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URIC ACID |
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Monitoring patients receiving cytotoxic drugs and a variety of other disorders, including gout, leukemia, psoriasis, starvation and other wasting conditions |
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Synonym | URIC ACID | |
Test Code | ||
Test Type | Biochemistry | |
Pre-Test Condition | Nothing special | |
Report Availability | Daily | |
# Test(s) | 1 | |
Test details | Sample Report |
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URIC ACID |
Synonym | URIC ACID | ||
Test Code | |||
Test Category | Biochemistry | ||
Pre-Test Condition | Nothing special | ||
Medical History | Share if any | ||
Report Availability | Daily | ||
Specimen/Sample | Blood | ||
Stability @21-26 deg. C | 4 Hrs | ||
Stability @ 2-8 deg. C | NA | ||
Stability @ Frozen | NA | ||
# Test(s) | 1 | ||
Processing Method | Uricase |
USEFUL FOR Diagnosis and treatment of renal failure Monitoring patients receiving cytotoxic drugs and a variety of other disorders, including gout, leukemia, psoriasis, starvation and other wasting conditions CLINICAL INFORMATION Uric acid is the final product of purine metabolism in humans. Purines, compounds that are vital components of nucleic acids and coenzymes, may be synthesized in the body or they may be obtained by ingesting foods rich in nucleic material (eg, liver, sweetbreads). Approximately 75% of the uric acid excreted is lost in the urine; most of the remainder is secreted into the gastrointestinal tract where it is degraded to allantoin and other compounds by bacterial enzymes. Asymptomatic hyperuricemia is frequently detected through biochemical screening. The major causes of hyperuricemia are increased purine synthesis, inherited metabolic disorder, excess dietary purine intake, increased nucleic acid turnover, malignancy, cytotoxic drugs, and decreased excretion due to chronic renal failure or increased renal reabsorption. Long-term follow-up of these patients is undertaken because many are at risk of developing renal disease; few of these patients ever develop the clinical syndrome of gout. Hypouricemia, often defined as serum urate below 2.0 mg/dL, is much less common than hyperuricemia. It may be secondary to severe hepatocellular disease with reduced purine synthesis, defective renal tubular reabsorption, overtreatment of hyperuricemia with allopurinol, as well as some cancer therapies (eg, 6-mercaptopurine). REFERENCE VALUES Males 1-10 years: 2.4-5.4 mg/dL 11 years: 2.7-5.9 mg/dL 12 years: 3.1-6.4 mg/dL 13 years: 3.4-6.9 mg/dL 14 years: 3.7-7.4 mg/dL 15 years: 4.0-7.8 mg/dL > or =16 years: 3.7-8.0 mg/dL Reference values have not been established for patients who are <12 months of age. Females 1 year: 2.1-4.9 mg/dL 2 years: 2.1-5.0 mg/dL 3 years: 2.2-5.1 mg/dL 4 years: 2.3-5.2 mg/dL 5 years: 2.3-5.3 mg/dL 6 years: 2.3-5.4 mg/dL 7-8 years: 2.3-5.5 mg/dL 9-10 years: 2.3-5.7 mg/dL 11 years: 2.3-5.8 mg/dL 12 years: 2.3-5.9 mg/dL > or =13 years: 2.7-6.1 mg/dL Reference values have not been established for patients who are <12 months of age. INTERPRETATION Hyperuricemia is most commonly defined by serum or plasma uric acid concentrations above 8.0 mg/dL in males or above 6.1 mg/dL in females. CAUTIONS The following drugs cause interference (falsely decreased levels) at therapeutic concentrations: -Alpha-methyldopa -Desferoxamine -Calcimdobesilate Results can be falsely decreased in patients with elevated levels of N-acetyl-p-benzoquinone imine (NAPQI, a metabolite of acetaminophen), N-acetylcysteine (NAC), and metamizole. CLINICAL REFERENCE Tietz Textbook of Clinical Chemistry. Chapter 24: Fourth edition, Edited by CA Burtis, ER Ashwood, WS Bruns. WB Saunders Company, Philadelphia, 2006, pp 803-807 |