Considered an indicator of cellular damage in liver disease, such as hepatitis or cirrhosis.
There are no food, fluid, activity, or medication restrictions unless by medical direction.
Method: Spectrophotometry, enzymatic at 37°C.
|Age||Conventional and SI Units||SI Units Expressed as microkat/L = (Units/L × 0.017)|
|Newborn||25–75 units/L||0.43–1.28 microkat/L|
|10 days–3 yr||15–60 units/L||0.26–1.02 microkat/L|
|Child||20–39 units/L||0.34–0.66 microkat/L|
| Male||20–40 units/L||0.34–0.68 microkat/L|
| Female||15–30 units/L||0.26–0.51 microkat/L|
|Values may be slightly elevated in older adults due to the effects of medications and the presence of multiple chronic or acute diseases with or without muted symptoms.|
Critical Findings and Potential Interventions
Overview(Study type: Blood collected in a gold-, red-, or red/gray-top tube; related body system: Digestive system.) Aspartate aminotransferase (AST) is an enzyme that catalyzes the reversible transfer of an amino group between aspartate and α-ketoglutaric acid in the citric acid or Krebs cycle, a powerful and essential biochemical pathway for releasing stored energy. AST exists in large amounts in liver and myocardial cells and in smaller but significant amounts in skeletal muscle, kidneys, pancreas, red blood cells, and the brain. Serum AST rises when there is damage to the tissues and cells where the enzyme is found, and levels directly reflect the extent of damage. AST values greater than 500 units/L (SI = 8.5 microkat/L) are usually associated with hepatitis and other hepatocellular diseases in an acute phase. AST levels are very elevated at birth, decrease with age to adulthood, and increase slightly in older adults.
- Compare serially with alanine aminotransferase levels to track the course of hepatitis.
- Monitor response to therapy with potentially hepatotoxic or nephrotoxic drugs.
- Monitor response to treatment for various disorders of hepatic function in which AST may be elevated, with tissue repair indicated by declining levels.
Factors that may alter the results of the study
- Drugs and other substances that may increase AST levels by causing cholestasis include amitriptyline, anabolic steroids, androgens, benzodiazepines, chlorothiazide, chlorpropamide, dapsone, erythromycin, estrogens, ethionamide, gold salts, imipramine, mercaptopurine, nitrofurans, oral contraceptives, penicillins, phenothiazines, progesterone, sulfonamides, tamoxifen, and tolbutamide.
- Drugs and other substances that may increase AST levels by causing hepatocellular damage include acetaminophen, acetylsalicylic acid, allopurinol, amiodarone, anabolic steroids, anticonvulsants, asparaginase, azithromycin, bromocriptine, captopril, cephalosporins, chloramphenicol, clindamycin, clofibrate, danazol, enflurane, ethambutol, ethionamide, fenofibrate, fluconazole, fluoroquinolones, foscarnet, gentamicin, indomethacin, interferon, interleukin-2, levamisole, levodopa, lincomycin, low-molecular-weight heparin, methyldopa, monoamine oxidase inhibitors, naproxen, nifedipine, nitrofurans, oral contraceptives, probenecid, procainamide, quinine, ranitidine, retinol, ritodrine, sulfonylureas, tetracyclines, tobramycin, and verapamil.
- Drugs and other substances that may decrease AST levels include allopurinol, cyclosporine, interferon alpha, naltrexone, progesterone, trifluoperazine, and ursodiol.
- Hemolysis falsely increases AST values.
- Hemodialysis falsely decreases AST values.
Potential Medical Diagnosis: Clinical Significance of Results
AST is released from any damaged cell in which it is stored, so conditions that affect the liver, kidneys, heart, pancreas, red blood cells, or skeletal muscle and cause cellular destruction demonstrate elevated AST levels.
Significantly increased (greater than five times normal levels) in:
- Acute hepatitis (AST is very elevated in acute viral hepatitis)
- Acute hepatocellular disease (especially related to chemical toxicity or drug overdose; moderate doses of acetaminophen have initiated severe hepatocellular disease in patients who are alcoholics)
- Acute pancreatitis
Moderately increased (three to five times normal levels) in:
- Alcohol misuse (chronic)
- Biliary tract obstruction
- Cardiac dysrhythmias
- Cardiac catheterization, angioplasty, or surgery
- Chronic hepatitis
- Heart failure
- HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome of pregnancy
- Infectious mononucleosis
- Liver tumors
- Muscle diseases (e.g., dermatomyositis, dystrophy, gangrene, polymyositis, trichinosis)
- Myocardial infarction
- Reye syndrome
- Trauma (related to injury or surgery of liver, head, and other sites where AST is found)
Slightly increased (two to three times normal) in:
- Cerebrovascular accident
- Cirrhosis, fatty liver (related to obesity, diabetes, jejunoileal bypass, administration of total parenteral nutrition)
- Delirium tremens
- Hemolytic anemia
- Pulmonary infarction
- Hemodialysis (presumed to be related to a corresponding deficiency of vitamin B6 observed in hemodialysis patients)
- Uremia (related to a buildup of toxins that modify the activity of coenzymes required for transaminase activity)
- Vitamin B6 deficiency (related to the lack of vitamin B6, a required cofactor for the transaminases)
Before the Study: Planning and Implementation
Teaching the Patient What to Expect
- Inform the patient this test can assist in assessing liver function.
- Explain that a blood sample is needed for the test.
Potential Nursing Actions
- Measuring and trending abdominal girth can assist in monitoring the progression of ascites with liver disease.
After the Study: Potential Nursing Actions
- The patient with cirrhosis should be observed carefully for the development of ascites, in which case fluid and electrolyte balance requires strict attention.
- Increased AST levels may be associated with liver disease. In general, patients should be encouraged to eat a well-balanced diet that includes foods high in fiber. Dietary recommendations will vary depending on the condition and its severity. For example, recommend a diet of soft foods if esophageal varices develop, fat substitutes for bile duct disease, or limitations on salt intake if ascites develop.
- Other options include enteral and parenteral nutrition as replacement strategies. Correlate laboratory values with IV fluid infusion and collaborate with the health-care provider and pharmacist to adjust to patient needs. Adequate pain and nausea control can improve caloric intake.
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