Reactive Arthritis: Clinical Aspects and Medical Management

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History of reactive arthritis

Considering the many terms and eponyms used in the literature to describe this condition, a brief review of the history of ReA is warranted. Although many attribute the earliest description of ReA to Hans Reiter in 1916, when he described the clinical triad of arthritis, nongonococcal urethritis, and conjunctivitis in a German soldier after an episode of bloody diarrhea,4 the syndrome also was described by two French physicians (Fiessinger and Leroy) in that same year.5 Therefore, it often was

Epidemiology

The lack of a disease definition or specific diagnostic criteria for ReA makes epidemiologic studies problematic.19, 20 An epidemiologic discussion of ReA not only should include the typical analyses of incidence and prevalence but also an analysis of attack rate, which is of equal importance. Because only a percentage of subjects exposed to the known causative organisms of ReA develop the disease, the attack rate refers to that percentage. The incidence, prevalence, and attack rate of ReA vary

Clinical features

The clinical features of ReA are well described and generally congruent for the postvenereal and the postenteric forms. The acute and chronic symptoms can include articular, tendon, mucosal, cutaneous, ocular, and occasionally cardiac manifestations (Table 1) or systemic features (fever, malaise, and weight loss); the latter usually are confined to the acute stage. Symptoms typically start within 1 to 4 weeks of the initial infection. As in the case of chlamydiae, however, the inciting

Triggering microbes

The triggering microbes of ReA are gram-negative bacteria with a lipopolysaccharide (LPS) component of their cell walls. All of these bacteria, or their bacterial products, have been demonstrated in the synovial tissue or fluid of patients who have ReA. This has been demonstrated in several studies involving many different laboratories.48, 49, 50, 51, 52, 53, 54, 55, 56 It is apparent that the entire bacteria or bacterial components traffic to the joints of patients who have ReA. Once these

Triggering Microbes Persist

The triggering microbes and their associated molecular biology in relation to arthritis, specifically ReA, are discussed elsewhere in this issue in the article by Gerard and colleagues. A brief review is warranted. PCR technology occasionally has demonstrated the presence of chromosomal DNA from the known triggers in the synovial tissue of patients who have the postdysentery form of ReA.48, 52, 53, 54 Recent studies from many laboratories have demonstrated that Ct and Cpn, such as Mycobacterium

Diagnostic tests

There are diagnostic criteria available, but these are broad and rely on clinical symptoms only. The American College of Rheumatology criteria, published in 1981, require the presence of a peripheral arthritis occurring in association with urethritis or cervicitis.2 The Third International Workshop on Reactive Arthritis in 1995 requires a peripheral arthritis with sacroiliac involvement and a preceding gastrointestinal or genitourinary infection.3 The current American College of Rheumatology

Nonsteroidal Anti-Inflammatory Drugs

A breadth of clinical experience suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) help with the inflammatory arthritis associated with ReA, but there are no well-designed prospective trials analyzing their efficacy for this indication. Although helpful for the articular symptoms, they are not believed efficacious for the potential extra-articular symptoms of ReA. Data suggest that continuous use of NSAIDs might reduce radiographic progression for other types of SpAs, in particular

Summary

Although environmental exposures have been implicated as potential causes for nearly all chronic diseases, ReA is one of the few with a known bacterial trigger. This insight into disease initiation has led to significant advances in the pathophysiology of this condition. As disease pathophysiology often stays one step ahead of science, however, many of the mysteries that surrounded ReA remain unsolved, including the clinical implications of bacterial persistence. In similar fashion, HLA-B27 is

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