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Gout

Posted by markferg@u.washington.edu, 7/12/04 at 11:25:23 AM.

Gout

What is it?

Gout is a form of peripheral arthritis resulting from the deposition of monosodium urate crystals secondary to hyperuricemia.

Prevalence in the United States: 1.6 to 13.6 per 1000
Typically occurs in middle aged or elderly males (90% of cases are in males).
It is particularly rare in premonpausal women.
Caucasians populations are more affected than those of African heritage.
Interestingly, gout is relatively frequent in young male Polynesians.

Hyperuricemia and gout are often associated with hypertension, obesity, hyperlipidemia, atherosclerosis, and ethanol abuse.

While all gout patients have a high serum uric acid concentration at some point in their disease progression, most hyperuricemic individuals never show clinical signs of urate crystal deposition.

What causes it?

Uric acid under excretion (90% of cases)
    Primary: Idiopathic reduced renal excretion
    Secondary:     Chronic renal failure
                           Thiazide use
                            Alcohol
                            Hyper or hypoparathyroidism

Uric acid overproduction (10% of cases)
    Primary: Enzyme defect in purine synthesis
    Secondary: Increased turnover of nucleic acids
                            Myeloproliferative and lymphoproliferative disorders
                            Hemolytic anemia
                            Chemotherapy
                           Alcohol

How does it present clinically?

The natural history of progressive urate crystal deposition manifests as three classic stages.

1. Acute gouty arthritis: 80% of attacks involve and single joint with severe pain, redness, and swelling.

2. Intercritical gout:     These are asymptomatic intervals between acute attacks most common early in    
                                    disease progression. This pattern is quite uncommon in other arthritic disorders
                                   and alone is very suggestive of gout.

3. Chronic tophaceous gout: Collections of solid urate in connective tissues, which may be calcified.

Attacks may occur for 4-6 years before radiographic evidence.

What are the radiographic features?

Location
    Lower extremity > upper extremity
    Small joints > large joints
    Random distribution in hands (helpful diagnostic distinction)
    First MTP most common (podagra)
Characteristics
    Marginal, pararticular or intra-articular erosions which may have overhanging edges
    Well-defined erosions that may have a sclerotic border
    Joint space preserved (unless very advanced)
    Not usually associated with osteoporosis
    Soft tissue and bursa deposition - tophi
    MRI - Tophus has low intensity on T1 and variable low to high intensity on T2 depending on the    
                amount of amorphous calcification.
    CT - Tophi have density similar to soft tissue.
Misc. Points
    Erosions and tophi usually only with longstanding disease
    40% of patients have concomitant CPPD
    Can have many different appearances, but is quite common so always keep in mind.

Examples:


Shows classic location at first MTP and small erosion with "overhanging" edge. Notice that the joint space and bone density are preserved.


Another appearance showing multiple erosion locations including first MTP, base of third and fourth metacarpals, and possibly the head of the fifth metacarpal and second proximal phalanx.


Advanced gout resulting in joint destruction from large erosions in first, fourth and fifth rays. Notice the large "overhanging" edges.


Example showing tophaceous gout of fifth MTP joint.


If you didn't appreciate the tophi on the last example, certainly you will here. Notice calcification of the tophus on the ulnar side of fifth MCP joint.


Patient with known gout. This example shows chondrocalcinosis of the triangular fibrocartilage. 40% of gout patients have concomitant CPPD. Also notice erosion of the head of the 5th proximal phalanx.


Tophaceous gout of the 1st MTP. Notice the tophi have a density similar to soft tissue and are both inside and surrounding the bone. Also note the cortical destruction of the proximal phalanx and the head of the metacarpal.


Treatment

First line is to control associated disorders such as hypertension, obesity, hyperlipidemia, atherosclerosis, and ethanol abuse.

Acute attack - Goal is to quickly alleviate pain. Anti-inflammatory therapy with NSAIDs, colchicine, or
                        Cox-2 inhibitors. Should resolve symptoms in hours to days.

Prophylactic - Goal is to prevent acute attacks. Indomethacin or colchicine. In patients without evident
                        tophi, prophylaxis can be safely discontinued 6 to 12 months after serum urate levels
                        have normalized.

Antihyperuricemic therapy - Goal is a serum urate concentration of 5 to 6 mg/dL which is below that at
                                            which monosodium urate is saturating in extracellular fluids. Uricosuric
                                           drugs and allopurinol can be used to lower the serum urate concentration.

Surgery is typically only indicated to treat the complications of tophaceous disease, which include infection, compression due to the mass effect of a tophus, joint deformity, and intractable pain. Tophaceous deposits may compress nerves or erode through the skin resulting in chronic ulcers which often lead to infection.



1. Becker MA. Clinical manifestations and diagnosis of gout. UpToDate Version 12.2

2. Becker MA. Treatment of gout. UpToDate Version 12.2

3. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology. 2nd ed. 1999 Lippincott Williams &
    Wilkins Philadelphia.

4. Manaster BJ, Disler DG, May DA. Musculoskeletal imaging: the requisites. 2nd ed. 2002 Mosby,
    Inc. St. Louis.

5. Ruddy et al. Kelley's Textbook of Rheumatology. 6th ed. 2001 W. B. Saunders Company

6. Weissleder R, Wittenberg J, Harisinghani MG. The Primer of Diagnostic Imaging. 3rd ed. 2003
    Mosby, Inc. Philadelphia.

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