Intermediate Uveitis Medication

  • Author: Robert H Janigian Jr, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Apr 29, 2011
 

Medication Summary

The goal is to suppress intraocular inflammation, which usually is accomplished with systemic corticosteroids. In some cases, this treatment is inadequate, and immunosuppressive or immune-modulating agents are required to control the disease. These agents can be used adjunctively with steroids or alone.

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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.

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Prednisone (Deltasone, Meticorten, Orasone)

 

Readily absorbed through the GI tract and inhibits phospholipase A2 (an enzyme that liberates arachidonic acid from phospholipids in the production of inflammatory mediators).

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Triamcinolone (Amcort)

 

A long-acting depo-steroid. For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Observe for ptosis or anterior dissection. Generic preparations appear to be equally efficacious compared to proprietary Kenalog.

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Prednisolone 1% (Pred Forte)

 

Has 3-5 times the anti-inflammatory action as hydrocortisone. Glucocorticoids inhibit the edema, fibrin deposition, capillary dilation and phagocytic migration of the acute inflammatory response. Steroids are also potent inhibitors of the inflammatory enzyme cascade, angiogenesis, and mast-cell degranulation. Steroids stabilize cell membranes.

Loteprednol etabonate binds to anti-inflammatory receptors 4.3 times more avidly than dexamethasone. Possible reduced risk of glaucoma due to ester substitution for ketone moiety at the 20 position on the steroid cholesterol ring. Shake well for susp (acetate).

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Immunosuppressives

Class Summary

Inhibit cell-mediated and (to a lesser degree) humoral immunity by arresting T-lymphocyte activity. The ultimate goal is to suppress inflammation.

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Cyclosporine (Sandimmune, Neoral)

 

A cyclic polypeptide produced as a fungus metabolite, capable of reversibly arresting the T-lymphocyte cell cycle in the G0 and G1 phases. Potent down-regulator of interleukin 2 production and receptor expression. Newer Neoral preparation is better absorbed and may require marked dosage reductions.

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Azathioprine (Imuran)

 

Antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. May decrease proliferation of immune cells, which results in lower autoimmune activity.

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Methotrexate (Folex PFS, Rheumatrex)

 

Antimetabolite that inhibits dihydrofolate reductase, thereby inhibiting DNA synthesis in rapidly replicating cells. Immunosuppressive actions may be related to reduction in cytokines. Available as 2.5-mg pills.

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Daclizumab (Zenepax)

 

A humanized monoclonal antibody blocking the IL-2 receptor alpha chain. Decreases inflammation by inhibiting IL-2 mediated biologic responses of activated lymphoid cells.

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Histamine H2-receptor antagonist

Class Summary

Reduces postprandial daytime and nighttime gastric acid secretion by about 50-80%. May increase gastromucosal defense and healing in acid-related disorders (ie, stress-induced ulcers) by increasing production of gastric mucus, increasing mucosal secretion of bicarbonate and gastric mucosal blood flow as well as increasing endogenous mucosal synthesis of prostaglandins. Histamine H2-receptor antagonists can be used prophylactically to prevent gastritis and ulcer disease in patients taking oral or intravenous corticosteroids.

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Cimetidine (Tagamet)

 

Used as prophylaxis against corticosteroid induced gastric and duodenal ulcer.

Consult with internist if patient has preexisting symptoms of GERD or peptic ulcer disease prior to beginning corticosteroid therapy.

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Ranitidine (Zantac)

 

Used as prophylaxis against corticosteroid-induced gastric and duodenal ulcer.

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Gastric pump inhibitors

Class Summary

Thought to be a gastric pump inhibitor in that it blocks the final step of acid production by inhibiting the H+/K+ -ATPase system at the secretory surface of the gastric parietal cell. Both basal and stimulated acid secretions are inhibited. Short-term (4-8 wk) treatment of active duodenal ulcer, active benign gastric ulcer, erosive esophagitis (all grades), and heartburn and other symptoms associated with GERD.

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Omeprazole (Prilosec)

 

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.

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Lansoprazole (Prevacid)

 

Inhibits gastric acid secretion.

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Esomeprazole magnesium (Nexium)

 

S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase enzyme system at secretory surface of gastric parietal cells.

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Contributor Information and Disclosures
Author

Robert H Janigian Jr, MD  Clinical Assistant Professor, Department of Surgery (Ophthalmology), Brown University Medical School

Robert H Janigian Jr, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, and Rhode Island Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Theodoros Filippopoulos, MD  Head of Glaucoma Clinic, Athens Vision Eye Institute; Clinical Lecturer, Department of Ophthalmology, Second Ophthalmology Clinic, University of Athens Medical School, Greece

Theodoros Filippopoulos, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, American Medical Association, American Society of Cataract and Refractive Surgery, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Brian A Welcome, MD  Staff Physician, Department of Ophthalmology, Rhode Island Hospital

Brian A Welcome, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, American Medical Association, and American Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

John D Sheppard Jr, MD, MMSc  Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Ophthalmology Residency Research Program Director, Eastern Virginia Medical School; President, Virginia Eye Consultants

John D Sheppard Jr, MD, MMSc is a member of the following medical societies: American Academy of Ophthalmology, American Society for Microbiology, American Society of Cataract and Refractive Surgery, American Uveitis Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

R Christopher Walton, MD  Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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