COX-3, a splice variant of COX-1, has been suggested to be the site of action of paracetamol, but genomic and kinetic analysis indicates that this selective interaction is unlikely to be clinically relevant. There is considerable evidence that the analgesic effect of paracetamol is central and is due to activation of descending serotonergic pathways, but its primary site of action may still be inhibition of PG synthesis. The action of paracetamol at a molecular level is unclear but could be related to the production of reactive metabolites by the peroxidase function of COX-2, which could deplete glutathione, a cofactor of enzymes such as PGE synthase.
But mainly, Acetominophen is an antipyretic and analgesic, but it is not antiinflammatory, so it wouldn't be useful for Niacin induced flushing.
Acetaminophen acts by inhibiting the COX-3 in the CNS and hence decreasing the body temperature, but not on the peripheral COX-1 & 2. hence, Aspirin is the better choice
submitted by โlfsuarez(160)
When patients are given Nicotinic acid(Niacin) they are told to expect common side effects to occur such as warmth and redness. One can avoid these side effects by taking aspirin