Uric acid level, Blood Uric Acid
Sample
- Get the venous blood and prepare the serum.
- The serum is preferred but this test can be done on the plasma.
- A random sample can be used.
- Serum/plasma is stable for 3 to 5 days at 4 °C.
Precautions
- EDTA and fluoride cause positive interference with the uricase method.
- Severe exercise increased the level of uric acid.
Indications
- This is done to diagnose gout.
- This test is also helpful to assess recurrent urinary stone formation.
- This test is done in leukemic patients and in renal failure.
Pathophysiology
- Uric acid is formed by the breakdown of nucleic acid.
- Uric acid is the end product of purine nucleoside, adenosine, and guanosine metabolism.
- Purine from dietary nucleic acid directly converted to uric acid.
- Uric acid formation from the Purine metabolism is 400 mg/day.
- The diet is 300 mg/day.
- Most of the body purines excreted as uric acid into the urine.
- Uric acid in the plasma found as monosodium urates.
- Uric acid is more soluble in plasma, synovial fluid, and urine than an aqueous solution.
- Patient with gout has urates pool of 18,000 to 30,000 mg.
- Mainly uric acid forms in the liver.
- The blood level of the uric acid depends upon:
- The rate of synthesis in the liver.
- The rate of excretion by the kidneys.
- Uric acid transported from the liver to the kidney through the blood.
- Uric acid removal:
- From the kidney, 75% is filtered.
- Rest 25 % excreted in the GI tract and degraded there.
- AT pH >5.57, most uric acid is in the urates form, this chemical form is soluble in the urine.
- Uricase enzyme deficiency accumulates uric acid in the body.
- Why there is an increased level of uric acid, that is due to:
- Excessive cell breakdown.
- catabolism of nucleic acid.
- Failure to excrete as in renal failure.
GOUT
- It leads to arthritis:
- There is the deposition of uric acid crystals in the periarticular joint tissue.
- At >6.4 mg/dL uric acid, plasma is saturated and the urate crystals precipitate in the tissue.
- They initiate acute inflammation with the presence of polys and macrophagic cells.
- The deposit of uric acid in soft tissue is called Tophi.
- When urine is supersaturated with uric acid leads to stone formation.
Signs and Symptoms of Gout:
- Asymptomatic Hyperuricemia is asymptomatic which is diagnosed by a lab test.
- These patients are at more risk to develop renal stones.
- Symptomatic patients may develop Gout (acute gouty arthritis).
- The deposits of urates are responsible for the signs and symptoms of inflammation.
- Gouty arthritis may associate with deposits of urates in the joint fluids.
- The patient may develop gouty nephropathy.
- May have urates nephrolithiasis.
- Pseudogout is caused by the deposition of calcium pyrophosphate dihydrate crystals.
- Gout is uncommon in children, menopausal women, and in males under the age of 30 years.
- Peak age is 40 to 50 years of age in males and later age group in females.
- Gout with the formation of Tophi. This is the third mode of presentation. This may begin at an early age or late age group.
- 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:
- Gout.
- renal diseases and Renal failure, prerenal Azotemia.
- Alcoholism.
- Lead poisoning.
- Leukemia, Multiple Myeloma, Lymphoma.
- Starvation, weight-loss diets.
- Metabolic acidosis. and Diabetic ketoacidosis
- Toxemia of pregnancy.
- Liver diseases.
- Hemolytic Anaemia.
- Following excessive cell destruction, as in chemotherapy and radiation therapy.
- Lead poisoning.
- Alcoholism.
- Hereditary gout.
- Hyperlipidemia and obesity.
- Hypothyroidism.
- Hypoparathyroidism.
- Hemolytic anemias.
- Psoriasis.
- Glycogen storage disease.
- Increased ingestion of purines in diet e.g. liver, sweetbreads, kidneys, and anchovies.
- A genetic inborn error in purine metabolism.
- Metastatic cancers.
- Rhabdomyolysis e.g. Heavy Exercise, Crush injury, burns, epileptic seizure, and myocardial infarction.
Hyperuricemia due to decreased excretion:
- Primary:
- Idiopathic.
- Secondary:
- Acidosis in diabetes and starvation.
- Hypothyroidism.
- Toxemia of pregnancy.
- Shock or chronic blood loss.
- Alcoholism.
- Hyperlipoproteinemia.
- Acute and Chronic renal failure.
- Lead poisoning.
- Salicylate due to low doses.
- Thiazide diuretics.
Decreased level of Uric acid seen in (Hypouricemia <2 mg/dL) :
- Fanconi’s syndrome
- Wilson’s disease
- Some malignancies like Hodgkin’s lymphoma and Myeloma.
- Deficiency of xanthine oxidase.
- Lead poisoning.
- Yellow atrophy of the liver.
- Salicylates in low doses.
- Thiazide diuretics.
- Increased renal reabsorption.
Treatment
- Prevent the acute attack.
- Prevent the stone formation.
- The acute attack needs anti-inflammatory, non-steroidal drugs, and allopurinol.
- Colchicine is used in patients who can tolerate NSAIDs.
- Cortisone can be injected into the joints.
- Ice -packs may be applied to relieve the pain.
- The patient has advised a low purine diet.
- Intake of fluid is encouraged to increase urinary output.
- Antihyperuricemic drugs like Zyloric is given.
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