Scleritis Medication

Updated: May 09, 2017
  • Author: Manolette R Roque, MD, MBA, FPAO; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Corticosteroids

Class Summary

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Rayos)

Inhibits phospholipase A and Fc receptor expression, activates the glucocorticoid receptor, reduces cytokine production, suppresses lymphocyte function, and redistributes circulating leukocytes. Also potent inhibitors of angiogenesis and potent stabilizer of cell membranes.

Prednisolone (FloPred, Millipred, Millipred DP, Prelone, Veripred 20)

Corticosteroids act as potent inhibitors of inflammation. They may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative corticosteroids may be used in equivalent dosage.

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Immunosuppressive drugs

Class Summary

Inhibit specific immune system pathways.

Methotrexate (Trexall Rheumatrex, Otrexup, Rasuvo)

Inhibits DHFR, causing a block in the reduction of dihydrofolate to tetrahydrofolate. This inhibits the formation of thymidylate and purines; arrests DNA, RNA, and protein synthesis. Patients should take adjunctive folic acid therapy up to 1000 mg per day to avoid hematopoietic complications.

Azathioprine (Imuran, Azasan)

Interferes with DNA synthesis and inhibits lymphocyte proliferation.

Cyclophosphamide

Chemically related to nitrogen mustards. As an alkylating agent, the mechanism of action of the active metabolites may involve cross linking of DNA, which may interfere with growth of normal and neoplastic cells. Drug of choice for granulomatosis with polyangiitis or polyarteritis nodosa.

Cyclosporine (Neoral, Sandimmune, Gengraf)

Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions, such as delayed hypersensitivity. For children and adults, base dosing on ideal body weight.

Mycophenolate mofetil (CellCept, Myfortic)

Inhibits purine synthesis and proliferation of human lymphocytes. Promising published case report of 3 patients with resistant disease treated with mycophenolate mofetil. Reduced toxicity makes this regimen an attractive alternative.

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Monoclonal antibodies

Class Summary

Selective immunomodulators that affect specific aspects of the inflammatory pathways.

Adalimumab (Humira)

Subcutaneous recombinant human IgG1 monoclonal antibody specific for human TNF. Indicated to reduce inflammation and inhibit progression of structural damage in moderate-to-severe rheumatoid arthritis. Reserved for those who experience inadequate response to one or more DMARDs. Can be used alone or in combination with MTX or other DMARDs. Binds specifically to TNF-alpha and blocks interaction with p55 and p75 cell-surface TNF receptors.

Infliximab (Remicade)

Intravenous chimeric IgG1k monoclonal antibody that neutralizes cytokine TNF-alpha and inhibits its binding to TNF-alpha receptor. Reduces infiltration of inflammatory cells and TNF-alpha production in inflamed areas. Used with MTX in patients who have had inadequate response to MTX monotherapy.

Rituximab (Rituxan)

Indicated to reduce signs and symptoms for moderately-to-severely active rheumatoid arthritis in combination with MTX. For use in adults who have experienced an inadequate response to one or more TNF antagonist therapies. Antibody genetically engineered. Chimeric murine/human monoclonal antibody directed against the CD20 antigen found on surface of B lymphocytes. Focal leukoencephalopathy is a lethal rare side effect that must be considered.

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Nonsteroidal anti-inflammatory drugs

Class Summary

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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