Rashes sulfonamides causing

Trimethoprim (Trimpex) interferes with the ability of bacteria to metabolize folinic acid, thereby exerting bacteriostatic activity. Trimethoprim is used for UTIs that are caused by susceptible microorganisms. Trimethoprim administration may result in rash, pruritus, epigastric distress, nausea, and vomiting. When trimethoprim is combined with sulfamethoxazole (Septra), the adverse effects associated with a sulfonamide may also occur. The adverse reactions seen with other anti-infectives, such as ampicillin, the sulfonamides, and cephalosporins, are given in their appropriate chapters. 

Note that in addition to the adverse events due to trimethoprim the combination trimethoprim-sulfamethoxazole may cause all of the untoward reactions associated with sulfonamides. In HIV positive patients the incidence of rashes can increase to 50%. Desensibilisation with increasing doses of co-trimoxazole has been successful. 

Serious adverse effects are rare except in AIDS patients. TMP-SMX can cause the same adverse effects as those associated with sulfonamide administration, including skin rashes, central nervous system (CNS) disturbances, and blood dyscrasias. Blood dyscrasias, hepatotoxicity, and skin rashes are particularly common in patients with AIDS. Most of the adverse effects of this combination are due to the sulfamethoxazole component. Trimethoprim may increase the hematological toxicity of sulfamethoxazole. Long-term use of trimethoprim in persons with borderline foUc acid deficiency, such as alcoholics and the malnourished, may result in megaloblastic anemia, thrombocytopenia, and granulocytopenia. 

Celecoxib is associated with fewer endoscopic ulcers than most other NSAIDs. Probably because it is a sulfonamide, celecoxib may cause rashes. It does not affect platelet aggregation at usual doses. It interacts occasionally with warfarin—as would be expected of a drug metabolized via CYP2C9. Adverse effects are the common toxicities listed above. 

Gastrointestinal distress frequently is caused by doses greater than 500 mg fom times a day, even with enteric-coated tablets. Painful and frequent micturition, albuminuria, hematuria, and rashes may result from doses of 4 to 8 g/day given for longer than 3 to 4 weeks. Once the urine is sterile, a high dose should be reduced. Because systemic methenamine has low toxicity at the typically used doses, renal insufficiency does not constitute a contraindication to the use of methenamine alone, but the acids given concurrently may be detrimental. Methenamine mandelate is contraindicated in renal insufficiency. CrystaUuria from the mandelate moiety can occur. Methenamine combines with sulfamethizole and perhaps other sulfonamides in the urine, which results in mutual antagonism. 

F. Toxicity of Trimethoprim Trimethoprim may cause the predictable adverse effects of an antifolate dmg, including megaloblastic anemia, leukopenia, and granulocytopenia. These effects are usually ameliorated by supplementary folinic acid. The combination of trimethoprim-sulfamethoxazole may cause any of the adverse effects associated with the sulfonamides. AIDS patients given TMP-SMZ have a high incidence of adverse effects, including fever, rashes, leukopenia, and diarrhea. 

Toxicity The toxic effects of sulfonamides include skin rashes, gastrointestinal distress, hemolysis, kidney damage, and drug interactions caused by competition for plasma protein binding sites. Pyrimethamine may cause folic acid deficiency when used in high doses. 

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