This poster is published under an
open license. Please read the
disclaimer for further details.
Type:
Educational Exhibit
Keywords:
Pathology, Developmental disease, Arthritides, Localisation, Diagnostic procedure, Complications, MR, CT, Conventional radiography, Musculoskeletal soft tissue, Musculoskeletal joint, Musculoskeletal bone
Authors:
R. Morcillo Carratalá1, Y. Herrero Gómez1, M. T. Fernández Taranilla2, V. Artiles1, S. FERNANDEZ1, M. Céspedes1; 1Toledo/ES, 2FUENLABRADA/ES
DOI:
10.1594/ecr2014/C-0601
Background
INTRODUCTION
Gout is a disorder of purine metabolism characterized by deposits of monosodium urate monohydrate crystals (tophi) in joints,
bones,
tendons,
bursae,
and periarticular tissue caused by longstanding hyperuricaemia.
Gout is the most common inflammatory arthritis in developed countries (it affects 1-2% of adults),
with a prevalence much higher in men than in women and increases with age,
especially in patients older than 30 years.
In women it mainly develops after menopause because the fall in estrogen (which is uricosuric) causes upper serum urate concentrations.
Hyperuricaemia is a risk factor for gout but most people remain asymptomatic throughout their lives.
Most patients with gout have a serum urate level above 6 mg/dL (in women) or 7 mg/dL (in men).
Gout and hyperuricaemia are associated with hypertension,
diabetes mellitus,
metabolic syndrome,
and renal and cardiovascular diseases.
Uric acid is the final product of endogenous and dietary purine metabolism.
Urate is produced in tissues that have the enzyme xanthine oxidase,
mainly in the liver and to a lesser extent in the small intestine.
Most uric acid produced daily is eliminated by the kidney (60-70%) and the rest is excreted through the gastrointestinal tract.
Renal mechanisms are responsible for hyperuricaemia in about 90% of individuals because impaired excretion of renal uric acid.
Hyperuricaemia results from several causes,
including:
- Idiopathic: the most common.
- Enzyme defects: overactivity of phosphoribosylpyrophosphate synthetase (overproduction of uric acid),
glucose-6 phosphatase deficiency (glycogen storage disease type 1),
hypoxanthine–guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome).
- Increased catabolism of purines: myeloproliferative and lymphoproliferative disorders,
psoriasis,
haemolytic anaemia.
- Decreased the renal excretion of uric acid: thiazide diuretics,
alcohol,
low-dose salicylates,
cyclosporine,
and renal disease.
- Diet: the prevalence of gout increases with consumption of alcohol and fructose (because of acceleration of ATP degradation to AMP,
a precursor of uric acid),
meat and seafood.
CLINICAL FEATURES
The disease is best described in four clinical phases:
- Asymptomatic hyperuricaemia: elevated uric acid levels without symptoms of arthritis,
tophi or uric acid stones.
Gout appears after 20 or 30 years of longstanding hyperuricaemia.
However,
about 5-10% of people with hyperuricaemia develop gout at some point in their lifetime.
- Acute gouty arthritis: risk of acute gout rises with urate concentration.
The arthritis is usually monoarticular and the initial attack is most often in the lower limbs (85–90% of cases),
usually the first metatarsophalangeal joint.
Factors that may increase the risk of acute attack of gout are alcohol,
meat and seafood consumption,
trauma,
and surgery.
Onset is abrupt,
and the affected joint is erythematous,
hot,
swollen,
and tender.
The most important differential diagnosis is septic arthritis.
Subsequent attacks frequently occur within shorter intervals and affect several joints,
especially the upper limbs.
- Intercritical gout: asymptomatic time between acute attacks of gout that can last months or years.
- Chronic tophaceous gout: tophaceous gout represents the chronic form of the disease (Fig. 1).
The arthritis is destructive poliarticular and tophi (deposits of monosodium urate crystals surrounded by chronic mononuclear and giant-cell reactions) can happen anywhere in the body: periarticular (tendons,
ligaments,
cartilages,
bones,
bursae,
synovial spaces),
paraarticular,
intraarticular,
or extraarticular tissues (subcutaneous tissue of the skin,
helix of the ear,
eyes,
breast,
vocal cords,
heart,
colon).
Tophi are painless and rarely become infected.
Identification of monosodium urate crystals in synovial fluid or tophus aspirates is the key diagnostic method for gout.
Such crystals appear as thin structures with pointed ends and they are strongly negative birefringent under direct polarised light.