Comprehensive Analysis of Gout Treatment Plan: From Dietary Control to Medication Selection

Gout is a group of diseases caused by long-term purine metabolism disorders due to hereditary or acquired factors, resulting in elevated blood uric acid levels accompanied by tissue damage. The prerequisite for its onset is hyperuricemia. However, 80% of people with hyperuricemia remain asymptomatic throughout their lives, a condition known as asymptomatic hyperuricemia. Only a small percentage develop clinical gout, characterized by: hyperuricemia, acute and chronic arthritis, tophi, gouty nephropathy, and kidney stones. These manifestations can appear alone or in combination.

Treatment of Gout: The principles of gout treatment are to terminate acute attacks and prevent recurrence; correct hyperuricemia; prevent kidney stones and kidney damage; and treat comorbidities. I. Dietary Control

(1) Limit daily total calorie intake to 100–120 kJ/kg to prevent obesity. (2) Carbohydrates should account for 65%–70% of daily calories; protein intake should be 0.5–1.0 g/kg; and fat intake should be 40–50 g/kg.

(3) Avoid high-purine foods such as heart, liver, kidney, brain, sardines, and yeast. Daily purine intake should be less than 100–150 mg.

(4) Drink plenty of water and eat more alkaline foods such as vegetables, citrus fruits, watermelon, winter melon, and milk. Alkaline medications may be taken as needed.

II. Drug Treatment Anti-gout drugs are divided into two main categories based on their clinical treatment purpose. One category includes gout inflammation interfering drugs, including colchicine, nonsteroidal anti-inflammatory drugs (NSAIDs), and glucocorticoids; the other category includes uric acid-lowering drugs, uric acid-inhibiting drugs, and dual-action drugs.

(I) Management of Asymptomatic Hyperuricemia
The main focus is on controlling diet and avoiding triggers, while actively treating coexisting conditions such as obesity, hypertension, and diabetes. However, for patients with serum uric acid > 0.54 mmol/L or uric acid levels > 5.9 mmol/L who may develop kidney stones, drug therapy should be considered.

(II) Management of the Acute Phase
The principle of management in this phase is to administer gout-inflammatories as early as possible to terminate the attack and relieve pain. After the acute inflammation subsides, uric acid-lowering drugs are used to prevent recurrence. However, it is crucial to note that uric acid-lowering drugs should not be used alone during this phase, as this can trigger so-called migratory gout attacks, worsening the condition and prolonging the attack. Commonly used medications to treat gout inflammation include:

1. Colchicine: Oral administration, initially 0.5–1.0 mg, then 0.5 mg/h until pain relief or severe gastrointestinal reactions occur and cannot be tolerated, at which point a maintenance dose of 0.5 mg is administered, 1–2 times daily. The usual dose for pain relief is 4–8 mg. For those who cannot tolerate oral administration, 2 mg of colchicine can be added to 20 ml of normal saline for intravenous infusion, with a total dose not exceeding 4–6 mg, and care should be taken to prevent leakage into the subcutaneous tissue.

Colchicine is the first-line drug for treating gout, especially severe attacks. It is a highly effective drug for treating acute gout attacks, causing pain and inflammation to subside in 90% of patients within 6–12 hours and disappear within 24–48 hours. Its mechanism may involve inhibiting leukocyte chemotaxis, proliferation, and phagocytosis of urate crystals, reducing the release of lysosomal enzymes, and increasing the pH value within the joint cavity, thus reducing urate precipitation. However, it does not reduce uric acid production or increase uric acid excretion. In addition to monitoring for severe diarrhea, vomiting, and other gastrointestinal reactions during treatment, regular blood tests and liver function tests are necessary to prevent leukopenia or drug-induced liver damage. Furthermore, intravenous leakage into the subcutaneous tissue can cause tissue necrosis, which requires caution.

2. Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

NSAIDs inhibit the synthesis and release of prostaglandins during inflammation, and are therefore used to treat gout attacks to reduce inflammation and relieve pain. Their side effects are less than colchicine, and they remain effective even several days after an attack.

Indomethacin: The initial dose is 25-50 mg, 3-4 times daily. It generally takes effect after 24 hours, and symptoms significantly improve after 2-3 days, after which the dosage can be gradually reduced.

Other drugs such as indomethacin, cyclophosphamide, phenylbutazone, hydroxyphenylbutazone, ibuprofen, piroxicam, and newer nonsteroidal anti-inflammatory drugs (NSAIDs) (such as diclofenac and chlorpheniramine) have all been proven effective for gout. The choice of which to use depends on the patient's condition and the potential side effects of the drugs.

3. Glucocorticoids
Glucocorticoids can rapidly relieve acute attacks, but a "rebound" phenomenon often occurs after discontinuation. Therefore, they are only used when colchicine or NSAIDs are ineffective, intolerable, or contraindicated.

ACTH 50U is added to 500ml of glucose for intravenous drip. Prednisone 30mg daily, divided into several oral doses, for 2-3 days. Prednisone 10mg once, 3-4 times daily.

In recent years, there has been a trend towards combining the above-mentioned gout-inhibiting drugs with appropriate low-dose uric acid-lowering drugs for acute gout. This can reduce the drug dosage, lessen side effects, and shorten the pain relief time.