Abstract
In the pathogenesis of reactive arthritis, infection through the mucosal route and genetic susceptibility (HLA-B27) are the most important contributing factors. With regard to non-specific urethritis, most probably caused by Chlamydia trachomatis infection, the use of early antimicrobial therapy has been shown to be effective in preventing arthritic recurrences. When the arthritis has been initiated, short-term conventional antimicrobial therapy seems unable to modify the course of the ongoing disease. In patients with acute reactive arthritis, a prolonged (3-month) treatment with tetracycline shortens the duration of arthritis when triggered by Chlamydia trachomatis, while such treatment has not proved effective in enteroarthritis. In patients with chronic reactive enteroarthritis, a prolonged course of quinolones, such as ciprofloxacin, might be of benefit. Sulfasalazine, which has an effect in the acute exacerbations of ankylosing spondylitis, is probably also effective in chronic reactive arthritis. An antimicrobial effect can be one of the mechanisms by which sulfasalazine exerts its therapeutic effect. Follow-up studies are necessary to assess the influence of antibiotic therapy on the late prognosis of patients with reactive arthritis.
Published Version
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