Gout

Gout is a type of inflammatory arthritis caused by uric acid crystals. It usually occurs after a period of high uric acid levels in the blood (over 6.8 mg/dL), but not everyone with high uric acid develops gout. High uric acid can lead to uric acid crystal accumulation in various body tissues, causing symptoms like joint inflammation, gout nodules or tophi, kidney stones, and reduced kidney function.

Uric acid levels and gout are related to genes, diet, and other diseases. Genes affect protein production that controls uric acid levels, particularly through its elimination in the kidneys, which is the most critical process for maintaining uric acid balance. Diet only partially influences blood uric acid levels.

Risk factors for gout include obesity, chronic kidney disease, genetics, certain medications like hydrochlorothiazide and pyrazinamide, and consuming too much alcohol, red meat, and sugary drinks.

Gout symptoms include severe, sudden joint inflammation and pain, with the joint becoming red, swollen, and tender. The pain typically peaks within 24 hours and can subside in a few days to two weeks even without treatment. Initially, gout may affect one joint at a time, like the big toe, ankle, or mid-foot. If untreated, flare-ups become more frequent and involve more joints. Over time, tophi can develop in various body parts, causing bone damage and deformity. Tophi are usually painless but can become inflamed.

Diagnosing gout involves considering the patient's history and physical exam. The most accurate diagnosis is confirmed by finding uric acid crystals in joint fluid under a microscope. If this isn't possible, ultrasound or dual-energy CT scans can detect uric acid deposits. High blood uric acid levels support the diagnosis, but levels can be normal during flare-ups.

Treating gout during flare-ups aims to reduce inflammation, pain, and swelling as quickly as possible. Treatment depends on factors like patient's other diseases, severity of inflammation, and history of gout. Options include cold compresses and rest, and avoiding massaging the affected joint.

Non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen, ibuprofen, and indomethacin reduce inflammation and pain. They have risks for patients with kidney, liver, heart diseases, stomach ulcers, or bleeding risks.

Colchicine reduces inflammation without increasing stomach ulcer risk but must be taken within the first 24 hours of a flare-up. It can cause side effects like diarrhea, nausea, and stomach pain.

Steroids like prednisolone are effective for severe, multi-joint inflammation and patients who can't take NSAIDs or colchicine. They temporarily increase blood sugar and suppress immunity, so they're used cautiously.

Preventing gout flare-ups involves low-dose colchicine, adjusting for kidney function. In the first 3-6 months of uric acid-lowering treatment, flare-ups might still occur. Long-term use of colchicine without uric acid-lowering medication can lead to tophi without warning inflammation. Low-dose NSAIDs or steroids may also prevent flare-ups in specific cases.

Long-term treatment involves lowering uric acid levels to prevent flare-ups, tophi, joint damage, and possibly slow kidney deterioration. The goal is a uric acid level below 6 mg/dL, possibly stricter in severe cases. Not all gout patients need this medication. It's for frequent, severe flare-ups, existing tophi, or concurrent kidney disease.

Uric acid-lowering drugs include allopurinol and febuxostat, which inhibit uric acid production. Allopurinol is first-line but can cause allergic reactions, especially in Thai or Chinese patients with specific genetic risks. Febuxostat is an alternative but more expensive and used cautiously in heart disease patients. Both require liver enzyme monitoring.

Drugs that increase uric acid elimination through urine include probenecid, sulfinpyrazone, and benzbromarone. They require high water intake to prevent kidney stones and have limitations in reduced kidney function patients. Benzbromarone is effective but can have severe liver side effects.

Losartan and hydrochlorothiazide, blood pressure medications, also affect uric acid elimination. Losartan helps lower uric acid, while hydrochlorothiazide can increase it.

Dietary changes can help manage gout. Limiting alcohol, red meat, and sugary drinks is recommended. For overweight patients, weight loss is crucial for reducing uric acid levels and overall health.

In summary, gout is a manageable condition with medication and lifestyle changes, focusing on reducing and controlling uric acid levels.