美国风湿学院(ACR)发布2012版痛风管理指南
2012年美国风湿病学会痛风治疗指南解读
的，在T 2相上大部分是中等信号，少数为高信号，并且造影后呈现明显的强化。
这种强化可能和组织学上看到的周围“纤维血管区”中占优势的血管成比例。
在T 2加权像上的低信号点倾向于钙化灶。
6痛风、其他结晶性关节病和感染的影像学区别临床上，痛风的表现可以和感染性关节炎相似，包括发热，关节红肿热痛，血白细胞计数增多，血沉、C 反应蛋白升高；但痛风骨侵蚀的典型表现，易发作部位及缺乏邻近软组织化脓，有助于痛风诊断的征象。
抽取关节腔积液在偏振光显微镜见绿色针样晶体，革兰染色为阴性，将有助于痛风诊断。
关节软骨表面的MSU 结晶沉积物在超声中表现平行于骨皮质的回波曲线带，形成“双轨征”。
这是和焦磷酸钙结晶疾病有明显区别的征象，焦磷酸盐沉积症通常导致结晶沉积在关节内而不是关节表面。
超声为能检查出这些区别的最敏感的方式。
7影像学监测治疗效果随着更多新型、有效降尿酸方法的出现，人们尝试用影像学手段监测治疗疗效。
影像学变化包括痛风石的缩小、“双轨征”的消失、滑膜增生停止、关节渗出和骨髓水肿的改善。
CT 和MRI 采用先进的痛风石3D 绘图，使CT 和MRI 描述病变更加准确和逼真。
DECT 基于化学成分能识别尿酸结晶，在治疗随访中，观察溶解的痛风石方面更确切、可靠。
MRI 在随访滑膜增生和骨髓水肿方面有它特殊的价值，而超声是可以显示上述（除骨髓水肿外）所有影像表现的一种极好的廉价的方法，从而可以替代评估方法，并能提供精确的细节和良好的空间分辨率。
尽管MRI 在临床和科研方面同样有助于监测疾病进展，但随访不便捷且花费高。
因此，超声有望成为监测治疗反应的最佳方法。
综上所述，长期以来，影像学在诊断和随访痛风疗效方面价值十分有限，随着影像学技术的发展和临床案例探索，超声可用来指导穿刺获得组织样本，甚至在深部组织中寻找尿酸沉积物，从而有助于诊断。
准确地评估痛风的疾病活动性，并能有助于非典型急性痛风及伴痛风石的慢性痛风的诊断，同时评估治疗反应。
解读2012年美国风湿病学会_欧洲抗风湿病联盟狼疮肾炎治疗指南_王立
肾脏病理分析和评判
近年来比较公认的国际肾脏病学会 肾脏病理学 会（ ISNRPS） 2003 年 LN 分类标准 （ 表 1 ） 也被 ACR 和 EULAR 一致推荐使用 。但 EULAR 客观地指出了 ， 该 分类系以肾小球病变为主 ，尚存在一定的局限性 ， 应 同时分析小管间质病变及与抗磷脂抗体相关的血管损 伤等病变 。
Ⅴ型 LN 对于合并Ⅲ型或 Ⅳ 型的 Ⅴ 型 LN， 治疗推荐与单 纯的Ⅲ型或Ⅳ型一致。 对于单纯的Ⅴ型 LN，ACR 和 EULAR 一致认为诱 导缓解治疗首选 MMF （ 2 3 gd ） + 泼尼松 （ 0. 5 mg · kg ·d ） ，6 个月后如改善则改用 MMF 1 2 gd 或 AZA 2 mg·kg － 1 ·d － 1 维持治疗 ，如无改善改用 CTX、 钙调磷酸酶抑制剂或利妥昔单抗 。 Ⅵ型 LN 以替代治疗为主 ，不推荐积极应用激素和免疫抑 制剂治疗，激素和免疫抑制剂依照患者其他脏器受累 情况使用。EULAR 指南中提及了替代治疗方式的选 择： 仍在使用免疫抑制剂的患者尽量避免腹膜透析 ， 以避免增加感染发生率 ； 而对于抗磷脂抗体阳性的患 者，如采取血液透析应警惕血管通路血栓形 成 。 另 外，如考虑行肾移植术 ，需选择患者狼疮活动度在较 低水平至少 3 6 个月的时机进行 。 其他 EULAR 推荐指出， 对于抗磷脂抗体综合征相关 肾病 （ APS-associated nephropathy ） 患 者， 需 给 予 羟 氯 喹（ hydroxychloroquine，HCQ） 和（ 或 ） 抗凝、 抗血小板 治 疗。 ACR 提 出 血 栓 性 微 血 管 病 （ thrombotic microangiopathy，TMA） 患者首选血浆置换治疗 。
2012年美国风湿病学会(ACR)痛风治疗指南解读
2012年ACR痛风治疗指南解读痛风性关节炎的发病率逐年增高，关于高尿酸血症及痛风性关节炎的规范治疗越来越受到人们的重视。
2012年美国风湿病学会（ACR）在2011年推出诊治共识的基础上，制定了最新的痛风治疗指南，该指南分为两部分：第一部分是痛风的系统治疗指南，第二部分是急性痛风性关节炎的治疗与预防性抗炎治疗，均发表于《关节炎护理与研究》[Arthritis Care Res 2012，64（10）：1431和1447]杂志。
此次治疗指南对过去各国治疗指南进行了总结更新，结合最新的文献证据和专家共识，制定出了不同证据级别的治疗方案。
痛风的非药物及药物治疗原则痛风的非药物治疗指南首先强调了患者宣教的重要性，单纯饮食及生活方式干预可在一定程度上起到降尿酸和（或）预防急性痛风关节炎发作的作用。
关于饮食控制，指南建议：①限制短时间内大量摄入富含嘌呤的食物，限制富含嘌呤的肉类、海鲜及果糖饮料的摄入，推荐低脂或脱脂乳制品和蔬菜；②减少酒精摄入（特别是啤酒、白酒和烈酒），避免酗酒，疾病活动的患者须戒酒，尤其是药物无法有效控制病情进展及慢性痛风性关节炎患者。
降尿酸治疗（ULT）非药物治疗适用于所有患者，经非药物治疗血尿酸（SUA）仍＞7 mg/dl 者，应予药物。
痛风患者ULT目标为SUA＜6 mg/dl；对于痛风性关节炎症状长期不缓解或有痛风石的患者，SUA应＜5 mg/dl。
推荐抑制尿酸生成的黄嘌呤氧化酶抑制剂（XOI）为首选用药，推荐别嘌醇或非布索坦单药治疗。
对XOI有禁忌或不耐受者可换用促尿酸排泄药，但肌酐清除率（CCr）＜50 ml/min者不宜使用。
注意，这里监测的是CCr而非血肌酐浓度（SCr）。
与传统观念不同，指南指出，在急性痛风性关节炎发作期，在恰当抗炎治疗后，可开始ULT。
该观点有待国内大量临床资料证实。
别嘌醇方案推荐初始剂量≤100 mg/d（慢性肾脏病4期及以上者为50mg/d）；每2~5周渐加量；维持最大治疗剂量（＞300mg/d）使SUA降至目标值以下，肾功能不全者，只要对其充分宣教及规律监测药物毒性反应，也可按此剂量治疗；建议用药前筛查人白细胞抗原（HLA）-B*5801基因型。
2012版ACR痛风管理指南-宋立军
(tophi) deposited chiefly in and around joints, which
sometimes lead to deformity and crippling
反应;
中国指南未提及。
4、痛风关节炎急性发作的抗炎 镇痛药选择：
ACR指南推荐NSAIDs、秋水仙碱和糖皮质激素，3种
药同等推荐，医师根据患者偏好、以前治疗反应、合
并症综合考虑;
中国指南建议糖皮质激素用于不能耐受NSAIDs和秋水
仙碱或肾功能不全者。
5、分层治疗的强调：
ACR指南强调分层治疗，痛风关节炎根据疼痛程度及
鼓励食用：低脂乳制品和蔬菜。
急性痛风性关节炎发作的基本治疗原则
急性痛风性关节炎发作必须采取药物治疗，且最好在
发病之初的24小时内开始。如果在ULT过程中出现急
性痛风性关节炎发作，不须暂停降尿酸药物。
要让患者知道诱发痛风性关节炎急性发作的原因，一
旦发作，患者应知晓基本处理原则；
要让患者认识到痛风是体内尿酸过度积累所致，只有
嘌呤的肉类、海鲜及果糖饮料的摄入，推荐低脂或脱
脂乳制品和蔬菜；
② 减少酒精摄入（特别是啤酒、白酒和烈酒），避免
酗酒，疾病活动的患者须戒酒，尤其是药物无法有效
控制病情进展及慢性痛风性关节炎患者。
研究人员将食物建议分为三类：避免食用、限制食用
和鼓励食用。
客观的说，这些建议都是来自某些孤立的临床研究，
受累关节数，决定选单药还是联合治疗，对联合治疗
方案也做了建议;
《美国风湿病学会欧洲抗风湿联盟痛风分类标准》解读
3、病理学标准
2、对于疑似痛风患者，医生可以根据该标准进行初步诊断。如果患者的临床 表现符合标准，则可以进一步进行影像学和病理学检查以明确诊断。如果患者的 临床表现不符合标准，则可能需要进一步检查以排除其他疾病的可能性。
Hale Waihona Puke 3、病理学标准3、在治疗方面，医生可以根据该标准对痛风患者进行分期治疗。对于急性发 作期患者，医生可以采取非甾体抗炎药、糖皮质激素等药物治疗以缓解疼痛和炎 症。对于慢性期患者，医生可以采取降尿酸治疗以降低血尿酸水平，预防痛风发 作。同时，医生还需要对患者进行生活方式的干预，如控制饮食、增加运动等， 以降低痛风复发的风险。
痛风概述
痛风概述
痛风是一种由于嘌呤代谢紊乱或尿酸排泄障碍导致的慢性代谢性疾病。根据 国家卫健委2019年的数据，我国痛风患病率呈逐年上升趋势，且发病年龄日趋年 轻化。痛风的主要病理生理机制是尿酸盐结晶沉积，导致急性痛风性关节炎和痛 风石形成。痛风患者常伴发高血压、糖尿病、肥胖、高血脂等代谢性疾病。
指南解读
要点分析
要点分析
1、分类：该指南将痛风分为急性发作期、间歇期和慢性期三个阶段，有助于 更好地理解患者的病情和制定相应的治疗方案。
要点分析
2、诊断：指南强调了病史采集、体格检查、实验室检查和影像学检查的重要 性，有助于提高诊断的准确性。
要点分析
3、治疗：该指南提出了针对不同阶段的治疗方案，包括抗炎、降尿酸和尿酸 盐溶解等治疗措施，具有很强的实操性。
在影像学方面，有以下两个标准： （1）关节超声：超声检查发现关节内有结晶沉积或痛风石；
2、影像学标准
（2）关节X线检查：X线平片显示关节周围有骨质破坏或囊性变。
3、病理学标准
3、病理学标准
2012美国ACR痛风指南(第一部分)
16North Mississippi Medical Center, Tupelo, MS 17Southern California Permanente Medical Group, Downey, CA 18University of Florida, Gainesville, FL 19Cleveland Clinic, Cleveland, OH 20University of Pennsylvania and VA Medical Center, Philadelphia, PA 21Harvard Vanguard Medical Associates/Atrius Health, Somerville, MA 22VA Medical Center. Birmingham, Alabama and University of Alabama, Birmingham, AL Keywords Allopurinol; Febuxostat; Probenecid; Pegloticase; Uricosuric; Xanthine Oxidase; Tophi INTRODUCTION Gout is a disorder that manifests as a spectrum of clinical and pathologic features built on a foundation of an excess body burden of uric acid, manifested in part by hyperuricemia,which is variably defined as serum urate greater than either 6.8 or 7.0 mg/dL (1;2). Tissue deposition of monosodium urate monohydrate crystals in supersaturated extracellular fluids of the joint, and certain other sites, mediates most of the clinical and pathologic features of gout. Typically, the disease first presents as arthritis that is acute and episodic, but can become recurrent in the majority of individuals. Gout also can manifest as chronic arthritis of one or more joints (1;2). Tophi, mainly in articular, periarticular, bursal, bone, auricular,and cutaneous tissues are a pathognomonic feature of gout, and are detectable by physical exam, and/or by imaging approaches and pathology examination (3;4;5). Renal manifestations of gout include urolithiasis, typically occurring with an acidic urine pH (1;2).Chronic interstitial nephropathy, mediated by monosodium urate monohydrate crystal deposition in the renal medulla, can occur in severe disease, but is currently considered to be an uncommon clinical manifestation of gout.Gout is one of the most common rheumatic diseases of adulthood, with self-reportedprevalence in the USA recently estimated at 3.9% of adults (~8.3 million people)(6).Prevalence of gout has risen in many countries (e.g., New Zealand), and especially in theUSA over the last few decades, mediated by factors such as increased prevalence of co-morbidities that promote hyperuricemia, including hypertension, obesity, metabolicsyndrome, type 2 diabetes, and chronic kidney disease (CKD)(7–10). Other factors in therising prevalence of gout include certain dietary trends and widespread prescription ofthiazide and loop diuretics for cardiovascular diseases (11). Many gout patients, includingthe growing subset of affected elderly, have complex co-morbidities and medication profilesthat complicate overall management (12). Long-term morbidity and impairment of health-related quality of life are now better appreciated in many gout patients, particularly thosewith multiple co-morbidities and/or chronic gouty arthritis (13;14). Despite advancedunderstanding of the molecular bases of hyperuricemia and gouty inflammation, and theextensive practice experience of many providers, substantial quality of care gaps exist ingout management (15). Moreover, significant shortfalls in patient education and adherencehave been identified in gout (16).On behalf of the American College of Rheumatology (ACR), we were charged withdeveloping systematic non-pharmacologic and pharmacologic recommendations foreffective treatments in gout with acceptable risk-benefit ratio. Our assignment was to focuson four specific domains in gout management. Two of these domains are addressed herein,(i) Urate-lowering therapy (ULT), and (ii) chronic gouty arthritis with tophaceous diseasedetected on physical examination (designated by the ACR with the terminology “chronictophaceous gouty arthropathy” (abbreviated CTGA), and specifically represented in theNIH-PA Author ManuscriptNIH-PA Author ManuscriptNIH-PA Author Manuscriptfundamental case scenarios 7–9 described herein). Domains iii-iv (analgesic and anti-inflammatory management of acute gouty arthritis, and pharmacologic anti-inflammatory prophylaxis of attacks of gouty arthritis, respectively) are addressed in a separate manuscript (Part II of the guidelines)(17).There are multiple lines of epidemiologic and experimental evidence that hyperuricemia, via effects of excess soluble urate, may play a role in some human renal, cardiovascular, and metabolic co-morbidities also frequently associated with gout (7–10). We did not address pharmacologic management of asymptomatic hyperuricemia, due to a paucity of prospective, randomized, controlled human research trials in that area (18).We were charged by the ACR with developing gout recommendations based on evidence as available, at an international level, for rheumatologists and other health care providers,including other subspecialists, primary care practitioners, nurse practitioners, physician assistants, and allied health professionals. The ACR requested that we apply the established Research and Development/University of California at Los Angeles (RAND/UCLA)Appropriateness Method (19) to generate recommendations, and engaged a diverse,international panel of experts. Creating novel classification of gout as a disease, new gout diagnostic criteria, or definition of treatment outcomes were beyond the scope of this work.Instead, we generated multifaceted case scenarios to elucidate decision-making based primarily on clinical and laboratory test-based data that can be obtained on a gout patient in an office practice setting.Guidelines for gout management have been generated in the last decade, at the national or multinational society level, by the European League Against Rheumatism (EULAR)(20;21),the Dutch College of General Practitioners (22), the Japanese Society of Gout and Nucleic Acid Metabolism (23), and the British Society for Rheumatology (BSR)(24). Moreover, the National Institute for Health and Clinical Excellence (NICE) single technology appraisal (STA) process has been applied to ULT in gout using febuxostat (25). New guidelines wererequested by the ACR, as the understanding of gout risk factors has been greatly augmented by recent clinical research (12). Moreover, ULT options recently increased via clinicaldevelopment, and drug regulatory agency approval of new pharmacologic agents (febuxostat and the biologic drug pegloticase)(26;27). New imaging approaches for gout that can detect radiographic changes of early disease not visualized by plain radiography (e.g., highresolution ultrasound, dual energy computed tomography (DECT)(28;29), are beinginvestigated for impact on gout diagnosis, and assessment of disease burden and severity,and choices and effectiveness of management. Developments such as these are considered in the work of this committee, which was built on several key assumptions (Table 1).The ACR gout guidelines are designed to emphasize safety, and quality of therapy, and to reflect best practice, as evaluated by a diverse group of experts that examine the level ofevidence available at the time. Importantly, societal cost of health care, and cost and cost-effectiveness differences between therapies are excluded from analysis by the RAND/UCLA Appropriateness Methodology (19) (Table 1). Individual results of this work are designated as “recommendations” rather than guidelines, in order to reflect the non-prescriptive nature of decision-making evaluated by experts, and based on available evidence at the time. The recommendations cannot substitute for individualized, direct assessment of the patient,coupled with clinical decision making by a competent health care practitioner. Treatment recommendations also assume appropriate attention to potential drug interactions (eg, with anticoagulants, azathioprine, amoxicillin), and effects of co-morbidities such as diabetes,and renal, cardiac, gastrointestinal, and hepatic disease (Table 1). The motivation, financial circumstances, and preferences of the gout patient play a very important role. Moreover, the NIH-PA Author ManuscriptNIH-PA Author ManuscriptNIH-PA Author Manuscriptrecommendations for gout management presented here are not intended to limit or denythird party payer coverage of health care costs for groups, or individual patients, with gout.METHODSProject design and development of recommendations and grading of evidence The overall design of the project is schematized in Supplemental Figure 1. The RAND/UCLA consensus methodology, developed in the 1980s, incorporates both Delphi and nominal group methods (19;30), and was successfully used to develop other guidelines commissioned by the ACR. The purpose of this methodology is to reach a consensus among experts, with an understanding that published literature may not be adequate to provide sufficient evidence for day-to-day clinical decision-making. The RAND/UCLA method requires 2 groups of experts—a core expert panel (CEP) that provides input into case scenario development and preparation of a scientific evidence report, and a task force panel (TFP) that votes on these case scenarios. Our CEP consisted of leaders for each domain (Supplemental Figure 2). Pharmacologic approaches, and diet, lifestyle and non-pharmacologic measures (e.g., weight loss, exercise) were addressed within each domain.The CEP leaders communicated with an international panel of gout experts, and the PIs, to develop initial case scenarios that reflect broad differences in severity of the disease and its clinical manifestations. In addition, there were weekly interactive teleconferences between domain leaders and PIs to refine case scenarios. Though previous systematic review for gout has been performed by EULAR, as a prime example, we performed our own systematic review of pertinent literature. The resultant scientific evidence report given to the TFP in conjunction with clinical scenarios representing a broad scope of disease, with multiple questions of interest, and alternative options, for each case scenario.By ACR mandate, the TFP had a majority of members without perceived potential conflict of interest (COI), and had diverse experience and expertise, as described in detail inSupplemental Figure 2. The TFP included 7 rheumatologists (one of whom is a Chair ofInternal Medicine, and one an Internal Medicine Residency Training Program Director), 2primary care physicians, a nephrologist, and a patient representative. There were 2 rounds of ratings, the first anonymously with the members of the TFP instructed to rank each of the potential elements of the guidelines on a risk-benefit basis ranging from 1 to 9 on a Likert scale using Delphi process, followed by a face-to-face group discussion and then re-voting of the same scenarios. A vote of 1–3 on the Likert Scale was rated as Inappropriate = risks clearly outweigh the benefits. A vote of 4–6 on the Likert Scale was considered Uncertain =risk-benefit ratio is uncertain. A vote of 7–9 on the Likert Scale was rated as Appropriate =benefits clearly outweigh the risks. Samples of votes taken and results are provided inSupplemental Figure 3. Votes on case scenarios were translated into recommendations if the median voting score was graded 7–9 (“appropriate”) and if there was no significantdisagreement, defined as no more than 1/3 of the votes graded (“inappropriate”) for thescenario. The final rating was done anonymously in a 2-day face-to-face meeting, facilitated by an experienced moderator (Neil Wenger). During the face-to-face TFP meeting, some case scenarios were clarified for content or verbiage, and re-voted on by the TFP.The level of evidence supporting each recommendation was ranked based on previousmethods used by the American College of Cardiology (31) and applied to recent ACRrecommendations (32;33). Level A grading was assigned to recommendations supported by multiple (i.e., more than one) randomized clinical trials or meta-analyses. Level B grading was assigned to the recommendations derived from a single randomized trial, ornonrandomized studies. Level C grading was assigned to consensus opinion of experts, case studies, or standard-of-care.NIH-PA Author ManuscriptNIH-PA Author ManuscriptNIH-PA Author ManuscriptSystematic reviewPubMed and Cochrane Central Register of Controlled Trials (CENTRAL) from the 1950s to the present were searched to find articles on gout with help of an experienced librarian(Rikke Ogawa). We used a search strategy based on the Cochrane Highly Sensitive Search Strategy for identifying randomized trials. The search was expanded to include articlesdiscussing research designs such as cohort, case control and cross sectional studies. Limits included English Language and the exclusion of “animal only” studies. The exact terms,process and results of the search are summarized in Supplemental Figure 4.Clinical Case DescriptionsThe TFP evaluated scenarios with a broad spectrum of clinical gout, similar to what aclinician might see in a busy practice, and divided into mild, moderate, and severe disease activity in each of three distinct “treatment groups” (Figure 1A–B). In generating these nine fundamental clinical case scenarios, mild disease activity levels in each “treatment group”were meant to represent patients at the lowest disease activity level for which mostclinicians would consider initiating or altering a specific medication regimen. Conversely,severe disease activity level was intended to represent patients with disease activity equal or greater to that of the “average” subject studied in a clinical trial. The case scenarios were not intended to serve as classification criteria. To allow the TFP to focus on managementdecisions, each case scenario had the assumption not only that the diagnosis of gout was correct, and that there was some clinical evidence of gout disease activity. This included intermittent symptoms of variable frequency, specifically presented to the TFP as episodes of acute gouty arthritis of at least moderate to severe pain intensity (17). Clinical evidence of gout disease activity, presented to the TFP, also included one or more tophi detected byphysical exam, or alternatively, chronic symptomatic arthritis (ie, “chronic arthropathy” or “synovitis”) due to gout, with or without confirmed joint damage (e.g., deformity, erosion due to gout on imaging study). Hyperuricemia was defined here as serum urate >6.8 mg/dL(2). We determined all aspects of case scenario definitions by a structured iterative process,using regular electronic mail, and teleconferences at least once per month. Multiplerevisions to the proposed parameters were carried out, until accepted by the CEP domain leaders.Definitions of pharmacologic therapeutic agentsMedication classes evaluated in the case scenarios were defined as follows: Xanthineoxidase inhibitor (XOI) refers to allopurinol or febuxostat; uricosuric agents were defined to include agents available in the USA (probenecid, and off-label use (as uricosuric therapy) of fenofibrate and losartan), but did not include sulfinpyrazone or benzbromarone. Other agents and modalities were self-explanatory. Evaluation by the TFP of effectiveness of a giventherapeutic option assumed that patients in case scenarios received the maximum tolerated typical dose for a period of time sufficient to accurately assess therapeutic response, unless otherwise indicated.Managing perceived potential COIPerceived potential COI was managed in a prospective and structured manner. Specifically,all participants intellectually involved in the project, whether authors or not, were required to fully, and prospectively disclose relationships with pharmaceutical companies with amaterial interest in gout (Supplemental Material Discussion). Disclosures were updatedevery 6 months, and for the PIs, CEP and TFP, updated just prior to the face-to-facemeeting. A summary listing of all perceived potential COI was disseminated to allparticipants in the project, and is available in the supplemental materials. Based on thepolicies of the ACR, which are aligned with those of many medical societies, no more than NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript49% of project participants could have COI at any given time. It was required that theproject PI (John FitzGerald) remain without perceived potential COI prior to and during the process.RESULTS Primary principles of management for all gout case scenarios The TFP generated recommendations for a systematic non-pharmacologic and pharmacologic management approach intended to be applicable to all patients with gout,which is summarized in Figure 3. This was based on the assumption that the diagnosis of gout was correct before initiation of management. The approach highlighted patient education on the disease and treatments and their objectives, and initiation of diet and lifestyle recommendations. The TFP also recommended elimination of prescription medication that were non-essential for the optimal management of co-morbidities (eg,hypertension, CHF, hyperlipidemia, or major organ transplant) in an individual patient,where such medication elevated serum urate levels; with prime examples being thiazide and loop diuretics, niacin, and calcineurin inhibitors (Evidence C). Though low dose acetylsalicylic acid (aspirin ≤ 325 mg daily) elevates serum urate, the TFP did not recommend discontinuation of this modality as cardiovascular disease prophylaxis in gout patients. In discussion, without a specific vote, the TFP viewed the relative risks specifically attributable to the modest effects of low dose aspirin on serum urate as negligible in gout management.The TFP recommended that clinicians consider causes of hyperuricemia for all gout patients,and recommended a specific co-morbidity checklist (Evidence C)(Table 2). In doing so, the TFP specially recommended consideration, and if indicated, medical evaluation of certain agents and disorders that cause uric acid underexcretion or overproduction, and thereby could merit laboratory investigations such as urinalysis, renal ultrasound, a completehemogram, or urine uric acid quantification as indicated. In this context, the TFPspecifically recommended screening for uric acid overproduction (by urine uric acidevaluation for uric acid overproduction), in patient subsets with gout clinical disease onset before age 25 (Evidence C), or a history of urolithiasis (Evidence C).The TFP provided guidance for referral to a specialist, with caution to avoid appearing self-serving. Though limited by the absence of outcomes data on potential benefits of referral,the TFP recommended that gout case scenarios including any of the following should be amongst those where referral to a specialist is considered (Evidence C for all): (i) Unclear etiology of hyperuricemia; (ii) Refractory signs or symptoms of gout; (iii) Difficulty inreaching the target serum urate level, particularly with renal impairment and a trial of XOI treatment; (iv) Multiple and/or serious adverse events from pharmacologic ULT.Clinical evaluation of gout disease activity and burdenThe TFP recommended clinical evaluation of gout disease symptom severity and burden in individual patients by history and thorough physical exam for symptoms of arthritis, and signs such as tophi and acute and chronic synovitis (Evidence C). To be actionable byclinicians, the authors, without a specific TFP vote, suggest that clinicians can work with patients to record and estimate the number per year, and severity (17) of acute attacks of gouty arthritis per year.Core recommendations for non-pharmacologic ULT measures in goutThe TFP recommended certain diet and lifestyle measures for the vast majority of patients with gout (Evidence B-C for individual measures) (Figure 4). Many of the diet and lifestyle NIH-PA Author ManuscriptNIH-PA Author ManuscriptNIH-PA Author Manuscriptmeasures were recommended for decreasing the risk and frequency of acute gout attacks(12) and lowering serum urate, but the primary emphasis of the TFP recommendations in Figure 4 was on diet and lifestyle choices for promotion and maintenance of ideal health,and prevention and optimal management of life-threatening comorbidities in gout patients,including coronary artery disease (34,35), and obesity, metabolic syndrome, diabetes,hyperlipidemia, and hypertension.Dietary recommendations were grouped into 3 simple qualitative categories, termed “limit”,“avoid”, or “encourage” (Figure 4). This approach, with rare exceptions (36,37), reflected a general lack of specific evidence from prospective, blinded, randomized clinical intervention trials that linked consumed quantities of individual dietary components to changes in either serum urate levels or gout outcomes. Notably, the replication of hazardous lifestyle riskfactors in a conventional clinical research trial would potentially pose both design andethical difficulties. As such, the TFP deliberated on evidence regarding the impact ofexposures to alcohol or purine-rich foods in a short time frame. The evidence sources were epidemiologic studies of hyperuricemia and incident gout, including long-term prospective analyses and internet-based case-crossover studies. The TFP recommended that goutpatients limit their consumption of purine-rich meat and seafood (Evidence B) as well as high fructose corn syrup sweetened soft drinks and energy drinks (Evidence C), andencouraged the consumption of low-fat or non-fat dairy products (Evidence B) (38)(Figure4). The TFP also recommended reduced consumption of alcohol (particularly beer, but also wine and spirits), and avoidance of alcohol overuse in all gout patients (Evidence B) (Figure4). The TFP further recommended abstinence from alcohol consumption for gout patients during periods of active arthritis, especially with inadequate medical control of the disorder and in CTGA (Evidence C)(39). Significantly, in discussion by the TFP, without a specific vote, the TFP recognized that diet and lifestyle measures alone provide therapeuticallyinsufficient serum urate-lowering effects and/or gout attack prophylaxis for a large fraction of individuals with gout (12). For example, some clinical trials on diet and fitness havereported only ~10–18% decrease in serum urate (38). In further discussion by the TFP, again without a specific vote, the TFP viewed this degree of serum urate-lowering as beneficial for all case scenarios, but insufficient to achieve an effective serum urate target in those with sustained hyperuricemia substantially above 7 mg/dL.Core recommendations for pharmacologic ULT, including the serum urate targetHere, and with all other recommendations for drug therapy in Parts I and II of the 2012 ACR Guidelines for gout, the recommendations assumed a lack of contra-indications, intolerance,serious adverse events, or drug-drug interactions for given agents. The TFP recommended gout with CKD stage 2–5, or end stage renal disease (ESRD), as an appropriate indication,by itself, for pharmacologic ULT (Evidence C) in patients with prior gout attacks andcurrent hyperuricemia. In pharmacologic ULT, certain treatment choices (e.g., probenecid)and drug dosing decisions (e.g., allopurinol) are impacted by the creatinine clearance. The TFP, without a direct vote, discussed and recognized the clinical value of accuratemeasurement of creatinine clearance, not simply the serum creatinine, in ascertaining the degree of renal impairment. However, the scope of the project did allow for detailed,prescriptive recommendations regarding specific ULT drug doses, or usage of individual agents in the presence of a given degree of either renal impairment, or other co-morbidities such as hepatic impairment.TFP recommendations for pharmacologic ULT, presented graphically in Figure 3, included recommendation of xanthine oxidase inhibitor (XOI) therapy with either allopurinol orfebuxostat as the first line pharmacologic approach (Evidence A). The panel did notpreferentially recommend either XOI over the other XOI drug. In doing so, the TFP weighed the lack of published safety data for febuxostat in the setting of stage 4 or worse CKD.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptProbenecid was recommended as an alternative first line pharmacologic ULT option, in the setting of contra-indication or intolerance to at least one XOI agent (Evidence B). However,the TFP did not recommend probenecid as a first line ULT monotherapy in those with acreatinine clearance below 50 ml/min.The TFP recommended that pharmacologic ULT could be started during an acute goutattack, providing that effective anti-inflammatory management has been instituted (EvidenceC). The TFP recommended regular monitoring of serum urate (every 2–5 weeks) duringULT titration, including continuing measurements once the serum urate target is achieved (every 6 months) (Evidence C). The TFP weighed this measure as particularly useful tomonitor adherence, given that poor adherence to ULT is a common problem in gout patients(16).The TFP recommended that the goal of ULT is to achieve a serum urate target, at aminimum, of < 6 mg/dL in all gout case scenarios (Evidence A). Moreover, the TFPrecommended that the target serum urate should be lowered sufficiently to durably improve signs and symptoms of gout, including palpable and visible tophi detected by physicalexamination, and that this may involve therapeutic serum urate-lowering to below 5 mg/dL (Evidence B).Recommendations specific to allopurinol dosing and pharmacogenetics TFP recommendations for use of allopurinol in gout are summarized in Table 3A.Importantly, the TFP recommended that the starting dose of allopurinol be no greater than 100 mg per day (Evidence B)(40), consistent with prior FDA and EULAR guidelines (21).The rationale of the TFP was partly that a low allopurinol starting dose could reduce early gout flares after ULT initiation, (26), and partly as a component of risk management with respect to the potential for severe hypersensitivity reaction to allopurinol (40), discussed in further detail below. The TFP recommended gradual upward titration of the allopurinolmaintenance dose every 2–5 weeks to an appropriate maximum dose for gout, in order to treat to the serum urate target appropriate for the individual patient (Evidence C).The TFP weighed robust evidence that allopurinol monotherapy at doses of 300 mg daily or less failed to achieve the serum urate target of <6 mg/dL (26,41), or < 5 mg/dL (42,43), in more than half of subjects with gout. The TFP reviewed small studies in which theallopurinol dose was titrated above 300 mg daily in gout with overall success in achieving the serum urate target (43,44). Importantly, in doing so, the TFP also recommended that the maintenance dose of allopurinol can be raised above 300 mg per day, even in those withrenal impairment, provided there is adequate patient education and regular monitoring for drug hypersensitivity and other adverse events, such as pruritis, rash, and elevated hepatic transaminases, as well as attention to potential development of eosinophilia (Evidence B).The TFP next considered the issue of measures to reduce the incidence of severe allopurinol hypersensitivity reactions, here termed allopurinol hypersensitivity syndrome (AHS). TFP discussion recognized the potential for hospitalization and severe morbidity, and thereported mortality rate of 20–25% in AHS (45,46). The estimated incidence of AHS is~1:1000 in the USA and its spectrum includes not only Stevens-Johnson Syndrome andToxic Epidermal Necrolysis, but also systemic disease with a clinical constellation offeatures such as eosinophilia, vasculitis, rash, and major end-organ disease (47). Concurrent thiazide use and renal impairment have been implicated as risk factors for AHS (48–50). A widely employed risk management strategy has been a non-evidence-based algorithm for allopurinol maintenance dosing, calibrated to renal impairment (51)(Evidence C);importantly, the TFP did not recommend this strategy,NIH-PA Author ManuscriptNIH-PA Author ManuscriptNIH-PA Author Manuscript。
ACR痛风指南解读ppt课件
6 months after achieving the target serum urate level, where there has been resolution of tophi previously detected on physical examination (evidence C)
预防用药 评述 以往临床上也都采用了上述预防药物，但是在疗程上均 明显不足 之所以将糖皮质激素列入二线预防药物，主要是考虑到 长期使用糖皮质激素可能带来的多种不良反应
• 过度饮酒（男性每天2份， • 饮酒（主要是啤酒，但 女性每天1份） 也包括葡萄酒和烈酒） （B级） （B级） • 任意量的酒（病情进展， 控制不佳，反复发作者） （C级）
• 蔬菜 （C级）
非药物治疗 评析 对患者进行积极有效的宣教是慢性疾病治疗的重要环节。 EULAR会议上流行病学调查数据显示：痛风患者在疾病认 识上广泛存在误区，缺乏规范降尿酸治疗的知识，而且 患者用药依从性较差。 家庭医生及非风湿科专科医生亦缺乏规范治疗的概念 “指南”特别强调“宣教”的重要性，同时提出积极控 制可以导致高尿酸血症的合并疾病是预防、治疗痛风的 重要环节，值得引起重视
有关节痛或痛风石均需长期抗炎预防治疗。 持续监测血尿酸水平和降尿酸药物的副作用。 专科医生规范化治疗。 小剂量阿司匹林允许使用，其他药物权衡利弊。
血尿酸监测 血尿酸监测对于痛风治疗是必需的 在调整降尿酸药物过程中，每2－5周测定一次 在达标后（血尿酸<6mg/dl），也要每6个月测定一次 尿酸测定是调整药物剂量的依据，也有利于判断患者对治疗 药物的依从性
定义 血尿酸
1mg/dl=59.45μmol/L
痛风指南：发达国家是这样治疗痛风的
痛风指南：发达国家是这样治疗痛风的前沿：痛风是一种最常见的炎症性关节病，在西方国家男性的患病率约为1%～2%。
随着我国人民生活水平的不断提高，痛风的患病率也呈逐年上升趋势，目前已经接近西方发达国家水平。
痛风是由于血尿酸水平持续升高，导致单钠尿酸盐在关节和其他组织中沉积所致。
高尿酸血症和痛风与糖尿病、高血压、心血管疾病、慢性肾脏病等密切相关，是上述疾病发生发展的独立危险因素，也直接导致了患者长期生活质量的下降。
2002～2008年荷兰全科医师学会、欧洲风湿病学会、英国风湿病学会以及日本痛风和核酸代谢学会均陆续颁布了痛风治疗指南，为合理规范化诊治痛风提供了重要依据。
治疗药物和新型影像学技术（高频超声和双能CT）的应用进一步推动了痛风诊治的发展。
2012年美国风湿病学会在循证医学证据基础上，结合专家根据患者具体临床情况给出的意见，针对痛风治疗提出了新的指南，包括非药物性干预和药物治疗。
2013年多个国家又联合提出了痛风诊断和治疗推荐。
为了更好地指导我国临床医师在实践中结合患者具体情况制订合理的治疗方案。
1痛风的治疗目标：普遍目标：痛风的治疗目标已经非常明确，最新的几项推荐或指南一致强调血尿酸水平降至360μmol/L（6mg/dl）以下是治疗的最低目标；痛风石患者目标：对于已有痛风石的痛风患者，为了更好地长期改善患者的临床症状和体征，应将血尿酸水平降至300μmol/L（5mg/dl）以下。
因此在治疗过程中需要严密监测患者血尿酸水平，另外也需要关注关节炎发作的频率和痛风石的大小。
最终目标：对于痛风患者，关节炎不再发作、痛风石逐渐被吸收也是治疗的重要目标。
2痛风的诊断：在关节积液或痛风石中发现单钠尿酸盐晶体仍然是诊断痛风的最有利依据。
临床发现典型痛风石或对秋水仙碱治疗反应好，支持痛风诊断，除此以外的多数情况下，临床、实验室以及传统X线检查对于诊断的帮助不大。
对于11项研究的荟萃分析显示：新型影像学技术（超声、双能CT）对于痛风诊断有帮助。
痛风管理指南acr指南
痛风管理指南: ACR指南简介痛风是一种常见的代谢性疾病，以高尿酸血症和尿酸盐沉积引起的关节炎为主要临床表现。
目前，美国风湿病学会〔ACR〕发布了一份痛风管理指南，旨在为临床医生和患者提供最新的痛风治疗和管理建议。
本文将以ACR指南为根底，介绍痛风的诊断、治疗和预防措施。
诊断根据ACR指南，痛风的诊断主要基于以下几个方面：1.临床病症：典型的痛风发作表现为急性关节炎，多累及大趾关节，常伴有剧烈疼痛和红、肿、热等病症。
2.尿酸水平：血尿酸水平升高是痛风的重要指标，但并非所有高尿酸血症患者都会开展为痛风。
ACR指南建议根据临床病症和尿酸水平来进行诊断。
3.关节液分析：关节液中尿酸结晶的检测是确诊痛风的金标准，但不是所有不明原因的急性关节炎都需要进行关节液分析。
治疗ACR指南给出了痛风治疗的详细建议，包括急性发作期的治疗和长期控制期的治疗。
急性发作期的治疗•非甾体类抗炎药〔NSDs〕：对于急性发作期的疼痛和炎症，NSDs是首选的治疗药物。
•秋水仙碱：秋水仙碱是一种可用于急性痛风发作的药物，常用于NSDs不能耐受或禁用的患者。
•肾上腺皮质激素：对于严重病症或其他药物无效的患者，肾上腺皮质激素是有效的选择。
长期控制期的治疗•尿酸降低治疗：ACR指南推荐在持续高尿酸血症的患者中进行尿酸降低治疗，以减少痛风发作的风险。
•遵循药物治疗原那么：ACR指南强调在进行药物治疗时应根据患者的肾功能和疗效来选择适宜的药物，并定期监测尿酸水平。
•饮食和生活方式管理：控制体重、限制酒精和高嘌呤食物的摄入，以及适当的运动可以帮助预防痛风和减轻病症。
预防ACR指南认为痛风是可以预防的，以下是一些预防痛风的措施：•饮食调整：限制酒精和高嘌呤食物的摄入，增加低脂鱼类和植物蛋白的摄入。
•体重控制：减轻过重和肥胖可以降低痛风的发病风险。
•健康生活方式：适量运动、戒烟和控制血压等生活方式改变有助于预防痛风。
结论ACR痛风管理指南为临床医生和患者提供了最新的痛风诊断、治疗和预防的指南。
ACR痛风指南与中国痛风指南比较
ACR痛风指南与中国痛风指南比较医学论坛网2013-12-21发表评论分享比较2012年ACR痛风治疗指南（ACR指南）和中华医学会风湿病学分会痛风诊疗指南（中国指南），主要有以下不同。
1、ACR指南推荐的一线降尿酸药物是别嘌醇和非布索坦，非布索坦首次作为一线药物推荐，丙磺舒是至少对一种黄嘌呤氧化酶抑制剂禁忌或不能耐受，才作为一线的促尿酸排泄药用于降尿酸治疗;而中国指南没有推荐非布索坦（中国未上市），中国指南推荐的苯溴马隆，ACR指南没有推荐（美国没有被批准上市）。
有尿路结石史和尿尿酸升高者，ACR 指南推荐禁用促尿酸排泄药物;中国指南推荐前者慎用，后者没有提及。
2、开始降尿酸时间，ACR指南建议在开始有效的抗炎治疗后就可以开始降尿酸治疗;中国指南建议在急性发作平熄。
3、ACR指南建议在高危人群（包括汉族人群）中，开始别嘌醇治疗前检测HLA.B'5801基因，避免AHS;而中国指南没有提及。
4、在急性痛风性关节炎抗炎治疗药物选择上，ACR指南推荐NSAIDs、秋水仙碱和糖皮质激素，3种药物作了同等推荐，建议医师根据患者的偏好、以前治疗的反应、合并症综合考虑药物的选择;中国指南建议糖皮质激素用于不能耐受NSAIDs、秋水仙碱或肾功能不全者。
5、ACR指南强调分层治疗，痛风性关节炎根据疼痛的程度及受累关节数确定严重程度，决定选用单药治疗还是联合治疗，对联合治疗方案也做了建议;中国指南没有强调分层治疗。
6、ACR 指南将小剂量强的松或强的松龙用于对秋水仙碱和NSAIDs不能耐受、有禁忌证、无效的患者预防痛风复发;中国指南没有提及。
由于种族差异，生活方式的不同，医疗环境及可供选择的药物不一样，ACR痛风指南是否能适用于中国临床实践，还需要临床医生验证。
关键词：痛风治疗指南ACR。
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美国风湿学院（ACR）发布2012版痛风管理指南
2012-11-01 15:11 来源：丁香园
近日，美国风湿学院（American College of Rheumatology，ACR）发布了2012版痛风管理指南，指导医生和患者如何更好应对痛风。
指南分为两个部分：
第一部分:痛风的药物和非药物治疗
痛风管理的基础性建议
·痛风患者应该学习合理的饮食习惯和生活习惯
·需要避免引起继发性高尿酸血症的因素
·除非必须，否则避免使用引起尿酸增高的药物
·需要评估痛风的严重程度（是否有痛风石，痛风的发作次数等等）
降尿酸药物治疗建议
·凡是确诊有痛风石的痛风患者都可以使用降尿酸药物（别嘌醇等）治疗
·频繁发作的痛风（每年发作大于等于2次）患者也可以使用此类药物
·痛风合并慢性肾病（2期或以上）或者过去有过尿路结石的患者也被推荐使用此类药物
·最低治疗目标是将血清尿素水平降低到6mg/dl以下，降到5mg/dl以下则更理想·推荐别嘌醇或非布索坦为一线降尿酸用药
·如果痛风已经发作则需要考虑联合使用降尿酸药物和抗炎药物
·别嘌醇的起始计量不要超过100mg/天，如果合并慢性肾病（4期或以上）则不超过50mg/天。
可每2～5周增加一次剂量，直到血清尿酸达到目标治疗水平
·丙磺舒是促进尿酸排泄的最佳选择
·如果尿酸水平顽固性增高，则可以考虑联用黄嘌呤氧化酶抑制剂（别嘌醇或布索坦）和促进尿酸排泄的药物（如丙磺舒）
饮食建议
研究人员将食物建议分为三类：避免食用、限制食用和鼓励食用。
客观的说，这些建议都是来自某些孤立的临床研究，而不是大规模多中心临床研究或meta分析。
关于某些食物（樱桃、坚果和豆类）的建议研究人员也有分歧。
避免食用：富含高嘌呤的动物内脏、果糖含量高的甜食饮料和汽水。
痛风发作期间避免饮酒，非发作期间也需严格限酒。
限制食用：牛肉、羊肉、猪肉、嘌呤含量高的海鲜（沙丁鱼和贝壳类）、自然很甜的果汁、食盐和酒（尤其是啤酒）
鼓励食用：低脂乳制品和蔬菜
第二部分：急性痛风发作期的治疗建议
·急性痛风发作24小时内开始药物治疗
·降尿酸药物需要继续服用
·非甾体类抗炎药（NSAID）、糖皮质激素和口服秋水仙碱是痛风急性发作期的一线推荐用药。
如果发作严重，则可联合使用这些药物。
不过不建议NSAID和糖皮质激素联用，因为这两个要的胃肠道副作用会叠加，有一定风险
·在疼痛的关节可以采用冰块外敷
·为预防痛风发作，降尿酸治疗的同时可以同时使用NSAID或秋水仙碱，如果这两个药物有禁忌症或患者不能耐受，则可以考虑使用强的松等糖皮质激素替代。