《2010年中国痛风临床诊治指南》解读

《2010年中国痛风临床诊治指南》指出,在诊断痛风时要特别注意痛风患者的病程阶段:即无症状高尿酸血症、急性痛风性关节炎或慢性痛风,强调关注患者是否为无症状高尿酸血症或痛风合并其它情况(糖尿病、高血压病,或心脑血管的危险因素)。除了合理应用非甾类抗炎药或糖皮质激素积极治疗急性关节炎急性发作外,痛风患者的综合管理尤为重要,包括对所有患者去除引起高尿酸血症的诱因及给予非药物干预(生活方式和饮食调整、减轻体重、适度饮酒,停用引起尿酸升高的药物等),有效控制合并症。对反复发作的、间歇期或慢性痛风患者给予降尿酸药物治疗以维持血尿酸水平低于327μmol/L,以及为严重的慢性痛风石患者寻找可能的手术治疗机会。     

应将痛风当作慢性进展性疾病进行量化评估和长期达标治疗

痛风是风湿科常见疾病,过去的5年开发了新的有效针对高尿酸血症(非布索坦、尿酸酶)和干扰痛风炎症[白细胞介素(IL)-1拮抗剂]的药物[1].尽管如此,在临床实践工作中,痛风炎症发作和高尿酸血症的处理不尽如人意,存在巨大的理想和现实的差距[2].为提高痛风患者治疗的依从性,改善痛风的预后,甚至“治愈”痛风,笔者提倡:首先应提高“痛风是慢性进展性疾病”的认识和警觉性,其次,在痛风炎症干扰、降尿酸治疗和预防发作三大主要治疗时期,进行翔实而具体的量化评估,根据评估结果采用规范、个体化、有的放矢的治疗策略.最后,坚持非药物和药物降尿酸的有机结合,长期达标控制血尿酸,达到减少痛风炎症发作、溶解痛风石,提高生活质量之目的.     

别嘌呤醇治疗心力衰竭的研究进展

别嘌呤醇目前在临床上主要用于治疗各种高尿酸血症和慢性痛风,但是近来许多研究表明别嘌呤醇还可以应用于心力衰竭的治疗。现对别嘌呤醇治疗心力衰竭的研究进展作简单介绍。     

高尿酸血症/痛风流行病学特点及危险因素

高尿酸血症/痛风的患病率逐年攀升,呈现高流行、年轻化、男性高于女性、沿海高于内地的流行趋势.肥胖、高血压、高血脂、高血糖等与高尿酸血症/痛风的发生、发展密切相关.小剂量阿司匹林、袢利尿剂和噻嗪类利尿剂等药物亦可促进血清尿酸水平的升高.高尿酸血症是2型糖尿病、高血压、动脉粥样硬化、心血管事件、脑卒中和慢性肾脏病等疾病的独立危险因素,是痛风发作的最主要生化基础和最直接病因.对于高尿酸血症/痛风患者,应强调早期发现和早期治疗.     

痛风/高尿酸血症患者生活习惯的危险因素

目的探讨痛风/高尿酸血症患者生活习惯中的危险因素。方法应用自行设计的调查表,分别对病例组和对照组进行问卷调查,调查内容包括一般的基线资料和可疑的生活习惯危险因素。结果秩相关分析结果显示,饮酒、周围人吸烟、疲劳、精神紧张、喝咖啡、作息情况、饮食等8个因素与研究对象是否患有痛风/高尿酸血症存在相关性(P<0.05)。Logistic回归分析结果显示,经常饮酒者发生痛风/高尿酸血症的危险性是不经常饮酒者的0.683倍;周围人经常吸烟者发生痛风/高尿酸血症的危险性是不经常吸烟者的0.653倍;经常感觉疲劳者发生痛风/高尿酸血症的危险性是不经常感觉疲劳者的0.605倍;经常喝咖啡者发生痛风/高尿酸血症的危险性是不经常喝咖啡的者0.498倍;作息不规律者发生痛风/高尿酸血症的危险性是作息规律者的1.645倍;饮食不规律者发生痛风/高尿酸血症的危险性是饮食规律者的2.212倍。结论有效控制饮酒、减少周围人吸烟量、减少疲劳状态的发生、降低喝咖啡的频率等可以有效预防痛风/高尿酸血症的发生;规律的作息制度和饮食可在一定程度上预防痛风/高尿酸血症的发生。     

原发性痛风治疗的现状

原发性痛风(简称痛风)治疗的目的,应该包括下述4点:①迅速终止痛风的急性发作;②预防痛风性关节炎的复发;③预防或治疗尿酸盐沉积于关节和肾实质中所引起的损害;④预防尿酸性肾结石的形成。本文根据文献对其治疗现状作一综述。无症状性高尿酸血症期的处理高尿酸血症是指血清尿酸含量大于6mg%,常见于有痛风家族史者。本期的处理主要是饮食治疗和降低血清尿酸药物的应用问题。传统的观点认为,低嘌呤饮食是痛风患者必须长期遵守的原则。控制嘌呤的摄入确能有效地降低痛风患者血清尿酸。但是,长期遵守低嘌呤的饮食原则,常会导致营养不足,患者不易耐受。所以不能期望限制嘌呤摄入对痛风治疗会有很大的作用。在临床实践中患者只     

别嘌呤醇对伴高尿酸血症慢性心力衰竭急性发作患者血浆B型利尿钠肽及尿酸浓度的影响

目的探讨别嘌呤醇对伴高尿酸血症慢性心力衰竭急性发作患者血浆B型利尿钠肽(BNP)及尿酸浓度的影响。方法选取慢性心力衰竭伴高尿酸血症急性发作患者58例,利用计算机进行随机分组,对照组29例,单纯给予常规抗心力衰竭药物治疗;观察组29例,在常规药物治疗基础上联合别嘌呤醇治疗。治疗12 w后,对比两组临床效果,并分析用药前后血流动力学指标及BNP、尿酸浓度变化。结果观察组治疗后血浆BNP、血尿酸、左室舒张末期内径(LVDd)、左室收缩末期内径(LVDs)、左室射血分数(LVEF)水平均低于对照组(均P<0.05),有效率明显高于对照组(P<0.05)。两组无明显不良反应发生。结论慢性心力衰竭伴高尿酸血症急性发作患者在常规抗心力衰竭药物治疗基础上联合别嘌呤醇疗效较好,改善患者血浆BNP及尿酸水平,促进患者恢复,值得推荐。     

别嘌呤醇治疗伴高尿酸血症的慢性心力衰竭疗效观察

慢性心力衰竭患者中常合并有高尿酸血症，高尿酸血症已作为心力衰竭预后不良的独立指标，且与心力衰竭存活率之间呈等级关系，可预测慢性心力衰竭的生存率。Stmthem等的报告长期服用大剂量别嘌呤醇可将血清尿酸高的心力衰竭患者的住院率和病死率降至血清尿酸正常的心力衰竭患者的水平，别嘌呤醇能改善心力衰竭患者的心功能及预后。本文旨在观察常规治疗基础上加服别嘌呤醇对慢性心力衰竭合并高尿酸血症患者心功能的影响，现报告如下。     

血尿酸水平与慢性心力衰竭患者心功能状态的相关性分析

摘要　目的 研究血尿酸水平与慢性心衰患者心功能状态的相关性。方法：回顾收集2012年10月至2014年10月航空总医院心内科因慢性心力衰竭住院的患者200例,同期收集非心衰入院患者180例为对照组,收集患者基本资料及检验结果,采用logistic回归,分析高尿酸血症与慢性心力衰竭发生的相关性。并依据尿酸水平,将200例心衰患者分为尿酸正常组、轻度高尿酸血症组、显著高尿酸血症组,统计分析心衰患者中血尿酸水平与患者心功能状态的关系。结果：慢性心力衰竭组血尿酸水平明显高于非心衰组患者。高尿酸血症与慢性心力衰竭发生的OR 值为2. 244 ( P <0. 05)。慢性心力衰竭患者中,高尿酸血症者较尿酸正常者,心功能状态更差,且随着尿酸水平的升高,心功能指标进一步恶化。结论: 慢性心力衰竭患者高尿酸血症发生率更高,高尿酸血症可能是慢性心衰的危险因素。血尿酸水平越高,患者心功能状态越差。     

痛风和高尿酸血症处理中的循证医学观点

随着人们生活水平的改善和生活方式的改变，我国患痛风或高尿酸血症的人数逐年增多。多项流行病学资料显示高尿酸血症和心血管疾病、高血压、肥胖、高脂血症、糖尿病经常同时出现，高尿酸血症与高血压发病密切相关，与心血管疾病的发生也有一定联系。然而，有不少医务人员和相关的高危人群对痛风和高尿酸血症的检查、监测、预防和治疗还是重视不够，在痛风预防和治疗上经常沿用一些经验疗法，     

CaseBook Challenges: Managing Gout,Hyperuricemia and Comorbidities—Dialogue with the Experts

The prevalence of gout and hyperuricemia are on the rise in the United States corresponding with an increase in risk factors for these conditions, such as obesity, metabolic syndrome, and the use of diuretics. A progressive disorder, untreated gout can be debilitating and result in tophi, chronic arthropathy, and recurrent kidney stones. Although joint aspiration is needed for a definitive diagnosis, the majority of patients are diagnosed presumptively based on medical history and presentation with characteristic signs and symptoms. Patients with gout also often have multiple comorbidities, and there is an increasing body of evidence that shows hyperuricemia is associated with incidence hypertension, diabetes, chronic kidney disease, and heart failure. Clinical strategies for the management of gout and hyperuricemia must include considerations for these and other common cardiometabolic and renal conditions. In addition to acute flare therapy and prophylaxis, the treatment of gout involves lowering serum uric acid (SUA) levels with the urate-lowering therapies (ULTs) allopurinol or febuxostat. Once begun, treatment with ULT is lifelong. However, inadequate dosing and patient nonadherence or intolerance to therapy often lead to treatment failure. Recent guidelines from the American College of Rheumatology stress tailoring therapy and target SUA level (traditionally <6 mg/dL, but lower levels may be needed for certain patients) based on gout severity and the presence of comorbid conditions. Because painful acute gout flares may result in trips to the emergency department and because the majority of gout cases are managed in primary care, it is important for clinicians practicing in these settings to be able to diagnose and treat this condition and communicate with patients to improve their understanding of the disease process and adherence to treatment.     

The effect of control and self-medication of chronic gout in a developing country. Outcome after 10 years

OBJECTIVE: We describe a 10 year observation of the effect of control of hyperuricemia compared with self-medication alone in patients with chronic gout. METHODS: We studied 299 consecutively self-referred Malayo-Polynesian men with chronic gout, mean age 35 +/- 14.3 SD years. Subjects comprised 228 cases with chronic gout without tophi or urolithiasis (Group 1) and 71 with those complications (Group 2). Attacks of acute gouty arthritis were treated with nonsteroidal antiinflammatory drugs (NSAID) and/or corticosteroids. After acute arthritis had settled, urate-lowering drugs were instituted in both groups combined with low dose colchicine and/or low dose NSAID for at least 0.5-2 years. Urate levels were maintained longterm at a mean of < 5 mg/dl. After 10 years, the dropouts were traced and evaluated for comparison with baseline and those who remained in the study. In Group 2 the urate-lowering drugs were continued. RESULTS: Control of gout and hyperuricemia was achieved in all patients who remained under control: 91.6% of the 299 patients for at least 2 years (short-term), up to 5 years in 87.5% (medium term), and up to 10 years in 79.6% (longterm). In Group 1 (chronic gout without complication) only 36.8% had no attacks during 8 years, after they had tapered urate-lowering drug after the first 2 years of the study. In the 61 dropouts the intermittent symptomatic treatment and/or self-medication without longterm control of hyperuricemia resulted after 1 decade in chronic gout with more complications and associated conditions leading to increased morbidity, disability, and comorbidity, and 3 early mortalities. CONCLUSION: By controlling hyperuricemia, improvement of the prognosis of chronic gout, comorbidity, and early death was achieved compared with self-medication alone. Self-medication in a developing country if continued unchecked may become a public health problem in a population with a high prevalence rate of gout.     

Difficult gout and new approaches for control of hyperuricemia in the allopurinol-allergic patient

A major obstacle to the treatment of hyperuricemia in patients allergic to allopurinol is the limited availability of suitable, equally effective, alternative, urate-lowering drugs. Conventional uricosuric drugs, including probenecid and sulfinpyrazone, are recommended for allopurinolintolerant patients with gout and “underexcretion” hyperuricemia who have normal renal function and no history of nephrolithiasis. Therapeutic options in those in whom traditional uricosuric drugs are contraindicated, ineffective, or poorly tolerated include slow oral desensitization to allopurinol and cautious administration of oxipurinol. Allopurinol desensitization is useful particularly in those who have failed other treatment modalities. If available (as in Europe, South Africa, and Japan), benzbromarone may be tried in patients with gout and mild-to-moderate renal insufficiency. Recombinant urate oxidase can be used in the short-term prophylaxis and treatment of chemotherapy-associated hyperuricemia in patients with lymphoproliferative and myeloproliferative disorders. Hyperuricemia and gout occur with increased frequency in cyclosporine-treated allograft transplant recipients. The management of gout in these patients is complicated by two main factors: cyclosporine-induced renal impairment, and interactions with medications used to preserve the allograft.     

Hyperuricemia, gout, and autosomal dominant polycystic kidney disease

The relationship between hyperuricemia, gout, and autosomal dominant polycystic kidney disease (ADPKD) is not widely recognized. In an attempt to further clarify this relationship, the authors have studied 17 patients with ADPKD, 9 controls, 9 patients with proven gout and chronic renal failure, 11 patients with gout and normal renal function, and 11 patients with chronic renal failure. The mean serum uric acid concentration was higher in patients with ADPKD as a group than in controls (8.0 +/- 1.7 mg/dl vs. 6.4 +/- 1.6 mg/dl, p less than .02). Clinical gout was identified in 24% of patients with ADPKD; none of the patients with chronic renal failure of other etiologies had gout. Fractional excretion of uric acid and the activity of the enzyme hypoxanthine guanine phosphoribosyl transferase (HGPRT) were not different among the groups studied. From this study the authors conclude that ADPKD should be included among those diseases associated with hyperuricemia and gout. A partial deficiency in HGPRT or abnormal renal handling of uric acid do not appear to be responsible for the increased incidence of gout in patients with ADPKD.     

抗痛风药的合理应用

痛风作为一种常见的关节炎,发病率在逐年上升。不恰当的治疗可以造成慢性疼痛、肾功能不全以及关节破坏和畸形,从而影响患者的生活质量。治疗痛风的药物主要包括控制痛风急性发作期的药物和降尿酸的药物。作者结合临床经验及国内外痛风指南,对治疗痛风药物的疗效、安全性及合理用药作一综述。     

Gout in the heart transplant recipient: physiologic puzzle and therapeutic challenge

PURPOSE: Hyperuricemia and gouty arthritis have been associated with cyclosporine use in renal transplant recipients. Patients requiring heart or heart-lung transplantation may have additional risk factors for the development of gout, yet it has not previously been described in this population. We share herein our clinical experience with gouty arthritis in six heart transplant recipients. PATIENTS AND METHODS: During a one-year period, six hospitalized male heart transplant patients were seen in consultation for gouty arthritis. Five were subsequently followed for gout as outpatients; the sixth died within six months. Management included trials of nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, allopurinol, and intra-articular steroid injections, as well as attempts to minimize cyclosporine nephrotoxicity. RESULTS: Three patients had gout in remission at time of transplant surgery, and three others developed gout for the first time two to 45 months after transplantation. Following transplant surgery, both pre-existing and new-onset gout appeared to exhibit an accelerated course, with unusually rapid development of chronic polyarticular disease and tophi in four of the five patients followed for more than six months. Peak serum uric acid levels ranged from 11.0 mg/dL to 16.5 mg/dL. NSAIDs produced reversible renal insufficiency in four patients. Gout-related infections occurred in three patients, one of whom died. CONCLUSION: Acute gouty arthritis may occur in the heart transplant recipient despite concomitant use of immunosuppressive drugs. Cyclosporine, with its attendant hypertension and nephrotoxicity, appears to be the major risk factor for hyperuricemia in this setting, leading to the accelerated development of tophi and chronic polyarthritis. Management is complicated by the patients' renal insufficiency and propensity to infection, as well as by interaction with transplant-related medications. Prevention of hyperuricemia by minimizing cyclosporine nephrotoxicity appears to be the best management strategy, with judicious use of allopurinol for those patients in whom this preventive approach fails.     

Characteristics of chronic gout in Northern Sulawesi, Indonesia

OBJECTIVE: To identify associations and possible risk factors for gout that may contribute to chronic tophaceous gout in rural and urban districts of North Sulawesi, Indonesia. METHODS: A total of 190 patients with chronic gout and 190 age and sex matched controls were selected from 28 community health centers. Potential risk factors including alcohol consumption, food habits, family history, body weight, related medical conditions, drug use, and laboratory investigations were sought. RESULTS: Alcohol consumption and certain food habits were associated with gout. A positive family history of gout and overweight were also significant risk factors. Renal impairment was found in 86.3% of patients and hyperuricemia in 92.1%. In controls, renal impairment and hyperuricemia were 7.4% and 32.6%, respectively. Patients with hypertension and nephrolithiasis were more at risk of having associated gout. There was a significant association between gout, hyperuricemia, hypercholesterolemia, hypertriglyceridemia, and higher levels of creatinine and urea. There was also a significantly lower level of urine uric acid in gout cases compared with controls. Gouty tophi were found in 91% of these cases with chronic gout. The use of diuretics for treating hypertension, continuing excessive alcohol consumption and purine-rich food habits in untreated gout, and hyperuricemia were associated with chronic and tophaceous gout. Urate-lowering drugs were not available in the community health centers. CONCLUSION: Severe tophaceous gout with deformities and disability is found in North Sulawesi. Prominent risk factors include alcohol, obesity, renal impairment, diet, hypertension, and family history. Improved education about gout seems needed. Urate-lowering drugs are not available in community health centers but are needed, especially in rural areas, as studied here.