Eurolac Drug Interactions

Concurrent treatment with probenecid is contraindicated because of increases in ketorolac trometamol plasma level and half-life. Because of an increased tendency to bleeding when oxpentifylline is administered concurrently, this combination is contraindicated. Concurrent treatment with lithium is contraindicated because there is a possible inhibition of renal lithium clearance, increased plasma lithium concentration, and potential lithium toxicity.
Ketorolac should not be used with other NSAIDs because of the potential for additive side effects.
Ketorolac trometamol is highly bound to human plasma protein (>99%) and binding is concentration-independent.
Because ketorolac trometamol is a highly potent drug and present in low concentrations in plasma, it would not be expected to displace other protein-bound drugs significantly.
Ketorolac trometamol did not alter digoxin protein binding.
In-vitro studies indicated that at therapeutic concentrations and above of salicylate (≥300 μg per mL), the binding of ketorolac trometamol was reduced from approximately 99.2 to 97.5%. Therapeutic concentrations of digoxin, warfarin, paracetamol, phenytoin and trometamol did not alter ketorolac trometamol protein binding.
There is no evidence in animal or human studies that ketorolac trometamol induces or inhibits the hepatic enzymes capable of metabolizing itself or other drugs. Hence Ketorolac would not be expected to alter the pharmacokinetics of other drugs due to enzyme induction or inhibition mechanisms.
In normovolemic healthy volunteers, ketorolac trometamol reduces the diuretic response to furosemide by approximately 20%, so particular care should be taken in patients with cardiac decompensation.
There is an increased risk of renal impairment when ketorolac trometamol is administered concurrently with ACE inhibitors, particularly in volume-depleted patients.
Caution is advised when methotrexate is administered concurrently, since some prostaglandin synthesis-inhibiting drugs have been reported to reduce the clearance of methotrexate, and thus, possibly enhance its toxicity.