History and exam

Key diagnostic factors

common

men ages >40 years

Gout is more common in men; incidence increases with age.[2][3][5][6][15]

use of gout-inducing medication

Use of drugs including aspirin, cyclosporine, tacrolimus, or pyrazinamide increase urate reabsorption.[11][12]

consumption of meat, seafood, or alcohol

Meta-analyses of prospective cohort and cross sectional studies report that increased serum urate levels or gout correlate with red meat, seafood, and alcohol intake.[14][16]

One prospective 12-year follow-up of 47,150 men reported a higher risk of gout among those in the highest versus lowest quintiles of seafood and meat consumption, relative risks 1.51 (95% CI 1.17 to 1.95) and 1.41 (95% CI 1.07 to 1.86), respectively.[15]

history of medical condition with high cell turnover rate

Conditions that lead to high endogenous purine metabolism include hematologic malignancies, myeloproliferative disorders, psoriasis, and chemotherapy-induced cell death.[10]

rapid-onset severe pain

Patients with an acute attack can often pinpoint the onset to the hour. They may describe the pain as the most severe they have ever experienced. Symptoms often develop overnight.[53]

joint stiffness

Joint stiffness in the morning is prominent and reflects the underlying inflammatory mechanism. Function may be limited because of pain and stiffness.

foot joint distribution

Most commonly involved are joints in the feet, especially the first metatarsophalangeal, tarsometatarsal, and ankle joints.[57]

few affected joints

Pattern is usually monoarticular or oligoarticular (<4 joints). Can be polyarticular, affecting multiple joints in the hands and feet, especially in older people.[57]

swelling and joint effusion

Reflect the inflammatory nature of the disease.

tenderness

Prominent diffuse joint tenderness usually exists.

tophi

May be present over extensor surface joints, especially the elbows, knees, and Achilles tendons.[57]

May also be evident over dorsal aspects of hands and feet, and in the helix of the ears.

Other diagnostic factors

common

erythema and warmth

May be subtle at times, requiring careful examination.

uncommon

family history of gout

Family history of gout may increase risk of hyperuricemia and gout.[50][51]

Risk factors

strong

older age

Annual incidence of gout increases with age.[2][15]

male sex

More common in men.[2][3][5][6]

menopausal status

Gout is rare in premenopausal women.[8]

consumption of meat, seafood, alcohol

Meta-analyses of prospective cohort and cross-sectional studies report that increased serum urate levels or gout correlate with red meat, seafood, and alcohol intake.[14][16]

One prospective 12-year follow-up of 47,150 men reported a higher risk of gout among those in the highest versus lowest quintiles of seafood and meat consumption, relative risks 1.51 (95% CI 1.17 to 1.95) and 1.41 (95% CI 1.07 to 1.86), respectively.[15]

use of diuretics

Thiazide and loop diuretics are associated with an increased risk of gout and of gout flares.[37]

One meta-analysis of cohort studies concluded that diuretic use more than doubles the risk of developing gout compared with no diuretic use.[13]

use of cyclosporine or tacrolimus

Lead to increased tubular reabsorption of urate as well as decreased glomerular filtration and interstitial nephropathy.[11][12]

use of pyrazinamide

Increases urate reabsorption.

use of aspirin

Doses of ≤325 mg elevate urate levels, while higher doses have uricosuric effects and lead to lower urate levels.[10]

genetic susceptibility

Some urate overproducers have specific genetic defects, such as hypoxanthine-guanine phosphoribosyl transferase (HPRT) deficiency, 5-phosphoribosyl-l-pyrophosphate (PRPP) synthetase hyperactivity, and glucose-6-phosphate dehydrogenase (G6PD) deficiency.[32][33][34]

The most complete form of HPRT deficiency is associated with Lesch-Nyhan syndrome (premature gout and learning disabilities in children).[38] The partial deficit of the enzyme is associated with gout and hyperuricemia without neurologic manifestations.

high cell turnover rate

Conditions that lead to high endogenous purine metabolism include hematologic malignancies, myeloproliferative disorders, psoriasis, and chemotherapy-induced cell death.[10]

weak

obesity

Increases the risk of gout.[17][18]

One meta-analysis of cohort studies reported that people with a body mass index of ≥30 are more than twice as likely to develop gout as people without this risk factor.[13]

adiposity and insulin resistance

Associated with hyperuricemia.[17][18][39][40][41]

Weight loss is associated with lower urate level and risk of gout, and reduced serum urate in those with gout.[42][43][44]

exogenous insulin

Exogenous pharmacologic insulin can reduce the renal excretion of urate.[45][46]

hypertension

An independent risk factor for gout.[17][37]

Renal urate excretion is inappropriately low relative to glomerular filtration rate.[47] This may reflect early nephrocalcinosis in hypertensive patients. Gout, in turn, may be associated with a higher incidence of hypertension and cardiovascular morbidity.[48]

One meta-analysis of cohort studies concluded that people with hypertension have more than double the risk of developing gout (relative risk 2.11) compared with normotensive individuals.[13]

renal insufficiency

Has been found to be associated with higher risk of incident gout or gout flares.[37]

diabetes mellitus

Epidemiologic studies suggest that patients with diabetes mellitus are at a higher risk of incident gout and/or gout flares.[37] However, a subsequent meta-analysis of observational studies concluded that diabetes mellitus may be a protective factor for the risk of gout.[49]

hyperlipidemia

Hypertriglyceridemia and hypercholesterolemia are associated with a higher risk of incident gout and/or gout flares in epidemiologic studies.[37] However, confounding factors may have influenced findings.

family history of gout

Risk of hyperuricemia and gout may be higher in people with a family history of gout.[50][51]

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