What Price Pain Relief?

Endurance training and chronic intermittent hypoxia modulate in vitro salicylate-induced hepatic mitochondrial dysfunction

“…Aspirin, of which salicylate is the active metabolite, is widely prescribed to decrease inflammation as well as in the treatment and prevention of cardiovascular diseases (Hochman and Shah, 2006;Juby and Davis, 2008). Aspirin can generate hepatotoxicity in a sub-set of patients (Juby and Davis, 2008) and, in fact, it has been demonstrated that salicylates have damaging effects on liver mitochondria causing uncoupling of oxidative phosphorylation (Charnock and Opit, 1962), structural alterations (Gutknecht, 1990), and calcium-induced MPTP Lemasters, 1996, 1997).…”

Association of Perioperative Use of Nonsteroidal Anti-Inflammatory Drugs With Postoperative Myocardial Infarction After Total Joint Replacement

“…1 Both nonselective and selective cyclooxygenase 2 inhibitors (COX2I) are associated with cardiovascular risk 2,3 and may impair bone healing and prosthesis fixation for total joint replacement. 4 COX2I agents, especially rofecoxib, 5 have received the most scrutiny for cardiovascular risk, but the US Food and Drug Administration requires a black box warning for cardiovascular risk for all nonselective NSAIDs.…”

COX‐2, but not COX‐1, activity is necessary for the induction of perforant path long‐term potentiation and spatial learning in vivo

“…Although there are conflicting reports of increased risk of cardiovascular toxicity (Hochman & Shah, 2006; Solomon et al , 2006), celecoxib remains on the market for the treatment of arthritis‐associated inflammation, and is preferred to non‐selective inhibitors such as aspirin because of its decreased ulcerogenic properties (Lai et al , 2005). Given accumulating evidence in animal models for a role of COX‐2 activity in learning and memory and normal synaptic function it would be interesting to test if such deficits are evident after long‐term use of COX‐2‐selective inhibitors by patients.…”