Gout comes from high uric acid, but high uric acid does not necessarily mean gout. It only happens when uric acid crystals in the blood deposit on the synovium of joints and cause synovitis. In fact, only about 10% patients with hyperuricemia have gout.
On the other hand, due to the complex pathogenic factors of gout, many patients may still have normal blood uric acid levels when gout attacks. At this time, don't be superstitious about the test results and delay the timely treatment of gout.
High uric acid can not only induce gout.
Uric acid is the metabolic end product of purine in human body, and high uric acid has harmful effects on many tissues and organs of human body. Excessive deposition of uric acid in bones and joints can cause gout; Deposition in the kidney will cause nephropathy and induce renal failure; High uric acid will also greatly increase the risk of various metabolic related diseases (such as obesity, diabetes, hyperlipidemia, etc.). ) and cardiovascular diseases.
"Normal" uric acid is not enough for gout patients.
According to international standards, the normal range of uric acid is: male.
High uric acid that does not cause gout also needs treatment.
There is a long-standing controversy about this issue, but at present, the academic circles basically agree that no matter how "healthy" a person is, as long as uric acid exceeds 520 μmol/L, uric acid should be treated; If this person is also complicated with risk factors of diabetes, chronic kidney disease or cardiovascular disease, then as long as uric acid exceeds the above normal range, even if there is no gout attack, treatment needs to be started.
Uric acid lowering drugs can also be used for acute gout attacks.
For a long time, it has been thought that if uric acid-lowering drugs are used in the acute stage of gout, the surface of tophus in the joint may dissolve, and insoluble crystals will be deposited in the tissue, which will aggravate the inflammatory reaction. Therefore, "acute gout can not use uric acid lowering drugs" has almost become the golden rule in gout treatment.
However, 20 12 American Gout Management Guidelines first proposed that under the protection of effective anti-inflammatory drugs, the treatment of acute uric acid reduction is not taboo. Then, 20 13 China's "experts on hyperuricemia and gout treatment" also recognized this view, thinking that you don't have to wait for two weeks after the acute symptoms of gout are relieved, but you can start the treatment of reducing uric acid immediately.
Clinicians generally tend to adopt a conservative attitude towards this "counterintuitive" avant-garde concept. After all, old ideas have a long history and are deeply rooted in people's hearts; The new viewpoint needs more evidence-based evidence, and its greater clinical significance lies in that patients with acute gout attack during taking uric acid-lowering drugs can stop uric acid-lowering treatment accordingly.
Simple diet control for gout patients is far from enough.
80% of uric acid in human blood comes from purine metabolism, and only 20% comes from food intake. Therefore, the effect of simple diet control on reducing serum uric acid level is very limited (most of them can only reduce 10%-20% or 70-90 μmol/L). Therefore, we must choose drugs reasonably according to the condition.
Many patients refuse to take medicine for fear of "side effects", which is a typical "choking on food".
As long as drugs are used scientifically and regularly, the risk of rare complications of drugs is not higher than that of going out to encounter a car accident. Who stays at home all day for fear of a car accident?
The treatment of hyperuricemia and gout cannot rely entirely on drugs.
After applying uric acid-lowering drugs, some patients think that they can rest easy and enjoy delicious food.
However, the idea that "one more slice is a big deal" is not only wrong, but also dangerous.
For chronic metabolic diseases such as gout, "low purine" diet is the premise and basis of treatment. Without reducing the intake of purine from the source, it is impossible to control the disease simply by relying on drugs. However, due to overeating, uric acid increased significantly, and the dosage of the drug had to be increased, which greatly increased the risk of adverse drug reactions.
Patients with hyperuricemia do not need to stop taking aspirin.
Aspirin is a century-old classic drug, which is widely used.
However, low-dose aspirin can inhibit the excretion of uric acid by renal tubules, which is considered to be an important cause of hyperuricemia. In the past, doctors often advised gout patients to stop taking aspirin. However, the new view holds that the negative effect of aspirin on gout patients is actually very weak, even negligible.
This has important guiding significance for clinical practice. For example, patients with gout take low-dose aspirin to prevent cardiovascular disease, and there is no need to stop taking medicine or change medicine.
Surgery can't cure tophi.
Tophus is a white crystal precipitated by uric acid exceeding its saturation, which occurs on the extension side of joints, tendons and bony processes. By taking uric acid-lowering drugs and maintaining uric acid