类风湿关节炎诊断及治疗指南(2010年)。
ACR与EULAR2010年RA新标准解读
ACR1987年标准的特异性和敏感性
观察结果：
98例确诊为RA，其中初次符合ACR1987年标准的有65例 (66%)
非RA的31/172(18%)达到了ACR1987年标准 2年后有85例符合ACR1987年标准，敏感性为87% 2年后172例非RA中有43例(25%)达到2年后标准，特异性
EULAR2009
专家共识
有滑膜炎表现并且有放射影像学骨侵蚀证 据者应视为RA
1990年在英国Norfolk的Norwich 卫生专署机构 调查了该地RA的患病率。结果显示，第5年符合 ACR标准的患病率与第1年相比，女性高45%，男 性高36%。这说明ACR1987年的标准对于1年内发 病的关节炎敏感性不够理想。
Harrison et al.J Rheum 1998;25: 2324-30
Emery P. ACR 2009.
数据采集
RA的早期诊断是否可行？
以下指标对于诊断RA意义很大
掌指、跖趾关节受累或3个 以上关节受累
晨僵大于30分钟 掌指关节握挤(Squeeze
Test)试验阳性
早期治疗能明显的提高疗效，改善预后
1、新的传统DMARDs，如来氟米特、米诺霉 素 2、生物制剂，特别是TNF-a抑制剂
Analytical approach Comparing disease in patients
1987年ACR分类标准产生的过程
由9个亚委员会委员和另外32个来自美国大 学或私人诊所的风湿病学专家对262例RA和 等量其它疾病的对照组进行平均7年的研究
ACR1987年RA分类标准
1、晨僵: 至少1小时 (≥6周) 2、多关节炎: 14个关节区中≥3个同时肿胀或积液 (≥6周) 3、手关节炎: 腕或掌指或近端指间关节肿胀(≥6周) 4、对称性关节炎(≥6周) 5、皮下结节： 6、X线:手和腕关节的X线改变 7、类风湿因子: 类风湿因子阳性(滴度正常人阳性率 <5%) *符合≥4条, 可诊断为RA
类风湿性关节炎中医诊断及治疗
气血两虚证
• 独活寄生汤加减。常用药物如寄生、独活、防风、
秦艽、细辛、当归、白芍、川芎、熟地、党参、 茯苓、甘草、杜仲、牛膝、桂枝、黄芪、灵仙、 鸡血藤等
肝肾虚损证
• 偏阳虚证：用右归丸合阳和汤加减。常用药物如
熟地、山萸、山药、枸杞、杜仲、肉桂、附子、 菟丝子、当归、鹿角霜、白芥子、麻黄、炮姜、 黄芪、党参、寄生、独活、威灵仙、鸡血藤等
类风湿性关节炎中医诊断及治疗
病因病机
• RA属中医“历节病”、“尪痹”的范畴，其
• 病程多反复发作缠绵难愈。 • 病因病机 • 肝肾不足，气血亏虚 ，正虚邪恋，感受风寒
湿邪，寒热错杂 ，痰瘀互结，阻滞经脉。
辨证分型
• 风寒湿型 • 风湿热型 • 分型论治 • 寒热错杂型 • 气血亏虚型 • 肝肾亏损型
合理的调摄和饮食
• 情绪要乐观，避免出现抑郁或焦虑，要有战胜疾 病的信心，才能提高依从性；
• 合理饮食，避免出现营养不Fra bibliotek。制定合理的治疗方案
• 早诊断早治疗（发病3月内，治疗效果和预后相对较好）。
• 根据患者的身体、经济状况制定一个安全、有效、经济的 治疗方案。
• 治疗方案要个体化，不能千篇一律把诊疗指南的用药都用 上。
• 越婢加术汤
• 多用于类风关急性发作期，表现为风湿热痹者。
• 防已黄芪汤
• 适用于气虚湿阻之RA。
• 麻黄细辛附子汤
• 以麻黄细辛附子汤合越婢加术汤治疗类风关风 寒湿型。
• 独治寄生汤
• 治类风关日久，正虚邪实者
• 三痹汤
• 适用于RA肝肾气血不足夹风寒湿痹的治疗。
• 宣痹汤
• 适用于RA湿热痹型，湿热较重者，可与二妙 散同用。
ACR2010诊断RA标准
ACR/EULAR2009年的类风湿关节炎诊断标准这个是临床诊断为骨性关节炎的病人，按Kellgren-Lawrence分期。
目前了解到Kellgren和Lawrence的放射学诊断标准，将骨性关节炎分为五级：0级：正常；Ⅰ级：关节间隙可疑变窄，可能有骨赘；Ⅱ级：有明显骨赘，关节间隙可疑变窄；Ⅲ级：中等量骨赘，关节间隙变窄较明显，有硬化性改变；Ⅳ级：大量骨赘，关节间隙明显变窄，严重硬化性病变及明显畸形。
膝关节炎的影像学评估与功能、疼痛及肌力评估的关系Para Español haga clic aquí.FAST FACTS∙OA is the most common form of joint disease in humans and is a leading cause of disability among the elderly.∙It typically occurs in the hand joints, spine, hips and knees.∙It is caused by cartilage breakdown and subsequent bony changes of the joints.∙Although the joint changes are irreversible, only a small number of patients will progress to the point that requires joint replacement surgery.∙OA symptoms can vary greatly among patients. Y our rheumatologist can make the diagnosis and prescribe appropriate treatment recommendations for you.In osteoarthritis, the cartilage between the bones in the joint breaks down, and bony enlargement occurs.WHA T IS OSTEOARTHRITIS?Osteoarthritis (OA) is a slowly progressive joint disease typically seen in middle-age to elderly people. It occurs when the joint cartilage breaks down, causing the underlying bone to fail. OA symptoms include joint pain, stiffness, knobby swelling, cracking noises with joint movements and decreased function. It typically affects the joints of the hands and spine and weight-bearing joints such as the hips and knees.WHO GETS OSTEOARTHRITIS?OA typically occurs in patients age 40 and above. However, some risk factors might cause it to occur sooner (see below). It affects people of all races and gender.WHA T ARE THE RISK FACTORS FOR OSTEOARTHRITIS?∙Older age∙Family members with OA∙Obesity∙Joint trauma or repetitive use of jointsHOW IS OSTEOARTHRITIS DIAGNOSED?OA usually is diagnosed by having typical symptoms and physical examination as described above. In some cases, imaging studies may be useful to tell the extent of disease or to help rule out other joint problems.The circles on this figure indicate joints that are commonly affected by osteoarthritis.HOW IS OSTEOARTHRITIS TREATED?The goal of treatment is to reduce pain and improve function of the affected joints. This can be achieved with a combination of physical measures, drug therapy and, sometimes, surgery.Physical measures– Exercise, support devices and thermal therapy are useful in OA. Some forms of unproven alternative treatment such as spa, massage, acupuncture and chiropractic manipulation can help relieve pain for a short duration, but usually are costly and require repeated treatments.Drug Therapy– Available forms of drug therapy include topical and oral agents. Topical drugs, which include capsaicin cream, lidocaine, and diclofenac gel, can be applied directly on the skin overlying the affected joints. Oral pain relievers such as acetaminophen, and nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used as first-line treatment. For more serious pain, stronger medications, such as narcotics, may be required. Joint injections with corticosteroids or a form of lubricant called hyaluronic acid (HA) derivatives have proven effective for some patients.Surgery– Arthroscopy and/or joint replacement is considered when the joint is seriously damaged, or the patient is in intractable pain and experiencing significant loss of function.Supplements– Many over-the-counter nutritional supplements have been used for treatment of OA, but most lack good research data to support their effectiveness and safety. Among the most widely used areglucosamine/chondroitin sulfate, calcium and vitamin D, and omega-3 fatty acids. To ensure safety and avoid drug interaction, consult your doctor or pharmacist before using any of these agents, especially in combination with prescribed drugs.LIVING WITH OSTEOARTHRITISThere is no cure for OA, but you can manage how it impacts your lifestyle. For instance, giving proper positioning and support to the neck and back during sitting or sleeping; adjusting furniture, such as raising a chair or toilet seat; and avoiding trauma and repetitive motions of the joint, especially frequent bending, are great starts.Adding regular exercise to your daily activities will improve muscle strength. Exercises that increase strength of the quadriceps muscles (the front thigh muscles) also can help decrease knee pain and reduce subsequent disability associated with osteoarthritis. Working with a physical or occupational therapist can help you learn the best exercises and choose appropriate assistive devices for your joints.Weight loss in obese people can reduce pain and progression of OA. Achieving and keeping an ideal weight will make a difference in your overall comfort levels.POINTS TO REMEMBER∙OA is the most common form of arthritis and can occur together with other types of arthritis.∙Evaluation by your doctor will help confirm the diagnosis and develop an appropriate treatment plan for your condition.∙The goal of treatment in OA is to reduce pain and improve function.∙At present, there is no available therapy that can reverse the damage of OA in the joint, but many studies are underway.TO FIND A RHEUMA TOLOGISTFor more information about rheumatologists, click here.Learn more about rheumatologists and rheumatology health professionals.FOR MORE INFORMATIONThe American College of Rheumatology has compiled this list to give you a starting point for your own additional research. The ACR does not endorse or maintain these Web sites, and is not responsible for any information or claims provided on them. It is always best to talk with your rheumatologist for more information and before making any decisions about your care.Arthritis FoundationUpdated August 2009Written by Thitinan Srikulmontree, MD, and reviewed by the American College of Rheumatology Patient Education Task Force.This patient fact sheet is provided for general education only. Individuals should consult a qualified health care provider for professional medical advice, diagnoses and treatment of a medical or health condition.© 2010 American College of Rheumatology5次坐-立试验在膝骨关节炎患者功能评估中的价值。
类风湿性关节炎的诊断标准
类风湿性关节炎的诊断标准风湿性关节炎（Rheumatoid Arthritis，RA）是一种慢性炎性关节病，全身性诊断标准（2010年版）可用于诊断RA。
诊断标准包括：1. 精确定义的弥漫性关节炎活动（至少4周）- 对应弥漫性关节炎列表（synovial joint lists）4项或更多关节的活动性的发炎。
2. 同一时间至少有1个细胞培养定量检测（Radiographic Quantitative Assay，RQA）阳性反应- 血清共行联合抗体（CommonAssociated Immunoglobulin，CAI-IgG或IgA）蛋白水平较正常检测值增高，或，用现代囊膜色素（Modern Mucopigment）测试显示抗体滴度大于常值。
3. 同时有至少2处活动性骨质结核损伤- 可用X光检查、磁共振成像（MRI）或其他影像学检查，根据发病规律判断多处骨质结核损伤。
4. 其他相关的免疫性和血清学检查的阳性反应- 这些检查包括：血清C-反应蛋白（CRP）水平高于正常范围；粪便抗IgA抗体检测（Fecal Antibody Test for IgA）阳性；180度双侧抗体评估测定（Double Blind Assessment，DBA）阳性；RQA测定的抗体IgG水平高于常规检查值；血清促炎因子（Serum Inflammatory Factors，SIF）测定高于正常范围；RA抗原（Rheumatoid Antigen）水平增高；抗核抗体（Anti-nuclear Antibody, ANA）阳性；抗类风湿抗体（Anti-Rheumatic Antibody，ARA）阳性。
以上8个检查项目，至少满足4条标准，同时兼具以上4个特征可以诊断RA。
另外，还需要更详细的检查，如血常规检查，白细胞介素-6（Interleukin—6，IL—6），粪便抗体测定，以及对病因的进一步研究，如肿瘤基因突变检查等。
2010年骨关节炎诊治指南(风湿免疫)
骨关节炎诊断及治疗指南中华医学会风湿病学分会1概述骨关节炎（Osteoarthritis，OA）是一种最常见的关节疾病。
是以关节软骨的变性、破坏及骨质增生为特征的慢性关节病。
本病的发生与衰老、肥胖、炎症、创伤、关节过度使用、代谢障碍及遗传等因素有关。
骨关节炎在中年以后多发，女性多于男性。
本病在40岁人群的患病率为10%-17%，60岁以上为50%，而在75岁以上人群则高达80%。
该病有一定的致残率。
本病按病因分为原发性骨关节炎和继发性骨关节炎。
前者是指原因不明的骨关节炎，与遗传和体质因素有一定关系，多见于中老年人；后者是指继发于关节外伤、先天性或遗传性疾病、内分泌及代谢病、炎性关节病、地方性关节病、其他骨关节病等。
有时很难鉴别原发性骨关节炎和继发性骨关节炎。
问诊和体格检查可以帮助判断病因。
影像学检查有助于继发性骨关节炎的诊断。
本病按是否伴有临床症状分为症状性骨关节炎和放射学骨关节炎。
前者伴有明显的骨关节炎临床症状，而后者无临床症状只有X线骨关节炎表现。
2临床表现2.1常见症状和体征本病好发于膝、髋、手（远端指间关节、第一腕掌关节）、足（第一跖趾关节、足跟）、脊柱（颈椎及腰椎）等负重或活动较多的关节。
2.1.1关节疼痛及压痛：本病最常见的表现是关节局部的疼痛和压痛。
负重关节及双手最易受累。
一般早期为轻度或中度间断性隐痛，休息时好转，活动后加重，随病情进展可出现持续性疼痛，或导致活动受限。
关节局部可有压痛，在伴有关节肿胀时尤为明显。
疼痛在阴冷、潮湿和雨天会加重。
2.1.2关节肿大：早期为关节周围的局限性肿胀，随病情进展可有关节弥漫性肿胀、滑囊增厚或伴关节积液。
后期可在关节部位触及骨赘。
2.1.3晨僵：患者可出现晨起或关节静止一段时间后僵硬感，称为晨僵，活动后可缓解。
本病的晨僵时间一般数分钟至十几分钟，很少超过半小时。
2.1.4关节摩擦音（感）：多见于膝关节。
由于软骨破坏、关节表面粗糙，出现关节活动时骨摩擦音（感）。
2010年美国风湿病学会联合欧洲抗风湿病联盟的类风湿关节炎分类标准解读
１９８７年ＲＡ分类标准的可靠性曾被进一
步验证。Ｅｍｅｒｙ等在１９９９年的研究结果显示，关节 炎病史小于１２周者只有５１％满足ＡＣＲ １９８７年 ＲＡ分类标准。１２周以内的早期患者往往达不到分 类标准．难以作出诊断。许多患者关节炎病史大于 １２周甚至１年才符合ＡＣＲｌ９８７年的ＲＡ分类标准 的条件。众所周知，所有的医师都希望在３个月以 内而不是在１年才作出诊断。１９９５至１９９７年法国 的Ｂｒｉｔｔａｎｙ等７所医院对病史小于１年的２７２例新 发病的关节炎患者进行前瞻性研究．应用这个标准 每６个月观察１次．在第２年末时评价分类标准的 准确性。在最后１次随访时，由５名专家作出诊断。 ２７２例新发病例共有９８例确诊为ＲＡ。其中初次符 合ＡＣＲ １９８７年ＲＡ分类标准的有６５例ｆ６６％），而 非ＲＡ有３１／１７２（１８％）达到了诊断标准。观察２年， ８５例符合分类标准。灵敏度为８７％。１７２例非ＲＡ 中有４３例ｆ２５％）达到ＡＣＲ １９８７年ＲＡ分类标准的 ４条标准。因而特异度只有７５％，其原因是ＡＣＲ １９８７年ＲＡ分类标准中没有排除标准。对于病史小 于１年的关节炎患者．该标准无法预测是否会发展 为ＲＡ。有些患者初次就诊符合标准，但２年后证实 并非ＲＡ。在另一项４８６例炎症性关节病的前瞻性 研究中发现，ＡＣＲ标准的灵敏度较好（７７％～８７％）。 但是在预测骨侵蚀的特异性方面很差。１９９０年在 英国Ｎｏｒｆｏｌｋ的Ｎｏｒｗｉｃｈ卫生专署机构调查了该地 ＲＡ的发病率。结果显示。第５年符合ＡＣＲ标准的 患病率与第１年相比，女性高出４５％，男性高出 ３６％。这说明ＡＣＲ １９８７年的ＲＡ分类标准对于１
ＡＣＲ
年内发病的关节炎灵敏度不够理想。人们希望在疾 病的早期作出诊断并给予早期治疗。以避免致残。 显然ＡＣＲｌ９８７年的ＲＡ分类标准不能满足这一要 求。对ＲＡ早期诊断、早期治疗、预防残废并保护关 节功能是努力争取的目标。但并非所有的ＲＡ患者 都需要联合使用ＤＭＡＲＤｓ和生物制剂。ＲＡ的治疗 应个体化，因此需对预后有效的评估。有少数ＲＡ 患者预后好，这些患者可能并不是真正的ＲＡ．不需 要用ＤＭＡＲＤｓｌ蝴。 新标准的背景、作用及内容 为发展新的ＲＡ分类标准，ＥＵＬＡＲ组织了“ＲＡ 早期疾病队列研究”（Ｉ期研究）。该研究针对分类 不明的炎性关节炎中那些高风险的慢性损伤。并且 迅速使用改善病程药物。参加单位有阿姆斯特丹、 维也纳、曼彻斯特、奥斯陆、利兹、荷兰莱顿、多伦多 等共９个团队，录入患者３ １１５例，条件是：①有炎
类风湿关节炎的诊断与治疗
• 病情活动度
• 预后不良相关的因素
达标治疗
2018中国类风湿关节炎诊疗指南
RA活动性判断
• 疲劳程度 • 晨僵持续时间 • 关节疼痛和肿胀的数目和程度
• 炎性指标：ESR、CRP
• DAS28 • 其他影响预后的因素：病程、躯体功能障碍(如HAQ 评分)、关节外表现、血清中自身抗体和HLADR1/DR4是否阳性，以及早期出现X线提示的骨破坏 等。
生物DMARDs治疗
1.TNF-a阻滞剂
– etanercept（益赛普、强克、安佰诺、恩利) – infliximab（类克） – adalimumab（修美乐）
2.IL-6单抗（雅美乐） 3.IL-1R拮抗剂 抗炎，防止骨质破坏，疗效确切 4.CTLA4-Ig融合蛋白 感染，昂贵 5.抗CD20单抗 6.JAK抑制剂（托法替布）
–患者血清自身抗体阴性，而血尿酸水平大多 增高。慢性患者可在关节周围和耳廓等部位 出现痛风石。
ห้องสมุดไป่ตู้
鉴别诊断
• 强直性脊柱炎
– 多见于男性青壮年
– 以非对称性的下肢大关节为主，骶髂关节及
脊柱受累明显。晚期脊柱呈竹节样改变，骶
髂关节间隙消失及骨性融合。 – 血清类风湿因子阴性， HLA-B27 90% 以上 阳性。
• 早期治疗 • 联合用药
• 方案个体化
• 功能锻炼 • 病人教育
治疗
• 一般治疗
–休息、关节制动及关节功能锻炼。
• 药物治疗
– 非甾体抗炎药（non-steroidal antiinflammatory drugs， NSAIDs） – 改善病情抗风湿药（disease modifying antirheumatic drugs，DMARDs）
类风湿关节炎诊断与治疗指南(2010年)
节半脱位，表现掌指关节向尺侧偏斜。除关节症状外， 还可出现皮下结节，称为类风湿结节；心、肺和神经 系统等受累。
第二页，共35页。
2.2 实验室检查
RA患者可有轻至中度贫血，红细胞沉降率 (ESR)增快、C反应蛋白(CRP)和血清IgG、 IgM、IgA升高，多数患者血清中可出现RF、 抗CCP抗体、抗修饰型瓜氨酸化波形蛋白 (MCV)抗体、抗P68抗体、抗瓜氨酸化纤维 蛋白原(ACF)抗体、抗角蛋白抗体(AKA)或抗 核周因子(APF)等多种自身抗体。这些实验 室检查对RA的诊断和预后评估有重要意义。
表1 RA x线分期
I期(早期) la.X线检查无骨质破坏性改变 ;X线显示骨质疏松，可有轻度的软骨破坏，伴或不
伴有 轻度的软骨下骨质破坏 ; 2a.可有关节活动受限，但 无关节畸形; 3.关节邻近肌肉萎缩; 4.有关节外软组织病变，
如结节或腱鞘炎
Ⅲ期(严重期)
4 对称性关节炎
左右两侧关节同时受累（两侧近端指间关节、掌指关节及跖
趾关节受累时，不一定绝对对称）
5 类风湿结节 医生观察到在骨突部位、促肌表面或关节周围有皮下结节
6 RF阳性
任何检测方法证明血清中RF含量升高（该方法在健
康人群中的阳性率 ＜5% )
7 影像学改变 在手和腕的后前位相上有典型的RA影像学改变：必须包括骨质侵蚀 或受累关节及其邻近部位有明确的骨质脱钙
概述
类风湿关节炎(rheumatoidarthritis．RA)是一种以侵蚀性
关节炎为主要表现的全身性自身免疫病。本病以女性多
发。男女患病比例约1：3。RA可发生于任何年龄， 以30～50岁为发病的高峰。我国大陆地区的RA患病率 约为0．32％-0．36％。本病临床表现多样，从主要的
2010类风关诊断标准
2010类风湿性关节炎诊断标准一、诊断标准概述类风湿性关节炎（RA）是一种慢性自身免疫性疾病，其主要特点是炎症性多系统损害，导致关节疼痛、肿胀和僵硬，并最终导致关节畸形。
RA的诊断通常基于临床、实验室和影像学检查的综合结果。
以下是2010年ACR/EULAR提出的类风湿性关节炎诊断标准。
二、疾病历史和家族史1. 至少一个关节肿胀或疼痛，持续至少6周；2. 至少一个关节活动受限或畸形；3. 炎症性滑膜炎的典型症状（如关节晨僵，活动后缓解，以及皮肤下的类风湿结节）；4. 类风湿因子（RF）阳性；5. 有RA的家族史。
注：满足以上至少四项可诊断为RA。
三、临床表现1. 关节表现：RA常影响多个关节，尤其是手足小关节，表现为肿胀、疼痛和僵硬。
随着病情发展，可出现关节活动受限、畸形和功能受损。
2. 系统表现：RA可累及身体其他器官和系统，如皮肤、眼睛、肺、心脏、血管等。
常见症状包括疲劳、体重减轻、发热、盗汗、贫血等。
四、实验室检查1. 类风湿因子（RF）：RF是一种自身抗体，在约70%的RA患者中可检测到。
但RF阳性并不一定意味着RA的诊断，因为其在其他自身免疫性疾病和感染性疾病中也可能出现。
2. 抗瓜氨酸抗体（ACAs）：包括抗CCP抗体和抗AKA抗体。
这些抗体在RA患者中具有较高的特异性，有助于早期诊断。
3. 其他实验室指标：包括血沉（ESR）、C反应蛋白（CRP）、白细胞计数等，这些指标可反映疾病活动度。
五、影像学检查1. X线检查：X线平片可显示关节炎症、增生和畸形等病变。
2. 超声检查：关节超声可用于评估滑膜炎的严重程度和治疗效果，且具有无创、便捷的优势。
3. MRI检查：MRI对软组织的显示能力优于X线和超声，可更早地发现关节病变。
六、病理学检查1. 滑膜活检：通过关节镜或切开手术获取滑膜组织样本进行病理检查，可观察到RA特征性的滑膜病理改变。
2. 皮下结节活检：类风湿结节是RA的典型表现，对其活检可显示类风湿性肉芽肿。
类风湿关节炎病证结合诊疗指南
类风湿关节炎病证结合诊疗指南1范围本《指南》规定了类风湿关节炎的流行病学、诊断要点、辨证论治、中成药选择、外治疗法、预防调摄、治疗推荐等。
本《指南》适用于类风湿关节炎病证结合诊断和治疗。
2规范性引用文件下列文件对于本规范的应用是必不可少的。
凡是注明日期的引用文件，仅所注明日期的版本适用于本规范。
凡是不注明日期的引用文件，其最新版本（包括所有的修改版本）适用于本文件。
证据推荐级别及证据水平，参照[1]2001年牛津证据分级与推荐意见强度。
GB/T1.1-2009《标准化工作导则第1部分：标准的结构和编写》《中医药标准制定管理办法（试行）》GB/T16751.1-1997《中医临床诊疗术语-疾病部分》GB/T16751.2-1997《中医临床诊疗术语-证候部分》2015American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis3术语及定义下列术语和定义适用于本规范。
3.1病证结合Combination of Diseaseand Syndrome辨病与辨证相结合的研究模式，主要是指现代医学诊断疾病结合辨证论治模式。
3.2药品不良反应adverse drug reaction，ADR合格药品在正常用法用量下出现的与用药目的无关的有害反应。
4流行病学类风湿关节炎（Rheumatoid arthritis,RA）是一种以对称性多关节炎为主要临床表现的自身免疫性疾病，以关节滑膜慢性炎症、关节的进行性破坏为特征。
目前发病原因不明，可能与遗传、免疫、感染、环境等因素有关，该病属于中医风湿病（痹证、痹病）范畴，中医诊断为“尪痹”[2]。
RA几乎见于世界所有的地区和各种族；目前患病人数约占世界总人口的1.0%，中国的发病率大约为0.28-0.4%[3]。
RA可以发生于任何年龄，女性高发年龄为45～54岁，男性随年龄增加而发病率上升，男女罹患本病的比例约为1:3[4]。
2010ACR EULAR 类风湿诊断指南
ARTHRITIS&RHEUMATISMVol.62,No.9,September2010,pp2569–2581DOI10.1002/art.27584©2010,American College of Rheumatology2010Rheumatoid Arthritis Classification CriteriaAn American College of Rheumatology/European League Against RheumatismCollaborative InitiativeDaniel Aletaha,1Tuhina Neogi,2Alan J.Silman,3Julia Funovits,1David T.Felson,2Clifton O.Bingham,III,4Neal S.Birnbaum,5Gerd R.Burmester,6Vivian P.Bykerk,7Marc D.Cohen,8Bernard Combe,9Karen H.Costenbader,10Maxime Dougados,11Paul Emery,12Gianfranco Ferraccioli,13Johanna M.W.Hazes,14Kathryn Hobbs,15Tom W.J.Huizinga,16Arthur Kavanaugh,17Jonathan Kay,18Tore K.Kvien,19Timothy Laing,20 Philip Mease,21Henri A.Ménard,22Larry W.Moreland,23Raymond L.Naden,24 Theodore Pincus,25Josef S.Smolen,1Ewa Stanislawska-Biernat,26Deborah Symmons,27 Paul P.Tak,28Katherine S.Upchurch,18JirˇíVencovsky´,29Frederick Wolfe,30and Gillian Hawker31This criteria set has been approved by the American College of Rheumatology(ACR)Board of Directors and the Euro-pean League Against Rheumatism(EULAR)Executive Committee.This signifies that the criteria set has been quantita-tively validated using patient data,and it has undergone validation based on an external data set.All ACR/EULAR-approved criteria sets are expected to undergo intermittent updates.The American College of Rheumatology is an independent,professional,medical and scientific society which does not guarantee,warrant,or endorse any commercial product or service.Objective.The1987American College of Rheuma-tology(ACR;formerly,the American Rheumatism As-sociation)classification criteria for rheumatoid arthri-tis(RA)have been criticized for their lack of sensitivity in early disease.This work was undertaken to develop new classification criteria for RA.Methods.A joint working group from the ACR and the European League Against Rheumatism devel-This article is published simultaneously in the September 2010issue of Annals of the Rheumatic Diseases.Supported by the American College of Rheumatology and the European League Against Rheumatism.1Daniel Aletaha,MD,MSc,Julia Funovits,Dipl.Ing,Josef S. Smolen,MD:Medical University of Vienna,Vienna,Austria;2Tuhina Neogi,MD,PhD,FRCPC,David T.Felson,MD,MPH:Boston University School of Medicine,Boston,Massachusetts;3Alan J.Sil-man,FRCP,FmedSci,DSc(Hons):Arthritis Research UK,Chester-field,UK;4Clifton O.Bingham,III,MD:Johns Hopkins University,Baltimore,Maryland;5Neal S.Birnbaum,MD:California PacificMedical Center and University of California,San Francisco;6Gerd R.Burmester,MD:Charite´Hospital–University Medicine Berlin,FreeUniversity and Humboldt University Berlin,Berlin,Germany;7VivianP.Bykerk,MD,FRCPC:Mount Sinai Hospital and University ofToronto,Toronto,Ontario,Canada;8Marc D.Cohen,MD:NationalJewish Medical and Research Center,Denver,Colorado;9BernardCombe,MD,PhD:Lapeyronie Hospital and Montpellier I University,Montpellier,France;10Karen H.Costenbader,MD,MPH:Brighamand Women’s Hospital and Harvard University,Boston,Massachu-setts;11Maxime Dougados,MD:Cochin Hospital,Assistance PubliqueHoˆpitaux de Paris,and Paris-Descartes University,Paris,France; 12Paul Emery,MD,MA,FRCP:University of Leeds and NIHR Leeds Musculoskeletal Biomedical Research Unit,Leeds,UK;13GianfrancoFerraccioli,MD:School of Medicine,Catholic University of theSacred Heart,Rome,Italy;14Johanna M.W.Hazes,MD,PhD:Erasmus Medical Center,University Medical Center Rotterdam,andUniversity of Rotterdam,Rotterdam,The Netherlands;15KathrynHobbs,MD:University of Colorado School of Medicine,Denver;Arthritis&Rheumatism An Official Journal of the American College of Rheumatology and 2569oped,in3phases,a new approach to classifying RA.The work focused on identifying,among patients newly presenting with undifferentiated inflammatory synovi-tis,factors that best discriminated between those who were and those who were not at high risk for persistent and/or erosive disease—this being the appropriate cur-rent paradigm underlying the disease construct“rheu-matoid arthritis.”Results.In the new criteria set,classification as “definite RA”is based on the confirmed presence of synovitis in at least1joint,absence of an alternative diagnosis that better explains the synovitis,and achieve-ment of a total score of6or greater(of a possible10) from the individual scores in4domains:number and site of involved joints(score range0–5),serologic abnormality(score range0–3),elevated acute-phase response(score range0–1),and symptom duration(2 levels;range0–1).Conclusion.This new classification system rede-fines the current paradigm of RA by focusing on fea-tures at earlier stages of disease that are associated with persistent and/or erosive disease,rather than defining the disease by its late-stage features.This will refocus attention on the important need for earlier diagnosis and institution of effective disease-suppressing therapy to prevent or minimize the occurrence of the undesir-able sequelae that currently comprise the paradigm underlying the disease construct“rheumatoid arthri-tis.”IntroductionRheumatoid arthritis(RA)is a chronic inflam-matory disease characterized by joint swelling,joint tenderness,and destruction of synovial joints,leading to severe disability and premature mortality(1–5).Given16Tom W.J.Huizinga,MD,PhD:Leiden University Medical Centre, Leiden,The Netherlands;17Arthur Kavanaugh,MD:University of California,San Diego;18Jonathan Kay,MD,Katherine S.Upchurch, MD:UMassMemorial Medical Center and University of Massachu-setts Medical School,Worcester;19Tore K.Kvien,MD,PhD:Diakon-hjemmet Hospital,Oslo,Norway;20Timothy Laing,MD:University of Michigan,Ann Arbor;21Philip Mease,MD:Swedish Medical Center and University of Washington,Seattle;22Henri A.Me´nard,MD: McGill University Health Centre and McGill University,Montreal, Quebec,Canada;23Larry W.Moreland,MD:University of Pittsburgh, Pittsburgh,Pennsylvania;24Raymond L.Naden,MB ChB,FRACP: Ministry of Health,Auckland,New Zealand;25Theodore Pincus,MD: New York University Hospital for Joint Diseases,New York,New York;26Ewa Stanislawska-Biernat,MD,PhD:Institute of Rheumatol-ogy,Warsaw,Poland;27Deborah Symmons,MD,FFPH,FRCP: University of Manchester,Manchester,UK;28Paul P.Tak,MD,PhD: Academic Medical Center,University of Amsterdam,Amsterdam, The Netherlands;29Jirˇı´Vencovsky´,MD,DSc:Institute of Rheumatol-ogy,Prague,Czech Republic;30Frederick Wolfe,MD:National Data Bank for Rheumatic Diseases and University of Kansas,Wichita; 31Gillian Hawker,MD,MSc,FRCPC:Women’s College Hospital and University of Toronto,Toronto,Ontario,Canada.Dr.Aletaha has received consulting fees,speaking fees, and/or honoraria from Abbott,Bristol-Myers Squibb,UCB,Schering-Plough,Wyeth,and Roche(less than$10,000each).Dr.Bingham has received consulting fees,speaking fees,and/or honoraria from UCB, Roche,Genentech,Celgene,and Merck Serono(less than$10,000 each);he has received research and/or educational grant support from Bristol-Myers Squibb,Genentech,UCB,Centocor,Abbott,and Am-gen.Dr.Birnbaum has received consulting fees,speaking fees,and/or honoraria from Amgen,Pfizer,Centocor,Abbott,and UCB(less than $10,000each).Dr.Burmester has received consulting fees,speaking fees,and/or honoraria from Abbott,Bristol-Myers Squibb,Pfizer, UCB,and Roche(less than$10,000each).Dr.Bykerk has received consulting fees,speaking fees,and/or honoraria from Amgen,Wyeth, Abbott,Schering-Plough,Roche,Bristol-Myers Squibb,and UCB(less than$10,000each);her spouse is employed by Genzyme and owns stock in the company.Dr.Cohen has received consulting fees, speaking fees,and/or honoraria from UCB,Genentech,Bristol-Myers Squibb,and Human Genome Sciences(less than$10,000each).Dr. Combe has received consulting fees,speaking fees,and/or honoraria from Abbott,Bristol-Myers Squibb,Pfizer,Roche,Schering-Plough, and Merck,Sharpe,and Dohme(less than$10,000each).Dr.Emeryhas received consulting fees,speaking fees,and/or honoraria from Pfizer,Abbott,Centocor,UCB,Roche,Bristol-Myers Squibb,and Merck,Sharpe,and Dohme(less than$10,000each).Dr.Ferraccioli holds a patent for T cell receptor clonotype analysis(PCT/IB2008/ 053152NP).Dr.Huizinga has received consulting fees,speaking fees, and/or honoraria from Schering-Plough,Bristol-Myers Squibb,UCB, Biotest AG,Wyeth/Pfizer,Novartis,Roche,Sanofi-Aventis,Abbott, and Axis-Shield(less than$10,000each).Dr.Kavanaugh has con-ducted clinical research for Amgen,Abbott,Bristol-Myers Squibb, UCB,Roche,Centocor,Genentech,and Sanofi-Aventis.Dr.Kay has received consulting fees from Array BioPharma,Bristol-Myers Squibb, Celgene,Centocor,Genentech,Roche,UCB,and Sanofi-Aventis(less than$10,000each).Dr.Mease has received consulting fees,speaking fees,and/or honoraria from Abbott,Amgen,Biogen Idec,Bristol-Myers Squibb,Centocor,Roche,Genentech,UCB,Pfizer,Novartis, and Eli Lilly(less than$10,000each).Dr.Me´nard has received un-restricted educational and research grants as well as consulting and speaking fees from Abbott,Amgen,Inova,Merck,Pfizer,Roche, Schering-Plough,UCB,and Wyeth(less than$10,000each)and investigator-initiated research grants from Bristol-Myers Squibb,Euro-Immun AG,and Roche(more than$10,000each);he owns stock or stock options in Merck;and he has a license agreement with Euro-Immun AG for an anti-Sa enzyme-linked immunosorbent assay.Dr. Moreland has received consulting fees,speaking fees,and/or honoraria from Biogen Idec,Centocor,Pfizer,Takeda,KaloBios,ChemoCen-tryx,UCB,Genentech,Incyte,and Eli Lilly(less than$10,000each). Dr.Naden has received consulting fees from the American College of Rheumatology in regard to the methodology of developing weighted scoring systems(more than$10,000).Dr.Pincus has received consult-ing fees,speaking fees,and/or honoraria from Amgen,Abbott,Bristol-Myers Squibb,Centocor,UCB,Wyeth,and Genentech(less than $10,000each)and investigator-initiated research grants from Amgen, Bristol-Myers Squibb,UCB,and Centocor.Dr.Stanislawska-Biernat has received speaking fees from Abbott and Pfizer(less than$10,000 each).Dr.Vencovsky´has received speaking fees from Pfizer,UCB, Abbott,Roche,and Merck,Sharpe,and Dohme(less than$10,000 each).Address correspondence and reprint requests to Alan J. Silman,MD,FRCP,Arthritis Research UK,Copeman House,Ches-terfield S417TD,UK.E-mail:a.silman@.Submitted for publication January22,2010;accepted in revised form May20,2010.2570ALETAHA ET ALthe presence of autoantibodies,such as rheumatoid factor(RF)and anti–citrullinated protein antibody (ACPA)(tested as anti–cyclic citrullinated peptide[anti-CCP]),which can precede the clinical manifestation of RA by many years(6–9),RA is considered an auto-immune disease(10,11).Autoimmunity and the overall systemic and articular inflammatory load drive the de-structive progression of the disease.However,although structural changes,which can be visualized by conven-tional radiography or other imaging techniques,best distinguish RA from other arthritic disorders(12),joint damage is rarely apparent in the very early stages of disease,but rather accumulates consistently over time (13–16).Over the last decade,the optimal use of disease-modifying antirheumatic drugs(DMARDs),in particu-lar the anchor DMARD methotrexate(MTX)(17–19), and the availability of new biologic agents(11,20),have dramatically enhanced the success of RA management. Moreover,it has been recognized that early therapeutic intervention improves clinical outcomes and reduces the accrual of joint damage and disability(21–23).Undoubt-edly,treating patients at a stage at which evolution of joint destruction can still be prevented would be ideal. However,at present,clinical trials of RA treatments are hampered by lack of criteria allowing for study enroll-ment of patients at early stages of disease.Thus,to date it has not been possible to effectively investigate the efficacy of early interventions in terms of their ability to prevent later-stage RA,since there are no validated or accepted uniform criteria to classify such individuals with early disease.The standard and accepted means of defining RA is by use of classification criteria.Classification criteria enable the stratification of groups of individuals into those with and those without RA in order to standardize recruitment into clinical trials and related studies,and provide the basis for a common approach to disease definition that can be used to compare across studies and centers.The classification criteria set that is in widespread international use to define RA is the1987 American College of Rheumatology(ACR;formerly the American Rheumatism Association)criteria(24).These criteria are well accepted as providing the benchmark for disease definition,but have a significant limitation in that they were derived by trying to discriminate patients with established RA from those with a combination of other definite rheumatologic diagnoses.They are there-fore not helpful in achieving the goal of identifying patients who would benefit from early effective interven-tion,as discussed above.Indeed,with modern therapies,the goal is to prevent individuals from reaching the chronic,erosive disease state that is exemplified in the 1987criteria for RA.A joint working group of the ACR and the European League Against Rheumatism(EULAR)was therefore formed to develop a new approach for classi-fication of RA.While classification criteria are poten-tially adopted for use as aids for diagnosis,the focus of this endeavor was not on developing diagnostic criteria or providing a referral tool for primary care physicians. Indeed,a separate body of work is needed to develop such tools,which may be informed by classification criteria.Thus,the specific charge was to develop new classification criteria for RA to facilitate the study of persons at earlier stages of the disease.It was with this framework in mind that the working group developed the2010ACR/EULAR classification criteria for RA. Overview on hypothesis and methods of Phases1and2A priori,the working group focused on develop-ing an approach that would be appropriate for newly presenting patients with undifferentiated inflammatory synovitis,in order to identify that subset of patients who are at sufficiently high risk of persistent and/or erosive disease—this being the appropriate current paradigm underlying the disease construct“rheumatoid arthritis”—to be classified as having RA.It was recog-nized that such a scheme should not be developed using existing criteria sets as the“gold standard,”because of the inherent circularity.The goal set forth was to develop a set of rules to be applied to newly presenting patients with undifferentiated synovitis that would1) identify the subset at high risk of chronicity and erosive damage;2)be used as a basis for initiating disease-modifying therapy;and3)not exclude the capture of patients later in the disease course.To achieve these goals,the working group de-vised a3-phase program.Phase1was a data-driven approach based on cohorts of real-world patients with early arthritis,to identify factors,and their relative weights,that were associated with the subsequent deci-sion by a physician to start MTX treatment.Phase2was a consensus-driven,decision science–based approach, informed by the data from Phase1,to refine these factors and their weights using a series of“paper pa-tients,”as well as to identify any other factors that may be of relevance based on current clinical thinking.Phase 3,which is the focus of this report,describes the derivation,from the previous2phases,of the finalACR/EULAR CLASSIFICATION CRITERIA FOR RA2571classification criteria set.The details of the methods and results from Phases1and2are provided elsewhere (25,26),and are briefly summarized below.Phase1.The aim of Phase1was to identify the contributions of clinical and laboratory variables that in practice were the most predictive of the decision to initiate DMARD therapy in a population of patients with early undifferentiated synovitis.Initiation of DMARD therapy was used as an indicator of the physician’s opinion that the patient was at risk of developing persistent and/or erosive arthritis that we would currently consider to be RA.Data on3,115 patients from9early arthritis cohorts who were consid-ered not to have evidence of another possible diagnosis explaining their presentation were obtained.Between July2007and November2008an expert working group developed an analysis strategy that related an agreed-upon list of standardized clinical and laboratory vari-ables collected at baseline to the initiation of DMARD treatment within the next12months.MTX initiation was used as the gold standard for this purpose.The analytical process aimed to identify the independent contribution of each variable on this list and included univariate regression modeling,a subsequent principal components analysis,and a multivariate regression model that included all identified components(25).The resulting list of informative variables identified during that process and the weights based on the odds ratios are shown in Table1.Phase2.Phase2consisted of a consensus-based, decision science–informed approach,which took place between November2008and June2009.The purpose of this phase was to derive a clinician-based judgment on the relative contribution of clinical and laboratory fac-tors deemed to be important in influencing the proba-bility of developing“persistent inflammatory and/or erosive arthritis that is currently considered to be RA”(hereinafter referred to as“developing RA”).An expert panel was assembled,comprising12 rheumatologists from Europe and12from North Amer-ica with extensive experience in the diagnosis and man-agement of RA.They provided real-life case scenarios of patients with early undifferentiated inflammatory arthri-tis representing low to high probability of developing RA.A2-day workshop was held in May2009in which domains(factors)and categories within those domains that were important in determining the probability of developing RA were identified.When appropriate, these judgments were informed by the results of Phase1 and other available literature.The relative importance or weights of these domains and their categories were determined by means of decision science theory and conjoint adaptive technology,using the computerized 1000Minds program()in an inter-active and iterative process(26).This analysis permitted the calculation of an individual’s score of the likelihood of developing RA from0to100,where a higher score indicated greater likelihood of RA development.The domains,categories,and weights derived during that initial process are shown in Table2.Objectives,methods,and results of Phase3Objectives of Phase3.In Phase3the working group integrated the findings of the first2phases, refined the scoring system,and determined the optimal cut point to define“definite RA.”The goal of this final phase was to utilize the results of Phases1and2to develop a scoring system that would be applicable to newly presenting patients with undifferentiated inflam-matory arthritis to permit identification of those with a high probability of developing persistent and/or erosive RA.Being intended for use with newly presenting patients,the scoring system should be robust enough that it could be applied repeatedly during the early course of disease,such that a patient identified as not classifiable as having definite RA at initial presentation might be classified as having definite RA at a subsequent time point.The work was not aimed at classifying subjects with established disease,either active or inac-tive.However,the working group recognized that pa-tients may present for the first time with disease that is at a later stage and being treated.Thus,although it was not the explicit charge of the working group to provideTable1.Summary of Phase1results*Variable Comparison Relative weight†Swollen MCP joint Present vs.absent 1.5Swollen PIP joint Present vs.absent 1.5Swollen wrist Present vs.absent 1.6Hand tenderness Present vs.absent 1.8Acute-phase response Low-level abnormal vs.normal 1.2Highly abnormal vs.normal 1.7Serology Low-positive vs.negative 2.2(RF or ACPA)High-positive vs.negative 3.9*MCPϭmetacarpophalangeal;RFϭrheumatoid factor;ACPAϭantiϪcitrullinated protein antibody.†Derived from odds ratios from the multivariate regression model,and interpreted as the increase in the odds of having rheumatoidarthritis(RA)with as opposed to without the respective feature(e.g.,weight of1.5for swelling of proximal interphalangeal[PIP]jointsmeans that the odds of having RA is1.5-fold in patients with asopposed to patients without swelling of a PIP joint).2572ALETAHA ET ALrules for the classification of such patients,it is appro-priate to have a single criteria system that could be applied to all patients;these issues were addressed by the expert panel during Phase3.Determination of the optimal cut point for defi-nite rheumatoid arthritis.Determination of the optimal cut point to classify an individual as having definite RA was achieved using2complementary approaches,mir-roring the approaches used in the first2phases:data-informed and consensus-based.From the consensus-based approach,the expert panel was asked to examine the rankings of case scenarios based on the new scoring system and to indicate,in their opinion,the point at which the cases changed from“probable”to“definite”RA.Four cases were excluded due to missing domain information(nϭ2)or ineligibility(2cases were more likely another diagnosis).For the remaining50cases,the mean cut point defining definite RA was65.7(median66.1;range60.0–70.3)of a total possible score of100.A data-driven verification of that cut point was then attempted,in which the new scoring system was applied to3of the existing cohorts used for Phase1(the Etude et Suivi des Polyarthrites Indifferenciees Re-centes data set from France,the Norwegian data set,and the Rotterdam Early Arthritis Cohort data set from Rotterdam)(25).These cohorts were chosen based on the completeness of data and the collected variables, enabling calculation of the patients’probability scores at baseline.The disease characteristics of these cohorts were not substantively different from those of the re-maining cohorts(data not shown).The area under the curve(AUC)for the3 receiver operating characteristic(ROC)curves(which plot sensitivity against1Ϫspecificity for the range of scores)indicated good discrimination of those who did versus those who did not receive MTX(or another DMARD/biologic agent)within a year(AUC0.82for Norway,0.66for France,and AUC0.69for Rotterdam; PϽ0.0001for all).The probability scores similarly discriminated between those who fulfilled the1987ACR criteria at12months and those who did not(AUC for the ROC curves0.88[Norway],0.67[France],and0.72 [Rotterdam]).Visual inspection of the diagnostic test parameters associated with curves that used MTX initi-ation as the outcome showed a maximum slope for both the positive and negative likelihood ratios between a score of60/100and70/100,with flattening thereafter(67 in the Norway cohort,66in the French cohort,and66in the Rotterdam cohort).The cut point of60–70that was derived from expert consensus was therefore supported by these data.Given the consistency with the consensus-based approach,and to maximize sensitivity of the criteria,a cut point of60was deemed to be most appropriate.Rationale for the composition and weight of the final criteria.For development of the final criteria set, the results and weights from the comprehensive Phase2 process(26)were used as a starting point.Based onTable2.Summary of Phase2results and subsequent modificationsExact (0Ϫ100)Rescaled(0Ϫ10)Rounded to0.5(0Ϫ10)Joint involvement*1large000Ͼ1Ϫ10large,asymmetric10.2 1.021Ͼ1Ϫ10large,symmetric16.1 1.61 1.51Ϫ3small21.2 2.1224Ϫ10small28.8 2.883Ͼ10,including at least1small joint50.8 5.085Serology†Negative RF andnegative ACPA000Low-positive RF orlow-positive ACPA22.0 2.202High-positive RF orhigh-positive ACPA33.9 3.39 3.5Acute-phase reactants‡Normal CRP andnormal ESR000Abnormal CRP orabnormal ESR5.90.590.5Duration of symptoms§Ͻ6weeks000Ն6weeks9.30.931*Joint involvement refers to any swollen or tender joint on examina-tion.Distal interphalangeal joints,first carpometacarpal joints,andfirst metatarsophalangeal joints are excluded from assessment.Catego-ries of joint distribution are classified according to the location andnumber of the involved joints,with placement into the highest categorypossible based on the pattern of joint involvement.“Large joints”refers to shoulders,elbows,hips,knees,and ankles.“Small joints”refers to the metacarpophalangeal joints,proximal interphalangealjoints,second through fifth metatarsophalangeal joints,thumb inter-phalangeal joints,and wrists.“Symmetric”is defined as bilateralinvolvement of at least1region.In the category“Ͼ10joints,”at least1of the involved joints must be a small joint;the other joints caninclude any combination of large and additional small joints,as well asother joints not specifically listed elsewhere(e.g.,temporomandibular,acromioclavicular,sternoclavicular,etc.).†Negative refers to IU values that are less than or equal to the upperlimit of normal(ULN)for the laboratory and assay;low-positive refersto IU values that are higher than the ULN butՅ3times the ULN forthe laboratory and assay;high-positive refers to IU values that areϾ3times the ULN for the laboratory and assay.Where rheumatoid factor(RF)information is only available as positive or negative,a positiveresult should be scored as low-positive for RF.ACPAϭantiϪcitrullinated protein antibody.‡Normal/abnormal is determined by local laboratory standards.CRPϭC-reactive protein;ESRϭerythrocyte sedimentation rate.§Duration of symptoms refers to patient self-report of the duration ofsigns or symptoms of synovitis(e.g.,pain,swelling,tenderness)ofjoints that are clinically involved at the time of assessment,regardlessof treatment status.ACR/EULAR CLASSIFICATION CRITERIA FOR RA2573these categories and weights,we aimed in the final steps of the project to simplify the criteria in order to ensure that they were user friendly.We used the results of the data-driven Phase1as a guide for these adaptations,and verified at each step that the main properties of the criteria were not altered and that classification of pa-tients remained unchanged.The general steps toward simplification are shownTable3.The2010American College of Rheumatology/European League Against Rheumatism classi-fication criteria for rheumatoid arthritisScoreTarget population(Who should be tested?):Patients who1)have at least1joint with definite clinical synovitis(swelling)*2)with the synovitis not better explained by another disease†Classification criteria for RA(score-based algorithm:add score of categories A–D;a score ofՆ6/10is needed for classification of a patient as having definite RA)‡A.Joint involvement§1large joint¶02Ϫ10large joints11Ϫ3small joints(with or without involvement of large joints)#24Ϫ10small joints(with or without involvement of large joints)3Ͼ10joints(at least1small joint)**5B.Serology(at least1test result is needed for classification)††Negative RF and negative ACPA0Low-positive RF or low-positive ACPA2High-positive RF or high-positive ACPA3C.Acute-phase reactants(at least1test result is needed for classification)‡‡Normal CRP and normal ESR0Abnormal CRP or abnormal ESR1D.Duration of symptoms§§Ͻ6weeks0Ն6weeks1*The criteria are aimed at classification of newly presenting patients.In addition,patients with erosivedisease typical of rheumatoid arthritis(RA)with a history compatible with prior fulfillment of the2010criteria should be classified as having RA.Patients with longstanding disease,including those whosedisease is inactive(with or without treatment)who,based on retrospectively available data,havepreviously fulfilled the2010criteria should be classified as having RA.†Differential diagnoses vary among patients with different presentations,but may include conditions suchas systemic lupus erythematosus,psoriatic arthritis,and gout.If it is unclear about the relevant differentialdiagnoses to consider,an expert rheumatologist should be consulted.‡Although patients with a score ofϽ6/10are not classifiable as having RA,their status can be reassessedand the criteria might be fulfilled cumulatively over time.§Joint involvement refers to any swollen or tender joint on examination,which may be confirmed byimaging evidence of synovitis.Distal interphalangeal joints,first carpometacarpal joints,and firstmetatarsophalangeal joints are excluded from assessment.Categories of joint distribution are classifiedaccording to the location and number of involved joints,with placement into the highest category possiblebased on the pattern of joint involvement.¶“Large joints”refers to shoulders,elbows,hips,knees,and ankles.#“Small joints”refers to the metacarpophalangeal joints,proximal interphalangeal joints,second throughfifth metatarsophalangeal joints,thumb interphalangeal joints,and wrists.**In this category,at least1of the involved joints must be a small joint;the other joints can include anycombination of large and additional small joints,as well as other joints not specifically listed elsewhere(e.g.,temporomandibular,acromioclavicular,sternoclavicular,etc.).††Negative refers to IU values that are less than or equal to the upper limit of normal(ULN)for thelaboratory and assay;low-positive refers to IU values that are higher than the ULN butՅ3times the ULNfor the laboratory and assay;high-positive refers to IU values that areϾ3times the ULN for thelaboratory and assay.Where rheumatoid factor(RF)information is only available as positive or negative,a positive result should be scored as low-positive for RF.ACPAϭantiϪcitrullinated protein antibody.‡‡Normal/abnormal is determined by local laboratory standards.CRPϭC-reactive protein;ESRϭerythrocyte sedimentation rate.§§Duration of symptoms refers to patient self-report of the duration of signs or symptoms of synovitis(e.g.,pain,swelling,tenderness)of joints that are clinically involved at the time of assessment,regardlessof treatment status.2574ALETAHA ET AL。
类风湿关节炎治疗指南
治
疗
非药物治疗
NSAIDS
影响药物选择的因素： 有效性、 安全性、 便利性、 影响药物选择的因素 ： 有效性 、 安全性 、 便利性 、 费用。 费用。 RA患者出现严重NSAIDS副作用的可能性是OA的将近 患者出现严重NSAIDS副作用的可能性是OA的将近2 RA患者出现严重NSAIDS副作用的可能性是OA的将近2 倍 危险因素： 高龄（ 75岁 溃疡病史、 危险因素 ： 高龄 （ 75 岁 ） 、 溃疡病史 、 合用激素或 抗凝药、 大剂量、 多种NSAIDS 合用、 NSAIDS合用 抗凝药 、 大剂量 、 多种 NSAIDS 合用 、 严重的基础 病 高危人群的药物选择： 小剂量的强的松、 高危人群的药物选择 ： 小剂量的强的松 、 非乙酰化 水杨酸盐、高选择性COX 抑制剂、NSAID+胃保护 COX水杨酸盐、高选择性COX-2抑制剂、NSAID+胃保护 剂
来氟米特
研究表明来氟米特可作为MTX的替代药，特别是不 研究表明来氟米特可作为MTX的替代药 MTX的替代药， 能耐受MTX的副作用或对MTX反应不好的。 MTX的副作用或对MTX反应不好的 能耐受MTX的副作用或对MTX反应不好的。 减轻 RA 活动性和延缓 X 线进展的程度与中等剂量 减轻RA 活动性和延缓X MTX相当 对于用足量的MTX 相当。 MTX未获完全临床缓解 的 MTX 相当 。 对于用足量的 MTX 未获完全临床缓解 联用来氟米特有益。 的，联用来氟米特有益。 肠肝循环在来氟米特的代谢方面有重要作用 ， 因 肠肝循环在来氟米特的代谢方面有重要作用， 此其半衰期长。 不用推荐的消胆胺脂清洗的方法， 此其半衰期长 。 不用推荐的消胆胺脂清洗的方法 ， 药物的消除可能要2年的时间。 药物的消除可能要2年的时间。
类风湿性关节炎诊疗指南
类风湿性关节炎诊疗指南一、疾病概述类风湿性关节炎通常会侵犯双侧对称性的多个关节，尤其是手、足小关节。
其病因尚不明确，但可能与遗传、环境、感染、内分泌等多种因素有关。
在病理上，主要表现为滑膜炎症、增生，形成血管翳，侵犯关节软骨、骨和肌腱等组织，导致关节破坏和畸形。
二、临床表现1、关节症状疼痛：常为对称性、持续性疼痛，关节活动时疼痛加剧。
肿胀：关节周围软组织肿胀，可伴有关节积液。
晨僵：晨起时关节僵硬，活动后逐渐减轻，持续时间常超过 1 小时。
畸形：晚期可出现关节畸形，如掌指关节半脱位、手指向尺侧偏斜等。
2、关节外表现类风湿结节：常见于关节伸侧、受压部位或经常摩擦处。
肺部病变：如间质性肺炎、胸膜炎等。
心脏病变：心包炎较为常见。
眼部病变：巩膜炎、角膜炎等。
神经系统病变：周围神经受压引起的感觉和运动障碍。
三、诊断标准目前常用的诊断标准包括：1、关节晨僵至少 1 小时，持续 6 周以上。
2、有 3 个或 3 个以上关节肿胀，持续 6 周以上。
3、掌指关节、近端指间关节或腕关节肿胀，持续 6 周以上。
4、对称性关节肿胀，持续 6 周以上。
5、皮下类风湿结节。
6、手和腕关节的 X 线片显示有骨侵蚀或骨质疏松。
7、血清类风湿因子阳性（滴度>1:32）。
符合以上 7 项中的 4 项即可诊断为类风湿性关节炎，但应注意排除其他疾病。
四、检查方法1、实验室检查类风湿因子（RF）：约 70% 80%的患者 RF 阳性，但 RF 阳性不一定都是类风湿性关节炎，其他疾病如干燥综合征、系统性红斑狼疮等也可阳性。
抗环瓜氨酸肽抗体（抗 CCP 抗体）：对类风湿性关节炎的诊断具有较高的特异性。
红细胞沉降率（ESR）和 C 反应蛋白（CRP）：可反映疾病的活动程度。
血常规：可出现贫血、血小板增多等。
2、影像学检查X 线：早期可见关节周围软组织肿胀，骨质疏松；晚期可见关节间隙狭窄、关节面破坏、关节畸形等。
磁共振成像（MRI）：能更早期发现滑膜炎症、骨髓水肿等病变。
2010-ACREULAR-类风湿关节炎分类标准
2010 ACR/EULAR 类风湿关节炎分类标准发表时间：2010-09-18 发表者：张昌丽 (访问人次：310)目标人群：有下列表现的患者：1、有至少一个关节具有明确的临床滑膜炎（肿胀)【新标准目的在于给新症患者分类。
另外，具有侵蚀性疾病如类风湿关节炎典型表现，其病史符合2010标准的，应该分类为类风湿关节炎。
患者有长期疾病，包括那些疾病处于非活动期（经过治疗或未经治疗），基于回顾性的可以获得的资料，先前符合2010年标准的，也应分类为类风湿关节炎。
】2、具有滑膜炎，用其他疾病不能得到更好解释的【不同表现的患者鉴别诊断也不同，但是系统性红斑狼疮，银屑病关节炎和痛风应该可以包括在内。
如果不清楚应该考虑哪些相关的鉴别诊断，应该咨询风湿病学专家】RA分类标准（评分算法：A-D的项目评分相加；患者如果按下列标准评分≥6/10，明确诊断为类风湿性关节炎)【虽然患者评分不足6分的不能分类为类风湿关节炎，但是他们的状态可以再次评价，随着时间推移，可能会符合标准。
】A：受累关节【指的是查体时发现的任何肿胀或触痛的关节，可通过滑膜炎的影像学证据证实。
在评估中，远端指间关节，第一腕掌和第一跖趾关节除外。
关节分布的分类根据受累关节的位置和数量，划入最可能受累关节类目。
】- 1个大关节（0分）【大关节指的是肩关节，肘关节，髋关节，膝关节和踝关节】- 2-10大关节（1分）- 1-3小关节（有或没有大关节）（2分）【小关节指的是掌指关节，近端指间关节，2-5跖趾关节，拇指指间关节和腕关节】- 4-10小关节（有或没有大关节）（3分）-超过10个小关节（至少一个小关节）（5分)【在这一条中，至少一个受累关节必须是小关节；其他关节可以包括任何大的或额外的小关节的组合，如其他别处未特别列出的关节（颞颌关节，肩峰锁骨关节，胸锁关节）】B：血清学（至少需要1项结果）【阴性指的是低于或等于当地实验室正常值的上限。
低滴度阳性指的是国际单位值高于正常值上限，但是低于正常值上限3倍。
类风湿关节炎(含各种评分标准)
健康调查问卷（HAQ）的内容
穿衣和梳理： － 能自己穿衣吗？包括系鞋带和扣釦 － 能自己洗头吗？ 个人卫生： － 能自己洗澡并擦干身体吗？ － 能洗盆浴吗？ － 能自己上厕所吗？
触物： － 能触到头顶高度５斤重的物体并 把它拿下来吗？ － 能弯腰从地上拾起衣服吗？ 握物： － 能开小汽车车门吗？ － 能打开已开启过的罐头瓶吗？ － 能开关水龙头吗？
RA治疗药物百年进展
针对性药物开始于生物治疗
RA的药物治疗
（一）非甾体抗炎药：抗炎止痛 （二）慢作用抗风湿药：控制病情发展 （三）糖皮质激素：作为慢作用药起效前的“桥治疗” （四）生物制剂：针对特定细胞因子的靶向治疗
目前传统治疗药物和靶点
van Vollenhoven, R. F. Nat. Rev. Rheumatol. 2009;5: 531–541.
DAS28>3.2为活动，>5.1高度活动，<2.6缓解
病情改善的评估： 治疗反应良好：Δ DAS28> 1.2； 治疗反应一般：0.6<Δ DAS28<=1.2 治疗无反应： Δ DAS28 <= 0.6
DAS28(4) = (0.56*sqrt(t28) + 0.28*sqrt(sw28) + 0.70*Ln(ESR) + 0.014*GH DAS28(3) = [0.56*sqrt(t28) + 0.28*sqrt(sw28) + 0.70*Ln(ESR)]*1.08 + 0.16
3、增加ESR和CRP
4、废除晨僵、皮下结节、对称性关节炎 5、不再把“持续6周”作为必要条件
RA的相关评分
美国风湿病学学会（ACR20/50/70）推荐的核心标准
类风湿性关节炎诊疗指南
3.CT：CT检查可清晰显示RA关节周围软组织 肿胀及其密度改变，以及骨端关节面小的侵 蚀性破坏和骨质破坏。对需要分辨关节间隙、 椎间盘、椎管及椎间孔的RA患者可选用CT 检查。
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3.糖皮质激素
糖皮质激素(简称激素)能迅速改善关节肿 痛和全身症状。在重症RA伴有心、肺或神 经系统等受累的患者，可给予短效激素， 其剂量依病情严重程度而定。针对的关节 病变，如需使用，通常为小剂量激素(泼尼 松≤7.5 mg/d)仅适用于少数RA患者。
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影像学检查1
1.X线检查：双手、腕关 节以及其他受累关节 的X线片对本病的诊 断有重要意义。早期 X线表现为关节周围 软组织肿胀及关节附 近骨质疏松；随病情 进展可出现关节面破 坏、关节间隙狭窄、 关节融合或脱位。根 据关节破坏程度可将 X线改变分为4期。
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X线表现
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影像学检查2
临床上对于RA患者应强调早期应DMARDs。病 情较重、有多关节受累、伴有关节外表现或 早期出现关节破坏等预后不良因素者应考虑 2种或2种以上 DMARDs的联合应用。主要联 合用药方法包括甲氨蝶呤、来氟米特、羟氯 喹及柳氮磺胺吡啶中任意2种或3种联合，亦 可考虑环孢素A、青霉胺等与上述药物联合 使用。但应根据患者的病情及个体情况选择 不同的联合用药方法。
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流行病学
类风湿性关节炎在不同人群中的发病率在0.01%0.05%之间，患病率为0.18%-1.07%不等。其发病 具有一定的种族差异，印第安人高于白种人，白 种人高于亚洲黄种人。
ACR与EULAR2010年RA新标准解读
Access To cohorts 人群 临床表现
定义类风湿关节炎的表型
正常/ 无症状
临床前
可能是 未分化 未分化 关节炎 关节炎
类风湿 关节炎
类风湿关节炎病程演进
大型人群 抗CCP抗体 数据???? 初级医疗
生物标记 CCP RF 细胞因子 遗传学 临床数据
观察指标：
关节肿(28个关节) 关节压痛(28个关节) 血沉 CRP HAQ CCP RF
结果
寡关节(2-6个关节)肿胀和压痛OR值分别为2.9和2.0 多关节(7-28个关节)肿胀和压痛OR值分别为：5.2和 3.3 C反应蛋白的意义大于血沉 血清学CCP和RF有价值
HAQ对疾病预后有意义
新的诊断措施 1、MRI、超声 2、CCP抗体阳性率达82%，特异性>90%以
及GPI等 3、CRP 早期诊断成为可能！！
×
ACR/EULAR2010年RA新分类标准
关节炎以排除其它疾病为前提 强调CCP抗体和RF，增加急性相反应物 保留受累关节数和滑膜炎持续时间 废除晨僵、皮下结节、对称性关节炎三个
ACR1987年标准的特异性和敏感性
观察结果：
98例确诊为RA，其中初次符合ACR1987年标准的有65例 (66%)
非RA的31/172(18%)达到了ACR1987年标准 2年后有85例符合ACR1987年标准，敏感性为87% 2年后172例非RA中有43例(25%)达到2年后标准，特异性
EULAR2009
专家共识
有滑膜炎表现并且有放射影像学骨侵蚀证 据者应视为RA
专家推荐
以下两种病人应分类为RA: 符合两项强制标准的病人（至少一个关节
类风湿关节炎诊断治疗的指南
类风湿关节炎诊断治疗指南【概述】类风湿关节炎(Rheumatoid arthritis，RA)是一种病因不明的自身免疫性疾病，多见于中年女性，我国的患病率约为0.32-0.36%。
主要表现为对称性、慢性、进行性多关节炎。
关节滑膜的慢性炎症、增生形成血管翳，侵犯关节软骨、软骨下骨、韧带和肌腱等，造成关节软骨、骨和关节囊破坏，最终导致关节畸形和功能丧失。
【临床表现】1、症状和体征病情和病程有个体差异，从短暂、轻微的少关节炎到急剧进行性多关节炎均可出现。
受累关节以近端指间关节、掌指关节、腕、肘、肩、膝和足趾关节最为多见；颈椎、颞颌关节、胸锁和肩锁关节也可受累，并伴活动受限；髋关节受累少见。
关节炎常表现为对称性、持续性肿胀和压痛，常常伴有晨僵。
最为常见的关节畸形是腕和肘关节强直、掌指关节的半脱位、手指向尺侧偏斜和呈“天鹅颈”样及钮扣花样表现。
重症患者关节呈纤维性或骨性强直，并因关节周围肌肉萎缩、痉挛失去关节功能，致使生活不能自理。
除关节症状外，还可出现类风湿结节和心、肺、肾、周围神经及眼等内脏病变。
2、实验检查多数活动期患者有轻至中度正细胞性贫血，白细胞数大多正常，有时可见嗜酸性粒细胞和血小板增多，血清免疫球蛋白IgG、IgM、IgA可升高，血清补体水平多数正常或轻度升高，60%—80%患者有高水平类风湿因子（RF），但RF阳性也见于慢性感染（肝炎、结核等）、其他结缔组织病和正常老年人。
其他如抗角质蛋白抗体（AKA）、抗核周因子（APF）和抗环瓜氨酸多肽（CCP）等自身抗体对类风湿关节炎有较高的诊断特异性，敏感性在30%~40%左右。
3、X线检查为明确本病的诊断、病期和发展情况，在病初应摄包括双腕关节和手及（或）表1 类风湿关节炎X线进展的分期I期（早期）1* X线检查无破坏性改变2 可见骨质疏松II期（中期）1* 骨质疏松，可有轻度的软骨破坏，有或没有轻度的软骨下骨质破坏2* 可见关节活动受限，但无关节畸形3 邻近肌肉萎缩4 有关节外软组织病损，如结节和腱鞘炎III期（严重期）1* 骨质疏松加上软骨或骨质破坏2* 关节畸形，如半脱位，尺侧偏斜，无纤维性或骨性强直3 广泛的肌萎缩4 有关节外软组织病损，如结节或腱鞘炎IV期（末期）1* 纤维性或骨性强直2 III期标准内各条标准前冠有*号者为病期分类的必备条件双足X线片，以及其他受累关节的X线片。
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吡喃羧酸类 依托度酸(etodolac)
非酸性类 萘丁美酮(nabumetone) 昔康类 吡罗昔康(piroxicam) 氯诺昔康(lornoxicam) 美洛昔康(meloxicam) 磺酰苯胺类 尼美舒利(mincaulide) 昔布类 塞来昔布(celecoxib) 依托考昔(etoricoxib) 50
3.2 病情的判断
判断RA活动性的指标包括疲劳的程度、晨 僵持续的时间、关节疼痛和肿胀的数目和 程度以及炎性指标(如ESR、CRP)等。临床 上可采用DAS28等标准判断病情活动程度。 此外，RA患者就诊时应对影响其预后的因 素进行分析。这些因素包括病程、躯体功 能障碍(如HAQ评分)、关节外表现、血清中 自身抗体和HLA—DRl／DR4是否阳性，以 及早期出现x线提示的骨破坏等。
4．2药物治疗
4．2．1非甾体抗炎药(NSAIDs) 这类药物主要通过抑制环氧化酶(COX)活性，减少前列腺 素合成而具有抗炎、止痛、退热及减轻关节肿胀的作用， 是临床最常用的RA治疗药物(表5o NSAIDs对缓解患者的关 节肿痛，改善伞身症状有重要作用。其主要不良反应包括 胃肠道症状、肝和肾功能损害以及可能增加的心血管不良 事件。根据现有的循证医学证据和专家共识，NSAIDs使 用中应注意以下几点：①注重NSAIDs的种类、剂量和剂 型的个体化；②尽可能用最低有效量、短疗程；③一般先 选用一种NSAID。应用数日至I周无明显疗效时应加到足 量。如仍然无效则再换用另一种制剂，避免同时服用2种 或2种以上NSAIDs；④对有消化性溃疡病史者，宜用选择 性COX一2抑制剂或其他NSAID加质子泵抑制剂；
⑤老年人可选用半衰期短或较小剂量的NSAID； ⑥心血管高危人群应谨慎选用NSAID，如需使用， 建议选用对乙酰氨基酚或萘普生；⑦肾功能不全 者应慎用NSAIDs；⑧注意血常规和肝肾功能魄定 期监测。 NSAIDs的外用制剂(如双氯芬酸二乙胺乳胶剂、 辣椒碱膏、酮洛芬凝胶、吡罗昔康贴剂等)以及植 物药膏剂等对缓解关节肿痛有一定作用，不良反 应较少，应提倡在临床上使用。
2.3 影像学检查
2.3.1 x线检查：双手、腕关节以及其他受累 关节的x线片对本病的诊断有重要意义。早 期X线表现为关节周围软组织肿胀及关节附 近骨质疏松；随病情进展可出现关节面破 坏、关节间隙狭窄、关节融合或脱位。根 据关节破坏程度可将x线改变分为4期(表1)。
表1 RA x线分期
表3 ACR／EULAR2009年RA分类标准和评分系统
关节受累情况 受累关节情况 中大关节
得分(0-5分) 受累关节数 1 2-lO 0 1
小关节
4-10 至少1个为小关节 >10
1-3
3 5
2
血清学 RF或抗CCP抗体均阴性 RF或抗CCP抗体至少l项低滴度阳性
得分(O-3分) 0 2 3
2.2 实验室检查
RA患者可有轻至中度贫血，红细胞沉降率 (ESR)增快、C反应蛋白(CRP)和血清IgG、 IgM、IgA升高，多数患者血清中可出现RF、 抗CCP抗体、抗修饰型瓜氨酸化波形蛋白 (MCV)抗体、抗P68抗体、抗瓜氨酸化纤维 蛋白原(ACF)抗体、抗角蛋白抗体(AKA)或 抗核周因子(APF)等多种自身抗体。这些实 验室检查对RA的诊断和预后评估有重要意 义。
2 临床表现
2.1 症状和体征 RA的主要临床表现为对称性、持续性关节肿和足趾关节最为多见；同时， 颈椎、颞颌关节、胸锁和肩锁关节也可受累。中、 晚期的患者可出现手指的“天鹅颈”及“钮扣花” 样畸形，关节强直和掌指关节半脱位，表现掌指 关节向尺侧偏斜。除关节症状外，还可出现皮下 结节，称为类风湿结节；心、肺和神经系统等受 累。
2009年ACR和欧洲抗风湿病联盟(EULAR)提出了新的RA分类标准和评 分系统，即： 至少1个关节肿痛，并有滑膜炎的证据(临床或超声或MRI)；同时排除 了其他疾病引起的关节炎，并有典型的常规放射学RA骨破坏的改变， 可诊断为RA。 另外，该标准对关节受累情况、血清学指标、滑膜炎持续时间和急 性时相反应物4个部分进行评分，总得分6分以上也可诊断RA(表3)。
3.3 缓解标准
判断RA的缓解标准有多种。表4列出了ACR 提出的RA临床缓解的标准，但有活动性血 管炎、心包炎、胸膜炎、肌炎和近期因RA 所致的体质量下降或发热，则不能认为临 床缓解。
3.4 鉴别诊断
在RA的诊断中。应注意与骨关节炎、痛风性关节炎、血 清阴性脊柱关节病(uSpA)、系统性红斑狼疮(SLE)、干燥综 合征(Ss)及硬皮病等其他结缔组织病所致的关节炎鉴别。 3.4.1 骨关节炎：该病在中老年人多发，主要累及膝、髋等 负重关节。活动时关节痛加重，可有关节肿胀和积液。部 分患者的远端指间关节出现特征性赫伯登(Heberden)结节， 而在近端指关节可出现布夏尔(Bouchard)结节。骨关节炎 患者很少出现对称性近端指问关节、腕关节受累，无类风 湿结节，晨僵时间短或无晨僵。此外，骨关节炎患者的 ESR多为轻度增快，而RF阴性。x线显示关节边缘增生或 骨赘形成，晚期町由于软骨破坏出现关节间隙狭窄。
最大剂量（mg/d） 2400 180 1.2 200 1500 150 150 200 180 60
每次剂量（mg） 服药次数 (次 400-800 3 3 3 3 2 3 3 2 30-60 3
0.2 50 250-500 25-50 25-50
苯乙酸类 双氯芬酸(diclofenac) 吲哚乙酸类(indometacin) 舒林酸(srlindac) 18 阿西美辛(acenetacin)
3 诊断要点
3.1 诊断标准 RA的诊断主要依靠临床表现、实验室检查及影像学检查。典型病例按 1987年美国风湿病学会(ACR)的分类标准 (表2)诊断并不困难，但对于 不典型及早期RA易出现误诊或漏诊。对这些患者，除RF和抗CCP抗体 等检查外，还可考虑MRI及超声检查，以利于早期诊断。对可疑RA的 患者要定期复查和随访。
表2 1987年美国风湿病学会的RA分类标准
条件
定义
1 晨僵 2 ≥3个以上关节区的关节炎
关节及其周围僵硬感至少持续1h
3 4 5 6 7
医生观察到下列14个关节区（两侧的近端指间 关节、掌指关 节、 腕、肘、膝、踝及跖趾关节）中至少3个有软组织肿 胀或积液（不是单纯骨隆起） 手关节炎 腕、掌指或近端指间关节区中，至少有一个关节区 肿胀 对称性关节炎 左右两侧关节同时受累（两侧近端指间关节、掌指 关节及跖趾关节受累时，不一定绝对对称） 类风湿结节 医生观察到在骨突部位、促肌表面或关节周围有皮下结节 RF阳性 任何检测方法证明血清中RF含量升高（该方法在 健康人群中的阳性率 ＜5% ) 影像学改变 在手和腕的后前位相上有典型的RA影像学改变：必须包括 骨质侵蚀或受累关节及其邻近部位有明确的骨质脱钙 注：以上7条满足4条或4条以上并排除其他关节炎可诊断RA，条件1-4必须 持续至少6周(引自Arthrifis RheⅡm。1988，31：315—324)
类风湿关节炎诊断及 治疗指南
概述
类风湿关节炎(rheumatoidarthritis．RA)是一种以侵 蚀性关节炎为主要表现的全身性自身免疫病。本 病以女性多发。男女患病比例约1：3。RA可发生 于任何年龄，以30～50岁为发病的高峰。我国大 陆地区的RA患病率约为0．32％-0．36％。本病临 床表现多样，从主要的关节症状到关节外多系统 受累的表现，。病理表现为关节滑膜的慢性炎症、 血管翳形成，并出现关节的软骨和骨破坏，最终 可导致关节畸形和功能丧失。此外，患者尚可有 发热及疲乏等全身表现。血清中可出现类风湿因 子(RF)及抗环瓜氨酸多肽(CCP)抗体等多种自身抗 体。
I期(早期) la.X线检查无骨质破坏性改变 ; 2.可见骨质 疏松 Ⅱ期(中期) la.X线显示骨质疏松，可有轻度的软骨破坏， 伴或不伴有 轻度的软骨下骨质破坏 ; 2a.可有关节活动 受限，但无关节畸形; 3.关节邻近肌肉萎缩; 4.有关节 外软组织病变，如结节或腱鞘炎 Ⅲ期(严重期) 1a.X线显示有骨质疏松伴软骨或骨质破 坏; 2a.关节畸形，如半脱位。尺侧偏斜或过伸。无纤维性 或骨性强直; 3.广泛的肌萎缩4有关节外软组织病变，如 结节或腱鞘炎 Ⅳ期(终末期) la.纤维性或骨性强直;2.Ⅲ期标准内各条 注：a各期标准的必备条件(引自JaMA．1949。140：659— 662．)
7.3
24 4 20 2-5 11 22
1200
2000 20 16 15 400 400 120
200-400
1000 20 8 7.5-15 100-200 100-200 120 1
3
1 2 1 2 2 1
2.3.2 磁共振成像(MRI)：
MRI在显示关节病变方面优于x线，近年 已越来越多地应用到RA的诊断中。MRI可 以显示关节炎性反应初期出现的滑膜增厚、 骨髓水肿和轻度关节面侵蚀，有益于RA的 早期诊断。
2.3.3 超声检查：
高频超声能清晰显示关节腔、关节滑膜、 滑囊、关节腔积液、关节软骨厚度及形态 等，彩色多普勒血流显像(CDFI)和彩色多普 勒能量图(CDE)能直观地检测关节组织内血 流的分布，反映滑膜增生的情况，并具有 很高的敏感性。超声检查还可以动态判断 关节积液量的多少和距体表的距离，用以 指导关节穿刺及治疗。
RF或抗CCP抗体至少1项高滴度(>正常上限3倍)阳性 滑膜炎持续时间 <6周 >6厨
得分(O-1分) 0 1
急性时相反应物
CRP或ESR均正常
得分(O-1分)
0