Gout is a common inflammatory arthropathy caused by purine metabolism disorders or uric acid excretion disorders, with a global incidence of 0.1% to 10%. In both men and women, a blood uric acid level of more than 420 micromol/L twice a day is hyperuricemia, and serum uric acid exceeding its saturation in the blood or tissue fluid can induce gout.
Elevated serum uric acid concentrations are the root cause of the occurrence and development of hyperuricemia and gout and their associated comorbidities. Long-term adherence to serum uric acid significantly reduces the frequency of gout attacks, prevents tophi formation, prevents bone destruction, reduces the risk of death and improves the quality of life of patients, which is the key to preventing gout and its associated comorbidities. Meta-analysis showed that the overall prevalence of hyperuricemia in China was 13.3%, and the prevalence of gout was 1.1%. There is a correlation between increased uric acid levels and the onset of gout.
Recently, a study published in The Lancet Rheumatology added new evidence to the association between serum uric acid and acute onset in gout patients, and once again emphasized that it is very important for patients with gout to achieve uric acid control standards regardless of symptoms. The results showed that when serum uric acid concentrations persisted averaged.
Screenshot source: The Lancet Rheumatology
The investigators analysed patient-level data from two randomized trials of uric acid reduction conducted in Nottingham, UK and New Zealand:
New Zealand trial: 71 participants with an average age of 60.1 years;
Nottingham trial: 517 participants in total, with an average age of 62.9 years.
Based on data at months 6, 9 and 12 months after baseline, average serum uric acid concentrations after treatment
The main result of the study was the proportion of patients who had at least one gout attack during the 12th to 24th month visit. Secondary results Average number of seizures per patient per month in months 12-24 (number of collections: 0-4 times/month). At month 24, the results of serum uric acid responders and non-responders were compared.
All patients in the New Zealand trial and 441 patients in the Nottingham trial completed all 24 months of follow-up.
Serum uric acid concentration
From pooled individual data from the two trials, the investigators identified 343 serum uric acid responders (uric acid compliance) and 245 serum uric acid non-responders (uric acid non-compliance). The data showed that during the 12-24-month period, the proportion of gout attacks in serum uric acid responders was significantly smaller than in those without serum uric acid responses, and the risk of gout attacks was reduced by 71% (adjusted OR 0.29, 95% CI 0.17-0.51, p
Gout attacks in 91 (27%) of the 343 serum uric acid responders;
Of the 245 patients with no response to serum uric acid, 156 (64%) had gout attacks.
Further analysis also found that this association was independent of the initial random treatment allocation. This suggests that a decrease in serum uric acid is the main cause of the absence of gout.
On the other hand, the mean number of episodes in serum uric acid responders at 12 to 24 months was significantly lower than that of serum uric acid responders (mean difference –0.41 [–1.77 to –1.04], p
Image credit: 123RF
Prevention and control of gout
Hyperuricemia and gout are systemic diseases with multisystem involvement, and patients need to focus on a number of aspects in addition to uric acid control. In the "Guidelines for the Diagnosis and Treatment of Hyperuricemia and Gout in China" (2019), normative guidance is given for the diagnosis, treatment and prevention of gout:
1. All patients with hyperuricemia and gout need to maintain a healthy lifestyle:
1) Control weight and exercise regularly;
2) Limit the intake of alcohol and high-purine and high-fructose diet;
3) Encourage the intake of dairy products and fresh vegetables and drink water in moderation;
4) It is not recommended or restricted to the intake of soy products (such as tofu).
2. Continue to pay attention to the influencing factors of serum uric acid level, always control the serum uric acid level in the target range: 240 ~ 420 μmol / L, and may take uric acid-lowering drugs for a long time or even for life.
3. Understand the possible hazards of the disease, regularly screen and monitor the target organ damage and deal with related comorbidities in a timely manner, so as to achieve early detection and early treatment, and improve the overall prognosis of patients.
Timing and control goals of initiation of uric acid-lowering drugs in patients with gout:
In patients with gout, when the serum uric acid ≥ 480 μmol/L, it is recommended to start uric acid-lowering drug therapy;
Serum uric acid ≥ 420 μmol/L and with any of the following, initiation of uric acid-lowering drug therapy: 2 episodes of gout attacks≥2 times/year, tophi, chronic gouty arthritis, nephrolithiasis, chronic kidney disease, hypertension, diabetes mellitus, dyslipidemia, stroke, ischemic heart disease, heart failure, and age of onset
It is recommended to start uric acid-lowering drug therapy 2 to 4 weeks after complete remission of the acute attack of gout, and it is not recommended to discontinue uric acid-lowering drugs in patients with acute attacks of gout who are taking uric acid-lowering drugs;
It is recommended that patients with gout control serum uric acid
It is not recommended to control serum uric acid in the long term
Resources:
[1] Lisa K Stamp, Christopher Frampton, JasvinderA Singh, et al., (2021). Association between serum urate and flares in peoplewith gout and evidence for surrogate status: a secondary analysis of tworandomised controlled trials. The Lancet Rheumatology. DOI: https://doi.org/10.1016/S2665-9913(21)00319-2
Chinese Medical Association Endocrinology Branch. Guidelines for the Diagnosis and Treatment of Hyperuricemia and Gout in China (2019). Chinese Journal of Endocrinology and Metabolism[J].2020,01(36):1-13.
Source | A new perspective on medicine
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