AIDS-associated Reiter's syndrome.

Classically, Reiter's syndrome was defined as a triad of arthritis, urethritis, and conjunctivitis. In 1981, the American Rheumatism Association revised its defining criteria for Reiter's syndrome as an episode of peripheral arthritis of more than 1 month's duration occurring in association with urethritis and/or cervicitis. Reiter's syndrome is also associated with mucocutaneous lesions. Reiter's syndrome was first described in association with the human immuno-deficiency virus (HIV) in 1987. The course of Reiter's syndrome in HIV is more severe, progressive, and refractory to treatment than in non-HIV-positive patients. The immunopathogenesis of Reiter's syndrome is linked to HLA-B27, which has been described as the disease susceptibility factor. The association of Reiter's syndrome and HLA-B27 positivity is 80%. Infectious agents may play a critical role in the initiation or perpetuation of Reiter's syndrome. It has been suggested that an amino acid sequence within the HLA-B27 molecule allows microbial peptides to bind and be presented to T cytotoxic cells (CD8), which results in a primary T cytotoxic cell response against various tissues. The role of the HIV in the pathogenesis of Reiter's syndrome is still being investigated. Human immunodeficiency virus may directly cause arthritis; it may increase the host's susceptibility to infection with arthritogenic organisms. Additionally, HIV infection increases the relative number of CD8 cells, which may play a key role in the pathogenesis of Reiter's syndrome. In this article, we present a case of Reiter's syndrome in an HLA-B27 and HIV-positive patient, and a review of the literature on the infectious, immunologic, and dermatologic aspects of Reiter's syndrome in HIV disease.