Interactions

NSAIDs give scope for interaction, by differing pharmacodynamic and pharmacokinetic mechanisms, with:

• ACE inhibitors and angiotensin II antagonists: there is risk of renal impairment and hyperkalemia.

• Quinolone antimicrobials: convulsions may occur if NSAIDs are co-administered.

• Anticoagulant (warfarin) and antiplatelet agents (ticlopidine, Clopidogrel): reduced platelet adhesiveness and GI tract damage by NSAIDs increase risk of alimentary bleeding (notably with azapropazone). Phenylbutazone, and probably azapropazone, inhibit the metabolism of warfarin, increasing its effect.

• Antidiabetics: azapropazone and phenylbutazone inhibit the metabolism of sulphonylurea hypoglycaemics, increasing their intensity and duration of action.

• Antiepileptics: azapropazone and phenylbutazone inhibit the metabolism of phenytoin and sodium valproate, increasing their risk of toxicity.

• Antifungal: fluconazole raises the plasma concentration of, and thus risk of toxicity from, celecoxib.

• Antihypertensives: their effect is lessened due to sodium retention by inhibition of renal prostaglandin formation.

• Antivirals: ritonavir may raise plasma concentration of piroxicam; NSAIDs may increase haematological toxicity from zidovudine.

• Ciclosporin: nephrotoxic effect is aggravated by NSAIDs.

• Cytotoxics: renal tubular excretion of methotrexate is reduced by competition with NSAIDs, with risk of methotrexate toxicity (low-dose methotrexate given weekly avoids this hazard).

• Diuretics: NSAIDs cause sodium retention and reduce diuretic and antihypertensive efficacy; risk of hyperkalaemia with potassium-sparing diuretics; increased nephrotoxicity risk (with indomethacin, ketorolac).

• Lithium: NSAIDs delay the excretion of lithium by the kidney and may cause lithium toxicity.

Individual NSAIDs

The currently available NSAIDs exhibit a variety of molecular structures and it is usual to classify these drugs by their chemical class. Clinical trials in rheumatoid arthritis and osteoarthritis, however, rarely find substantial differences in response to average doses of NSAIDs whatever their structure, and this no doubt reflects their common mode of action. Some 60% of patients will respond to any NSAID and many of the remainder will respond to a drug from another group. A structural classification is nevertheless used here as it provides a logical framework; furthermore, specific toxicity profiles tend also to relate to chemical group (see below). Summary data on NSAIDs licenced in the UK are given in Table 15.2.

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