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H. RALPH SCHUMACHER, Jr, MD
Professor of Medicine, University of Pennsylvania, Philadelphia, PA

The pathogenesis of gout
■ ABSTRACT
An elevated serum urate level, together with local factors, can result in the deposition of urate crystals into the joints. Once crystals are deposited into a joint, they can be released into the joint space and initiate an inflammatory cascade causing acutegouty arthritis. These acute flares resolve, but the crystals remain in the joint. The way to ultimately correct the underlying metabolic problem of hyperuricemia and the crystal deposition is to lower the serum urate level and dissolve the crystal deposits. This will stop both the acute attacks and the progressive joint damage.

these crystals into the joint space, where they may initiate anacute inflammatory reaction recognized as acute gouty arthritis. The acute attack is self-limited, but crystals remain in the joint and low-grade, often subclinical, inflammation persists even between acute attacks. Although acute attacks can be treated with anti-inflammatory medications, the underlying cause of the disease can be treated only by lowering the serum urate level.

■ KEY POINTS
Aserum urate level of approximately 6.8 mg/dL is the concentration at which urate crystals begin to precipitate. The higher the urate level, the more likely that crystals will deposit into joints. Local factors that combine with hyperuricemia to contribute to the development of gout are trauma, irritation, reduced temperature, and prior joint disease. Because acute attacks of gout typically resolvespontaneously, especially early in the disease course, evaluating the efficacy of acute therapies can be difficult. Lowering the serum urate to less than 6 mg/dL will dissolve crystals out of the joints, ultimately preventing acute gout attacks and joint damage.

■ CRYSTAL DEPOSITION AND THE DEVELOPMENT OF GOUT Asymptomatic hyperuricemia is not a disease but rather is the underlying factor that canpredispose to gout. A serum urate level of approximately 6.8 mg/dL is the concentration at which monosodium urate crystals begin to precipitate.1,2 Although this level is based on in vitro studies, it suggests a reasonable biological threshold for clinicians assessing patients for hyperuricemia. It should be noted that there are often no manifestations of gout during an extended period ofhyperuricemia even though urate crystals are beginning to deposit into joints. The higher the serum urate level, the more likely that crystals will deposit into joints. Predisposition is not causation In the Normative Aging Study, 22% of men who had serum urate levels greater than 9 mg/dL developed gout during a 5-year period⎯a much higher rate than among men with serum urate levels less than 9 mg/dL.3Nevertheless, a full 78% of the men in this study with serum urate levels greater than 9 mg/dL did not develop gout over the 5-year period, illustrating that while hyperuricemia predisposes to gout, it does not automatically cause gout. Contributing factors beyond serum urate Other factors, when combined with hyperuricemia, contribute to crystal deposition and the development of gout. Trauma orirritation. Patients with hyperuricemia tend to have monosodium urate crystal deposition at
input on the content of presentations at the symposium or on this article. This article is based on Dr. Schumacher’s lecture on this subject at the symposium that formed the basis of this supplement. Dr. Schumacher reported that he prepared his lecture, Fallon Medica transcribed his lecture, and he alonedeveloped the transcript into this article without assistance from undeclared contributors.The article underwent formatting and nonsubstantive copyediting by Fallon prior to submission to the Journal.
JULY 2008

serum urate level greater than approximately 6.8 mg/dL, the saturation point of urate in biological fluids, is the underlying cause of gout. Hyperuricemia, along with other factors...
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