Gout Disease

BASICS

DESCRIPTION

Inflammatory reaction to urate crystals in joints, bones and subcutaneous structures. Initially, a hyperacute arthritis which may progress to a chronic arthritis. Rarely it may present as a chronic arthritis. Recognition of the crystals in fluid is pathognomonic.

Primary gout - the most common: underexcretion or overproduction of uric acid
Secondary gout - related to myeloproliferative diseases or their treatment, therapeutic regimens producing hyperuricemia, renal failure, renal tubular disorders, lead poisoning, hyperproliferative skin disorders, enzymatic defects (e.g., deficient hypoxanthine guanine phosphoribosyltransferase, glycogen storage diseases)
System(s) affected: Musculoskeletal, Endocrine/Metabolic, Renal/Urologic
Genetics: N/A
Incidence/Prevalence in USA: 100/100,000. Under age 18: rare; age 18-44: 3; age 45-64: 21; age over 65: 35
Predominant age: 30-60
Predominant sex: Male > Female (20:1)

SIGNS AND SYMPTOMS

Hyperacute onset (within 24 hours) of severe pain, swelling, redness, and warmth in one or two joints (75% are monoarticular)
Soft tissue redness, swelling, warmth
Exquisite tenderness
Propensity for first MTP joint, symptomatic in 50% of initial attacks; eventually in 75%
Acute untreated attacks last 2–21 days
Attack may be isolated; more often repetitive. Second attack may not occur for years.
Recurrent attacks last longer and occur more frequently with each recurrence
Between critical periods – absence of inflammation (until the chronic or tophaceous phase occurs)
Rarely polyarticular – proximal interphalangeal, distal interphalangeal, metacarpal phalangeal, wrist, knee, ankle, midtarsal joints, heel
Migratory polyarthritis is a rare presentation
50% of untreated patients develop a chronic arthritis within 3–42 years
Inflammatory synovial effusion
Subcutaneous or intraosseous nodules (20%), referred to as tophi – may affect ears (antihelix), extensor aspects of peripheral joints (e.g., olecranon), rarely fingertips, cornea, aorta, spine, or even intracranial
Subcutaneous nodules may have a creamy (urate) discharge
Fever, chills
Carpal tunnel syndrome
Kidney stones

CAUSES

Hyperuricemia
Dietary excess (e.g., anchovies, sardines, sweetbreads, kidney, liver, and meat extracts)
Inborn errors of metabolism
Lead poisoning (Saturnine gout from moonshine)
Kidney disease
Hemoproliferative disorders

RISK FACTORS

Ethanol ingestion
Family history
Polynesian extraction (e.g., Samoan gout)
Medications – aminophylline, caffeine, corticosteroids, cytotoxic drugs (cyclosporine), diazepam, diphenhydramine, diuretics, L-dopa, dopamine, epinephrine, ethambutol, methaqualone, alpha-methyl dopa, nicotinic acid, probenecid (low dose), pyrazinamide, salicylates (< 10/dL blood levels), sulfinpyrazone (low dose), vitamins B12 and C
Diuretics may be responsible for 20% of secondary gout
Ketosis
Surgery or trauma
Obesity (50%)
Hypertension (50%)
Vascular disease
Diabetes
Renal failure
Hypothyroidism
Hyperparathyroidism; hypoparathyroidism
Hyperlipidemia types II, IV, V
Paget's disease
Hyperproliferative skin disorders (e.g., psoriasis)
Lymphoproliferative disorders
Calcium pyrophosphate deposition disease
Sarcoidosis
Hemolytic anemia
Hemoglobinopathies
Pernicious anemia
Radiation treatment
Type I glycogen storage disease
Down syndrome
Gut sterilization by antibiotics

DIAGNOSIS

LABORATORY

WBC usually elevated with left shift during acute attacks
ESR usually elevated during acute attacks
Hyperuricemia may be present, although not diagnostic

Drugs that may alter lab results:

Intra-articular steroids – many have inherent birefringence, which will cause confusion on synovial fluid analysis
Hyperuricemia – induced by drugs that reduce effective circulating blood volume (induced by low dose aspirin, probenecid or sulfinpyrazone)
Cyclosporine – induced renal insufficiency

Disorders that may alter lab results: Alcoholism, sarcoidosis, lead poisoning, kidney failure, psoriasis, hemoglobinopathy

PATHOLOGICAL FINDINGS

Urate crystals in synovial membrane (98% of specimens processed entirely anhydrously [urate is water soluble])
Tophus in 29% of individuals with untreated gout of 5 years duration, in 74% of individuals with untreated gout of 40 years duration

SPECIAL TESTS

Synovial fluid white blood cell count is usually inflammatory (10,000–70,000 cells/dL), but may have as few as 1,000 WBC/dL
Wet mounts of synovial fluid reveal negatively birefringent urate crystals on polarizing exam
Gout crystals may be identified in asymptomatic joints

IMAGING

X-ray is usually normal in the first year of uncontrolled disease.
X-ray in chronic gout reveals "punched-out" erosions (lytic areas) often with periosteum overgrowing the erosion ("overhanging edge" sign). This is highly suggestive, but may also be caused by amyloidosis, type IIa hyperlipoproteinemia, and by multicentric reticulohistiocytosis.
X-ray erosions with preservation of joint space is similarly characteristic. X-ray rarely reveals intraosseous lytic areas (tophi).
Bone scan reveals increased nuclide concentration at affected sites

DIAGNOSTIC PROCEDURES

Arthrocentesis with polarizing optical examination
Biopsy of synovial membrane or subcutaneous nodule, processing the specimen anhydrously (urate is water soluble) and examining with polarizing optics

TREATMENT

APPROPRIATE HEALTH CARE

Outpatient, except for consideration of associated joint infection or for therapeutic unresponsiveness

GENERAL MEASURES

Control the acute attack of gout
Addressing the underlying cause

SURGICAL MEASURES

N/A

ACTIVITY

Affected joint(s) at rest until hyperacute phase is controlled

DIET

Reduce ingestion of fat, alcoholic beverages, sardines, anchovies, liver, sweetbreads

PATIENT EDUCATION

Arthritis Foundation pamphlet on gout
Rothschild, BM.: Hyperuricemia in the elderly. Geriatric Consultant, 4:14-16, 31, 1985.

FOLLOW UP

PREVENTION/AVOIDANCE

Avoidance of exacerbating medications/diets/habits

POSSIBLE COMPLICATIONS

Increased susceptibility to infection
Urate nephropathy
Uric acid nephropathy
Renal stones
Nerve/spinal cord impingement
Recognition of urate crystals does not preclude concomitant infectious arthritis

EXPECTED COURSE AND PROGNOSIS

With early treatment, total control
If recurrent attacks, successful uric acid adjustment (requiring lifelong use of uricosuric or allopurinol medication) usually effective
During the first 6–24 months of uricosuric or allopurinol therapy, acute gout may occur

MISCELLANEOUS

ASSOCIATED CONDITIONS

Myeloproliferative disorders
Lymphoproliferative disorders
Alcoholism
Hyperlipidemia
Obesity
Hypertension
Diabetes
Lesch-Nyhan syndrome – chorea, spasticity, self-mutilation in childhood

AGE-RELATED FACTORS

Pediatric: Onset in this age group identifies gout secondary to an inborn error of metabolism or underlying disease process
Geriatric: Usually related to medications
Others: N/A

PREGNANCY

Usual pregnancy precautions

OTHER NOTES

N/A

ABBREVIATIONS

MP = metatarsal phalangeal
NSAID = nonsteroidal anti-inflammatory drug

Clinical Investigations

ROLE OF HOMOEOPATHY

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