Đăng xuất
Probenecid slows down the elimination of naproxen by competing for glucuronidation and biliary and tubular secretion. If these active substances are used concomitantly in the treatment of e.g. gout, a reduction in naproxen dosage and careful monitoring of the patient for possible adverse reactions are recommended.
Concomitant administration of antacid or cholestyramine can delay the absorption of naproxen but does not affect its extent.
Concomitant administration of food can delay the absorption of naproxen but does not affect its extent.
NSAIDs should not be used for 8–12 days after mifepristone administration as NSAIDs can reduce the effects of mifepristone.
Due to the high plasma protein binding of naproxen, patients simultaneously receiving hydantoins, anticoagulants, other NSAIDs, aspirin or a highly protein-bound sulphonamide should be observed for signs of overdosage of these drugs. Patients simultaneously receiving naproxen and a hydantoin, sulphonamide or sulfonylurea should be observed for adjustment of dose if required. No interactions have been observed in clinical studies with naproxen and anticoagulants or sulfonylureas, but caution is nevertheless advised since interaction has been seen with other non-steroidal agents of this class. Animal data indicate that NSAIDs can increase the risk of convulsions associated with quinolone antibiotics. Patients taking quinolones may have an increased risk of developing convulsions.
Concomitant use of bisphosphonates and NSAIDs may increase the risk of gastric mucosal damage.
Combination use with diuretics, ACE inhibitors and angiotensin II antagonists: NSAIDs may reduce the antihypertensive effect of diuretics and other antihypertensive drugs. In some patients with compromised renal function (e.g. dehydrated patients or elderly patients with compromised renal function) the coadministration of an ACE inhibitor or Angiotensin II antagonist and agents that inhibit cyclo-oxygenase may result in further deterioration of renal function, including possible acute renal failure, which is usually reversible. Therefore, the combination should be administered with caution, especially in the elderly. Patients should be adequately hydrated and consideration should be given to monitoring of renal function after initiation of concomitant therapy, and periodically thereafter. Diuretics may increase the renal toxicity of anti-inflammatory analgesics.
Furthermore, the effect of other antihypertensive drugs (beta blockers) may be reduced. This should be taken into account at the onset of antihypertensive medication.
Naproxen should not be used concomitantly with other anti-inflammatory analgesics as this may increase adverse effects.
Acetylsalicylic acid: Clinical pharmacodynamic data suggest that concomitant naproxen usage for more than one day consecutively may inhibit the effect of low-dose acetylsalicylic acid on platelet activity and this inhibition may persist for up to several days after stopping naproxen therapy. The clinical relevance of this interaction is not known.
Acetylsalicylic acid displaces naproxen from protein binding sites in plasma, which accelerates the elimination of naproxen.
Corticosteroids: Increased risk of a gastrointestinal ulcer or hemorrhage. If these drugs are used concomitantly, the patient's status should be monitored carefully.
Anticoagulants: Anti-inflammatory analgesics may enhance the effect of anticoagulants, such as warfarin.
Anti-platelet agents and selective serotonin reuptake inhibitors (SSRIs): Increased risk of gastrointestinal bleeding.
Significant interactions between naproxen and oral hypoglycaemic drugs or antiepileptics are unlikely. Naproxen has been shown to displace valproic acid from protein binding sites in plasma, but the clinical significance of this phenomenon is likely to be minor.
Serum digoxin concentrations should be monitored in patients with renal failure and on digitalis treatment, and the digoxin dose should be adjusted if needed if naproxen is added to or removed from the medication.
Naproxen slows down the elimination of lithium. Serum lithium concentrations should be monitored and the lithium dosage adjusted if needed, if naproxen is added to or removed from the patient's medication.
Naproxen may slow down the elimination of methotrexate, ciclosporin and aminoglycoside antibiotics (directly dependent on glomerular filtration) and increase their toxicity. Interaction is, however, unlikely in connection with a low-dose (at doses used in the treatment of rheumatic diseases) methotrexate treatment.
Naproxen may change plasma protein binding of tacrolimus and expose to renal toxicity. Caution is advised in combination use, and if possible, the drug doses should be adjusted based on serum concentration determinations.
Naproxen may change the metabolism of zidovudine. The clinical significance of this phenomenon is not known.
Naproxen may interfere with urinary tests for 17-ketogenic steroids and 5-hydroxy-indoleacetic acid (diagnostics in adrenal gland diseases). This is avoided by discontinuing naproxen 72 hours before sampling.
