Skin reactions sulfonamides causing

Upon systemic distribution, many drugs evoke skin reactions that are caused on an immunological basis. Moreover, cutaneous injury can also arise from nonimmunological mechanisms. Cutaneous side effects vary in severity from harmless to lethal. Cutaneous reactions are a common form of drug adverse reaction. Nearly half of them are attributed to antibiotics or sulfonamides, and one-third to nonsteroidal anti-inflammatory agents, with many other pharmaceuticals joining the list... 

Severe adverse drug reactions with trimethoprim and co-trimoxazole are rare (12-14). This also applies to children (15). The adverse effects of co-trimoxazole correspond to those expected from a sulfonamide (16). In HIV-infected patients, adverse effects of co-trimox-azole are more frequent and more severe (17-19). Hematological disturbances due to co-trimoxazole include mild anemia, leukopenia, and thrombocytopenia, which may be due to folic acid antagonism. Serious metabolic disturbances that are associated with trimethoprim include hyperkalemia and metabolic acidosis. Trimethoprim can cause hypersensitivity reactions. However, with co-trimoxazole, the sulfonamide is generally believed to be more allergenic (12). Generalized skin reactions predominate. Other effects, such as anaphylactic shock, are extremely rare (20-22). Carcinogenicity due to trimethoprim or co-trimoxazole has not been reported. 

Immune vasculitis can also be induced by drugs. The sulfonamides, penicillin, thiouracil, anticonvulsants, and iodides have all been implicated in the initiation of hypersensitivity angiitis. Erythema multiforme is a relatively mild vasculitic skin disorder that may be secondary to drug hypersensitivity. Stevens-Johnson syndrome is probably a more severe form of this hypersensitivity reaction and consists of erythema multiforme, arthritis, nephritis, central nervous system abnormalities, and myocarditis. It has frequently been associated with sulfonamide therapy. Administration of nonhuman monoclonal or polyclonal antibodies such as rattlesnake antivenin may cause serum sickness. 

Except for drugs especially designed for local gastrointestinal (GI) effects (see Chapter 38), the sulfonamides are absorbed rapidly and well from the GI tract. Peak plasma levels are achieved in 2-6 hours, depending on the drug. Absorption from sites such as the vagina, respiratory tract, or abraded skin is unrehable, but sufficient drug may enter the body to cause toxic reactions in susceptible persons or to produce sensitization. 

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