Nonsteroidal anti-inflammatory drugs: prostaglandins, indications, and side effects

Abstract

For centuries, nonsteroidal anti-inflammatory drugs (NSAIDs) have been part of our clinical practice. They started out as drugs with anti-inflammatory and analgesic action, and gradually their use has been expanded to new therapeutic targets, some of which are unrelated to their primary mode of action. Today, our armamentarium includes a large range of compounds, attesting to their utility in the treatment of clinical pathologies ranging from pain and inflammation to prevention and treatment of cancer. On the other hand, although NSAIDs share many common properties, their use poses risks, and physicians should be cognizant of their subtle differences and potential complications. In this context, this review article presents insight into NSAIDs' pathophysiology and mode of action in the clinical setting, their indications, and their potential side effects.

The Incidence of Upper Gastrointestinal Complications of Non-Steroidal Anti-Inflammatory Drugs in Elderly Patients

“…Evidently, the most common side effect of NSAIDs use is gastrointestinal toxicity, which is the primary limiting factor for their use [10][11].…”

Inibidores seletivos da cox-2 na odontologia: limitações e efeitos adversos

“…This imbalance results in high blood pressure and risk of thrombus formation, which tend to increase with the progression of the treatment, with a higher incidence of ischemic events after a few months of use of these drugs [7,8,9].…”

“…Such events are a result of this selectivity that provides an unbalance between anti-and pro-thrombotic factors, with the action of thromboxane (TXA2) predominating at the expense of prostacyclin (PGI2), a potent vasodilator and platelet anti-aggregant, which triggers a series of cardiovascular complications. Among these drugs are the celecoxib, etoricoxib, valdecoxib, parecoxib and lumiracoxib [6,7,8,9].…”

NSAIDs induce peripheral antinociception by interaction with the adrenergic system

“…Many synthesis in inflamed tissues [28,29]. Other studies have demonstrated 49 that endogenous opioids and the NO/cGMP/KATP pathway may be 50 involved in the antinociceptive mechanisms of NSAIDs [2,20,25,31].…”

“…inhibition of cyclooxygenase activity and thus decreased 189 prostaglandin synthesis[28]. However, the profiles of the analgesic190 activities of dipyrone and diclofenac differ from those of other common 191 NSAIDs due to their direct antagonistic effects on PGE 2 -induced 192 hyperalgesia.…”