Uric Acid

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Part Number: 001057

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Description

12-Hour Fasting Required: NO

CPT Codes for this test: 84450

Labcorp's information for this test:

Synonyms

UA
Urate

Expected Turnaround Time

Within 1 day

Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.

Specimen Requirements

Specimen

Serum (preferred) or plasma

Volume

1 mL

Minimum Volume

0.7 mL (Note: This volume does not allow for repeat testing.)

Container

Red-top tube, gel-barrier tube, or green-top (lithium heparin) tube. Do not use oxalate, EDTA, or citrate plasma.

Collection

Separate serum or plasma from cells within 45 minutes of collection.

Storage Instructions

Maintain specimen at room temperature.¹

Stability Requirements

Temperature	Period
Room temperature	14 days
Refrigerated	14 days
Frozen	14 days
Freeze/thaw cycles	Stable x3

Causes for Rejection

Improper labeling

Test Details

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 <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 diuretics, 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, hypouricemia, hypercalciuria, and decreased bone density.⁹

Methodology

Uricase

Reference Interval

• Male:¹

- 0 to 30 days: 3.9-7.8 mg/dL

- 1 to 6 months: 1.9-8.1 mg/dL

- 7 to 11 months: 2.0-6.5 mg/dL

- 1 to 11 years: 2.2-5.5 mg/dL

- 12 years: 2.9-7.0 mg/dL

– 13 to 17 years: 3.9–7.7 mg/dL

– 18 years and older: 3.8–8.4 mg/dL

• Female:

- 0 to 30 days: 2.7-6.5 mg/dL

- 1 to 6 months: 2.0-6.6 mg/dL

- 7 to 11 months: 2.1-5.7 mg/dL

- 1 to 5 years: 2.0-5.0 mg/dL

- 6 to 11 years: 2.4-5.6 mg/dL

– 12 to 17 years: 2.9–6.1 mg/dL

– 18 to 50 years: 2.6–6.2 mg/dL

– 51 to 70 years: 3.0–7.2 mg/dL

– 71 years and older: 3.1–7.9 mg/dL

Therapeutic target for gout patients: <6.0²

Additional Information

Drug effects have been summarized.¹⁰

Footnotes

1. LabCorp internal studies

2. Zhang W, Doherty M, Bardin T, Suárez DH, Aristimuno GG. 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 Oct; 65(10):1301-1311. PubMed 16707532

3. Messerli FH, Frohlich ED, Dreslinski GR, Suárez DH, Aristimuno GG. Serum uric acid in essential hypertension: An indicator of renal vascular involvement. Ann Intern Med. 1980 Dec; 93(6):817-821. PubMed 7447188

4. Cameron JS, Simmonds HA. Uric acid, gout and the kidney. J Clin Pathol. 1981 Nov; 34(11):1245-1254. PubMed 7320221

5. Lin HY, Rocker LL, McQuillan MA, Schmaltz S, Palella TD, Fox IH. Cyclosporine-induced hyperuricemia and gout. N Engl J Med. 1989 Aug 3; 321(5):287-292. PubMed 2664517

6. Lugassy G, Michaeli J. Hypouricemia in the hypereosinophilic syndrome. Response to treatment. JAMA. 1983 Aug 19; 250(7):937-938. PubMed 6864977

7. Pollard A. Disorders of purine and pyrimidine metabolism. In: Gornall AG, ed. Applied Biochemistry of Clinical Disorders. Hagerstown, Md: Harper & Row Publishers;1980:335-344. PubMed 16707533

8. Ramsdell CM, Kelley WN. The clinical significance of hypouricemia. Ann Intern Med. 1973 Feb; 78(2):239-242. PubMed 4683752

9. Steele TH. Hypouricemia. N Engl J Med. 1979 Sep 6; 301(10):549-550. PubMed 460310

10. Zhiri A, Jouanel P. Urates. In: Siest G, Galteau MM, eds. Drug Effects on Laboratory Test Results. Analytical Interferences and Pharmacological Effects. Littleton, Mass: PSG Publishing Co;1988:423-438. PubMed 3606290