Reactive arthritis
Inflammatory arthritis triggered by infection, often with eye and urinary involvement.
Reactive arthritis is an inflammatory arthritis that arises after an infection elsewhere in the body, often when the original infection has already resolved. It is notable as a seronegative spondyloarthropathy associated with the HLA-B27 gene and can present with a classic triad of arthritis, eye inflammation, and urogenital symptoms.
Quick Facts
- Field
- Rheumatology
Facts from the source article.
Did You Know?
- Patients with HIV have an increased risk of developing reactive arthritis.
- Reactive arthritis may be self-limiting, frequently recurring, chronic, or progressive; 15 to 50 percent of cases involve recurrent bouts of arthritis.
- The clinical mnemonic for reactive arthritis is 'Can't see, can't pee, can't climb a tree.'
Signs and symptoms
Symptoms generally appear within 1–3 weeks but can range from 4 to 35 days after the inciting episode. The classic triad includes conjunctivitis, nongonococcal urethritis, and asymmetric oligoarthritis. Urinary symptoms such as dysuria or increased frequency often appear first; men may develop prostatitis, and women cervicitis, salpingitis, or vulvovaginitis. Arthritis typically affects fewer than five joints, commonly the knees or sacroiliac joint, and may be additive or migratory. Enthesitis can cause heel pain, Achilles tendinitis, or plantar fasciitis. About 20 to 40 percent of men develop circinate balanitis. Keratoderma blennorrhagicum—small hard nodules on the soles or palms—is diagnostic when the classic triad is absent. Ocular involvement, usually mild bilateral conjunctivitis, occurs in about 50% of men with urogenital reactive arthritis and about 75% of men with enteric reactive arthritis; uveitis may also occur. Dactylitis, or sausage digit, is a distinctive feature. Mucocutaneous lesions include oral ulcers, recurrent aphthous stomatitis, geographic tongue, and migratory stomatitis.
Causes
Reactive arthritis is associated with the HLA-B27 gene and is triggered by a preceding infection. The most common trigger in the US is genital infection with Chlamydia trachomatis. Other bacteria include Ureaplasma urealyticum, Salmonella spp., Shigella spp., Yersinia spp., and Campylobacter spp. Shigella is the most common cause following diarrhea, while Chlamydia trachomatis is the most common cause following urethritis. The interaction between pathogen and immune system involves the innate immune response: synovial macrophages interact with the pathogen, initiating T-cell activation and release of proinflammatory cytokines. Synovial fluid cultures are negative, suggesting an autoimmune response involving cross-reactivity of bacterial antigens with joint tissues or deposition of bacterial antigens in the joints.
Diagnosis
Diagnosis is based on clinical presentation, dominated by arthritis in one or more joints causing pain, swelling, redness, and heat. Swabs of the urethra, cervix, and throat may be cultured, along with urine, stool, or synovial fluid. Non-specific tests such as C-reactive protein and erythrocyte sedimentation rate can support the diagnosis. A blood test for HLA-B27 is performed; about 75 percent of patients have this gene. No definitive diagnostic criteria exist, but the American College of Rheumatology has published sensitivity and specificity guidelines.
History
When the triad includes ophthalmic and urogenital manifestations, the eponym Reiter's syndrome is often applied, after German physician Hans Conrad Julius Reiter, who described the condition in a soldier during World War I. Many physicians have argued the eponym is undeserved due to Reiter's Nazi Party affiliation and involvement in forced human experimentation at Buchenwald concentration camp. The full triad was described by another physician in the 19th century, and names such as arthritis urethritica, venereal arthritis, and polyarteritis enterica had been used previously.
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