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Gout and Pseudogout

Practice Essentials

Gout and pseudogout are the 2 most common crystal-induced arthropathies. Gout (see the image below) is caused by monosodium urate monohydrate crystals; pseudogout is caused by calcium pyrophosphate crystals and is more accurately termed calcium pyrophosphate disease.

Gout. Acute podagra due to gout in elderly man.

Gout. Acute podagra due to gout in elderly man.

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Signs and symptoms

Symptoms of gout or pseudogout include the following:

Podagra (initial joint manifestation in 50% of gout cases and eventually involved in 90%; also observed in patients with pseudogout and other conditions)

Arthritis in other sites – In gout, the instep, ankle, wrist, finger joints, and knee; in pseudogout, large joints (eg, the knee, wrist, elbow, or ankle)

Monoarticular involvement most commonly, though polyarticular acute flares are not rare, and many different joints may be involved simultaneously or in rapid succession

In gout, attacks that begin abruptly and typically reach maximum intensity within 8-12 hours; in pseudogout, attacks resembling those of acute gout or a more insidious onset that occurs over several days

Without treatment, symptom patterns that change over time; attacks can become more polyarticular, involve more proximal and upper-extremity joints, occur more often, and last longer

In some cases, eventual development of chronic polyarticular arthritis that can resemble rheumatoid arthritis

Physical findings may include the following:

Involvement of a single (most common) or multiple joints

Signs of inflammation – Swelling, warmth, erythema (sometimes resembling cellulitis), and tenderness

Fever (also consider infectious arthritis)

Migratory polyarthritis (rare)

Posterior interosseous nerve syndrome (rare)

Tophi in soft tissues (helix of the ear, fingers, toes, prepatellar bursa, olecranon)

Eye involvement – Tophi, crystal-containing conjunctival nodules, band keratopathy, blurred vision, anterior uveitis (rare), scleritis

Complications of gout include the following:

Severe degenerative arthritis

Secondary infections

Urate or uric acid nephropathy

Increased susceptibility to infection

Urate nephropathy

Renal stones

Nerve or spinal cord impingement

Fractures in joints with tophaceous gout

See Presentation for more detail.


Studies that may be helpful include the following:

Joint aspiration and synovial fluid analysis

Serum uric acid measurement (though hyperuricemia is not diagnostic of gout)

24-hour urinary uric acid evaluation

Blood studies (including white blood cells [WBCs, triglyceride, high-density lipoprotein, glucose, and renal and liver function tests)

Plain radiographs may show findings consistent with gout. Erosions with overhanging edges are generally considered pathognomonic for gout (though also found in other diseases). Characteristics of erosions typical of gout include the following:

Maintenance of the joint space

Absence of periarticular osteopenia

Location outside the joint capsule

Sclerotic (cookie-cutter, punched-out) borders

Asymmetric distribution among the joints, with a strong predilection for distal joints, especially in the lower extremities

Ultrasonographic findings in established gout include the following:

A “double-contour” sign, consisting of a hyperechoic, irregular line of MSU crystals on the surface of articular cartilage overlying an adjacent hyperechoic bony contour

“Wet clumps of sugar,” representing tophaceous material, described as hyperechoic and hypoechoic heterogeneous material with an anechoic rim

Bony erosions adjacent to tophaceous deposits

Other imaging modalities that may be considered include the following:

Computed tomography (CT) – Complementary to plain radiography for recognizing erosions in gout

Magnetic resonance imaging (MRI) – MRI with gadolinium is recommended when tendon sheath involvement must be evaluated and when osteomyelitis is in the differential diagnosis

See Workup for more detail.


Gout is managed in the following 3 stages:

Treating the acute attack

Providing prophylaxis to prevent acute flares

Lowering excess stores of urate to prevent flares of gouty arthritis and to prevent tissue deposition of urate crystals

Acute treatment of proven crystal-induced arthritis is directed at relief of the pain and inflammation. Agents used in this setting include the following:

Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin


Colchicine (now less commonly used for acute gout than it once was)

Adrenocorticotropic hormone (ACTH)

Combinations of drugs (colchicine plus NSAIDs, oral corticosteroids plus colchicine, intra-articular steroids plus colchicine or NSAIDs)

Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled (unless kidneys are at risk because of an unusually heavy uric acid load).

Long-term management of gout is focused on lowering uric acid levels. Agents used include the following:




Because these agents change serum and tissue uric acid levels, they may precipitate acute attacks of gout. This undesired effect may be reduced by prophylaxis with the following:

Colchicine or low-dose NSAIDs

Low-dose prednisone (if patients cannot take colchicine or NSAIDs)

Other therapeutic agents that may be considered include the following:

Uricase and pegloticase

Vitamin C




Nonpharmacologic measures that may be warranted are as follows:

Avoidance or restricted consumption of high-purine foods

Avoidance of excess ingestion of alcoholic drinks, particularly beer

Avoidance of sodas and other beverages or foods sweetened with high-fructose corn syrup

Limited use of naturally sweet fruit juices, table sugar, and sweetened beverages and desserts, as well as table salt

Maintenance of a high level of hydration with water (≥8 glasses of liquids daily)

A low-cholesterol, low-fat diet, if such a diet is otherwise appropriate for the patient

Weight reduction in patients who are obese

See Treatment and Medication for more detail.

For patient education information, see Gout and Gout and Diet.




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