08/09/2026
GOUT - it is more than joint a pain in the big toe!
Gout is a crystal-induced inflammatory arthritis caused by deposition of monosodium urate crystals in joints and surrounding tissues. It develops in the setting of hyperuricemia, when the body’s uric acid levels in blood become high enough for crystals to form.
Although the first metatarsophalangeal joint—the big toe—is the classic location, gout can affect literally ANY JOINT as well as bursae and tendons.
An acute gout attack often comes on rapidly, sometimes overnight, with very intense pain, swelling, warmth, redness, and extreme tenderness. Your joint becomes a TENDER BAKED TOMATO. It can be concerning for an infection as even the pressure of a bedsheet can hurt! 🍅☠
**Why does uric acid become elevated?**
For most people with gout, the primary problem is not producing too much uric acid, it is the inability to get rid of it through the kidneys. Genetics play an important role. Kidney disease, obesity, metabolic syndrome, certain medications such as diuretics, alcohol intake, hormones, and dietary factors can also contribute. Diet is a big factor for causing flares. This is where fall fun comes in. Common instigators include alcohol (beer at a tailgate🍻), high fructose corn syrup (candy at halloween🎃, pies at thanksgiving, pastries at Christmas 🍪🎅🏻), shellfish and organ meats (potluck dinners 🍽).
A few important notes:
• A high serum uric acid level alone does NOT diagnose gout. Many people have hyperuricemia and never develop gout. I see this a lot in Psoriasis.
• Uric acid levels are typically normal during an acute gout attack, so a normal result at that moment does not exclude the diagnosis.
• We look for needle-shaped, negatively birefringent monosodium urate crystals in synovial fluid under a microscope as the gold standard of diagnosis.
**Treating the flare and treating gout are two different things.**
During an acute attack, treatment is aimed at controlling inflammation. Depending on the individual patient, this may include colchicine, NSAIDs, or corticosteroids.
Long-term treatment is different. For patients who meet criteria for urate-lowering therapy, medications such as allopurinol are used to reduce the body's urate burden and prevent future crystal formation.
The goal is generally to keep a **serum urate below 6 mg/dL**, with lower targets sometimes considered in patients with severe or tophaceous (nodules under the skin around joints) disease.
An important concept is that starting urate-lowering therapy can temporarily **increase the risk of gout flares** as existing urate deposits begin to mobilize. This does not necessarily mean the medication is failing. Anti-inflammatory prophylaxis should be recommended until goal urate levels are achieved and maintained for 3 months.
Untreated or inadequately controlled gout can progress from intermittent attacks to **chronic gouty arthritis**, with significant joint damage and functional impairment.
The encouraging part is that gout is one of the few inflammatory arthritides where we can directly target the underlying culprit. It is so simple: Treat the disease to prevent the flare!🎉
