Author: Feng He
Source: Rheumatism and Immunity Channel of the Medical Community< p>According to the Meta analysis cited in the “2019 Guidelines for Diagnosis and Treatment of Hyperuricemia and Gout in China”, the overall prevalence of hyperuricemia in China was 13.3%, Gout was 1.1%. In 2017 “China Gout Status Report White Paper” pointed out that the number of hyperuricemia patients in my country has reached 170 million, and the number of patients with gout has exceeded 80 million.
According to the courseware of Professor Wu Zhenbiao, Xijing Hospital of Air Force Military Medical University, we have sorted out the important points for gout diagnosis and treatment matters to readers.
01
High uric acid≠gout,but it is also very harmful!
Uric acid is the final metabolite formed by a series of oxidative decomposition of purine, and its 60 % or more needs to be excreted by the kidneys. A large increase in uric acid production and/or insufficient excretion can lead to its accumulation in the blood, resulting in hyperuricemia that is, under a normal diet, the fasting blood uric acid level is >420 μmol/L twice on different days.
Graph of wind pain
<600> Causes
Gout is an inflammatory disease caused by long-term purine metabolism disorder leading to increased blood uric acid and tissue damage caused by urate crystal deposition. Recurrent acute and chronic arthritis, joint deformity and severe pain are clinical features. In severe cases, joint destruction and even uric acid nephropathy occur.
Gout and hyperuricemia are two different concepts. Hyperuricemia occurs when serum uric acid (SUA) is elevated but there is no gout attack. Urate crystal deposition is the result of hyperuricemia. The incidence of gout was significantly positively correlated with the level of SUA; the lower the SUA, the faster the dissolution rate of tophi and the lower the recurrence rate of gout.
Professor Wu Zhenbiao pointed out that a large number of epidemiological and clinical studies at home and abroad have shown that elevated blood uric acid can not only cause gout It is also related to the occurrence and development of kidney, endocrine metabolism, cardiovascular and cerebrovascular diseases, and is even an independent risk factor for these diseases.
02
Diagnostics Gout, These 10 characteristics should be kept in mind!
Gout was first diagnosed using the 1977 ACR classification criteria, but due to sensitivity and specificity In 2015, the American College of Rheumatology proposed 10 diagnostic features of gout, which have become commonly used clinical diagnostic criteria; tophi and synovial fluid with urate crystals are the gold standard for gout diagnosis, but many primary hospitals have problems in medical facilities. More inclined to the evaluation of clinical symptoms, dual-energy CT and polarized light examination are also helpful for the early detection of tophi or urate crystals in synovial fluid; however, it should be noted that recurrent rheumatism, pseudogout and infectious arthritis should be excluded.
diagnostic features of gout p>
Figure 4: Imaging of gout
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Special attention should be paid here. The low level of uric acid during the attack cannot rule out gout!!!
During a gout attack, 70% of patients had high uric acid levels, but 30% had normal uric acid levels.
Normal reasons include stress response to excessive secretion of corticosteroids to promote uric acid excretion, taking diuretics or antihypertensive drugs.
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03
5 doubts about the treatment of gout, solve them one by one!
▎What should I do during an acute attack of gout? Don’t panic!
: span>Principles for the management of acute gout attacks
Non-steroidal anti-inflammatory drugs (NSAIDs) are the mainstay of gout First-line medication in the acute phase, it is recommended to take a sufficient amount in the early stage. Drugs with fast onset of action and few gastrointestinal adverse reactions are preferred. It should be used with caution in patients with old age, renal insufficiency, previous peptic ulcer, bleeding and perforation.
for NSA6 >Gout
Colchicine was the first anti-inflammatory and analgesic drug for gout, and it is still an acute attack of gout first-line medication. Studies have shown that compared with high-dose drugs, low-dose colchicine is equally effective in treating acute gout, and the adverse reactions are significantly reduced. Therefore, it is recommended that in acute gout attack, the first dose of colchicine is 1 mg, followed by 0.5 mg after 1 hour, and then changed to 0.5 mg qd or bid after 12 hours.
Figure 7: Colchicine for goutgout
Glucocorticoids have similar analgesic effects to NSAIDs in acute gout attacks, but can better relieve joint pain. Currently, European and American guidelines recommend glucocorticoids as first-line anti-inflammatory analgesics Glucocorticoids are recommended as second-line analgesics in order to prevent hormone abuse and repeated use from increasing the incidence of tophi.
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Figure 8: Glucocorticoids for gout
In recent years, IL-1 antagonists, a new type of gout anti-inflammatory and analgesic drug, have been gradually used in the treatment and prevention of gout. 1 The main antagonists are Anakinra, Canakinumab and Rilonacept, all of which are not listed in China.
▎Uric acid-lowering therapy Treatment, these 3 drugs must be mastered!
When choosing uric acid-lowering drugs, the indications, contraindications and types of hyperuricemia should be comprehensively considered. Allopurinol, febuxostat or benzbromarone are the first-line drugs for lowering uric acid in patients with gout; allopurinol or benzbromarone are first-line drugs for lowering uric acid in patients with asymptomatic hyperuricemia.
The treatment goal of gout /p>
Figure10: Comparison of uric acid lowering drugs
uric acid reduction period
Long-term uric acid-lowering therapy is the key to cure gout. After gout patients start taking uric acid-lowering drugs, the fluctuation of blood uric acid level can cause the dissolution of tophi or urate crystals inside and outside the joints, resulting in recurrent gouty arthritis. At the initial stage of uric acid lowering treatment (3 to 6 months), the level of blood uric acid was significantly reduced, and about 12% to 61% of patients had recurrent gout attacks. Continuing treatment for 8 to 12 months, the frequency of gout attacks could be significantly reduced.
In the initial stage of uric acid-lowering treatment for gout patients, low-dose (0.5-1 mg/d) colchicine is the first choice to prevent gout attacks, and maintain at least 3- 6 months; for patients with renal insufficiency, it is recommended to adjust the colchicine dosage according to eGFR; for patients who cannot tolerate colchicine, low-dose NSAIDs (not more than 50% of the conventional dose) or glucocorticoids (prednisone ≤ 10 mg/d) to prevent seizures for at least 3 to 6 months. In addition, uric acid-lowering drugs should be started in small doses and increased slowly to avoid or reduce gout attacks.
▎Gout is refractory, is there any other way?
Refractory gout is defined as having at least one of the following three:
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Single or combined with conventional uric acid-lowering drugs with sufficient dose and full course of treatment, but blood uric acid is still ≥360 μmol/L;< /span>
Gout attacks ≥2 times/year after receiving standardized treatment;
Multiple and/or progressive tophi present.
In terms of treatment, it is recommended to use polyethylene glycol recombinant uricase preparation for uric acid lowering in refractory gout Treatment; IL-1 or tumor necrosis factor alpha (TNF-α) antagonists may be considered in patients with refractory gout with recurrent pain that cannot be controlled by conventional drugs;Such as local complications (infection, rupture, nerve compression, etc.) of tophi or serious impact on the quality of life, surgery can be considered.
▎Comprehensive treatment is the key!
In patients with hyperuricemia and gout combined with chronic kidney disease, it is recommended to select uric acid-lowering drugs individually according to the stage of chronic kidney disease and dose; it is suggested that febuxostat should be given priority to urate-lowering drugs when eGFR<30 ml·min-1·(1.73 m2)-1. Hyperuricemia and gout are often associated with hypertension, lipid metabolism disorders, and diabetes. These diseases affect each other and cause each other. Therefore, adhere to the principle of “comprehensive treatment”, choose drugs with both uric acid-lowering effects, and avoid uric acid-raising drugs.
Finally, Professor Wu Zhenbiao mentioned in his lecture that for gout patients, lifestyle management is as important as standard gout diagnosis and treatment. Gout patients should adhere to a healthy lifestyle, such as drinking more water, alkalizing urine, and controlling dietary intake of total purines.
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