Which medications in the drug class Nonsteroidal anti-inflammatory drugs are used in the treatment of Scleritis?

Updated: Aug 29, 2019
  • Author: Manolette R Roque, MD, MBA, FPAO; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Answer

Nonsteroidal anti-inflammatory drugs

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions. Systemic therapy with NSAIDs, corticosteroids, and immunosuppressive agents, alone or in combination, may be effective in patients with noninfectious scleritis.

Ibuprofen (Motrin, Provil, Addaprin, Caldolor, Advil, Dyspel)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Indomethacin (Indocin, Tivorbex)

Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.

Naproxen (Naprosyn, Naprelan, Aleve, Anaprox DS)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Piroxicam (Feldene)

Decreases activity of cyclooxygenase, which, in turn, inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Celecoxib (Celebrex)

Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared to nonselective NSAIDs. Seek lowest dose for each patient.

Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates proinflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; may increase CSF IgG (10%).

Has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.


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