 or 2; avoid liver tests within 72 hours of a race or heavy weights session.

Vitamin E (800 IU a day) in biopsy-proven steatohepatitis without diabetes

Moderate evidence

In the PIVENS trial, 800 IU a day of natural vitamin E for 96 weeks improved steatohepatitis in 43 percent of non-diabetic adults compared with 19 percent on placebo and significantly lowered ALT and AST, though it did not improve fibrosis. Liver guidelines list it as an option for this specific group under specialist supervision. It has not been shown to help people with simple fatty liver, diabetes or cirrhosis.

High-dose vitamin E was associated with a 17 percent increase in prostate cancer in the SELECT trial and with a small increase in haemorrhagic stroke in meta-analyses; it is not recommended without a biopsy-based diagnosis and a specialist's agreement.

When to see a clinician promptly

  • AST or ALT above about 1,000 U/L, or any level with jaundice, confusion, drowsiness or easy bleeding: possible acute liver failure, needs same-day emergency assessment.
  • A ratio above 2 with raised enzymes and fever, jaundice, abdominal swelling or a tender liver after a period of heavy drinking: severe alcoholic hepatitis carries a high short-term mortality and is treated in hospital.
  • A high ratio with muscle pain, weakness and dark or cola-coloured urine, especially after extreme exertion, a fall or starting a statin: possible rhabdomyolysis.
  • A ratio above 1 with a platelet count below 150,000, low albumin, raised bilirubin or an enlarged spleen on imaging, which together suggest cirrhosis.
  • A high ratio with chest pain, breathlessness or palpitations, in case the AST is coming from the heart.
  • Any persistently raised enzymes, whatever the ratio, that have not been explained within 3 to 6 months, so that hepatitis, iron, coeliac, thyroid and metabolic causes can be worked through and a FIB-4 calculated.

Frequently asked questions

What is a normal AST/ALT ratio?

In healthy adults ALT is usually slightly higher than AST, giving a ratio below 1, typically around 0.7 to 1.0. The ratio is only worth interpreting when AST or ALT is above the normal range. Many perfectly healthy people, particularly lean older adults and women, have AST a little above ALT and a ratio of 1.0 to 1.3 with both enzymes normal, which means nothing.

What does an AST/ALT ratio greater than 2 mean?

With raised enzymes, a ratio above 2 most often indicates alcohol-related liver disease, particularly when AST is below 300 U/L and GGT and MCV are also high; about 70 percent of people with alcoholic hepatitis or cirrhosis show this pattern. It can also come from muscle injury or heavy exercise, a heart attack, cirrhosis of any cause, Wilson's disease or ischaemic liver injury. A creatine kinase and GGT usually settle which it is.

Does a high AST/ALT ratio always mean alcohol?

No. The ratio rises above 2 in alcohol-related liver disease because alcohol damages mitochondria and depletes vitamin B6, but AST is also abundant in skeletal muscle, heart and red cells, so a hard workout, rhabdomyolysis, inflammatory muscle disease, hypothyroidism, a heart attack or a haemolysed blood sample all produce a high ratio with a healthy liver. Cirrhosis from any cause pushes the ratio above 1 too. Clinicians use GGT, creatine kinase, MCV and your own account of drinking to sort these out.

What AST/ALT ratio suggests fatty liver disease?

Fatty liver disease usually produces a ratio below 1, often 0.5 to 0.9, because ALT rises more than AST. If the ratio climbs above 0.8 to 1 in someone with fatty liver, the chance of significant scarring increases, which is why a ratio of 0.8 or more scores points in the BARD fibrosis score and why a FIB-4 calculation and often a FibroScan follow. A ratio below 1 is reassuring but does not exclude advanced fibrosis on its own.

What does AST higher than ALT mean if both are normal?

Usually nothing. When both enzymes are within the normal range, the ratio carries no diagnostic information, and AST modestly above ALT is the normal pattern for many lean, older or female adults. The ratio becomes meaningful only when at least one enzyme is raised. If you have risk factors for liver disease (fatty liver, diabetes, heavy alcohol use, hepatitis), a FIB-4 score, which combines age, AST, ALT and platelets, is a better screen than the ratio alone.

What is the De Ritis ratio?

The De Ritis ratio is another name for the AST/ALT ratio, after Fernando De Ritis, who described in 1957 that the two transaminases rise in different proportions in different liver diseases, originally to distinguish viral hepatitis (ratio below 1) from other causes. It is still used as a quick clue to alcohol-related disease (above 2), to cirrhosis (rising above 1 in chronic disease) and, in recent research, as a prognostic marker in several cancers and in kidney disease.

Can the AST/ALT ratio diagnose cirrhosis?

Not on its own, but it helps. In chronic hepatitis C a ratio of 1 or more had 100 percent specificity for cirrhosis in one study, though it missed about half of cases, and in fatty liver a ratio above 1 raises the probability of advanced fibrosis. Cirrhosis is diagnosed with a combination of a low platelet count, low albumin, raised bilirubin or INR, FIB-4 or other fibrosis scores, elastography (FibroScan) and imaging, with biopsy reserved for uncertain cases.

How quickly does the ratio change if I stop drinking?

Quickly, if alcohol is the cause. AST has a half-life of about 17 hours and typically returns to normal within one to two weeks of stopping; ALT follows within two to four weeks, GGT within two to six weeks and MCV over about three months. If the enzymes and ratio stay abnormal after six to eight weeks of genuine abstinence, another cause or established cirrhosis is likely and further tests are needed.

References

  1. Cohen JA, Kaplan MM. The SGOT/SGPT ratio: an indicator of alcoholic liver disease. Digestive Diseases and Sciences (1979)
  2. De Ritis F, Coltorti M, Giusti G. An enzymic test for the diagnosis of viral hepatitis: the transaminase serum activities. Clinica Chimica Acta (1957)
  3. Botros M, Sikaris KA. The De Ritis ratio: the test of time. Clinical Biochemist Reviews (2013)
  4. Sheth SG, Flamm SL, Gordon FD, Chopra S. AST/ALT ratio predicts cirrhosis in patients with chronic hepatitis C virus infection. American Journal of Gastroenterology (1998)
  5. Diehl AM, Potter J, Boitnott J, Van Duyn MA, Herlong HF, Mezey E. Relationship between pyridoxal 5'-phosphate deficiency and aminotransferase levels in alcoholic hepatitis. Gastroenterology (1984)
  6. Kwo PY, Cohen SM, Lim JK. ACG Clinical Guideline: evaluation of abnormal liver chemistries. American Journal of Gastroenterology (2017)
  7. Harrison SA, Oliver D, Arnold HL, Gogia S, Neuschwander-Tetri BA. Development and validation of a simple NAFLD clinical scoring system for identifying patients without advanced disease. Gut (2008)
  8. Vilar-Gomez E, Martinez-Perez Y, Calzadilla-Bertot L, et al.. Weight loss through lifestyle modification significantly reduces features of nonalcoholic steatohepatitis. Gastroenterology (2015)
  9. Sanyal AJ, Chalasani N, Kowdley KV, et al.. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis (PIVENS). New England Journal of Medicine (2010)
  10. Kennedy OJ, Roderick P, Buchanan R, Fallowfield JA, Hayes PC, Parkes J. Systematic review with meta-analysis: coffee consumption and the risk of cirrhosis. Alimentary Pharmacology and Therapeutics (2016)
  11. Rinella ME, Neuschwander-Tetri BA, Siddiqui MS, et al.. AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology (2023)
  12. Liver function tests. MedlinePlus, US National Library of Medicine (2023)View source

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