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Diagnosis and management of gout: An update

Diagnosis and management of gout: An update

Gout, “the king of diseases and the disease of kings,” was one of the earliest disorders to be recognized as a clinical entity.1 No longer discriminating among socioeconomic classes, it has more than doubled in prevalence over the past 2 decades.2 A disorder of purine metabolism, gout now is the most common inflammatory arthropathy. It occurs in men more than in women (ratio, about 3 or 4:1).2

Even in this setting of a rising prevalence, primary care management of gout does not always adhere to evidence-based best practice.3 In addition, a significant number of patients do not respond to appropriate therapy or do not achieve optimal response to treatment, even in the hands of experienced rheumatologists (R. T. Keenan, M. H. Pillinger, unpublished data).

Recently, after almost 50 years of dormancy, new therapeutic agents for the management of gout have entered the market or are in clinical development. In this article, we review current guidelines for the diagnosis and management of gout.

DIAGNOSIS
The diagnosis of gout is not always easy to make. The original American College of Rheumatology criteria4 have been shown to have limited validity (sensitivity, 0.80; specificity, 0.64; positive predictive value, 0.80; and negative predictive value, 0.65).5 More recently, the European League Against Rheumatism (EULAR) also developed recommendations.6

Visualization of crystals
The gold standard for making a diagnosis of gouty arthropathy is visualization of negatively birefringent, needle-shaped crystals. This is done with arthrocentesis and analysis of synovial fluid (SF) or tophus aspirate and identification of monosodium urate (MSU) crystals, particularly intracellular crystals in neutrophils.6,7 MSU crystals also may be identified in SF obtained from asymptomatic joints, especially the knees and the first metatarsophalangeal (MTP) joints.7,8

Of note, acute gouty arthritis may coexist with another joint disease, such as septic arthritis or pseudogout. Therefore, arthrocentesis should be performed in almost all circumstances.

Serum uric acid (SUA) levels may be obtained during an acute attack (a high SUA level supports the possibility that a patient has gout). However, SUA levels may be paradoxically low during an acute attack (because of an increase in renal excretion); they typically are highest about 2 weeks after.

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