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Response to use of nonsteroidal analgesics. *Ibuprofen and celecoxib, respectively, were considered analgesics separately. †There was no information available about the choice of patient by better response to NSAID or placebo used. Data represent the number of patients who did not make use of supplementary rescue analgesia.

Box plots for visual analog scale (VAS) scores at 4, 5, and 6 hours after administration of study drug. Data are expressed as medians, percentiles, and ranges. *p < .05 compared with the placebo group; **p < .01 compared with the placebo group by Kruskal-Wallis H test and Mann-Whitney U test with Bonferroni correction.

Consumption of fentanyl up to 4, 5, and 6 hours after administration of study drug. Data are expressed as mean ± SD. *p < .05 compared with the placebo group; **p < .01 compared with the placebo group by non–repeated-measures analysis of variance and Student-Newman-Keuls test.

Synthesis and function of prostanoids. Perturbation of cell membranes can be mediated by diverse endogenous and exogenous stimuli. This triggers activity of phospholipase A₂, releasing arachidonic acid from the phospholipids making up the membrane. Two families of cyclooxygenases (COX-1 and COX-2) convert this fatty acid to a variety of so-called prostanoids that are unique to the particular cell or tissue and include prostaglandins, thromboxanes, and prostacyclin. Each of these prostanoids has specific physiological functions, some of which are listed in the table within this figure. Most nonsteroidal anti-inflammatory drugs (NSAIDs) are nonselective and inhibit both COX-1 and COX-2 families. Celecoxib (Celebrex) is representative of agents that selectively inhibit COX-2; it reduces pain and inflammation with little or no influence on gastric mucosa. However, this selective inhibition may promote greater synthesis of prostanoids derived from COX-1, including thromboxane-mediated effects leading to possible thrombotic events (eg, myocardial infarction, stroke). Arachidonic acid is also a substrate for lipoxygenase that catalyzes the formation of leukotrienes known for their anaphylactoid effects, including bronchospasm and upper airway edema. As NSAIDs inhibit the activity of cyclooxygenases, a greater portion of arachidonic acid can be converted to leukotrienes by lipoxygenase. This may not be tolerated by patients with atopy because they experience pseudoallergic syndromes.