Gout is one of the most common and painful forms of arthritis — caused by the deposition of monosodium urate crystals in joints and surrounding tissues when uric acid levels in the blood are chronically elevated. The classic presentation is an excruciating attack of joint pain (most often the big toe) that begins suddenly, often at night, and produces exquisite tenderness, redness, warmth, and swelling. Medical clinics diagnose gout, treat acute attacks, and provide long-term management to prevent recurrent attacks and joint damage. This guide explains comprehensive gout care.
Why Uric Acid Levels Rise
Uric acid is the end product of purine metabolism — purines are compounds found in certain foods (red meat, organ meats, shellfish, beer) and produced by the body’s cell turnover. Hyperuricemia (elevated serum uric acid) results from overproduction, underexcretion (the most common mechanism), or both. Risk factors include male sex, older age, obesity, hypertension, kidney disease, diuretic use, and high-purine diet.
Treating an Acute Gout Attack
Acute gout attacks are treated with: NSAIDs (indomethacin or naproxen) at full doses, colchicine (anti-inflammatory specific to gout), or corticosteroids (for patients who cannot use NSAIDs or colchicine). Treatment started within 24 hours of attack onset significantly shortens duration and severity. Ice application and joint rest complement medication. Urate-lowering therapy is NOT started during an acute attack — initiating it during a flare can prolong or worsen the attack.
Long-Term Urate-Lowering Therapy
Patients with recurrent gout attacks, tophi (urate crystal deposits under skin), or gout-related joint damage require long-term urate-lowering therapy to maintain serum uric acid below 6 mg/dL. Allopurinol (first-line) or febuxostat (alternative) reduce uric acid production. Probenecid increases renal uric acid excretion. Starting urate-lowering therapy is accompanied by prophylactic low-dose colchicine or NSAIDs for 3–6 months to prevent attack precipitation during the serum uric acid reduction period.
Conclusion
Gout is entirely manageable with appropriate clinic care — acute attacks can be rapidly controlled, and long-term urate-lowering therapy prevents further attacks and joint damage. Many patients continue to experience recurrent attacks simply because they do not receive or adhere to preventive treatment. Work with your clinic to establish the urate-lowering strategy that keeps your uric acid in the target range.
FAQs – Gout
Q1. What foods trigger gout attacks?
A: High-purine foods (red meat, organ meats, shellfish, sardines, anchovies), alcohol (particularly beer), and high-fructose beverages are the most common dietary triggers. A low-purine diet can reduce attack frequency but is rarely sufficient without medication for patients with frequent attacks.
Q2. Does drinking water help gout?
A: Adequate hydration (8+ glasses daily) helps kidneys excrete uric acid more effectively and reduces crystal formation risk. Staying well-hydrated is a simple, beneficial component of gout management.
Q3. Can gout affect joints other than the big toe?
A: Yes. While the big toe (first metatarsophalangeal joint) is most commonly affected, gout can involve the ankle, knee, wrist, and finger joints, particularly with long-standing disease or inadequate treatment.
Q4. Is gout related to kidney disease?
A: Bidirectionally. Kidney disease reduces uric acid excretion, raising serum levels. Chronic hyperuricemia and urate crystal deposition can damage kidneys over time. Managing both conditions together is important.
Q5. Can women get gout?
A: Yes, though gout is much more common in men (ratio 3–4:1). Estrogen promotes uric acid excretion, so postmenopausal women lose this protection and their gout incidence approaches that of men. Women with gout often have more joint involvement and may be sicker when first diagnosed.
