迷思破解：类风湿关节炎患者可发生痛风

华盛顿——在美国风湿病学会(ACR)年会上，Adlene Jebakumar博士报告的一项人群队列研究显示，类风湿性关节炎(RA)患者确实可发生痛风，只不过发生率低于一般人群。

Eric L. Matteson博士

这项研究纳入813例1980~2007年被诊断为RA的患者。根据临床标准(包括滑液中检出典型尿酸单钠晶体)或ACR前身美国风湿病学会的1977 标准进行诊断。纵向追踪所有患者的完整社区病历直至2012年4月或直至患者死亡或搬家。

在该队列中，537例(66%)为类风湿因子阳性，33%有类风湿结节，53%有侵蚀性关节病。在总共9771个随访人-年(平均每例RA患者12年)期间，22例患者发生根据临床标准诊断的痛风。大拇趾是最常见的痛风部位(12例/22例)。根据临床标准诊断的痛风的25年累计发生率为5.3%。在22例急性痛风患者中，9例存在典型细胞内尿酸单钠晶体；所有这些患者均在RA发生后罹患痛风。根据包括存在尿酸单钠晶体在内的临床标准诊断的痛风的25年累计发生率为1.3%。2008年1月1日，RA患者的痛风患病率为1.9%(11例/582例)，而根据美国全国健康与营养调查数据及采用年龄和性别特异性患病率得出的预期患病率为5.2%(30例)。

RA患者的痛风危险因素包括：老龄[危险比(HR)=1.5/增加10岁；P=0.04]、男性(HR=3.18；P=0.03)和肥胖(HR=3.5；P=0.03)。侵蚀性RA关节病患者的痛风风险较低(HR=0.24；P=0.03)。近几年来(1995~2007年)RA患者的痛风发生率高于以前(1980~1994年；HR=5.6；P=0.007)。

梅奥医院风湿病科主任Eric L. Matteson博士在接受采访时指出，在风湿病领域存在一个“迷思”，即RA患者不可能发生痛风，因此在遇到大脚趾热痛的RA患者时，风湿病科医生可能将此现象视为RA急性加重。该研究结果显示，大脚趾热痛可能提示痛风。最佳的做法是抽取脚趾关节滑液，检查有无晶体。在治疗RA患者的痛风时，可考虑使用强的松、阿那白滞素、别嘌呤醇或非布索坦。在一些患者中，可能会出现痛风治疗药物与RA治疗药物之间的相互作用问题。一些RA治疗药物或可解释为什么RA患者较少出现痛风急性加重。大剂量阿司匹林常用于治疗RA，其可显著降低尿酸水平。根据推测，放弃长期使用和大剂量使用非甾体类固醇可能是导致RA患者较多发生痛风急性加重的原因。

Jebakumar博士和Matteson博士均声明无相关经济利益冲突。

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By: SALLY KOCH KUBETIN, Internal Medicine News Digital Network

WASHINGTON – Gout does occur in patients with rheumatoid arthritis, though at a lower rate than in the general population, Dr. Adlene Jebakumar said at the annual meeting of the American College of Rheumatology.

This finding comes from a review of a population-based cohort of 813 people diagnosed with rheumatoid arthritis (RA) between 1980 and 2007. Diagnoses were made either clinically including typical monosodium urate crystal positivity in synovial fluid or 1977 criteria developed by an ACR precursor organization, the American Rheumatology Association criteria. All subjects were longitudinally followed through their complete community medical records until April 2012 or they died or moved away.
 
Of the study cohort, 537 (66%) were rheumatoid factor positive; 33% had rheumatoid nodules, and 53% had erosive joint disease. During 9,771 total person-years of follow-up (mean 12 years per RA patient), 22 patients developed gout as defined by clinical criteria. The great toe was the most common site of gout (12 of 22 patients). The 25-year cumulative incidence of gout diagnosed by clinical criteria was 5.3%. Typical intracellular monosodium urate crystals were present in 9 of 22 patients with acute gout; all had developed gout after the RA incidence date. The 25-year cumulative incidence of gout diagnosed by clinical criteria including presence of urate crystals is 1.3%. The prevalence of gout in RA on Jan 1, 2008, was 1.9% (11 of 582 patients) as opposed to expected prevalence of 5.2% (or 30 patients) based on National Health and Nutrition Examination Survey data using age and sex-specific prevalence rates.

Risk factors for gout in RA were: older age (hazard ratio, 1.5/10-year increase; P = .04), male sex (HR, 3.18; P = .03) and obesity (HR, 3.5; P = .03). The presence of erosive RA joint disease reduced the risk of gout (HR, 0.24; P = .03). Gout has become more common in patients diagnosed with RA in recent years (1995-2007) than in previous years (1980-1994; HR, 5.6; P = .007).

Dr. Eric L. Matteson noted in an interview that when an RA patient develops a hot and tender big toe, rheumatologists are likely to presume it is an RA flare. In part, this is because there is a myth in rheumatology that patients with RA cannot get gout, Dr. Eric L. Matteson noted in an interview. The literature contains reports of only 30 such cases. In fact, as the study findings show, that hot and tender toe may be gout. The best course of action is to aspirate the toe joint and look at the synovial fluid for crystals.

The treatment of gout in an RA patient can involve administration of prednisone, anakinra, allopurinol, or febuxostat. Drug-drug interactions between the agents used to treat gout and those for RA may be a problem in some cases.

Some of the treatments used in RA may explain why there are so few gout flares in RA patients. High doses of aspirin, which are an RA treatment, significantly lower uric acid levels. In what he described as being speculation, Dr. Matteson, chair of the department of rheumatology at the Mayo Clinic, Rochester, Minn., suggested that the "push away" from use of NSAIDs long term and in high doses to help manage RA may be resulting in more gout flares in these patients.

Dr. Jebakumar and Dr. Matteson reported having no relevant financial conflicts of interest.