Clinical Pharmacology of A nti-inflammatory Agents. RHEUMATIC DISEASES. Rheumatic diseases (rheumatism) are painful conditions that affect millions. These diseases cause inflammation, swelling, and pain in the joints or muscles.
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Clinical Pharmacology of Anti-inflammatory Agents
Venus Williams Diagnosed With Sjogren’s Syndrome
Propionic acid derivatives
Acetic acid derivatives
Enolic acid (Oxicam) derivatives
Fenamic acid derivatives
( Fenamates )
Selective COX-2 inhibitors (Coxibs)
The cell damage associated with inflammation acts on cell membranes to cause leukocytes to release lysosomal enzymes; arachidonic acid is then liberated from precursor compounds, and various eicosanoids are synthesized. The cyclooxygenase (COX) pathway of arachidonate metabolism produces prostaglandins, which have a variety of effects on blood vessels, on nerve endings, and on cells involved in inflammation. The lipoxygenase pathway of arachidonate metabolism yields leukotrienes, which have a powerful chemotactic effect on eosinophils, neutrophils, and macrophages and promote bronchoconstriction and alterations in vascular permeability.
The discovery of two cyclooxygenase isoforms (COX-1 and COX-2) led to the concept that the constitutive COX-1 isoform tends to be homeostatic in function, while COX-2 is induced during inflammation and tends to facilitate the inflammatory response. On this basis, highly selective COX-2 inhibitors have been developed and marketed on the assumption that such selective inhibitors would be safer than nonselective COX-1 inhibitors but without loss of efficacy.
The more an NSAID blocks COX-1, the greater is its tendency to cause ulcers and promote bleeding. Butcelecoxib (Celebrex), blocks COX-2 and has little effect on COX-1, and is therefore further classified as a selective COX-2 inhibitor. Selective COX-2 inhibitors cause less bleeding and fewer ulcers than other NSAIDs.