Gout is the most common form of inflammatory arthritis, affecting millions of adults. The condition develops when excessive uric acid in the blood leads to the formation and deposition of monosodium urate (MSU) crystals within joints and surrounding tissues. This crystal buildup triggers sudden, painful episodes of swelling, often starting in the big toe, though any joint can be affected. The American College of Rheumatology (ACR) develops guidelines to standardize gout care, covering diagnosis, treatment of active flares, and long-term disease control.
How Gout is Diagnosed
Confirming a gout diagnosis centers on the direct identification of the causative crystals. The standard method involves joint aspiration, where fluid is drawn from the affected joint. This synovial fluid is examined under a polarized light microscope to visualize the negatively birefringent, needle-shaped monosodium urate crystals. Finding these specific crystals definitively confirms gout, distinguishing it from other types of arthritis.
When joint aspiration is not feasible or the diagnosis is uncertain, clinicians may rely on clinical features and advanced imaging. Clinical criteria consider the patient’s history, the location of the attack, and the speed of symptom development. Imaging, particularly musculoskeletal ultrasound, can serve as an adjunctive tool to visualize MSU crystal deposits.
Treating Acute Gout Attacks
Managing an acute gout flare requires the rapid reduction of inflammation. The ACR recommends starting treatment within 24 hours of symptom onset using three primary anti-inflammatory drug classes: nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and colchicine.
Corticosteroids can be administered orally, intramuscularly, or directly into the affected joint (intra-articularly). If colchicine is selected, the guidelines specify using a low-dose regimen, which offers similar effectiveness to higher doses with fewer side effects. For severe attacks or poor response to a single agent, combination therapy is allowed, such as combining colchicine with an NSAID or oral corticosteroid.
Strategies for Long-Term Uric Acid Management
Long-term gout control focuses on lowering the serum uric acid (SU) level to prevent future flares and dissolve existing crystal deposits. The ACR recommends initiating urate-lowering therapy (ULT) for patients with frequent flares (two or more per year) or evidence of chronic disease, such as tophi or radiographic damage. A “treat-to-target” strategy is recommended: the ULT dose should be adjusted until the SU concentration is consistently below 6 mg/dL. Maintaining this target promotes the dissolution of urate crystals.
Allopurinol is the preferred first-line ULT agent for all patients, including those with moderate-to-severe chronic kidney disease. Treatment should begin at a low dose (typically 100 mg per day or less) to avoid adverse reactions and minimize the risk of triggering a flare. If patients cannot tolerate allopurinol or do not reach the target SU level, second-line options like febuxostat or uricosuric agents may be used. Febuxostat also requires a low starting dose (generally 40 mg per day or less), with subsequent titration based on SU levels.
When starting ULT, anti-inflammatory prophylaxis is recommended to prevent flares, which can occur as crystals dissolve. This prophylaxis, often low-dose colchicine, NSAIDs, or corticosteroids, should continue for at least three to six months after ULT initiation. If oral ULT agents fail to achieve the target or for patients with severe, non-resolving tophi, switching to a more potent intravenous therapy may be necessary.
Lifestyle Recommendations Supporting Treatment
Prescription medication is the foundation of long-term gout management, but the ACR guidelines also address lifestyle adjustments. These adjustments are beneficial but do not replace the need for ULT in patients with established gout. Patients who are overweight or obese should consider a weight-loss program, as reducing body mass can help lower uric acid levels.
Dietary modifications are recommended to reduce the intake of substances that can raise uric acid or trigger a flare.
- Limiting the consumption of high-purine foods, such as certain meats and seafood, is advised.
- Restricting alcohol intake is advised.
- Limiting consumption of high-fructose corn syrup, a common ingredient in sweetened beverages, is advised.
- Consuming low-fat dairy products may be beneficial, as they are associated with a lower risk of gout flares.
Beyond diet, patients taking certain medications for other conditions may need adjustments. For instance, switching from the diuretic hydrochlorothiazide to an alternative antihypertensive agent like losartan is recommended to help manage uric acid levels.

