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NSAID drug metabolism

Impaired NSAID drug metabolism is believed to be caused by several genes. To assess the risk of having an impaired NSAID metabolism, these genes are grouped into a set called genoset. If you have a risk genoset then it means you have 3x higher risk for developing gastrointestinal bleedings or ulcers during treatment with NSAIDs. In this case, enzymes responsible for the clearance of NSAIDs are impaired, which causes gastrointestinal toxicity resulting in ulcers and bleeding.

NSAIDs used in Estonia and internationally:

Salicylates (Aspirin, Diflunisal, Salicylic acid, Salsalate)
Propionic acid derivatives (Ibuprofen, Dexibuprofen, Naproxen, Fenoprofen, Ketoprofen, Dexketoprofen, Flurbiprofen, Oxaprozin, Loxoprofen)
Acetic acid derivatives (Indomethacin, Tolmetin, Sulindac, Etodolac, Ketorolac, Diclofenac, Aceclofenac)
Enolic acid derivatives (Piroxicam, Meloxicam, Tenoxicam, Droxicam, Lornoxicam)
Coxibs (Celecoxib, Rofecoxib, Valdecoxib, Parecoxib, Etoricoxib, Lumiracoxib)
Fenamates (Mefenamic acid, Tolfenamic acid, Flufenamic acid, Meclofenamic acid)

If you have a risk genoset, then you should consult with your doctor about which NSAIDs to use and in what doses. NSAIDs can also increase bleeding through decreasing the ability of blood to clot. Therefore, people who are taking drugs that also increase bleedings, such as Warfarin, should avoid prolonged use of NSAIDs. Also, patients with rheumatoid arthritis are at high risk for developing gastrointestinal bleedings because of the prolonged use of NSAIDs.