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Home / Drugs / Starting with S / Salicylate-sodium
 
Salicylate-sodium
 

Sodium salicylate is a sodium salt of salicylic acid. It can be prepared from sodium phenolate and carbon dioxide under higher temperature and pressure. It is used in medicine as an analgesic and antipyretic. Sodium salicylate also acts as non-steroidal anti-inflammatory drug (NSAID) and induces apoptosis in cancer cells. It is also potential replacement for aspirin for people sensitive to it.
CategoriesNonsteroidal Anti-inflammatory Agents (NSAIAs)
Salicylates
PackagersJ
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indication

It is used in medicine as an analgesic and antipyretic. Sodium salicylate also acts as non-steroidal anti-inflammatory drug (NSAID)

pharmacology

Non-steroidal anti-inflammatory drugs such as Salicylate-sodium work by inhibiting the enzyme cyclooxygenase (COX), which converts arachidonic acid to prostaglandin H2 (PGH2). PGH2, in turn, is converted by other enzymes to several other prostaglandins (which are mediators of pain, inflammation, and fever)

mechanism of action

Salicylate-sodium is considered a non-selective COX inhibitor—that is, it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to be achieved mainly through inhibition of COX-2, whereas inhibition of COX-1 would be responsible for unwanted effects on platelet aggregation and the gastrointestinal tract. However, the role of the individual COX isoforms in the analgesic, anti-inflammatory, and gastric damage effects of NSAIDs is uncertain and different compounds cause different degrees of analgesia and gastric damage. Salicylate-sodium directly and irreversibly inhibits the activity of both types of cyclo-oxygenases (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. Salicylate may competitively inhibit prostaglandin formation. Salicylate's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms.

drug interactions

Betamethasone: The corticosteroid, betamethasone, may decrease the effect of the salicylate, salicylate-sodium.

Fludrocortisone: The corticosteroid, fludrocortisone, may decrease the effect of the salicylate, salicylate-sodium.

Gliclazide: The salicylate, salicylate-sodium, increases the effect of the sulfonylurea, gliclazide.

Glyburide: The salicylate, salicylate-sodium, increases the effect of the sulfonylurea, glibenclamide.

Hydrocortisone: The corticosteroid, hydrocortisone, may decrease the effect of the salicylate, salicylate-sodium.

Methazolamide: The salicylate, salicylate-sodium, at high dose increases the effect of the carbonic anhydrase inhibitor, methazolamide.

Methotrexate: The salicylate, salicylate-sodium, increases the effect and toxicity of methotrexate.

Prednisolone: The corticosteroid, prednisolone, may decrease the effect of the salicylate, salicylate-sodium.

Prednisone: The corticosteroid, prednisone, may decrease the effect of the salicylate, salicylate-sodium.

Probenecid: The salicylate, salicylate-sodium, decreases the uricosuric effect of probenecid.

Sulindac: Risk of additive toxicity (e.g. bleed risk). Salicylate-sodium may decrease the serum concentration of sulindac. Consider alternate therapy or monitor for changes in the therapeutic effects of sulindac and adverse effects of both agents if the interacting agent is initiated, discontinued or dose changed.

Triamcinolone: The corticosteroid, triamcinolone, may decrease the effect of the salicylate, salicylate-sodium.

Warfarin: The antiplatelet effects of sodium salicylate may increase the bleed risk associated with warfarin.