Continuing from today’s in-depth article on tophi gout, here are some of the questions you may be asking about tophi gout. If you and someone in your family suffer from tophi gout, it may be helpful to read the following questions and answers carefully.
1. Should I treat asymptomatic hyperuricemia?
There is still a lot of controversy over whether uric acid-lowering drugs should be used in asymptomatic hyperuricemia patients. In general, high levels of uric acid in the blood but no gout are usually observed without medication. In most cases, the first seizure of acute gout occurs after at least 20 years of persistent hyperuricemia. In addition, most people with hyperuricemia remain asymptomatic for almost life, and gouty arthritis only occurs in about 4.9% of those with uric acid above 9 mg/dL a year. This is because there are few benefits compared to the side effects and costs of administering the drug. However, recently, hyperuricemia itself is known as a risk factor for cardiovascular disease, and there are reports that it promotes the progression of chronic renal failure. Therefore, the administration of drugs for each patient will be judged according to the situation, but in particular, in the case of so-called metabolic syndrome such as obesity, insulin resistance, high blood pressure, and hyperlipidemia, administration can be considered in terms of preventing cardiovascular disease.
2. Can I have tophi gout even if my blood uric acid level is low?
It is clear that tophi gout occurs in patients with hyperuricemia. However, it should be noted that blood uric acid levels may be normal when acute gout occurs. Inducers of acute gout include diuretics that increase serum uric acid levels, drugs such as cyclosporine, alcohol, cytotoxic chemotherapy, overeating, as well as surgery that can temporarily reduce blood uric acid levels, fasting and severe diet, and uric acid-lowering drugs. This is because use, etc. can also cause acute gout attacks.
3. Can tophi gout be treated only when it is sick?
Most of the tophi gouts are treated only for an acute gout attack and are often terminated. However, 20 years after the first seizure of gout occurred, 28% of patients with gouttophi were severely disabled, and 2-3% of those patients were severely disabled. In addition, about 10% of the causes of death in gout patients are renal failure, and hyperuricemia itself acts as a risk factor for deteriorating renal function and may also cause urinary tract stones. Consistent treatment to reduce uric acid reduces gouttophi, which can prevent disability and prevent worsening of renal function. In addition, since most of gout patients are accompanied by diseases such as high blood pressure, diabetes, cardiovascular disease, and obesity, constant and continuous management of metabolic syndrome along with control of gout is required.
4. Is a strict purine restriction diet essential to prevent tophi gout?
Until recently, foods were classified according to the level of purine content, and strict restrictions were recommended for foods with a high content of purine. However, it is known that the strict limit of purine intake, which is the traditional gout diet, is not only difficult for actual patients to adhere to, and the effect of lowering uric acid is not significant. As obesity and carbohydrates (especially foods high in fructose) have been known to be closely related to the increase in gout incidence, nowadays, low purine, low calorie, low carb diets are recommended for gout patients with adequate weight loss. Adequate dairy and protein intakes are being used in parallel.
5. What drugs should be watched for in patients with tophi gout?
Several commonly used drugs affect the level of uric acid in the blood, and aspirin is a representative of them. High doses of aspirin promote uric acid excretion, but low doses of aspirin may increase blood uric acid levels as uric acid excretion decreases. Therefore, when low doses of aspirin are administered to prevent cardiovascular disease, serum uric acid levels must be carefully monitored. In patients who are already taking uric acid-lowering drugs, low doses of aspirin are known to have little effect on the patient’s blood uric acid levels. In addition, ACE (Angiotensin or its receptor) inhibitors and vitamin C promote uric acid excretion, but diuretics and tuberculosis drugs such as pyrazinamide and ethambutol, and cyclosporine are known as drugs that inhibit uric acid excretion.
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