What is a normal ast and alt level: High, Low & Normal Results, Symptoms & Causes

14.08.202321.06.2023 by alexxlab

Aspartate aminotransferase (AST) blood test

Definition

The aspartate aminotransferase (AST) blood test measures the level of the enzyme AST in the blood.

Alternative Names

Aspartate aminotransferase; Serum glutamic-oxaloacetic transaminase; SGOT

How the Test is Performed

A blood sample is needed.

How to Prepare for the Test

No special preparation is needed.

How the Test will Feel

When the needle is inserted to draw blood, some people feel moderate pain. Others feel only a prick or stinging. Afterward, there may be some throbbing or a slight bruise. This soon goes away.

Why the Test is Performed

AST is an enzyme found in high levels in the liver, heart, and muscles. It is also found in lesser amounts in other tissues. An enzyme is a protein that causes a specific chemical change in the body.

Injury to the liver results in release of AST into the blood.

This test is mainly done along with other tests (such as ALT, ALP, and bilirubin) to diagnose and monitor liver disease.

Normal Results

The normal range is 8 to 33 U/L.

Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or may test different samples. Talk to your health care provider about the meaning of your specific test results.

What Abnormal Results Mean

An increased AST level is often a sign of liver disease. Liver disease is even more likely when the levels of substances checked by other liver blood tests have also increased.

An increased AST level may be due to any of the following:

Scarring of the liver (cirrhosis)
Death of liver tissue
Heart attack
Too much iron in the body (hemochromatosis)
Swollen and inflamed liver (hepatitis)
Lack of blood flow to the liver (liver ischemia)
Liver cancer or tumor
Use of drugs that are toxic to the liver, especially alcohol use
Mononucleosis (“mono”)
Muscle disease or trauma
Swollen and inflamed pancreas (pancreatitis)

AST level may also increase after:

Burns (deep)
Heart procedures
Seizure
Surgery

Pregnancy and exercise may also cause an increased AST level.

Risks

There is little risk involved with having your blood taken. Veins vary in size from one person to another and from one side of the body to the other. Taking blood from some people may be more difficult than from others.

Risks associated with having blood drawn are slight, but may include:

Fainting or feeling lightheaded
Excessive bleeding
Multiple punctures to locate veins
Hematoma (blood collecting under the skin)
Infection (a slight risk any time the skin is broken)

Images

References

Chernecky CC, Berger BJ. Aspartate aminotransferase (AST, aspartate transaminase, SGOT) – serum. In: Chernecky CC, Berger BJ, eds. Laboratory Tests and Diagnostic Procedures. 6th ed. St Louis, MO: Elsevier Saunders; 2013:172-173.

Daniels L, Khalili M, Goldstein E, Bluth MH, Bowne WB, Pincus MR. Evaluation of liver function. In: McPherson RA, Pincus MR, eds. Henry’s Clinical Diagnosis and Management by Laboratory Methods. 24th ed. Philadelphia, PA: Elsevier; 2022:chap 22.

Pratt DS. Liver chemistry and function tests. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 11th ed. Philadelphia, PA: Elsevier; 2021:chap 73.

Last reviewed January 24, 2021 by David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, WA. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team..

Related specialties

5-year-old boy • behavioral issues • elevated ALT and AST levels • Dx?

Case Reports

Jeffrey Taylor, MD, MS

Thomas Flass, MD, MS

Author and Disclosure Information

► Behavioral issues (impulsiveness, aggression)
► Liver edge 1 cm below costal margin
► Elevated ALT and AST levels

References

1. Wu F, Wang J, Pu C, et al. Wilson’s disease: a comprehensive review of the molecular mechanisms. Int J Mol Sci. 2015;16:6419-6431.

2. Merle U, Stremmel W, Gessner R. Influence of homozygosity for methionine at codon 129 of the human prion gene on the onset of neurological and hepatic symptoms in Wilson disease. Arch Neurol. 2006;63:982-985.

3. Compston A. Progressive lenticular degeneration: a familial nervous disease associated with cirrhosis of the liver, by S. A. Kinnier Wilson, (From the National Hospital, and the Laboratory of the National Hospital, Queen Square, London) Brain 1912: 34; 295-509. Brain. 2009;132(pt 8):1997-2001.

4. Thomas R, Sanders S, Doust J, et al. Prevalence of attention-deficit/hyperactivity disorder: a systematic review and meta-analysis. Pediatrics. 2015;135:e994-e1001.

5. Kang K. Abnormality on liver function test. Pediatr Gastroenterol Hepatol Nutr. 2013;16:225-232.

6. Lorincz M. Neurologic Wilson’s disease. Ann NY Acad Sci. 2010;1184:173-187.

7. Dening TR, Berrios GE, Walshe JM. Wilson’s disease and epilepsy. Brain. 1988;111(pt 5):1139-1155.

8. Socha P, Janczyk W, Dhawan A, et al. Wilson’s disease in children: a position paper by the Hepatology Committee of the European Society for Paediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutrit. 2018;66:334-344.

9. Bull PC, Thomas GR, Rommens JM, et al. The Wilson disease gene is a putative copper transporting P-type ATPase similar to the Menkes gene. Nat Genet. 1993;5:327-337.

10. Ala A, Schilsky ML. Wilson disease: pathophysiology, diagnosis, treatment and screening. Clin Liver Dis. 2004;8:787-805, viii.

11. Thomas GR, Forbes JR, Roberts EA, et al. The Wilson disease gene: spectrum of mutations and their consequences. Nat Genet. 1995;9:210-217.

12. Pfeiffer RF. Wilson’s disease. Semin Neurol. 2007;27:123-132.

13. Das SK, Ray K. Wilson’s disease: an update. Nat Clin Pract Neurol. 2006;2:482-493.

14. Morgan HG, Stewart WK, Lowe KG, et al. Wilson’s disease and the Fanconi syndrome. Q J Med. 1962;31:361-384.

15. Wiebers DO, Hollenhorst RW, Goldstein NP. The ophthalmologic manifestations of Wilson’s disease. Mayo Clin Proc. 1977;52:409-416.

16. Jackson GH, Meyer A, Lippmann S. Wilson’s disease: psychiatric manifestations may be the clinical presentation. Postgrad Med. 1994;95:135-138.

17. O’Conner JA, Sokol RJ. Copper metabolism and copper storage disorders. In: Suchy FJ, Sokol RJ, Balistreri WF, eds. Liver Disease in Children. 3rd ed. New York, NY: Cambridge University Press; 2007:626-660.

18. Dening TR, Berrios GE. Wilson’s disease: a longitudinal study of psychiatric symptoms. Biol Psychiatry. 1990;28:255-265.

THE CASE

A 5-year-old boy was brought into his primary care clinic by his mother, who expressed concern about her son’s increasing impulsiveness, aggression, and difficulty staying on task at preschool and at home. The child’s medical history was unremarkable, and he was taking no medications. The family history was negative for hepatic or metabolic disease and positive for attention deficit-hyperactivity disorder (ADHD; father).

The child’s growth was normal. His physical exam was remarkable for a liver edge 1 cm below his costal margin. No Kayser-Fleischer rings were present.

Screening included a complete metabolic panel. Notable results included an alanine aminotransferase (ALT) level of 208 U/dL (normal range, < 30 U/dL), an aspartate transaminase (AST) level of 125 U/dL (normal range, 10-34 U/dL), and an alkaline phosphatase (ALP) of 470 U/dL (normal range, 93-309 U/dL). Subsequent repeat laboratory testing confirmed these elevations (ALT, 248 U/dL; AST, 137 U/dL; ALP, 462 U/dL). Ceruloplasmin levels were low (11 mg/dL; normal range, 18-35 mg/dL), and 24-hour urinary copper was not obtainable. Prothrombin/partial thromboplastin time, ammonia, lactate, total and direct bilirubin, and gamma-glutamyltransferase levels were normal.

Further evaluation included abdominal ultrasound and brain magnetic resonance imaging, both of which yielded normal results. Testing for Epstein-Barr virus; cytomegalovirus; hepatitis A, B, and C titers; and antinuclear, anti-smooth muscle, and anti–liver-kidney microsomal antibodies was negative.

THE DIAGNOSIS

The patient’s low ceruloplasmin prompted referral to Pediatric Gastroenterology for consultation and liver biopsy due to concern for Wilson disease. Biopsy results were consistent with, and quantitative liver copper confirmatory for, this diagnosis (FIGURE).

Genetic testing for mutations in the ATP7B gene was performed on the patient, his mother, and his siblings (his father was unavailable). The patient, his mother, and his sister were all positive for His1069Gln mutation; only the patient was positive for a 3990_3993 del mutation (his half-brother was negative for both mutations). The presence of 2 different mutant alleles for the ATP7B gene, one on each chromosome—the common substitution mutation, His1069Gln, in exon 14 and a 3990_3993 del TTAT mutation in exon 19—qualified the patient as a compound heterozygote.

The 3990_3993 del TTAT mutation—which to our knowledge has not been previously reported—produced a translational frame shift and premature stop codon. As others have pointed out, frame shift and missense mutations produce a more severe phenotype.¹

Continue to: Further testing was prompted…

ALT (alanine aminotransferase) – SanaTest laboratory

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Rules for preparing for tests

An intracellular enzyme involved in amino acid metabolism.

Functions. Catalyzes the transfer of the amino group of alanine to alpha-ketoglutaric acid with the formation of pyruvic acid and glutamic acid. Transamination occurs in the presence of a coenzyme – pyridoxal phosphate – a derivative of vitamin B6. The highest activity of ALT is detected in the liver and kidneys, the lower one is in the pancreas, heart, and skeletal muscles. Enzyme activity in women is slightly lower than in men.

ALT is an intracellular enzyme and its content in the blood serum of healthy people is low. But when cells rich in ALT (liver, heart muscle, skeletal muscles, kidneys) are damaged or destroyed, these enzymes are released into the bloodstream, which leads to an increase in their activity in the blood. In viral hepatitis, the degree of increase in ALT activity is usually proportional to the severity of the disease. In acute cases, the activity of the enzyme in the blood serum may exceed normal values by 5-10 times or more. With viral hepatitis, an increase in enzyme activity occurs at a very early time – even before the onset of jaundice. Enzyme activity is also increased in patients with the anicteric form of the disease. In dynamics, with a favorable course of the process, ALT activity slowly decreases to its original values over several weeks. But a rapid decrease in enzyme activity, combined with increasing hyperbilirubinemia, indicates an unfavorable prognosis.

ALT is also increased in myocardial infarction: the simultaneous determination of the activity of two aminotransferases (ALT and AST) is a valuable diagnostic test. Normally, the ratio of AST/ALT activities (de Ritis coefficient) is 1.33±0.42. With viral hepatitis, this ratio decreases, and with acute myocardial infarction, it rises sharply.

Indications for the purpose of the analysis:

Diagnostics and differential diagnostics of liver diseases; Donor screening; Examination of contacts in the focus of viral hepatitis; Myocardial pathology; Skeletal diseases

Increased ALT level:

Necrosis of liver cells of any etiology (viral hepatitis, toxic liver damage). Shock. Heart failure. Extensive trauma and necrosis of skeletal muscles. Cirrhosis of the liver. Cholestatic and obstructive jaundice. Liver cancer (primary and metastatic). Extensive myocardial infarction. Myocarditis. Myositis. Myodystrophy. fatty hepatosis. Chronic alcoholism. Severe pancreatitis. Severe burns. Primary lack of carnitine. Treatment with hepatotoxic drugs (psychotropic drugs, anabolic steroids, contraceptives, salicylates, sulfonamides, antibiotics, immunosuppressants, antitumor drugs, chemotherapy and anesthesia drugs).

Decreased ALT level:

Severe liver damage – extensive necrosis, cirrhosis (when the number of cells synthesizing ALT is significantly reduced). Deficiency of pyridoxal phosphate (vitamin B6)

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Add to cart functions of internal organs (liver, kidneys , thyroid gland). Diagnosis is based on methods for detecting the level of sugar, cholesterol, electrolyte indicators (potassium, sodium, chloride). Also, blood biochemistry includes tests to clarify the hormonal balance, the presence of narcotic substances in the body (chemical and toxicological studies).

Blood chemistry: liver profile and kidney test

Liver function can be measured by looking at the levels of enzymes AST , ALT , ALP , and body. High levels indicate that unwanted changes are taking place in the body. The data obtained may show various diseases :

viral hepatitis or infections;
a tumor developing in the body;
diabetes mellitus, pre-diabetic changes;
degradation of internal organs due to alcoholism.

Before taking a blood test for biochemistry, specify the specifics of preparation for the analysis. Some laboratory tests require certain conditions to be met (no food 12 hours before the test).

Liver tests allow you to clarify the specifics of the work of the kidneys. This includes tests such as a serum creatinine and urea test. The laboratory assistant measures the concentration of these substances in serum or plasma. Other studies include the study of potassium, sodium. High levels of uric acid, for example, can cause gout (an inflammatory disease of the joints). Before such screening, you can eat and drink normally.

What information does general blood chemistry provide?

As part of biochemical analyzes, you can find out about the state of many organs and systems. For example, thyroid function tests in an adult measure TSH (thyroid-stimulating hormone) and T4 (free thyroxine). Thanks to this, it is possible to get an idea of \u200b\u200bthe endocrine system and metabolism. The measurement of enzymes in general blood biochemistry also provides a lot of information :

Creatine kinase – Elevated levels of this enzyme can be caused by excessive exercise, muscle damage, and viral infections. In addition, this indicator alone can already signal a myocardial infarction that has occurred.
Troponins are also elevated after a heart attack.

What other information does the general blood test give biochemistry and what diseases can it report? The test may indicate diabetes. The amount of sugar in the blood is controlled by insulin, a hormone produced by the pancreas. The level of sugar (glucose) can be measured after a 12-hour fast or after a meal. The decoding of the analyzes is carried out according to a special table with the designation of the obtained indicators and the existing norm.

In addition to the listed options, you can donate blood for biochemistry to measure the level of cholesterol and triglycerides. A high level of LDL is associated with heart disease, blockage of blood vessels. The concentration of a drug in the body can be measured. This is usually used to check the effects of heart and anticonvulsant drugs, COPD and asthma treatments. Screening is useful in identifying the causes of infertility, problems with the menstrual cycle, and menopause.

What is a normal ast and alt level: High, Low & Normal Results, Symptoms & Causes

Aspartate aminotransferase (AST) blood test

Definition

Alternative Names

How the Test is Performed

How to Prepare for the Test

How the Test will Feel

Why the Test is Performed

Normal Results

What Abnormal Results Mean

Risks

Images

References

Related specialties

5-year-old boy • behavioral issues • elevated ALT and AST levels • Dx?

References

THE DIAGNOSIS

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ALT (alanine aminotransferase) – SanaTest laboratory

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Blood chemistry: liver profile and kidney test

What information does general blood chemistry provide?

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