eGFR: estimated glomerular filtration rate; IL-1: interleukin 1; NSAID: nonsteroidal antiinflammatory drug; PPI: proton pump inhibitor.
* For additional information, refer to the UpToDate topic on the clinical manifestations and diagnosis of gout.
¶ Arthrocentesis and synovial fluid studies are required for further evaluation. For additional information, refer to UpToDate content on septic arthritis.
Δ This assumes the absence of contraindications to specific therapies. For rationale and second-line therapies, refer to UpToDate content on the treatment of gout flares.
◊ Systemic glucocorticoids are administered orally unless patients require parenteral administration (ie, intramuscular or intravenous, depending on the care setting).
§ Patients at increased risk of NSAID gastropathy may require a concurrent PPI. Risk factors for gastrointestinal bleeding on NSAIDs include expectation of a prolonged treatment course (eg, from a flare of long duration [eg, >48 hours]), history of peptic ulcer or gastrointestinal bleeding, age >65, and concurrent use of aspirin or glucocorticoids. Refer to UpToDate topics on primary prevention of gastroduodenal toxicity and secondary prevention of gastroduodenal toxicity in patients on NSAIDs.
¥ For additional information, refer to UpToDate content on pharmacologic urate-lowering therapy and nonpharmacologic strategies to treat gout.
‡ Indications to start urate-lowering pharmacotherapy include frequent (eg, ≥2 flares per year) or disabling gout flares, tophi and structural joint damage, and selected patients without recurrent attacks or tophi who have a high future risk of severe gout. For more information, refer to UpToDate content on urate-lowering therapy.
† Nonpharmacologic strategies include management of certain comorbid conditions (eg, obesity, hypertension, diabetes mellitus), addressing medications that affect urate balance (eg, diuretics and other antihypertensives), and modifying diet (eg, reducing intake of purines, alcohol, and high-fructose corn syrup).