Prevention and treatment of gouty arthritis: both diet and drug therapyFive perspectives of clinical anatomy in the treatment of gouty arthr
Prevention and treatment of gouty arthritis: both diet and drug therapy
Five perspectives of clinical anatomy in the treatment of gouty arthritis
Summary of medical records
Men with a history of 60 years old, obese type. Feel the sting left by great toe the day before eating seafood and drinking a lot of beer, then give local massage and hot compress, the symptoms were not improved obviously. Early in patients with sudden left hallux toe pain, can not sleep, immediately oral allopurinol did not improve.
Previous history of hypertension for 10 years, currently taking thiazide diuretics and calcium antagonists. 6 years of hyperlipidemia, taking atorvastatin calcium treatment. 1 years ago found elevated serum uric acid (512 mol/L), were not given attention, occasionally taking uric acid lowering drugs allopurinol.
The diagnosis and treatment of emergency after physical examination: the temperature of 38 DEG C, the blood pressure of 150/95 mm Hg, BMI 33 kg/m2; heart, lung and abdominal examination were normal; the left hallux toe swelling, refused to press. Laboratory examination: peripheral blood white blood cells 12 * 109/L, serum uric acid 408 mol/L. Considering the possibility of excluding erysipelas, gouty arthritis, given intravenous infusion of penicillin 1 D. Because the symptom is not relieved given Fenbid, 2 d after swelling improved, body temperature returned to normal.
Are patients with acute gouty arthritis?
The patients were elderly men, obesity, is gouty arthritis good hair; previous patients with elevated serum uric acid, but the treatment is not normal, there is the pathological basis of the onset of arthritis gout; arthritis patients before the onset of eating a lot of seafood and beer, a clear cause of gout arthritis; analysis from arthritis part of patients with left hallux toe pain with redness, is the most typical site of acute gouty arthritis attacks, also in line with the single joint attack characteristics of swelling and heat pain, so considering can be diagnosed with acute gouty arthritis.
The differential diagnosis should be considered in patients without local erysipelas, but the trauma and the history of mosquito bites, no other systemic infection, use of antibiotics is invalid, so the basic rule of erysipelas.
What are the causes of this acute disease?
Epidemiological studies have shown that middle-aged and older men, obese people are high risk of hyperuricemia and gout, hypertension and hyperlipidemia patients are also high incidence of hyperuricemia and gout. In addition, thiazide diuretics, which are used to control blood pressure, can cause elevated serum uric acid. A large number of studies have shown that eating high purine foods can cause elevated blood uric acid or induce gouty arthritis attacks, seafood and beer are likely to induce acute gout attack, the patient is the cause of this attack.
It should be noted that normal uric acid levels do not exclude acute gouty arthritis. On the other hand, elevated serum uric acid levels are not the only diagnostic criteria for gout. Most patients with hyperuricemia do not have acute gouty arthritis.
What kind of diet can induce gouty arthritis?
Diet was closely related to serum uric acid level. Liquor, beer, liquor can make blood uric acid increased significantly, while the appropriate drinking red wine can slightly reduce the level of serum uric acid. A beverage, fructose containing beverages make blood uric acid, blood uric acid does not affect non sugar drinks; coffee can reduce uric acid, but not the effect of caffeine, caffeine and tea had no effect on blood uric acid; dairy products also decrease uric acid; vitamin C can slightly reduce uric acid. Food, meat and seafood can increase the level of blood uric acid, and fruits, vegetables, such as no effect on blood uric acid, animal and vegetable protein also has little effect on blood uric acid.
What is the principle of treatment of acute gouty arthritis?
The correct principle of treatment of acute gout, appropriate for the rest of the cold, water, fasting, high purine foods as soon as possible adequate anti-inflammatory analgesic drugs to alleviate the pain as soon as possible. The acute phase of commonly used anti-inflammatory analgesic drugs including oral NSAIDs, colchicine, corticosteroids, single joint involvement may also be local injection of glucocorticoid.
Give uric acid lowering drugs on acute patients should not be so sore, symptoms disappeared after small doses given uric acid drug reasonable. This patient received massage and hot compress in pain, may cause local pain exacerbated or prolonged pain.
How to prevent gout arthritis again?
Gouty arthritis is a chronic disease, patients with uncontrolled blood uric acid may relapse. In order to prevent the recurrence of the disease, it is necessary to use the uric acid lowering drugs to reduce the level of serum uric acid in the ideal level. Commonly used drugs include allopurinol inhibit uric acid synthesis and promote the excretion of uric acid in benzene bromine Malone, should be started in small dose, gradually increase the amount, so that the blood uric acid reached 300~350 mol/L. In addition to regular monitoring of blood uric acid and pay attention to the function of liver and kidney and blood, if there is abnormal function of the liver and kidney or bone marrow suppression, should be promptly discontinued or replace other drugs.
Application of uric acid drugs in the early stage, patients may be due to the rapid decline in serum uric acid joint pain again, should be combined with anti-inflammatory analgesic drugs until pain relief. After the blood uric acid standards can reduce the amount of uric acid drugs, the maintenance time is not yet conclusive, multinational related recommendations should be maintained for life.
Guide article interpretation of three key recommendations to grasp the essence of treatment
With the improvement of people's living standards, hyperuricemia and gout incidence increased year by year, is expected to present the incidence of hyperuricemia in the total population of 1/10, in which 10%~15% patients may develop acute gouty arthritis. In recent years, in order to standardize the treatment of hyperuricemia and gout, countries have introduced a number of consensus. In 2012, the American College of Rheumatology has developed the new "2012 American College of Rheumatology guidelines" in the management of gout summarized recent research progress on the basis of the guide is divided into two parts: the first part is the guide system for the treatment of gout, the second part is the anti-inflammatory treatment and prevention of acute gouty arthritis. The guidelines are critical in regulating the treatment of gout, emphasizing the importance of serum uric acid levels in the prevention of acute gouty arthritis, and the importance of early anti-inflammatory treatment for acute gouty arthritis. Therefore, it is of great significance to deepen the understanding of guidelines for the treatment of hyperuricemia and gouty arthritis.
Principle of non drug treatment of hyperuricemia
The principle of non drug treatment of gout, emphasizing the importance of the first guide in health education for all patients, simple diet and lifestyle intervention can reduce uric acid and to a certain extent (or) can be used to prevent acute gouty arthritis attacks means.
With regard to dietary control, the guidelines recommend limiting the intake of purine rich foods, such as meat, seafood, and fructose, in a short period of time. In addition, all patients should reduce alcohol intake (especially beer, liquor and spirits), avoid alcohol. Patients with active disease need to stop drinking, especially the drugs can not effectively control the progression of disease and chronic gouty arthritis patients.
Strategies for reducing uric acid
In regard to the treatment of uric acid, the guidelines indicate that non drug measures of reducing uric acid are beneficial to all patients, but should be given to patients who have been treated with non drug therapy for 420 mol/L. All patients with gout uric acid should be treated from the blood uric acid concentration was less than 360 mol/L as a target; for gouty arthritis symptoms or long-term remission in patients with gout, uric acid levels should be maintained below 300 mol/L.
The guide will inhibit the formation of uric acid by xanthine oxidase inhibitors as the preferred drug, including allopurinol or febuxostat monotherapy. The xanthine oxidase inhibitor taboo or intolerant patients, can be replaced by a uricosuric drug, such as probenecid, but creatinine clearance rate is less than 50 ml/min were not recommended.
At the same time, to put forward how to prevent allopurinol severe allergic reactions. In addition to a small dose as a starting dose, a particular reference to the screening of the HLA-B*5801 genotype. The research confirmed that the HLA-B*5801 gene frequency of Han population is higher, and the HLA-B*5801 positive alopurinol alcohol is one of the risk factors of allergy. According to this characteristic, in the domestic application of rapid polymerase chain reaction method for screening of the HLA-B*5801 gene may be a effective way to prevent serious allergic reaction to allopurinol.
For the single agent in the treatment of blood uric acid is still not standard, the guidelines recommend lowering uric acid combined with oral drug treatment, such as a xanthine oxidase inhibitor (allopurinol or febuxostat) and a uricosuric drug (probenecid, fenofibrate or losartan) combined with.
Treatment of acute gouty arthritis
Acute gouty arthritis must be treated with medication, and preferably within 24 h after onset. If acute gouty arthritis occurs in reducing uric acid in the treatment process, does not need to stop uric acid lowering drugs, drug control acute attack include non steroidal anti-inflammatory drugs, colchicine, corticosteroids.
Non steroidal anti-inflammatory drugs need to be taken until complete remission of acute arthritis, while suffering from other diseases or patients with liver and kidney damage should be reduced as appropriate.
The guidelines recommend taking colchicine to within 36 h after onset. In view of the adverse drug reaction is obvious, the more likely the small dose, the initial dose of 1.2 mg, 1 h after taking 0.6 mg, 12 h according to a preventive anti-inflammatory treatment dose (0.6 mg, 1~2 /d) until complete remission of symptoms. For moderate to severe renal insufficiency, colchicine required reduction.
The guidelines recommend that glucocorticoid can be used to control the symptoms of acute gouty arthritis, 1~2 large joint involvement in patients with intraarticular injection; multiple joint involvement or joint position is not suitable for intra-articular injection of patients taken orally prednisone; not oral prednisone were given intravenous or intramuscular injection of methylprednisolone.