AST/ALT ratio

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AST/ALT ratio
LOINC 16325-3, 1916-6

The AST/ALT ratio or De Ritis ratio is the ratio between the concentrations of two enzymes, aspartate transaminase (AST) and alanine transaminase, aka alanine aminotransferase (ALT), in the blood of a human or animal. It is used as one of several liver function tests, and measured with a blood test. It is sometimes useful in medical diagnosis for elevated transaminases to differentiate between causes of liver damage, or hepatotoxicity. [1] [2] [3]

Contents

Most causes of liver cell injury are associated with a greater increase in ALT than AST, but an AST/ALT ratio of 2:1 or greater is suggestive of alcoholic liver disease, particularly in the setting of an elevated gamma-glutamyl transferase. [4]

The AST/ALT ratio can also occasionally be elevated in a liver disease pattern in patients with nonalcoholic steatohepatitis, and it is frequently elevated in an alcoholic liver disease pattern in patients with hepatitis C who have developed cirrhosis. In addition, patients with Wilson's disease or cirrhosis due to viral hepatitis may have an AST that is greater than the ALT, though the ratio typically is not greater than two.[ citation needed ]

When the AST is higher than ALT, a muscle source of these enzymes should be considered. For example, muscle inflammation due to dermatomyositis may cause AST > ALT. This is a good reminder that AST and ALT are not good measures of liver function when other sources may influence AST and/or ALT, because they do not reliably reflect the synthesizing ability of the liver, and they may come from tissues other than liver (such as muscle). [5] For example, intense exercise such as weightlifting can increase ALT to 50–200 U/L, and AST to 100–1000 U/L (and raise AST to about four times ALT) for the week following the exercise. [6]

History

Pathophysiology sample values
BMP/ELECTROLYTES:
Na+ = 140 Cl− = 100 BUN = 20 /
Glu = 150
\
K+ = 4 CO2 = 22 PCr = 1.0
ARTERIAL BLOOD GAS:
HCO3− = 24 p a CO2 = 40 p a O2 = 95 pH = 7.40
ALVEOLAR GAS:
p A CO2 = 36 p A O2 = 105 A-a g = 10
OTHER:
Ca = 9.5 Mg2+ = 2.0 PO4 = 1
CK = 55 BE = −0.36 AG = 16
SERUM OSMOLARITY/RENAL:
PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20
URINALYSIS:
UNa+ = 80 UCl− = 100 UAG = 5 FENa = 0.95
UK+ = 25 USG = 1.01 UCr = 60 UO = 800
PROTEIN/GI/LIVER FUNCTION TESTS:
LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7
ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5
AST/ALT = 0.6 BU = 0.2
AF alb = 3.0 SAAG = 1.0 SOG = 60
CSF:
CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.6

The De Ritis ratio [7] [8] is named after Fernando De Ritis, who performed analysis on transaminases in 1957. [8]

Mechanism

AST/ALT ratioAssociated conditions
>5extrahepatic causes
>2alcoholic hepatitis
hepatocellular carcinoma
early-stage viral hepatitis
<1late-stage viral hepatitis

The proportion of AST to ALT in hepatocytes is about 2.5:1, but because AST is removed from serum by the liver sinusoidal cells twice as quickly (serum half-life t1/2 = 18 hr) compared to ALT (t1/2 = 36 hr), so the resulting serum levels of AST and ALT are about equal in healthy individuals, resulting in a normal AST/ALT ratio around 1.

An AST/ALT ratio >5 necessarily involves extrahepatic tissue, as death of hepatocytes alone would produce an AST/ALT ratio no greater than 2.5. [9] Because the primary cause is extrahepatic, typically an isolated elevated AST is seen, with no change in ALT. Common causes include bone disease, chronic renal failure, lymphoma, and congestive heart failure. [10]

When hepatocellular death is increased beyond the usual "background" levels, the serum levels of AST compared to ALT tend to reflect the cellular proportions, yielding AST that is over twice as prevalent as ALT (AST/ALT >2) in conditions with chronic, constant hepatocyte damage (such as alcoholic hepatitis, hepatocellular carcinoma) and during early-stage acute liver damage (such as viral hepatitis).

In late-stage acute liver damage, the body has had adequate time to clear AST, but not ALT, often resulting in an AST/ALT <1. Since testing typically occurs late in acute viral hepatitis, it is conventionally associated with an AST/ALT ratio <1, though early in the disease, the AST/ALT ratio is often elevated. As the acute liver damage resolves, the body has more time to clear ALT, so in the absence of chronic liver disease, the AST/ALT ratio gradually returns to baseline levels. [11]

See also

Related Research Articles

<span class="mw-page-title-main">Hepatitis</span> Inflammation of the liver

Hepatitis is inflammation of the liver tissue. Some people or animals with hepatitis have no symptoms, whereas others develop yellow discoloration of the skin and whites of the eyes (jaundice), poor appetite, vomiting, tiredness, abdominal pain, and diarrhea. Hepatitis is acute if it resolves within six months, and chronic if it lasts longer than six months. Acute hepatitis can resolve on its own, progress to chronic hepatitis, or (rarely) result in acute liver failure. Chronic hepatitis may progress to scarring of the liver (cirrhosis), liver failure, and liver cancer.

<span class="mw-page-title-main">Jaundice</span> Abnormal pigmentation symptom for disease of the liver

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<span class="mw-page-title-main">Hepatitis C</span> Human viral infection

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Liver function tests, also referred to as a hepatic panel, are groups of blood tests that provide information about the state of a patient's liver. These tests include prothrombin time (PT/INR), activated partial thromboplastin time (aPTT), albumin, bilirubin, and others. The liver transaminases aspartate transaminase and alanine transaminase are useful biomarkers of liver injury in a patient with some degree of intact liver function.

<span class="mw-page-title-main">Alanine transaminase</span> Mammalian protein

Alanine transaminase (ALT) is a transaminase enzyme. It is also called alanine aminotransferase and was formerly called serum glutamate-pyruvate transaminase or serum glutamic-pyruvic transaminase (SGPT) and was first characterized in the mid-1950s by Arthur Karmen and colleagues. ALT is found in plasma and in various body tissues but is most common in the liver. It catalyzes the two parts of the alanine cycle. Serum ALT level, serum AST level, and their ratio are routinely measured clinically as biomarkers for liver health.

<span class="mw-page-title-main">Alcoholic liver disease</span> Medical condition

Alcoholic liver disease (ALD), also called alcohol-related liver disease (ARLD), is a term that encompasses the liver manifestations of alcohol overconsumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis or cirrhosis.

<span class="mw-page-title-main">Hepatotoxicity</span> Liver damage caused by a drug or chemical

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<span class="mw-page-title-main">Alcoholic hepatitis</span> Medical condition

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Chronic liver disease in the clinical context is a disease process of the liver that involves a process of progressive destruction and regeneration of the liver parenchyma leading to fibrosis and cirrhosis. "Chronic liver disease" refers to disease of the liver which lasts over a period of six months. It consists of a wide range of liver pathologies which include inflammation, liver cirrhosis, and hepatocellular carcinoma. The entire spectrum need not be experienced.

In medicine, the presence of elevated transaminases, commonly the transaminases alanine transaminase (ALT) and aspartate transaminase (AST), may be an indicator of liver dysfunction. Other terms include transaminasemia, transaminitis, and elevatedliver enzymes. Normal ranges for both ALT and AST vary by gender, age, and geography and are roughly 8-40 U/L. Mild transaminesemia refers to levels up to 250 U/L. Drug-induced increases such as that found with the use of anti-tuberculosis agents such as isoniazid are limited typically to below 100 U/L for either ALT or AST. Muscle sources of the enzymes, such as intense exercise, are unrelated to liver function and can markedly increase AST and ALT. Cirrhosis of the liver or fulminant liver failure secondary to hepatitis commonly reach values for both ALT and AST in the >1000 U/L range; however, many people with liver disease have normal transaminases. Elevated transaminases that persist less than six months are termed "acute" in nature, and those values that persist for six months or more are termed "chronic" in nature.

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<span class="mw-page-title-main">Cirrhosis</span> Chronic disease of the liver, characterized by fibrosis

Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, and end-stage liver disease, is the impaired liver function caused by the formation of scar tissue known as fibrosis due to damage caused by liver disease. Damage to the liver leads to repair of liver tissue and subsequent formation of scar tissue. Over time, scar tissue can replace normal functioning tissue, leading to the impaired liver function of cirrhosis. The disease typically develops slowly over months or years. Early symptoms may include tiredness, weakness, loss of appetite, unexplained weight loss, nausea and vomiting, and discomfort in the right upper quadrant of the abdomen. As the disease worsens, symptoms may include itchiness, swelling in the lower legs, fluid build-up in the abdomen, jaundice, bruising easily, and the development of spider-like blood vessels in the skin. The fluid build-up in the abdomen may develop into spontaneous infections. More serious complications include hepatic encephalopathy, bleeding from dilated veins in the esophagus, stomach, or intestines, and liver cancer. Stages of cirrhosis include compensated cirrhosis and decompensated cirrhosis.

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Hyperbilirubinemia is a clinical condition describing an elevation of blood bilirubin level due to the inability to properly metabolise or excrete bilirubin, a product of erythrocytes breakdown. In severe cases, it is manifested as jaundice, the yellowing of tissues like skin and the sclera when excess bilirubin deposits in them. The US records 52,500 jaundice patients annually. By definition, bilirubin concentration of greater than 3 mg/ml is considered hyperbilirubinemia, following which jaundice progressively develops and becomes apparent when plasma levels reach 20 mg/ml. Rather than a disease itself, hyperbilirubinemia is indicative of multifactorial underlying disorders that trace back to deviations from regular bilirubin metabolism. Diagnosis of hyperbilirubinemia depends on physical examination, urinalysis, serum tests, medical history and imaging to identify the cause. Genetic diseases, alcohol, pregnancy and hepatitis viruses affect the likelihood of hyperbilirubinemia. Causes of hyperbilirubinemia mainly arise from the liver. These include haemolytic anaemias, enzymatic disorders, liver damage and gallstones. Hyperbilirubinemia itself is often benign. Only in extreme cases does kernicterus, a type of brain injury, occur. Therapy for adult hyperbilirubinemia targets the underlying diseases but patients with jaundice often have poor outcomes.

References

  1. ↑ Nyblom H, Berggren U, Balldin J, Olsson R (2004). "High AST/ALT ratio may indicate advanced alcoholic liver disease rather than heavy drinking". Alcohol and Alcoholism. 39 (4): 336–9. doi: 10.1093/alcalc/agh074 . PMID   15208167.
  2. ↑ Nyblom H, Björnsson E, Simrén M, Aldenborg F, Almer S, Olsson R (September 2006). "The AST/ALT ratio as an indicator of cirrhosis in patients with PBC". Liver International. 26 (7): 840–5. doi:10.1111/j.1478-3231.2006.01304.x. PMID   16911467. S2CID   3126986.
  3. ↑ Gopal DV, Rosen HR (February 2000). "Abnormal findings on liver function tests. Interpreting results to narrow the diagnosis and establish a prognosis". Postgraduate Medicine. 107 (2): 100–2, 105–9, 113–4. doi:10.3810/pgm.2000.02.869. PMID   10689411. S2CID   30483587.[ permanent dead link ]
  4. ↑ Moussavian, S. N.; Becker, R. C.; Piepmeyer, J. L.; Mezey, E.; Bozian, R. C. (Mar 1985). "Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease". Digestive Diseases and Sciences. 30 (3): 211–4. doi:10.1007/bf01347885. PMID   2857631. S2CID   24588657.
  5. ↑ Giboney, Paul T. (2005-03-15). "Mildly Elevated Liver Transaminase Levels in the Asymptomatic Patient". American Family Physician. 71 (6): 1105–1110. ISSN   0002-838X. PMID   15791889.
  6. ↑ Pettersson, J.; et al. (2007). "Muscular exercise can cause highly pathological liver function tests in healthy men". British Journal of Clinical Pharmacology. 65 (2): 253–259. doi:10.1111/j.1365-2125.2007.03001.x. PMC   2291230 . PMID   17764474.
  7. ↑ Kenneth D. McClatchey (2002). Clinical laboratory medicine. Lippincott Williams & Wilkins. pp. 288–. ISBN   978-0-683-30751-1 . Retrieved 21 May 2010.
  8. 1 2 De Ritis F, Coltorti M, Giusti G (July 2006). "An enzymic test for the diagnosis of viral hepatitis: the transaminase serum activities. 1957". Clinica Chimica Acta. 369 (2): 148–52. doi:10.1016/j.cca.2006.05.001. PMID   16781697.
  9. ↑ Botros, Mona; Sikaris, Kenneth (November 2013). "The De Ritis Ratio: The Test of Time". The Clinical Biochemist. Reviews. 34 (3): 117–130. PMC   3866949 . PMID   24353357.
  10. ↑ Lazo, Mariana. "Liver Function". Johns Hopkins Medicine. Retrieved 7 July 2022.
  11. ↑ Botros, Mona; Sikaris, Kenneth (November 2013). "The De Ritis Ratio: The Test of Time". The Clinical Biochemist. Reviews. 34 (3): 117–130. PMC   3866949 . PMID   24353357.
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