Gout is an ancient disease, with uric acid crystals found in Egyptian mummified joints thousands of years ago, and its pathogenesis and pathophysiology have long been elucidated in detail. Despite this, the management of gout and hyperuricemia remains unsatisfactory both nationally and internationally, with problems of inadequate patient education, inadequate management, and poor adherence noted in Becker and Chohan’s 2008 monograph in Curr Opin Rheumatol and Hamburger et al.’s 2011 recommendations for the management of gout and hyperuricemia, in particular, the existence of Some ambiguous or controversial issues remain. 1. Aspirin and uric acid excretion In 2007, the British Society for Rheumatology and British rheumatology health professionals developed guidelines for the treatment of gout, suggesting that “small doses of aspirin (75-150 mg/d) have no significant effect on blood uric acid and can be used for cardiovascular disease prevention, but high doses of aspirin (600-2400 mg/d) can interfere with uric acid excretion and should be avoided. and should be avoided”. The recommendations for the management of cardiovascular disease combined with asymptomatic hyperuricemia (2nd edition) also suggest that “prolonged application of certain drugs can lead to increased blood uric acid, e.g. aspirin above 300 mg daily ……”. This is contrary to the previous concept that “small doses of aspirin interfere with uric acid excretion and large doses promote uric acid excretion”, and given that small doses of aspirin are widely used, including in a large number of elderly healthy people who use it prophylactically, it is of great clinical importance to clarify this issue. However, no references are given in these papers. The idea that “small doses of aspirin inhibit uric acid excretion and large doses promote uric acid excretion” is based on trial data, so it is impossible to disprove the traditional claim until there is new evidence to the contrary. In addition, the belief that “low-dose aspirin inhibits uric acid excretion” does not mean that patients with hyperuricemia who are taking low-dose aspirin must stop using aspirin, and the decision should be based on risk/benefit. 2. Whether vitamin C can lower blood uric acid Studies suggest that oral high-dose vitamin C is an independent low risk factor for gout. This makes the causal chain of vitamin C supplementation – reduced blood uric acid – reduced incidence of gout clear. Studies have shown that the pro-uric acid excretory effect of vitamin C may be related to its increased glomerular filtration rate and inhibition of uric acid reabsorption in the proximal renal tubules. This causal chain would be more complete if it could be demonstrated that urinary uric acid excretion is increased with oral vitamin C, but the literature on this has not been identified. Urinary acid excretion, urine volume, and pH of urine are associated with stone formation. Previous studies have shown that vitamin C supplementation (even 500 mg/day) significantly lowers urinary pH below 6, and that vitamin C lowers uric acid by promoting excretion. A decrease in urinary pH and an increase in uric acid excretion theoretically creates the conditions for uric acid stone formation. Will vitamin supplementation not promote urinary stone formation? Stone formation takes a long time and the observation period is too short to answer this question definitively yet. Second, vitamin C can interfere with uric acid measurements, leading to unreliable uric acid data is this question is more complicated. 3. The relationship between corticosteroids and uric acid and uric acid stones An expert consensus in China concluded that “patients with hyperuricemia should avoid the application of drugs that elevate blood uric acid such as diuretics (especially thiazides) and corticosteroids ……”. In a limited literature search, no discussion that corticosteroids can elevate blood uric acid was found. According to our clinical practice: 1. Almost all textbooks and guidelines suggest the use of corticosteroids for the treatment of acute gout, but none of them warn that it can elevate blood uric acid. 2. Patients with SLE who use a large amount of corticosteroids for a long time rarely have elevated uric acid, and most of those with hyperuricemia are related to renal involvement and diuretic use. 3. Studies on Cushing’s disease strongly suggest that excessive endogenous glucocorticoids stimulate uric acid excretion; uric acid excretion increases in people with normal renal function after receiving pro-adrenocorticosteroids or glucocorticoids. Thus, it appears that short-term corticosteroids do not increase uric acid. Are there any other problems with long-term glucocorticoid use? There is no unanimous conclusion. In conclusion, the prevailing view is that “small doses of aspirin interfere with uric acid excretion and large doses promote uric acid excretion”. The available articles and monographs mention that “vitamin C reduces uric acid levels”, but several questions need to be further investigated: Is this an artifact of the test? Is there an increase in urinary uric acid excretion? Can it reduce the incidence of gout? How feasible is it? Short-term corticosteroids do not increase uric acid, and more evidence is needed to determine whether long-term use promotes stone formation.