Uric acid level, Blood Uric Acid

Sample

1. Get the venous blood and prepare the serum.
2. The serum is preferred but this test can be done on the plasma.
3. A random sample can be used.
4. Serum/plasma is stable for 3 to 5 days at 4 °C.

Precautions

1. EDTA and fluoride cause positive interference with the uricase method.
2. Severe exercise increased the level of uric acid.

Indications

1. This is done to diagnose gout.
2. This test is also helpful to assess recurrent urinary stone formation.
3. This test is done in leukemic patients and in renal failure.

Pathophysiology

1. Uric acid is formed by the breakdown of nucleic acid.
2. Uric acid is the end product of purine nucleoside, adenosine, and guanosine metabolism.
3. Purine from dietary nucleic acid directly converted to uric acid.
4. Uric acid formation from the Purine metabolism is 400 mg/day.
   1. The diet is 300 mg/day.

5. Most of the body purines excreted as uric acid into the urine.
   1. Uric acid in the plasma found as monosodium urates.

6. Uric acid is more soluble in plasma, synovial fluid, and urine than an aqueous solution.
7. Patient with gout has urates pool of 18,000 to 30,000 mg.
8. Mainly uric acid forms in the liver.
9. The blood level of the uric acid depends upon:
   1. The rate of synthesis in the liver.
   2. The rate of excretion by the kidneys.

10. Uric acid transported from the liver to the kidney through the blood.
11. Uric acid removal:
    1. From the kidney, 75% is filtered.
    2. Rest 25 % excreted in the GI tract and degraded there.
    3. AT pH >5.57, most uric acid is in the urates form, this chemical form is soluble in the urine.
12. Uricase enzyme deficiency accumulates uric acid in the body.
13. Why there is an increased level of uric acid, that is due to:
    1. Excessive cell breakdown.
    2. catabolism of nucleic acid.
    3. Failure to excrete as in renal failure.

GOUT

1. It  leads to arthritis:
2. There is the deposition of uric acid crystals in the periarticular joint tissue.
   1. At >6.4 mg/dL uric acid, plasma is saturated and the urate crystals precipitate in the tissue.
3. They initiate acute inflammation with the presence of polys and macrophagic cells.
4. The deposit of uric acid in soft tissue is called Tophi.
5. When urine is supersaturated with uric acid leads to stone formation.

Signs and Symptoms of Gout:

1. Asymptomatic Hyperuricemia is asymptomatic which is diagnosed by a lab test.
   1. These patients are at more risk to develop renal stones.
2. Symptomatic patients may develop Gout (acute gouty arthritis).
   1. The deposits of urates are responsible for the signs and symptoms of inflammation.
   2. Gouty arthritis may associate with deposits of urates in the joint fluids.
   3. The patient may develop gouty nephropathy.
   4. May have urates nephrolithiasis.
   5. Pseudogout is caused by the deposition of calcium pyrophosphate dihydrate crystals.
   6. Gout is uncommon in children, menopausal women, and in males under the age of 30 years.
   7. Peak age is 40 to 50 years of age in males and later age group in females.
3. Gout with the formation of Tophi. This is the third mode of presentation. This may begin at an early age or late age group.
   1. Progressive inability to excrete uric acid and increase the urates crystal pool which appears Tophi in the cartilage, synovial membrane, tendons, and soft tissue.

Normal

Source 1

Age	mg/dL
Child <12 years	2.0 to 5.5
	Male	Female
Adult	4.4 to 7.6	2.3 to 6.6
60 to 90 years	4.2 to 8.0	3.5 to 7.3
>90 years	3.5 to 8.3	2.2 to 7.7

Source 2

• Male = 4.0 to 8.5 mg/dL
• Female = 2.7 to 7.3 mg/dL
• Old people = Values may be slightly increased.
• Child = 2.5 to 5.5 mg/dL
• Newborn = 2.0 to 6.2 mg/dL

Another source

• Male = 3.4 to 7.0 mg/dL.
• Female = 2.4 to 6.0 mg/dL.
• Children = 2.0 to 5.5 mg/dL.
• Hyperuricemia: most books defined the uric acid level:
  • Men = > 7 mg/dL.
  • Women = > 6 mg/dL.
• (Some of the books gives higher values)

Increased Uric acid level (Hyperuricemia >7 mg/dL in males and >6 mg/dL in female) is seen in:

1. Gout.
2. renal diseases and Renal failure, prerenal Azotemia.
3. Alcoholism.
4. Lead poisoning.
5. Leukemia, Multiple Myeloma, Lymphoma.
6. Starvation, weight-loss diets.
7. Metabolic acidosis. and Diabetic ketoacidosis
8. Toxemia of pregnancy.
9. Liver diseases.
10. Hemolytic Anaemia.
11. Following excessive cell destruction, as in chemotherapy and radiation therapy.
12. Lead poisoning.
13. Alcoholism.
14. Hereditary gout.
15. Hyperlipidemia and obesity.
16. Hypothyroidism.
17. Hypoparathyroidism.
18. Hemolytic anemias.
19. Psoriasis.
20. Glycogen storage disease.
21. Increased ingestion of purines in diet e.g. liver, sweetbreads, kidneys, and anchovies.
22. A genetic inborn error in purine metabolism.
23. Metastatic cancers.
24. Rhabdomyolysis e.g. Heavy Exercise, Crush injury, burns, epileptic seizure, and myocardial infarction.

Hyperuricemia due to decreased excretion:

1. Primary:
   1. Idiopathic.
2. Secondary:
   1. Acidosis in diabetes and starvation.
   2. Hypothyroidism.
   3. Toxemia of pregnancy.
   4. Shock or chronic blood loss.
   5. Alcoholism.
   6. Hyperlipoproteinemia.
   7. Acute and Chronic renal failure.
   8. Lead poisoning.
   9. Salicylate due to low doses.
   10. Thiazide diuretics.

Decreased level of Uric acid seen in (Hypouricemia <2 mg/dL) :

1. Fanconi’s syndrome
2. Wilson’s disease
3. Some malignancies like Hodgkin’s lymphoma and Myeloma.
4. Deficiency of xanthine oxidase.
5. Lead poisoning.
6. Yellow atrophy of the liver.
7. Salicylates in low doses.
8. Thiazide diuretics.
9. Increased renal reabsorption.

Treatment

1. Prevent the acute attack.
2. Prevent the stone formation.
3. The acute attack needs anti-inflammatory,  non-steroidal drugs, and allopurinol.
4. Colchicine is used in patients who can tolerate NSAIDs.
5. Cortisone can be injected into the joints.
6. Ice -packs may be applied to relieve the pain.
7. The patient has advised a low purine diet.
8. Intake of fluid is encouraged to increase urinary output.
9. Antihyperuricemic drugs like Zyloric is given.

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