Piussan C, Pautard-Muchemble B, Pautard J C, Lenaerts C, Boudailliez B, Risbourg B
Sem Hop. 1984 Jan 12;60(1):52-62.
Reactive arthritis is arthritis in which, although the nature of the responsible infection is known or suspected upon serological grounds, attempts at recovering the pathogen from the synovial fluid have failed. One of the main pathogenetic problems is the multiplicity of etiologic agents. Some are exogenous and may be related to the articular tropism of certain microorganisms, to immunologic depression due to an antecedent or coincident infection, and to successive reinfections by the same pathogen or by others which may promote an exacerbation of the disease. Others are endogenous and attention should be given to the local or systemic presence of an antigen as well as, in some instances, to the persistence of residual forms of infecting agents, which are more readily demonstrated with current bacteriological and serological methods. Although reactive arthritis is to be distinguished from septic arthritis, it can no longer be clearly differentiated from the classical post-infectious rheumatism. Once it has been produced, the antigenic stimulation is responsible for an immunologic response which tends to check systemic extension but may also produce tissue damage in the host. Some patients have circulating immune complexes which may bind to the joint, thereby damaging it. In other patients, particularly those who are HLA B27 positive, host-pathogen cross-reactions are demonstrated. Actually, the most frequent pathogenetic sequence seems to be a combination of two or more of these mechanisms, as there are reasons to believe that presence of the pathogen in situ is not required for the persistence of the inflammatory process. Reactive arthritis was first reported in adults following either sexually transmitted urethritis due to chlamydiae, mycoplasma or gonococci, or hepatitis B or an intestinal infection due to Yersinia, Campylobacter, Shigella, Klebsiella or Salmonella. Later, it was described in pediatric patients, particularly in Scandinavia where, for genetic reasons, the HLA B27 group is prevailing. Reactive arthritis seems less frequent in caucasian ethnic groups and above all in Latin Americans among whom HLA B27 carriers are more uncommon; however, it must be pointed out that they have not been as extensively studied and that other etiologic factors may still remain to be discovered. The course and etiology of the different forms of arthritis share certain characteristics which have been determined through a better knowledge of these conditions: onset occurs one or several weeks after a respiratory, urinary or, most often in children, digestive infection. This episode is unremarkable or latent and often overlooked.(ABSTRACT TRUNCATED AT 400 WORDS)
反应性关节炎是一种关节炎,尽管根据血清学依据已知或怀疑其相关感染的性质,但从滑液中分离出病原体的尝试均告失败。主要的发病机制问题之一是病因的多样性。有些病因是外源性的,可能与某些微生物的关节嗜性、先前或同时发生的感染所致的免疫抑制以及同一病原体或其他病原体的连续再感染有关,这些再感染可能会促使疾病加重。其他病因是内源性的,应关注抗原在局部或全身的存在,以及在某些情况下感染因子残余形式的持续存在,目前的细菌学和血清学方法更容易证实这一点。尽管反应性关节炎应与化脓性关节炎相鉴别,但它已无法与经典的感染后风湿病明确区分。一旦产生抗原刺激,就会引发免疫反应,这种反应往往会抑制全身扩散,但也可能对宿主造成组织损伤。一些患者有循环免疫复合物,它们可能与关节结合,从而损害关节。在其他患者中,尤其是那些 HLA B27 阳性的患者,存在宿主 - 病原体交叉反应。实际上,最常见的发病机制似乎是这些机制中的两种或更多种的组合,因为有理由相信炎症过程的持续并不需要病原体在原位存在。反应性关节炎最早是在成人中报道的,继发于衣原体、支原体或淋球菌引起的性传播尿道炎、乙型肝炎或耶尔森菌、弯曲杆菌、志贺菌、克雷伯菌或沙门菌引起的肠道感染。后来,在儿科患者中也有描述,特别是在斯堪的纳维亚半岛,由于遗传原因,HLA B27 群体较为常见。反应性关节炎在白种人群体中似乎较少见,尤其是在拉丁美洲人中,HLA B27 携带者更为罕见;然而,必须指出的是,对他们的研究还不够广泛,可能仍有其他病因有待发现。不同形式关节炎的病程和病因具有某些共同特征,这些特征是通过对这些病症的更深入了解而确定的:发病发生在呼吸道、泌尿系统感染后一周或数周,或者在儿童中最常见的是消化系统感染后。这一发作并不明显或呈潜伏性,常常被忽视。