反應性關節炎 (Reactive arthritis，簡稱ReA) 屬於血清陰性脊椎關節病變。發生病變的原因爲人體內經由腸道、泌尿系統、女性陰道或上呼吸道感染的病菌，經過抗原表現細胞之內處理與特殊的HLA alleles（如HLA-B27等）結合，表現於target之組織（如關節），而引發關節炎或關節周邊之軟組織發炎（如肌腱附著點發炎或黏液囊炎等）。常見引發 ReA 菌包括Chlamydia、Salmonella、Shigella、Yersinia、Campylobacter等。其中Chlamydia是以泌尿系統感染爲主，而其他的細菌則經由腸道感染進入體內。在兒童或年輕之成人可因上呼吸道鏈球菌感染而引發 ReA。因 ReA 病患 80%以上會出現 HLA-B27 基因，故 B27 或其他之基因如B7等，在ReA病變發生之過程扮演重要之角色。反應性關節炎其診斷仍是基於病人先前有明顯之泌尿道或腸道感染，經過2到4星期，引發周邊關節炎（或另有薦腸骨關節炎）。其治療仍以非類固醇抗發炎藥物(NSAID)爲主，常用者包括 indomethacin、diclofenac 或 naposin等。80% 左右之病患症狀可得到適度地改善，如 NSAIDs 使用無效，則可考慮 DMARDS，如 sulfasalazine 或 methotrexate 等，再無效，則近年來國外報告少數使用生物製劑 TNF-α 抑制劑，得到有效地治療效果。至於抗生素在 ReA 治療之結果，目前未有明顯之定論，需再作進一步研究，方可瞭解。

Reactive arthritis (ReA) is one of the seronegative spondyloarthropathy. The mechanism of the disease may be mediated through the following immunologic process: the specific HLA alleles (HLA-B27) on the antigen presenting cells may bind a pathogenic peptide which can be derived from some bacteria strains, e.g. microorganism coming from either gastrointestinal (Salmonella, shighella, Yersinia, Campylobacter, etc.) or genitourinary urinary (Chlamydia) or upper respiratory treat (strepotcoccus, etc.) and then present to T cells or targeting tissues. The major clinical features are peripheral arthritis, enthesitis and bursitis, etc. Since the prevalence rate of HLA-B27 was 80% in ReA, the disease can be referred as a genetic-determined disease. The diagnosis of ReA was based upon remote infection first, either through GU or GI tract and 2 to 4 weeks later developing arthritis or enthesitis. The infection must be definite. The treatment is mainly using nonsteroid anti-inflammatory drugs (NSAIDs), which includes indomethcacin, diclofenac, and naposin and 80% of patients can gain a substantial effect. If fail, disease modifying anti-rheumatic drugs (DMARDs) are considered. The most common drugs to use are methotrexate and sulfasalazine. When all medicines cannot suppress the clinical symptoms, recently, TNF-α inhibitors have been tried and a good efficacy was confirmed.