When it comes to the “three highs” that pose a great threat to people’s health in modern society – high blood sugar, high blood pressure and high blood cholesterol – no one will be unfamiliar with them. Now, the fourth high after the “three highs” – high uric acid has also surfaced and is coming on strong. “The first step to defeat the enemy is to know the enemy. There are a lot of common misconceptions about high uric acid and gout in the society, so it is necessary to sort out and learn with you. High uric acid does not necessarily mean gout, and gout does not necessarily mean high uric acid. Gout originates from high uric acid, but it does not necessarily mean that gout will occur when high uric acid is present, only when uric acid crystals in the blood are deposited in the synovial membrane and cause synovial inflammation. In fact, only about 10 percent of patients with high uric acid develop gout. Conversely, due to the complexity of the causative factors of gout, many patients’ blood uric acid levels may still be within the normal range when they have a gout attack. High uric acid does not only trigger gout. Uric acid is the end product of purine metabolism in the body, and high uric acid has harmful effects on many tissues and organs. Excessive uric acid deposited in bones and joints can cause gout; deposited in kidneys can cause kidney disease and kidney failure; high uric acid can also greatly increase the risk of many metabolic-related diseases (such as obesity, diabetes, hyperlipidemia, etc.) and cardiovascular diseases. For gout patients, “normal” uric acid is not enough According to international standards, the normal range of uric acid is < 420 μmol/L for men and < 360 μmol/L for women, however, for gout patients, controlling uric acid in this "normal" range is not enough. The latest guidelines recommend that the blood uric acid level of gout patients should be stabilized at 300 μmol/L for a long period of time to promote the dissolution of gout stones and prevent gout attacks. High uric acid levels that do not cause gout also need to be treated There has been a long-standing controversy on this issue, but the academic community is now basically unanimous: no matter how "healthy" a person is, as long as the uric acid exceeds 520 μmol/L, uric acid-lowering treatment should be carried out; if the person also has diabetes, chronic kidney disease or risk factors for cardiovascular disease, then as long as the uric acid exceeds the above-mentioned normal range, the person needs to be treated. Treatment needs to be initiated even if there is no gout attack. Uric acid-lowering drugs can also be used during acute gout attacks It has long been believed that if uric acid-lowering drugs are used during acute gout attacks, they may lead to the dissolution of gout stones on the surface of the joints and the formation of insoluble crystals in the tissues to aggravate the inflammatory response. Therefore, "no uric acid-lowering drugs should be used during the acute phase of gout" has almost become a golden rule in gout treatment. However, in 2012, the U.S. Gout Management Guidelines proposed for the first time that uric acid-lowering therapy in the acute phase is not contraindicated under the "protection" of effective anti-inflammatory drugs. This was followed by the 2013 Chinese Expert Consensus on the Treatment of Hyperuricemia and Gout, which also endorsed the idea that it is not necessary to wait until two weeks after the acute symptoms of gout have resolved, but that uric acid-lowering therapy can be started immediately. Clinicians generally tend to take a conservative approach to this "counterintuitive" avant-garde concept. After all, the old idea has been around for a long time, and the new idea needs more evidence-based evidence. The greater clinical significance of the new idea is that patients who have an acute attack of gout while taking uric acid-lowering drugs can be treated without stopping uric acid-lowering therapy. Dietary control alone is not enough for gout patients. 80% of uric acid in human blood is metabolized by our own purines and only 20% by food intake. Therefore, dietary control alone has a very limited effect on reducing blood uric acid levels (most of them can only be reduced by 10% - 20% or 70 - 90 μmol/L). Therefore, it is necessary to choose the right medication according to the condition. Many patients refuse to take medication because they are worried about "side effects", which is a typical case of "choking on food". As long as the medication is used scientifically and regularly, the risk of rare complications from medication is no higher than the risk of being in a car accident, and who would stay home all day for fear of a car accident? The treatment of high uric acid and gout should not rely entirely on medication. After taking uric acid-lowering medication, some patients think that they can rest easy and enjoy their diet. However, the idea that "the big deal is to take more pills" is not only wrong but also dangerous. For a chronic metabolic disease like gout, a "low purine" diet is the prerequisite and foundation of treatment. Without reducing purine intake at the source, the disease cannot be controlled by medication alone. The risk of adverse drug reactions is greatly increased when the dose of medication has to be increased due to the significant increase in uric acid caused by an inappropriate diet. Patients with high uric acid do not need to stop using aspirin Aspirin is a century-old classic drug with a very wide range of applications. However, small doses of aspirin inhibit the excretion of uric acid by the renal tubules and are considered an important trigger for hyperuricemia. Previously, doctors often recommended discontinuing the drug for patients who had gout but needed to take aspirin. However, the new view is that for patients who have developed gout, the negative effect of aspirin is actually very weak or even negligible. This has important implications for clinical practice, for example, gout patients who take small doses of aspirin to prevent cardiovascular disease hazards may not need to stop or change their medication. Surgery does not cure gout stones. Gout stones are white crystals of uric acid that have exceeded their saturation level and are found on the extensor surfaces of joints, tendons and bony prominences. Gout stones can be reduced by taking uric acid-lowering medication and keeping uric acid < 300 μmol/L. However, surgery does not solve the root of the problem. However, surgery does not solve the root of the problem. If the uric acid level remains high, the gout stone will recur after removal, and the surgical incision is difficult to heal, which can lead to infection. Therefore, unless the gout stone is huge, or affects the function of the joint or presses the nerve, it is generally not recommended to remove it through surgery. In conclusion, high uric acid and gout, with their high incidence and danger, are a matter of health and safety and should not be ignored. However, as with many common diseases, the Internet is full of rumors and falsehoods, and it is not easy to find reliable knowledge without a certain background of professional knowledge and time to investigate the truth.