I. What every physician needs to know.
Gout is a rheumatologic disorder characterized by supersaturation of uric acid in the serum (hyperuricemia) accompanied by attacks of acute, markedly painful monoarticular or polyarticular joint inflammation.
Humans lack the enzyme uricase (breaks down uric acid into allantoin); consequently, our serum uric acid levels are close to the limits of solubility. Uric acid levels can be increased by factors including decreased urate excretion (renal insufficiency, medications including diuretics) and/or increased urate production (dietary excess, obesity, ethanol, malignancy/chemotherapy). Flares may be precipitated by decreased uric acid excretion or increased production. In addition, since serum uric acid concentration is often close to the limits of solubility, any rapid change in urate concentration may cause precipitation/gout flare (for example, initiation of treatment with urate-lowering therapy).
Gout is characterized by four stages: asymptomatic tissue deposition, acute flares, intercritical periods (between flares), and chronic gouty arthritis.
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II. Diagnostic Confirmation: Are you sure your patient has gout?
The gold standard for diagnosis of gout is arthrocentesis, with aspiration of synovial fluid and microscopic examination looking for crystals and inflammatory cells (neutrophils). Under polarized microscopic exam, needle-like negatively birefringent crystals are visible.
The diagnosis of gout can also be made on a clinical basis. Key clinical criteria for the diagnosis of gout include:
- A classic history of one or more episodes of monoarticular arthritis followed by intercritical period(s) completely free of symptoms
- Maximum inflammation within 24 hours
- Rapid resolution of synovitis after colchicine therapy
- Unilateral first metatrasophalangeal joint attack (podagra)
- Presence of a visible or palpable lesion, which by location or appearance is likely to be a tophus
- Hyperuricemia (serum uric acid >7.0mg/dL)
A. History Part I: Pattern Recognition:
The typical patient with gout presents with recurrent attacks of acute, markedly painful monoarticular or oligoarticular inflammatory arthritis. Comonly affected joints include the hands, feet (1st metatarsophalangeal joint commonly affected, termed “podagra”), elbows, wrists (carpometacarpal joint), knees, shoulders, hips and sacroiliac joints.
Flares typically have maximal onset within 24 hours, and are separated in time by asymptomatic “intercritical periods.”
Other common clinical manifestations of gout include olecranon bursitis and tophi (typical locations include the pinna of the ear, juxtaarticular locations, tendons, and bursae). With longstanding gout, polyarthritis and chronic arthritis changes may develop, in addition to tophi deposition (tophaceous gout).
B. History Part 2: Prevalence:
Gout represents 5% of arthritis cases in the United States. It affects approximately 1% of men, and has increasing incidence with age (affects 9% of men over the age of 80). Gout affects men more frequently than women (M:F ratio 7:1); it is thought that this is in large part due to estrogen stimulation of urinary urate excretion. Gout is increasing in prevalence, and has been shown to parallel increases in obesity, diabetes and hypertension.
C. History Part 3: Competing diagnoses that can mimic gout.
The differential diagnosis of gout includes other causes of infectious and inflammatory arthritis. The most common competing diagnoses (which can also coexist with gout) include osteoarthritis, rheumatoid arthritis, calcium pyrophosphate deposition disease (CPPD) and septic arthritis. Traumatic arthritis should also be considered while taking the history of onset.
E. What diagnostic tests should be performed?
The gold standard for diagnosis of gout is arthrocentesis, with aspiration of synovial fluid and microscopic examination looking for crystals and inflammatory cells (neutrophils.) Under polarized microscopic exam, needle-like negatively birefringent crystals are visible.
When sending synovial fluid for laboratory analysis, it is important to order gram stain and culture in addition to cell count and differential and crystal examination. Septic arthritis is high in the differential diagnosis for gout, and the two processes can occur concurrently. Septic arthritis should be considered if the synovial fluid white blood cell (WBC) is greater than 20,000.
Synovial fluid glucose, protein and lactate dehydrogenase (LDH) are not informative in differentiating between gout and other inflammatory/infectious causes of arthritis, and should not be ordered.
What’s the evidence?
Shmerling, RH. Rheum Dis Clin North Am. vol. 20. 1994. pp. 503-512.
Zhang, W, Doherty, M, Bardin, T, Pascual, E, Barskova, V, Conaghan, P, Gerster, J, Jacobs, J, Leeb, B, Lioté, F, McCarthy, G, Netter, P, Nuki, G, Perez-Ruiz, F, Pignone, A, Pimentão, J, Punzi, L, Roddy, E, Uhlig, T, Zimmermann-Gòrska, I. “EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT)”. Ann Rheum Dis. vol. 65. 2006. pp. 1312-24.
Zhang, W, Doherty, M, Pascual, E, Bardin, T, Barskova, V, Conaghan, P, Gerster, J, Jacobs, J, Leeb, B, Lioté, F, McCarthy, G, Netter, P, Nuki, G, Perez-Ruiz, F, Pignone, A, Pimentão, J, Punzi, L, Roddy, E, Uhlig, T, Zimmermann-Gòrska, I. “EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT)”. Ann Rheum Dis. vol. 65. 2006. pp. 1301-11.
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