patients with renal impairment, heart failure, hypertension, and edema. The use of NSAIDs is contraindicated in persons who have had a hypersensitivity reaction to salicylates or any other NSAID. Asthmatics are at particular risk for these reactions. NSAIDs should be used during pregnancy only if the potential benefit justifies the risk to the fetus.

A significant number of drug interactions are common to most of the NSAIDs. The likelihood of NSAID-induced GI toxicity is increased by concomitant treatment with corticosteroids (long term), other NSAIDs, bisphosphonates, or anticoagulants. Certain NSAIDs can also compete for protein binding sites with warfarin, compounding the risk of GI bleeding if these drugs are coprescribed. Agents that cause thrombocy-topenia (e.g., myelosuppressive antineoplastic drugs) can also increase the likelihood that NSAIDs will cause bleeding. NSAIDs can decrease the clearance of methotrexate, resulting in severe hematological and GI toxicity. This does not appear to be a significant problem with low-dose methotrexate used in the treatment of rheumatoid arthritis; however, higher methotrexate doses used in the treatment of psoriasis or cancer may produce this toxicity. NSAIDs, when used in conjunction with immunosuppressive agents, can mask fever and other signs of infection.

Because NSAIDs decrease prostaglandin synthesis in the kidney, these drugs can increase the nephrotox-

icity of agents such as aminoglycosides, amphotericin B, cidofovir, cisplatin, cyclosporine, foscarnet, ganciclovir, pentamidine, and vancomycin. NSAIDs can decrease the renal excretion of drugs such as lithium. NSAIDs can decrease the effectiveness of antihyper-tensive drugs such as p-blockers and diuretics.The elderly and those with decreased renal function are at particular risk for this interaction. Elevated hepatic enzymes and hepatic toxicity can occur with some drugs.

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