Abstract

PIP: Nonsteroidal antiinflammatory agents (NSAID) are reviewed. Aspirin, indomethacin, and salicylate have all been shown to interfere or prevent the synthesis of prostaglandins (PGs), a main tissue inflammatory substance. However, an exception to the correlation of PG-synthetase inhibition with antiinflammatory activity has been noted with certain arylacetic acids. Studies on the role of lysosomes in the inflammation are criticized in this review, mainly because of improper understanding of the role of lysosomes in a physiological system. Since lysosomes are not a specific body, but an activator, attempts to isolate lysosomes to study functions are doomed to failure; i.e., a lysosome has no definition without the rest of its self-regulating system. NSAIDs work in 2 main ways; either via antiaggregation or antiinflammation. This may result in drug interactions between various types of NSAIDs. For example, simultaneous administration of aspirin with indomethacine did not produce an additive effect; rather they produced no effect in the rat paw edema test dissimilar to the action of either drug separately. However, hydrocortisone combined with another NSAID enhanced its antiinflammatory effects. Albumin binding theories of NSAID mechanism of action state that drugs are active only when albumin-bound because it has displaced tryptophane, or urate, or some other normally bound substance. The only way to discover an efficient antiinflammatory agent is to obviate the need for it by discovering the actual mechanism of inflammation, for when specific anti-etiologic therapy is developed, the need for treatment with NSAIDs is irrelevant.