NSAIDs are among the most widely used and prescribed drugs in
the U.S. This class contains approximately 20 drugs that share inhibition
of the cyclooxygenase enzyme as a mechanism of action. Although
this class also contains acetaminophen and salicylates, these two
drugs possess unique toxicity and are considered in separate chapters
(see Chapter 183, Aspirin and Salicylates,
and Chapter 184, Acetaminophen). NSAIDs are
effective antipyretics, analgesics, and anti-inflammatory agents.
Because of their large therapeutic window, NSAIDs are relatively safe
agents with respect to acute ingestion and overdose, rarely producing
serious complications.1–3 Several agents
are now available without prescription (over the counter), and the
world sales for NSAIDs is reported to be $6 billion per
year in U.S. dollars.4
During 2008, the American Association of Poison Control Centers
received reports of 107,115 NSAID exposures (excluding aspirin and
acetaminophen) resulting in 65 (0.05%) major outcomes (life-threatening signs
and symptoms or significant residual disability).5 There
were 44 deaths where NSAIDs were mentioned and 5 deaths associated
with single exposure. This experience compares favorably with the
toxicity reported with isolated aspirin or acetaminophen ingestions
during 2008: 99,210 exposures with 84 deaths.5 It
should be remembered that poison center data are gathered passively
and likely underrepresent the true number of exposed persons. The
morbidity from NSAIDs in acute overdose is far overshadowed by complications
of NSAIDs at therapeutic doses, including GI bleeding, drug-induced
renal failure, and ischemic heart disease.6–8 Due
to an increased risk for cardiovascular disease with therapeutic
doses, the selective cyclooxygenase-2 inhibitors rofecoxib and valdecoxib were
withdrawn from the U.S. market in 2004 and 2005, respectively.
NSAIDs are structurally varied compounds with common therapeutic effects
(Table 185-1). With the exception of aspirin
and other salicylates, NSAIDs reversibly inhibit the enzyme cyclooxygenase,
which is responsible for the production of prostaglandins from arachidonic
acid (Figure 185-1). The anti-inflammatory
effect of NSAIDs is through the inhibition of prostaglandin production,
but they may also inhibit neutrophils via mechanisms unrelated to
prostaglandin. NSAIDs work as antipyretics through inhibition of prostaglandin
E2 in the hypothalamus. NSAIDs also appear to attenuate
prostaglandin-mediated hyperalgesia and local pain fiber stimulus.
Table 185-1 Classes
of Nonsteroidal Agents Available in the U.S.
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