History History Male, 60 years old, obese body type. A day ago, after eating seafood and drinking a lot of beer, he felt tingling pain in his left [toe], and was immediately given local massage and hot compresses, but his symptoms did not improve significantly. In the early morning, the patient had a sudden onset of severe pain in the left [toe] and could not sleep, and immediately took oral allopurinol without improvement. Past history A 10-year history of hypertension, currently treated with thiazide diuretics and calcium antagonists. The patient has been treated with atorvastatin calcium for 6 years for hyperlipidemia. 1 year ago, elevated blood uric acid (512 μmol/L) was found on physical examination, but the patient did not pay attention to it and took allopurinol occasionally as a uric acid-lowering drug. The patient was not given any attention and was taking occasional allopurinol as a hyponatremic drug. Emergency physical examination: temperature 38°C, blood pressure 150/95 mm Hg, body mass index 33 kg/m2; cardiac, pulmonary and abdominal examinations were normal; left toe was red and swollen and refused to be pressed. Laboratory examination: peripheral blood leukocytes 12×109/L, blood uric acid 408 μmol/L. Considering the possibility of dengue, gouty arthritis was not excluded, and penicillin was given intravenously for 1 d. Oral fenpropathrin was given because the symptoms were not relieved, and the swelling and pain improved after 2 d. The body temperature returned to normal. Is the patient suffering from acute gouty arthritis? The patient was a middle-aged male with an obese body type, which is a good candidate for gouty arthritis; the patient’s blood uric acid was elevated in the past, but it was not treated regularly, so there was a pathological basis for gouty arthritis attack; the patient consumed a lot of seafood and beer before the arthritis attack, so there was a clear trigger for gouty arthritis attack; from the analysis of the site of arthritis, the patient presented with severe pain and redness in the left [toe, which is the most typical site for acute gouty arthritis attack Therefore, the diagnosis of acute gouty arthritis can be confirmed by comprehensive consideration. The differential diagnosis should consider the possibility of dengue, but the patient has no history of local trauma and mosquito bites, no history of other systemic infections, and the application of antibiotics is ineffective, so dengue can be basically excluded. What are the triggers for this acute onset of the patient? Current epidemiological studies show that middle-aged and elderly men and obese body types are at high risk for hyperuricemia and gout, and patients with hypertension and hyperlipidemia are also at high risk for hyperuricemia and gout. In addition, thiazide diuretics applied by patients to control blood pressure can cause an increase in blood uric acid. Numerous studies have shown that eating high purine foods can cause elevated blood uric acid or trigger a gouty arthritis attack, and seafood and beer can trigger an acute attack of gout, which is a trigger for this attack. It is important to note that a normal uric acid level does not exclude acute gouty arthritis, as some patients with acute gout have normal blood uric acid levels. Conversely, elevated serum uric acid levels alone are not the only diagnostic criterion for gout, and most patients with hyperuricemia do not have acute gouty arthritis attacks throughout their lives. What type of diet can trigger gouty arthritis? Diet is closely related to blood uric acid levels. Among alcohol, beer and white wine can significantly increase blood uric acid, while appropriate red wine consumption can slightly reduce blood uric acid levels. Among beverages, fructose-containing beverages raise blood uric acid, while sugar-free beverages do not affect blood uric acid; coffee can lower uric acid, but it is not the effect of caffeine, as caffeine and tea have no effect on blood uric acid; dairy products also have the effect of lowering blood uric acid; vitamin C can slightly lower uric acid. Among foods, meat and seafood can raise blood uric acid, while fruits and vegetables have no effect on blood uric acid, and animal and vegetable proteins have little effect on blood uric acid. What are the principles of management of acute gouty arthritis? The correct management principles for the acute stage of gout are rest, appropriate cold compresses, drinking more water, abstaining from high purine foods, and giving sufficient anti-inflammatory and pain-relieving drugs as soon as possible to relieve swelling and pain. The commonly used anti-inflammatory and analgesic drugs in the acute stage include oral NSAIDs, colchicine, glucocorticoids, and local injection of glucocorticoids in patients with single large joint involvement. Uric acid-lowering drugs should not be given to patients in the acute phase, and reasonable uric acid-lowering drugs should be given starting from small doses after the symptoms of swelling and pain have disappeared. In this case, massage and hot compresses were given when the pain appeared, which may cause local swelling and pain to increase or prolong the pain. How to prevent the recurrence of gouty arthritis? Gouty arthritis is a chronic disease, and patients with uncontrolled uric acid may have recurrent attacks. To prevent recurrence, uric acid-lowering medications should be used to keep blood uric acid at the desired level over time after the arthritis has resolved. In addition, the blood uric acid should be monitored regularly and the liver and kidney function and blood count should be reviewed, and if abnormal liver and kidney function or bone marrow suppression occurs, the drug should be discontinued or replaced in time. In the early stage of applying uric acid-lowering drugs, patients may have joint pain again due to the rapid decrease of blood uric acid, so anti-inflammatory and pain-relieving drugs should be added until the pain is relieved. The duration of maintenance is still inconclusive, but the relevant guidelines of many countries suggest that lifelong maintenance should be maintained. With the improvement of people’s living standard in China, the incidence of hyperuricemia and gout has been increasing year by year, and it is expected that the incidence of hyperuricemia in China is nearly 1/10 of the total population, among which 10-15% of patients may develop into gouty arthritis. In 2012, the American College of Rheumatology developed the latest 2012 American College of Rheumatology Guidelines for the Management of Gout based on recent research progress, which is divided into two parts: the first part is a guideline for the systematic treatment of gout, and the second part is the treatment and prophylaxis of acute gouty arthritis. Anti-inflammatory. The guidelines are essential for standardizing the treatment of gout, emphasizing the importance of meeting blood uric acid targets to prevent acute attacks of gouty arthritis and the importance of early anti-inflammatory therapy for acute gouty arthritis. Therefore, a deeper understanding of the guidelines is of great significance for the treatment of hyperuricemia and gouty arthritis. Principles of nonpharmacologic treatment of hyperuricemia Among the principles of nonpharmacologic treatment of gout, the guidelines first emphasize the importance of disease awareness for all patients, and that diet and lifestyle interventions alone can reduce uric acid to some extent and/or can be used as a means of preventing acute gouty arthritis attacks. Regarding dietary control, the guideline recommends limiting the patient’s high intake of purine-rich foods, i.e., meat, seafood, and fructose-based beverages for a short period of time, and recommends low-fat or nonfat dairy products and vegetables. In addition, all patients should reduce alcohol intake (especially beer, liquor and spirits) and avoid alcohol abuse. Patients with active disease need to abstain from alcohol, especially in patients whose disease progression cannot be effectively controlled by medications and those with chronic gouty arthritis. Uric acid-lowering management strategy Regarding uric acid-lowering treatment, the guideline states that non-pharmacologic uric acid-lowering measures are beneficial for all patients, but should be given to patients with blood uric acid > 420 μmol/L after non-pharmacologic treatment. All patients with gout should target a blood uric acid concentration of < 360 μmol/L for uric acid-lowering therapy; for patients with prolonged unremitting gouty arthritis symptoms or gout stones, blood uric acid levels should be maintained below 300 μmol/L. The guidelines include xanthine oxidase inhibitors that inhibit uric acid production as the drug of choice, including allopurinol or febuxostat monotherapy. Patients who are contraindicated or intolerant to xanthine oxidase inhibitors may be switched to a pro-uric acid excretory drug, such as probenecid, but it is not recommended for patients with a creatinine clearance of less than 50 ml/min. Also, the guidelines suggest how to prevent severe allopurinol allergic reactions. In addition to using a smaller dose as a starting dose, screening for HLA-B*5801 genotype is specifically mentioned. Studies have confirmed that the frequency of HLA-B*5801 gene is higher in Han Chinese population and that HLA-B*5801 positivity is one of the high risk factors for allopurinol allergy. To address this feature, screening for HLA-B*5801 gene by rapid polymerase chain reaction method may be an effective means to prevent severe allopurinol allergic reactions in China. For those who fail to achieve the blood uric acid target with the above monotherapy, the guideline recommends a combination of oral uric acid-lowering drugs, such as a xanthine oxidase inhibitor (allopurinol or febuxostat) with a pro-uric acid excretory drug (propofol, fenofibrate or cloxacin). Acute gouty arthritis treatment is recommended Acute gouty arthritis attacks must be treated with medication, preferably starting within 24 h of onset. If acute gouty arthritis occurs during uric acid-lowering therapy, uric acid-lowering drugs do not need to be discontinued. Drugs used to control acute attacks include NSAIDs, colchicine, and glucocorticoids. NSAIDs should be taken until the acute arthritis is completely relieved. Patients with other diseases or liver or kidney impairment should reduce the dosage as appropriate. Guidelines recommend that colchicine be taken within 36 h of an attack. In view of the significant adverse effects of the drug, the current preference is for low-dose therapy, i.e., a starting dose of 1.2 mg, followed by 0.6 mg 1 h later and a prophylactic anti-inflammatory dose (0.6 mg 1-2 times/d) after 12 h until complete resolution of symptoms. Colchicine needs to be reduced in those with moderate or severe renal insufficiency. The guidelines recommend that glucocorticoids be used to control symptoms of acute gouty arthritis. Intra-articular injections may be given to patients with one to two large joints involved; oral prednisone may be given to patients with multiple joints involved or whose joints are not suitable to receive intra-articular injections; intravenous or intramuscular methylprednisolone may be given to patients who cannot receive oral prednisone.