Myth 1, high blood uric acid must get gouty arthritis Many people find high blood uric acid, also known as hyperuricemia, during physical examination, they think they must get gouty arthritis, but in fact, they do not. According to reports on the prevalence of hyperuricemia in recent years, there are currently about 100 million or 200 million people with hyperuricemia in China, accounting for about 10% of the total population, and the incidence is trending younger. Hyperuricemia is the basis and the most direct cause of gouty arthritis, and gouty arthritis is considered to develop when uric acid is deposited in the body’s synovial fluid, causing redness, swelling, and pain in the joints. However, blood uric acid levels are not always high during acute attacks of gouty arthritis. For patients with gouty arthritis, blood uric acid needs to be controlled at a certain level, generally below 360umol/l. Patients with combined gouty stones need to drop even lower, below 300umol/l, in order to facilitate the dissolution and discharge of gouty stones. Misconception 2, gouty arthritis acute attack to lower uric acid treatment Many patients in the acute attack of gout desperately want to reduce the blood uric acid level to normal, this idea is not right. This is because the main reason for an acute attack of gouty arthritis is the dramatic fluctuation of uric acid levels in the body. The solubility of uric acid in body fluids is low. At high concentrations, it becomes supersaturated and is deposited in joint cartilage, synovium and other tissues in the form of uric acid salts, mainly because these tissues have fewer blood vessels, lower tissue fluid pH, and a matrix rich in mucopolysaccharides and connective tissue, making it easy for uric acid salts to be deposited, causing a non-specific inflammatory response, resulting in dissolution of joint cartilage and damage to soft tissue. When there is excessive purine intake in the body, it can cause an elevation of uric acid, and the deposition of urate on the surface of the joint triggers an inflammatory response, causing an acute attack of gout. After the application of uric acid-lowering drugs, the level of uric acid in the blood drops sharply. This causes the dissolution of urate deposited in joint cartilage and other tissues and its re-release into the blood, stimulating the phagocytosis of inflammatory cells and the release of inflammatory factors, which further leads to the exacerbation of arthritis. Therefore, uric acid-lowering therapy is generally not recommended during the acute phase of gouty arthritis, and the addition of uric acid-lowering drugs should be considered only after the disappearance of joint pain symptoms for more than 2 weeks, and the dosage should be increased gradually from small doses to the full amount. It is important to note that the process of lowering uric acid may cause an attack of gouty arthritis at any time, so it is important to monitor the changes in joint symptoms during the treatment process and add NSAIDs to inhibit a major attack of gouty arthritis if necessary. Myth 3: Gouty arthritis does not need treatment after the attack period Clinically, many patients with gouty arthritis can be seen in the acute phase of the disease attack joint redness, swelling and pain, seriously affecting their normal life and work, so pay more attention to the anti-inflammatory and pain relief treatment, it is believed that the disease is not pain, no need to continue treatment. This understanding is not correct. In fact, gouty arthritis, like diabetes, also requires long-term medication. After the acute period of anti-inflammatory and pain relief, alkalinization of urine and other treatment, the inflammation of the joints can be slowly absorbed, joint pain healed, but the uric acid in the body is still at a high level, which is like an “untimely bomb” and may cause another attack of gouty arthritis at any time. High levels of uric acid are deposited in joints, cartilage and soft tissues, which can cause gout stones to develop. Therefore, after the acute phase of gouty arthritis, colleagues who continue to control the diet after the joint pain disappears still need to take medication, and it is the uric acid-lowering drugs that are effective at this time. The choice of uric acid-lowering drugs is not random, but depends on the different conditions of the patient. There are two kinds of drugs, one is to promote uric acid excretion, such as benzbromarone tablets, and the other is to inhibit uric acid production, such as allopurinol. If the patient’s ultrasound shows urinary tract stones, the drug to promote uric acid excretion cannot be applied to prevent further increase of urinary tract stones; drugs to inhibit uric acid production can be chosen for mild to moderate renal abnormalities and urinary tract stones, but attention should be paid to the occurrence of allergic reactions. Myth 4: Antibiotics can be used in the acute phase of gouty arthritis Some patients with gouty arthritis believe that the redness and swelling of the joints are caused by bacterial infection and antibiotics can be applied for antibacterial treatment, in fact, antibiotics do not work for the metabolism of blood uric acid. If there is relief of symptoms, it may also be caused by the fact that the initial gouty arthritis can heal on its own. Generally speaking, for the acute stage of gouty arthritis with red, swollen and painful joints, you can consider adding non-steroidal anti-inflammatory drugs such as diclofenac, ibuprofen, etoricoxib, etc. You can also choose colchicine, but because the therapeutic and toxic doses of colchicine are similar, you need to use it under the guidance of a doctor. Then add sodium bicarbonate tablets to alkalize the urine to facilitate the discharge of urate crystals. Myth 5, strict control of diet gout will not attack Most patients believe that since gout is induced by excessive intake of high purine food, I do not eat purine containing food, gout will not attack? In clinical practice, it is also common for patients to say, “I basically eat cabbage every day, but I still have gout attacks”. They think that if they do not consume purine-containing foods and strictly control their diet, then they will not have gout attacks. In fact, this is not true. The human body produces about 750mg of uric acid every day, of which 80% comes from the metabolism of purines by itself and only 20% comes from food intake. The amount of uric acid excreted daily is 500mg-1000mg, of which two-thirds is excreted by the kidneys and one-third is broken down in the intestines. Excessive production and low excretion of uric acid will lead to an increase in blood uric acid blood in the body. High purine diet is only a precipitating factor of gouty arthritis attack, strict restriction of purine food intake to reduce blood uric acid is limited, it can only reduce blood uric acid concentration by 1mg/dl, most patients cannot reach the ideal target value of serum uric acid concentration, so it does not fundamentally eliminate the primary cause of gout attack, but also need to rely on drugs to reduce uric acid, but it should be emphasized that diet control is the basis of gout treatment. However, it should be emphasized that dietary control is the basis of gout treatment. During the acute phase of gout attack, the intake of medium and high purine food should be strictly controlled, while during the interval, the standard can be relaxed appropriately to ensure the daily nutritional intake. Myth 6: Asymptomatic hyperuricemia does not need treatment Because hyperuricemia can cause kidney function damage and cardiovascular events, asymptomatic hyperuricemia needs to be treated according to the specific situation to choose whether intervention is needed. The following treatment recommendations for asymptomatic hyperuricemia are provided in the Chinese Expert Consensus on Recommendations for the Diagnosis and Treatment of Hyperuricemia in Combined Cardiovascular Disease: 1. Routine blood uric acid monitoring during physical examination to detect asymptomatic hyperuricemia as early as possible; 2. All patients with asymptomatic hyperuricemia need to undergo therapeutic lifestyle changes and avoid drugs that elevate uric acid as much as possible; 3. When combined with cardiovascular risk factors or cardiovascular disease (including hypertension, abnormal glucose tolerance or diabetes, hyperlipidemia, coronary heart disease, stroke, heart failure or renal abnormalities, drug therapy is given when blood uric acid is greater than 8mg/dl; in hyperuricemia without cardiovascular risk factors or cardiovascular disease, drug therapy is given when blood uric acid value is greater than 9mg/dl; 4. The target value of blood uric acid therapy is less than 357umol/L; 5. Active control of coexisting cardiovascular risk factors in asymptomatic hyperuric acid patients. In addition, patients with a family history of gout should also be treated with uric acid-lowering therapy.