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Printed on 7/19/2026
For informational purposes only. This is not medical advice.
The AST/ALT (De Ritis) ratio is a simple enzyme ratio used as an adjunct in liver disease pattern assessment. Different ratio ranges can suggest different injury patterns but must be interpreted with full laboratory and clinical context.
Formula: AST/ALT Ratio = AST / ALT.
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Obtain AST (aspartate aminotransferase) and ALT (alanine aminotransferase) levels from the patient's basic metabolic panel or comprehensive metabolic panel — two of the most commonly ordered liver function tests. Ensure both values are from the same blood draw and expressed in the same units (U/L). These are standard components of every routine chemistry panel.
Divide AST by ALT to obtain the De Ritis ratio. For example, AST 80 U/L ÷ ALT 40 U/L = ratio of 2.0. The calculation is straightforward — no logarithms or additional variables required. The result is a dimensionless ratio that indicates which enzyme is relatively more elevated.
Use the ratio as one component of liver injury pattern recognition: Ratio <0.8 = typical of non-alcoholic causes (NAFLD, viral hepatitis) where ALT predominates. Ratio ~1.0 = equivocal; may represent advanced NAFLD fibrosis or mixed injury. Ratio 1.0–2.0 = suggestive of increasing fibrosis or early alcoholic injury. Ratio >2.0 = classically associated with alcoholic liver disease (De Ritis ratio). Ratio >3.0 = strongly suggestive of alcoholic hepatitis. Importantly, in cirrhosis from any cause (viral, NAFLD, autoimmune), the ratio tends to rise above 1.0 as fibrosis replaces hepatocytes. Always combine with GGT, ALP, bilirubin, INR, and clinical history.
Primary care physicians and hepatologists
The De Ritis ratio >2.0 is a classic screening marker for alcoholic liver disease. Combined with elevated GGT, clinical history of alcohol use, and elevated MCV, it supports — but does not confirm — alcohol-related hepatocellular injury.
Hepatologists and gastroenterologists
As NAFLD, HCV, or other chronic liver diseases progress from simple steatosis to cirrhosis, the AST:ALT ratio rises from below 1 toward and above 1. A rising ratio over serial measurements in a known chronic liver disease patient suggests advancing fibrosis.
Primary care physicians and hospitalists
Use the ratio to quickly characterize the liver injury pattern when a patient presents with abnormal LFTs: ALT > AST (ratio <1) points toward NAFLD, viral hepatitis, or drug-induced liver injury; AST > ALT (ratio >2) prompts alcohol history and GGT measurement.
All clinicians ordering liver function panels
When faced with elevated AST and ALT, the AST:ALT ratio is the first pattern-recognition step. It narrows the differential diagnosis and guides which additional tests to order: GGT for alcohol, hepatitis serologies for viral disease, ANA/ASMA for autoimmune hepatitis, ceruloplasmin for Wilson disease.
Hospitalists and internists
Elevated AST and ALT with ratio >1 vs elevated ALP and GGT: the pattern distinguishes hepatocellular injury (AST/ALT dominated) from cholestatic injury (ALP/GGT dominated). Combining both patterns helps localize injury to hepatocytes vs bile ducts.
The classic threshold of AST:ALT >2 for alcoholic liver disease has sensitivity of approximately 54% and specificity of approximately 70% — meaning nearly half of alcoholic liver disease cases have a ratio <2, and 30% of non-alcoholic cases have a ratio >2. It is a pattern-recognition aid, not a standalone diagnostic test. Always integrate with GGT, clinical alcohol history, and additional testing.
GGT is elevated disproportionately in alcoholic liver disease (induced by alcohol independently of hepatocyte injury) and more specifically than AST/ALT alone. A GGT that is 3-5x the upper limit of normal, combined with AST:ALT >2, strongly supports alcoholic liver disease. GGT normalization after abstinence (within 4-6 weeks) can also be used to assess treatment response.
Hepatitis A, B, and C characteristically produce a pattern where ALT is higher than AST (hepatocytes preferentially release ALT). An AST:ALT <1 in a patient with transaminase elevations should prompt hepatitis serology testing. If the ratio is >1 in viral hepatitis, consider advanced fibrosis as a contributor.
Early NAFLD (steatosis only) typically shows ratio <0.8 with ALT-dominant elevation. As fibrosis progresses toward F2-F3 and cirrhosis, the ratio approaches and exceeds 1.0. A rising AST:ALT ratio in a known NAFLD patient is a signal to calculate FIB-4 and consider FibroScan.
ALT synthesis requires pyridoxal-5'-phosphate (vitamin B6) as a cofactor. Alcoholics are frequently B6-deficient, which impairs ALT synthesis and artificially lowers ALT levels — thereby artificially elevating the AST:ALT ratio even in the absence of severe hepatocellular injury. This was documented by Diehl et al. (Gastroenterology 1984) and partially explains why alcoholic liver disease cases have elevated ratios.
Fibrosis replaces functional hepatocytes, disproportionately reducing ALT (which is almost exclusively hepatic) compared to AST (which has significant cardiac and muscle sources). This means that in end-stage liver disease from NAFLD, HCV, HBV, autoimmune hepatitis, or PBC/PSC, the ratio commonly exceeds 1.0 even without alcohol use.
AST is found in skeletal muscle, cardiac muscle, red blood cells, kidney, and brain — not just the liver. Myocardial infarction, rhabdomyolysis, vigorous exercise, or myopathy can produce AST elevations with normal ALT, yielding very high AST:ALT ratios. Always check creatine kinase (CK) and cardiac troponins when AST elevation is unexplained or disproportionate.
Isolated elevation of ALP and GGT with normal or mildly elevated transaminases suggests cholestatic injury (bile duct obstruction, PBC, PSC, drug cholestasis). Elevated transaminases with relatively normal ALP suggests hepatocellular injury. The ratio helps within the hepatocellular category to suggest alcohol vs non-alcohol.
The AST/ALT (De Ritis) ratio was described by De Ritis et al. in Italy in the 1950s as a hepatocellular injury marker. The ratio >2 for alcoholic hepatitis was validated by Cohen and Kaplan (Gastroenterology 1979) in a prospective study of liver disease etiology. Pyridoxine (B6) deficiency effects on ALT in alcoholics were characterized by Diehl et al. (Gastroenterology 1984). The ratio has AUROC approximately 0.75 for alcoholic vs non-alcoholic liver disease and should be interpreted with GGT, clinical history, and full hepatic assessment.
The ratio helps describe liver enzyme pattern but should be interpreted alongside absolute AST/ALT values and full hepatic assessment.
Use as a quick adjunct in liver enzyme interpretation, chronic liver disease follow-up, and hepatology triage discussions.
The ratio is non-specific and influenced by non-hepatic AST sources (muscle injury, hemolysis), assay timing, and mixed disease processes.
For related assessments, see FIB-4, MELD Score and Child-Pugh Score.
Disclaimer: This tool is for educational and informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about your health.
April 21, 2026 · trust-baseline
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