CPT Test code: 84550
Specimen: | Serum (preferred) or plasma |
Volume: | 1 mL |
Minimum Volume: | 0.5 mL |
Container: | Red-top tube, gel-barrier tube, green-top (heparin) tube, or lavender-top (EDTA) tube |
Collection: | Separate serum or plasma from cells within 45 minutes of collection. |
Storage Instructions: | Maintain specimen at room temperature.1 |
Patient Preparation: | At least four-hour fast preferred |
Causes for Rejection: | Improper labeling |
Reference Interval: | Male:1
• 0-1 month: 3.3-8.4 mg/dL • 1-12 months: 1.9-8.1 mg/dL • 1-12 years: 1.9-5.8 mg/dL • 12-18 years: 3.4-7.8 mg/dL • 18 years and older: 3.7-8.6 mg/dL Female: • 0-1 month: 2.4-6.5 mg/dL • 1-12 months: 2.1-6.5 mg/dL • 1-12 years: 2.0-5.8 mg/dL • 12-18 years: 2.4-6.3 mg/dL • 18 years and older: 2.5-7.1 mg/dL Therapeutic target for gout patients: <6.02 |
Use: | Uric acid measurements are useful in the diagnosis and treatment of gout, renal failure, and a variety of other disorders including leukemia, psoriasis, starvation, and other wasting conditions. Patients receiving cytotoxic drugs may be monitored with uric acid measurements. Only a minority of individuals with hyperuricemia develop gout. An increased uric acid level does not necessarily translate to a diagnosis of gout.3 The therapeutic goal for uric acid-lowering therapy is to promote crystal dissolution and prevent crystal formation. This is achieved by maintaining a uric acid level of less than 6 mg/dL.2
Elevated uric acid: Elevations of uric acid occur with increased purine synthesis, inherited metabolic disorders, excess dietary purine intake, increased nucleic acid turnover, malignancy, cytotoxic drugs, decreased excretion due to chronic renal failure, and increased renal reabsorption. Drugs: Drugs causing increased uric acid concentration include diurectics, pyrazinamide, ethambutol, and nicotinic acid.3 Endocrine: Hypothyroidism, hypoparathyroidism, hyperparathyroidism, pseudohypoparathyroidism, diabetes insipidus of nephrogenic type, and Addison disease can cause uric acid elevation. Lead poisoning from paint, batteries, and moonshine can cause elevated uric acid.4 Toxemia of pregnancy, diet, weight loss, fasting, or starvation can elevate uric acid levels.5 Decreased uric acid: Drugs bearing a relationship to low serum uric acid levels include aspirin (high doses), x-ray contrast agents, glyceryl guaiacolate, allopurinol corticosteroids, and probenecid.6 Massive doses of vitamin C increase urine uric acid secretion, lowering serum uric acid.4 Poor dietary intake of purines and protein can decrease serum uric acid. Diabetes, Fanconi syndrome, Wilson’s disease, cystinosis, galactosemia, hypophosphatemia, heavy metal poisoning, malignant neoplasms, hypereosinophilic syndrome, and Xanthinuria (deficiency of xanthine oxidase) can lower serum uric acid.4,6,7 Hypouricemia is reported with acute intermittent porphyria and severe liver disease (especially obstructive biliary disease).8 Isolated defects in the tubular transport of uric acid have been associated with increased renal clearance of urate, hyprouricemia, hypercalciuria, and decreased bone density.9 |
Additional Information: | Drug effects have been summarized.10 |
Footnotes: | 1. LabCorp Internal Studies
2. Zhang W, Doherty M, Bardin T, et al, “EULAR Evidence Based Recommendations for Gout. Part II: Management Report of a Task Force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT),” Ann Rheum Dis, 2006, 65(10):1301-11.PubMed 7447188 3. Messerli FH, Frohlich ED, Dreslinski GR, et al, “Serum Uric Acid in Essential Hypertension: An Indicator of Renal Vascular Involvement,” Ann Intern Med, 1980, 93(6):817-21.PubMed 7320221 4. Cameron JS, Simmonds HA, “Uric Acid, Gout and the Kidney,” J Clin Pathol, 1981, 34(11):1245-54.PubMed 6338384 5. Lin HY, Rocker LL, McQuillan MA, et al, “Cyclosporine-Induced Hyperuricemia and Gout,” N Engl J Med, 1989, 321(5):287-92.PubMed 2664517 6. Lugassy G, Michaeli J, “Hypouricemia in the Hypereosinophilic Syndrome. Response to Treatment,” JAMA, 1983, 250(7):937-8.PubMed 7144847 7. Pollard A, “Disorders of Purine and Pyrimidine Metabolism,” Applied Biochemistry of Clinical Disorders, Gornall AG, ed, Hagerstown, MD: Harper & Row Publishers, 1980, 335-44.PubMed 16707533 8. Ramsdell CM, Kelley WN, “The Clinical Significance of Hypouricemia, Ann Intern Med, 1973, 78(2):239-42.PubMed 3473283 9. Steele TH, “Hypouricemia,” N Engl J Med, 1979, 301(10):549-50 (editorial).PubMed 2664517 10. Zhiri A, Jouanel P, “Urates,” Drug Effects on Laboratory Test Results Analytical Interferences and Pharmacological Effects, Siest G, Galteau MM, eds, Littleton, MA PSG Publishing Co, Inc, 1988, 423-38.PubMed 3606290 |