IMMUNE-RESPONSE TO SULFAMETHOXAZOLE IN PATIENTS WITH AIDS

Antibody- and cell-mediated responses to sulfamethoxazole (SMX) were a nalyzed in AIDS patients with or without a history of hypersensitivity and in negative controls. In 20 of 20 (P < 0.01) human immunodeficien cy virus (HIV)-seropositive patients with skin reactions to cotrimoxaz ole, we found SMX-specific antibodies, while only 9 of 20 and 17 of 20 HIV-seropositive patients without a history of hypersensitivity to co trimoxazole had SMX-specific immunoglobulin M (IgM) and IgG, respectiv ely. The levels of specific IgM and IgG were higher in patients with s kin reactions than in patients without reactions (IgM, 1.0 +/- 0.19 ve rsus 0.47 +/- 0.23 [P < 0.001]; IgG, 0.68 +/- 0.15 versus 0.47 +/- 0.1 4 [P < 0.001] [mean optical density values +/- standard deviations]). Seronegative controls with no history of exposure to sulfa compounds d id not have SMX-specific IgG or IgM antibodies, and controls with a hi story of intake of SMX with or without reactions had low levels of IgG and IgM. The SMX-specific IgG subclasses were exclusively IgG1 and Ig G3. None of the patients had detectable SMX-specific IgE or IgA antibo dies nor did they exhibit a cell-mediated response as measured by a ly mphocyte proliferation assay. Antibodies to SMX recognized N-acetyl-su Ifonamide, N-(2-thiazolyl)-sulfanilamide, sulfadiazine, and sulfisoxaz ole but did not recognize sulfanilamide or 3-amino-5-methyl isoxazole in an inhibition assay. It is not known whether the SMX-specific antib odies associated with hypersensitivity reactions to SMX in HIV-seropos itive patients have a pathogenic role in these reactions. Sulfanilamid e or 3-amino-5-methyl isoxazole, on the other hand, could be potential alternative therapies in HIV-seropositive patients with a history of skin reactions to SMX.