Explanation:
Reactive arthritis consists of a triad of nonspecific urethritis, conjunctivitis, and asymmetric arthritis, usually involving the large joints of the lower extremities. Genitourinary causes of reactive arthritis include Chlamydia or Ureaplasma. GI infections due to Salmonella, Shigella, Yersinia, Klebsiella, and Campylobacter can also cause reactive arthritis. Gout attacks are typically monoarticular and begin abruptly with the affected joint being exquisitely painful, warm, red, and swollen. These attacks often spontaneously resolve in 310 days. While the symptoms from pseudogout may mimic those of gout, they tend to be less painful and take longer to reach peak intensity. Gonococcal arthritis is seen more often in females, is associated with migratory arthralgia, tends to favor the upper limbs and knees and may be associated with cutaneous lesions (pustules). The absence of attacks and joint distribution makes gout and pseudogout less likely. The history of conjunctivitis and association with diarrhea makes the diagnosis of reactive arthritis more likely than resistant gonococcal arthritis. His clinical symptoms do not suggest ankylosing spondylitis, although if he was HLA-B27 positive he would be at increased risk of developing spondylitis. This patient has the classic symptoms and exposure risk (GI infection) to suggest reactive arthritis. For the articular symptoms, reduction of inflammation and restoration of function can be achieved with nonsteroidal antiinflammatories alone. A sufficient number of patients with reactive arthritis will not be HLA-B27 positive, thus rendering this test useless as a screening test. However, it may be useful when the clinical picture is incomplete (such as absence of antecedent infection or lack of extraarticular features). Once an antecedent infection has triggered reactive arthritis, it is unlikely that antibiotics will affect the course of the illness (except in the case of chlamydiaassociated urogenital disease where a trial of prolonged antibiotic therapy may be reasonable).
Systemic corticosteroids are usually ineffective in reactive arthritis, but may be tried for resistant disease or conditions such as AIDS in which cytotoxic therapy is contraindicated. Given the absence of skin lesions, penile discharge, or urogenital symptoms, one would be hard-pressed to challenge the patient's statement that he has not engaged in unprotected sex at the risk of jeopardizing the physicianpatient relationship. Reactive arthritis may be the first manifestation of HIV infection. Therefore, HIV antibody status should be determined when the appropriate risk factors and/or clinical features are present. As mentioned previously, systemic steroids are usually ineffective for reactive arthritis and, with the possibility of joint infection, would necessitate ruling out infection by arthrocentesis of the affected joints. Joint infection cannot be ruled out based on his presentation, and joint sepsis must be excluded prior to corticosteroid injection. The clinical presentation is classic for reactive arthritis, and the absence of systemic symptoms makes the likelihood of disseminated bacterial infection low. Indomethacin, at a dose of 150200 mg/day, is the prototypic NSAID medication for treatment of reactive arthritis. Doses higher than this are associated with significant GI complications and do not improve efficacy in a patient resistant to the standard dose. In the event that the patient does not respond to 200 mg of indomethacin or alternative NSAIDs, disease- modifying antirheumatic drugs (DMARD) such as methotrexate, azathioprine, or sulfasalazine may be used, provided that HIV test results are negative, as these immunosuppressants have been reported to precipitate the onset of AIDS in HIV-positive patients.