An inherited disorder of purine metabolism, occurring
especially in men, characterized by a raised but variable blood uric
acid level and severe recurrent acute arthritis of sudden onset
resulting from deposition of crystals of sodium urate in connective
tissues and articular cartilage.
Gout most commonly affects joints in the following areas: feet,
ankles, hands, wrists, elbows, and knees. Less commonly affected
areas include the sacroiliac, sternoclavicular, and shoulder joints.
Also, gout rarely affects the hip and spine. One systemic area of
involvement in gout involves the kidneys, as a result of crystal
deposition with resulting sequelae
Plain-film radiography may be used to evaluate gout;
however, findings generally do not appear until after at least 1
year of uncontrolled disease. Bone scanning may also be used to
examine gout; the key finding on bone scans is an increased
radionuclide concentration at affected sites.
|Early-phase 1 findings in gout are limited
to the soft tissues. The typical finding is an asymmetric
swelling around the affected joint. Another finding that may be
evident in the early phase of gout is edema of the soft tissues
around the joints. In a patient who has had multiple episodes of
gouty arthritis in the same joint, a cloudy area of increased
opacity may be seen on plain-film radiographs
|In the intermediate phase 2 of gout, the
earliest bony changes appear. Most commonly, the bony changes
initially appear in the first metatarsophalangeal joint area.
These early changes are generally seen outside the joint or in
the juxta-articular area. These intermediate-phase findings are
often described as punched-out lesions, which can progress to
become sclerotic as they increase in size. Fractures may be
present in affected areas in severe cases of intermediate-phase
||In late-phase 3 gout, the hallmark findings
are numerous interosseous tophi.
Another change evident on plain-film radiographs in late-stage
disease is joint-space narrowing, which can be severe and
symptomatic. Marked deformities and subluxation may also be
noted in affected areas during the late stage of disease.
Calcific deposits in the soft tissues also can be observed in
The criterion standard in the diagnosis of gout is the analysis
of synovial fluid samples obtained with aspiration. Wet mounts of
the synovial fluid in gout reveal negatively birefringent urate
crystals. Also, the synovial fluid usually reveals an inflammatory
process, with a white blood cell count in the range of 7,000-10,000
x 103 per microliter.
Limitations of Techniques: In general, plain-film radiography is
useful in the evaluation of gout only after at least 1 year of
uncontrolled disease. CT is often used to follow up the development
of gout in areas that are difficult to assess; generally, CT is not
used as a screening examination for the disease. MRI has not been
studied with regard to its benefit in the evaluation of gout;
however, MRI may have promise in the study of this disease.
Chronic gout may be mistaken for rheumatoid arthritis as the joint
spaces narrow. However, in rheumatoid arthritis, joint involvement
is symmetric, erosions do not have sclerotic margins, and
juxta-articular osteoporosis may be present. Osteoarthritis may also
be mistaken for gout and can also occur concurrently.
Gout is a disease process that results from a central metabolic
abnormality, namely, hyperuricemia. In the early stages of the
disease, acute attacks of gouty arthritis occur. As gout progresses,
chronic arthritis develops; tophi in the affected joint spaces are
the hallmark findings.
Primary gout due to an inborn error of metabolism accounts for about
90% of cases of the disease, and approximately 10% of cases are due
to secondary gout. In 85-90% of cases of primary gout, the enzyme
defect responsible for hyperuricemia is unknown. Common causes of
secondary gout include renal disease, conditions with increased
nucleic-acid turnover, and inborn errors of metabolism.
Gout develops in less than 5% of people with hyperuricemia,
according to some estimates. This finding leads to the question
about why some affected individuals have gout and others do not.
Several factors are believed to predispose individuals to gout,
including the following: genetic predisposition,
obesity, use of pharmacologic agents, age, and duration of hyperuricemia
Acute attacks of gout are generally treated with nonsteroidal
anti-inflammatory drugs (NSAIDs), particularly indomethacin. Options
for the long-term treatment of gout include the administration of
probenecid, colchicines, and/or allopurinol. Patients should rest
the affected joints until the acute attack subsides. Attacks may be
prevented with dietary changes, specifically the avoidance of
dietary fats, alcohol, sardines, anchovies, liver, and sweetbreads.