Sign Out
Other nonsteroidal anti-inflammatory drugs including COX-2 inhibitors and/or glucocorticoids and alcohol: Augmentation of gastrointestinal side effects, increased risk of gastrointestinal haemorrhage. Salicylic acid displaces ibuprofen from protein binding. Caution is recommended with concomitant use, as this may increase the risk of adverse gastrointestinal effects.
Acetylsalicylic acid (low dosage): Experimental data suggest that ibuprofen may inhibit the efficacy of low dose acetylsalicylic acid on platelet aggregation when used concomitantly. However, the data are limited and the extrapolation of ex vivo data to the clinical situation is uncertain.
Therefore, no clear conclusions can be drawn regarding the regular use of ibuprofen; a clinically relevant effect with the occasional intake of ibuprofen is unlikely (see Properties/Effects).
Probenecid, Sulfinpyrazone: The elimination of ibuprofen is delayed; the uricosuric effect of probenecid and sulfinpyrazone is attenuated.
Oral anticoagulants: Non-steroidal anti-inflammatory drugs may increase the effects of anticoagulants such as warfarin.
Platelet aggregation inhibitors and selective serotonin reuptake inhibitors: Increased risk of gastrointestinal haemorrhage.
Anti-diabetic medicinal products: Ibuprofen enhances the hypoglycemic effect of oral antidiabetic medication and insulin. It may be necessary to adjust the dosage.
Aminoglycosides: NSAID's may decrease the excretion of aminoglycosides.
Diuretics: The efficacy of furosemide and thiazide diuretics can be decreased, probably due to sodium retention, related to an inhibition of prostaglandin synthesis in the kidneys.
Anti-hypertensive agents: A weakening of the efficacy of anti-hypertensive drugs is to be expected. As a result, concomitant treatment with NSAIDs and ACE inhibitors or beta-blocker agents may increase the risk of acute renal insufficiency.
Histamine H2-receptor antagonists: A clinically meaningful interaction of ibuprofen with cimetidine or ranitidine has not been established.
Digoxin: The plasma concentration of digoxin may increase.
Phenytoin: The plasma concentration of phenytoin may increase.
Lithium: The plasma concentration of lithium may increase.
Methotrexate: Increased methotrexate toxicity.
Zidovudine: The concomitant use of zidovudine and ibuprofen increases the risk of haemarthrosis and haematoma in HIV (+) haemophilic patients.
Tacrolimus: The risk of nephrotoxicity may be increased with concomitant use of tacrolimus and ibuprofen.
Voriconazole and Fluconazole: Concomitant use of voriconazole, fluconazole and ibuprofen may lead to an increase in the exposure and plasma concentration of ibuprofen.
Mifepristone: Co-administration of NSAIDs may increase NSAID exposure. A decrease in the efficacy of mifepristone can occur theoretically due to the anti-prostaglandin properties of NSAIDs. Studies suggest that co-administration of ibuprofen on the same day prostaglandins are administered (or as needed), has no adverse influence on the action of mifepristone or on the clinical efficacy of the pregnancy termination.
Baclofen: Increased baclofen toxicity.
Chinolone: Co-administration of NSAIDs may increase the risk of seizures.
Ciclosporin: The toxic effect on kidneys may increase.
Herbal extracts: Ginkgo biloba may potentiate the risk of bleeding associated with NSAIDs.
Interactions with diagnostic tests: Bleeding time (bleeding time may be prolonged until 1 day after discontinuation of therapy);
Serum glucose concentration (may decrease);
Creatinine clearance (may decrease);
Hematocrit or hemoglobin (may decrease);
BUN, serum creatinine concentrations and kaliemia (may increase);
Liver function test (increase in transaminases).
