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THE LABORATORY INVESTIGATION OF HYPERURICAEMIA AND GOUT


THE LABORATORY INVESTIGATION OF HYPERURICAEMIA AND GOUT
Definition

Hyperuricaemia is defined as a serum uric acid concentration above the upper level of normal for your laboratory. These levels differ for males and females. 

Hyperuricaemia is a risk factor for the development of gout; the exact relationship between hyperuricaemia and acute gout is unclear since acute gouty arthritis can occur in the presence of normal serum uric acid concentrations, and conversely, many persons with hyperuricaemia never experience an attack of gout.
Hyperuricaemia has been associated with hypertriglyceridaemia and diabetes mellitus, and it may be a risk factor for the development of coronary artery disease.

Initial laboratory investigations

Once the diagnosis of hyperuricaemia has been confirmed, the causes of this condition should be evaluated in order to correct these - see below for details
In addition, because patients with hyperuricaemia often have hypertension and impaired renal function, examination of the renal and cardiovascular system is essential. 

Baseline tests should include:
FBC
Urinalysis
U&E, creatinine
Serum uric acid
24-urine uric acid determination

 
CLINICAL FEATURES LABORATORY INVESTIGATIONS
  Hyperuricaemia progresses through the following clinical phases.
1. Asymptomatic hyperuricaemia Asymptomatic hyperuricaemia is the term for an abnormally high serum urate level (higher than the upper level of normal for your laboratory) without gouty arthritis or nephrolithiasis.
2. Acute gouty arthritis

Acute gout is characterised by the sudden 
onset of pain, erythema, limited range of motion and swelling of the involved joint, usually the first metatarsophalangeal joint, but may also involve other joints such as the ankle, the wrist and the fingers.
Demonstration of intra-articular monosodium urate crystals is necessary to establish the definitive diagnosis of gouty arthritis. Reliance on the clinical presentation and the serum uric acid level alone may lead to an inaccurate diagnosis, since rheumatoid arthritis, pseudogout (calcium pyrophosphate deposition) and osteoarthritis may mimic gouty arthritis.

3. Intercritical gout (intervals between acute attacks)

Following recovery from an acute gouty attack the patient reenters an asymptomatic phase of disease = "intercritical gout". During this phase the clinician should investigate the secondary causes of gout - see below

4. Chronic tophaceous gout

Tophi are deposits of sodium urate that are large enough to be seen on X-rays and may occur at virtually any site, especially the joints of the hands and feets, the helix of the ear, the olecranon bursa and the Achilles tendon. Usually occurs in patients with a polyarticular presentation, a serum uric levels more than 0.535 mmol/L (9.0 mg/dL), and with disease onset in persons less than 40 years.

4. Nephrolithiasis
 
CAUSES LABORATORY INVESTIGATIONS
  Baseline tests should include:
FBC
Urinalysis
U&E and creatinine
Blood urea
Serum uric acid
24-urine uric acid determination
Primary

Glucose-6-phosphate dehydrogenase deficiency
Fructose-1-phosphate aldolase deficiency
Hypoxanthine-guanine phosphoribosyltransferase deficiency 
(Lesch-Nyhan sydrome).
Primary idiopathic hyperuricaemia
Secondary A practical approach to differentiate
between overproduction of urate and 
decreased excretion is to obtain a 24-urine uric acid determination without dietary restriction.
Overproduction of uric acid
Haemolytic processes
Lymphoproliferative diseases
Myeloproliferative diseases
Polycythemia vera
Psoriasis
Paget's disease
Rhabdomyolysis
Exercise
Obesity
Purine-rich diet especially meat
Decreased excretion of uric acid      This is the most common abnormality
Renal insufficiency
Diabetes insipidus
Hypertension
Starvation ketosis
Sarcoidosis
Lead intoxication
Hyperparathyoidism
Hypothyroidism
Bartter's syndrome
Drugs e.g. salicylates diuretics levodopa ethambutol pyrazinamide cyclosporine nicotinic acid
Combined mechanism
Alcohol
Shock
 
REFERENCES
  1. Harris MD et al. Gout and hyperuricemia. Am. Fam. Phy 1999; Feb 15
  2. Pittman JR et al. Diagnosis and management of gout. Am.Fam.Phy 1999; Apr 1
  3. Sturrock RD. Gout. BMJ 2000; 320: 132 - 133
  4. Harrison's Principles of Internal Medicine. 12th edition.
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