How to apply aspirin in patients with gout and renal insufficiency
Release date: 2007-08-24
How to apply aspirin in patients with gout and renal insufficiency Recently, many readers have written that they have encountered many specific problems in the process of using aspirin, and hope to get expert guidance. Here, we focus on two aspects of how to focus on how to use aspirin and patients with renal insufficiency in patients with gout. Whether we can apply aspirin to the aspirin Chinese expert consensus drafter and the director of the Department of Geriatric Cardiology of the PLA General Hospital.
Professor Li Xiaoying is the director, chief physician, professor and doctoral tutor of the Department of Geriatric Cardiology of the General Hospital of the People's Liberation Army. He has been engaged in cardiovascular medicine for 34 years. Professor Li has published more than 140 academic papers, edited eight monographs, won five second prizes for provincial and ministerial level science and technology and medical achievements, and invented a patent, won the title of the national three-eighth red flag bearer, and won the second-class merit once and three times. After twice the work, he won the special contribution award from the Central Health Care Committee. He is currently a member of the Chinese Medical Association Cardiovascular Branch, a member of the Geriatrics Branch and a cardiovascular professional group, a member of the People's Liberation Army Health Medicine Committee, an adjunct professor at the Tsinghua University School of Medicine, and a vice president of three journals such as the Chinese Journal of Geriatrics. Editor, 12 journal editors such as Chinese Journal of Cardiovascular Diseases.
How do you apply aspirin to patients with gout? The incidence of hyperuricemia in patients with cardiovascular disease such as hypertension or coronary heart disease can reach about 18%.1 Because these patients often take aspirin, whether aspirin increases the risk of gout is doctor and Patients often worry about the problem. From the perspective of pharmacokinetics, aspirin weakens the role of uric acid excretion and anti-gout drugs (such as probenecid, sulfinpyrazone), which may lead to decreased uric acid excretion and increased blood uric acid levels. However, clinical studies have shown that aspirin has a dual effect on uric acid metabolism. High-dose aspirin (>3 g/d) can significantly inhibit renal tubular reabsorption of uric acid and increase uric acid excretion; medium-dose aspirin (1 to 2 g/ d) mainly inhibits renal tubular excretion of uric acid, which can lead to hyperuricemia; while low-dose aspirin (<0.5 g/d) has little effect on uric acid.
Caspi et al2 conducted a study of 49 elderly (61-94 years) patients without kidney disease, gout or hyperuricemia who took low-dose aspirin (75 mg/d for the first week, week 2) Use 150 mg/d, use 325 mg/d for the third week, and discontinue at week 4). The results of the study showed that: 1 The effect of aspirin on uric acid and uric acid clearance rate was: after taking aspirin 75 mg/d in the first week, the average blood uric acid level increased by 6.2%, and the average uric acid clearance rate decreased by 22.8%. At 2 weeks, although the dose of aspirin increased to 150 mg/d, uric acid concentration and uric acid clearance gradually returned to near baseline, and aspirin dose increased to 325 mg/d in the third week, blood uric acid concentration and uric acid clearance and baseline levels. No significant difference. 2 The effect of aspirin on creatinine and urea nitrogen was: the baseline value of serum creatinine clearance was (47±28) ml/min, and blood urea nitrogen and creatinine increased by 12.6% after taking aspirin 75 mg/d in the first week. And 4.8%, creatinine clearance decreased by 13.8%. After taking aspirin and 1 week after discontinuation of aspirin, renal function did not recover as quickly as uric acid, creatinine clearance was still 13.2% lower than baseline, blood urea nitrogen and creatinine increased by 14% and 8.3%, respectively. Most of the changes occur in patients with hypoproteinemia and in patients with diuretics. Seqal et al3 studied the effects of low-dose aspirin (100 mg/d) on renal function in 106 elderly patients aged 56-98 years with stable disease. Patients were treated with aspirin (100 mg/d) for the first 2 weeks of the study and were followed for 3 weeks. The results showed that after taking low-dose aspirin for 2 weeks, serum creatinine and uric acid levels increased by 4%, glomerular filtration rate (CG value) decreased by 3%, and blood urea nitrogen increased by 17% (both P< 0.05). After 3 weeks of discontinuation of aspirin, the above indicators improved, but 67% of patients still failed to fully recover.
Harris et al.4 In a prospective study, we observed whether low-dose aspirin enteric-coated tablets significantly affected the therapeutic effect of probenecid by observing serum uric acid levels and uric acid excretion. The study included patients with gouty arthritis who had been taking probenecid for at least 3 months. After 14 days of taking probenecid and aspirin (325 mg/d) daily, serum uric acid levels and uric acid excretion in the urine were measured. The results showed that the addition of aspirin to the administration of probenecid did not significantly affect blood uric acid levels and 24-hour uric acid output. The study concluded that daily administration of low-dose aspirin did not significantly affect the efficacy of fenvalate in uric acid excretion. Summary 1. Low-dose aspirin can still affect the renal excretion of uric acid, resulting in a slight increase in blood uric acid levels, which occurs in patients with hypoproteinemia and diuretics; 2. On the basis of taking probenecid, Adding small doses of aspirin daily does not significantly affect the uric acid excretion effect of probenecid; 3. Aspirin should be avoided when acute gout attacks occur; 4. For patients with acute coronary syndrome, when antiplatelet drugs must be applied, Weigh the pros and cons not to stop aspirin or switch to clopidogrel; 5. In elderly patients with hyperuricemia, low-dose aspirin should also be used to monitor uric acid levels and renal function. Can patients with renal insufficiency use aspirin? Renal insufficiency is more common in patients with heart failure and coronary heart disease, and these patients are basically taking aspirin. The effect of aspirin on renal insufficiency is also a common concern for clinicians. Several long-term aspirin treatment trials 5-8 also suggest that low-dose aspirin does not affect renal function. Because the prostacyclin (PGI2) of the kidney is mainly derived from COX-29, low-dose aspirin does not affect COX-2. When high-dose aspirin is used, especially when the blood concentration is >250 mg/ml, the patient is prone to renal damage, but the damage is reversible and can be recovered after stopping the drug.
Cardiovascular risk is significantly elevated in patients with renal dysfunction with arteriosclerotic disease, and aspirin can benefit, but the benefits of aspirin and the risk of bleeding should be weighed. The subgroup analysis of the HOT study showed that the incidence of cardiovascular events and myocardial infarction was significantly lower in hypertensive patients with serum creatinine >1.3 mg/dl, and the risk of bleeding was not significantly elevated. A study by Baigent et al11 showed that patients with serum creatinine ≥1.7 mg/dl used aspirin (100 mg/d) for 12 months without increasing the risk of major bleeding. This suggests that low-dose aspirin can be beneficial for hypertensive patients with mild to moderate increases in serum creatinine levels.
A prospective study12 confirmed that patients with renal insufficiency (creatinine ≥ 1.5 mg/dl) who received aspirin before coronary artery bypass surgery protected renal function. 94 patients were divided into aspirin treatment group and control group before operation. Serum creatinine level, urine output and creatinine clearance rate were matched between the two groups. The results showed that the creatinine level of the control group was significantly increased on the second day after surgery [(3.7±1.6) mg/dl vs (2.9±1.7) mg/dl, P=0.03], while the aspirin group was on the first postoperative day. On day 2, the creatinine level was significantly reduced, and the creatinine clearance rate was higher on day 1 [(34.3±14.3) ml/min versus (30.9±13.1) ml/min, P=0.01], and the clearance rate was also higher on the second day [ (32.6 ± 13.8) ml/min vs. (26.4 ± 9.8) ml/min, P < 0.0001]. At the time of discharge, the serum creatinine level was higher in the control group, while the serum creatinine level was lower in the aspirin group [(2.6 ± 1.4) mg/dl versus (3.8 ± 1.6) mg/dl, P < 0.0001]. Patients in the aspirin group had more urine on the first day after surgery, and the amount of postoperative bleeding increased slightly (P=0.01). The study concluded that continuous administration of aspirin before surgery can protect the patient's renal function, although there is negligible increased bleeding. This may be related to anti-platelet aggregation of aspirin, inhibition of angiogenic factor production, and increased renal blood perfusion and decreased blood viscosity. A randomized, double-blind trial13 showed that patients with chronic hemodialysis received daily low-dose aspirin (160 mg/d), and the monthly risk of thrombosis decreased from 0.46 to 0.16 per patient. This shows that for chronic hemodialysis patients, daily use of low-dose aspirin is an effective and harmless antithrombotic method.
In addition, a retrospective clinical study14 analyzed 4722 blood culture specimens from 872 patients who underwent hemodialysis. The results showed that patients in the aspirin-treated group had a lower chance of developing sputum-associated S. aureus bacteremia than those who did not take the aspirin group (0.17 events/patient-catheter-year vs. 0.34 events/patient-catheter-year), while others There is no significant difference in bacteria. The authors believe that patients receiving hemodialysis have an increased risk of S. aureus bacteremia, and that aspirin is resistant to S. aureus bacteremia in such patients. The reason is that in vivo studies have found that aspirin activates the sigma B-factor stress-inducing operon, thereby inhibiting the expression of a toxin and matrix adhesion genes. Therefore, aspirin has a direct inhibitory effect on Staphylococcus aureus. Despite this, a significant proportion of patients currently receiving chronic hemodialysis do not have aspirin. Dempster et al 15 investigated the use of aspirin in dialysis patients at a hemodialysis center in New York. The results showed that although 74 patients had a history of cardiovascular disease, only 38 (51%) were treated with aspirin. Of the patients who did not receive aspirin, 19 (53%) had no clear contraindications for aspirin for secondary prevention. certificate. Of the 98 patients with no history of cardiovascular disease, 18 (18%) received aspirin. Of the patients who did not receive aspirin, 57 (71%) had no clear contraindications for aspirin for primary prevention of cardiovascular disease. . This suggests that aspirin is not fully utilized in cardiovascular primary and secondary prevention in hemodialysis patients. Summary The benefits of aspirin are generally greater than their risk for patients with cardiovascular disease with renal insufficiency. In the 2005 British Guidelines for Adult Chronic Kidney Disease, patients with chronic kidney disease with a coronary heart disease risk >20% should take aspirin to prevent cardiovascular events. The Royal College of Physicians of London recommends that all dialysis patients with myocardial infarction, cerebral infarction, peripheral vascular disease, acute coronary syndrome or coronary revascularization should take aspirin.
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