The main reason for using a “coxib” (Selective COX-2 inhibitor) rather than a nonselective COX-inhibitor (aspirin) is that the “coxib” (AIIMS Nov 2010)
|A||Are associated with a lower risk of gastric or duodenal ulcerations|
|B||Cure arthritis, rather than just given symptom relief|
|C||Effectively inhibit uric acid synthesis|
|D||Have a lower risk of cardiotoxicity|
a. Celecoxib and related drugs, by virtue of their selective COX-2 inhibition, do not interfere as much with synthesis of PGE, which normally suppresses a component of gastric acid secretion and mucus production.
b. Overall, then, the risks of gastric and duodenal ulcers are reduced. The selectivity also means that the COX-2 inhibitors do not interfere with the production of other eicosanoids, such as TXA. That is both good and bad, clinically.
c. COX-2 inhibitors don’t cause antiplatelet effects and increase the risk of excessive or spontaneous bleeding.
d. On the other hand, this lack of effect renders them unsuitable for causing antiplatelet-aggregatory effects, as might be wanted when we administer aspirin.
e. COX-2 inhibitors, like the nonselective alternatives, aren’t cures for arthritis; they just alleviate symptoms. Compared with (and like) aspirin and other older NSAIDs, they have no effect on uric acid metabolism or excretion and cause no cardiotoxicity, and their onsets of action are, over all, not faster.