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Atopic Keratoconjunctivitis Medication

  • Author: Anne Chang-Godinich, MD, FACS; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Mar 17, 2015
 

Medication Summary

The goals of pharmacotherapy in the treatment of atopic keratoconjunctivitis are to reduce morbidity and to prevent complications, such as significant keratopathy, conjunctival fornix foreshortening, and corneal scarring or thinning requiring penetrating keratoplasty.

Mast cell stabilizers and antihistamines are the mainstays of prophylactic therapy. Antihistamines, steroids, and other immunosuppressives are used for immediate control of symptoms.

When medically treating patients with steroids or cyclosporine, a regular interval survey for drug-related adverse effects and complications is indicated.

For additional information, see PDR.net.

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Topical mast cell stabilizers

Class Summary

Topical mast cell stabilizers inhibit degranulation of sensitized mast cells upon exposure to specific antigens.

Lodoxamide tromethamine 0.1% (Alomide)

 

Lodoxamide stabilizes mast cells and inhibits increased vascular permeability, which is associated with immunoglobulin E (IgE) and antigen-mediated reactions. Alomide has been reported to prevent calcium influx into mast cells upon antigen stimulation without intrinsic anti-inflammatory, antihistamine, or vasoconstrictive effects.

Nedocromil sodium 2% (Alocril)

 

Nedocromil interferes with mast cell degranulation, specifically with the release of leukotrienes and platelet activating factor.

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Topical antihistamines

Class Summary

Topical antihistamine agents act by competitive inhibition of histamine at the H1 receptor. These medications are used for prophylaxis and symptomatic relief.

Ketotifen fumarate 0.025% (Zaditor, Alaway, Claritin Eye, Zyrtec Itchy Eye)

 

Ketotifen is a selective H1 histamine receptor antagonist and mast cell stabilizer that acts by inhibiting the release of mediators from cells involved in hypersensitivity reactions.

Olopatadine hydrochloride 0.1% (Patanol, Pataday)

 

Olopatadine inhibits histamine release through both selective H1 histamine receptor antagonism and less-specific mast cell stabilization.

Epinastine hydrochloride 0.05% (Elestat)

 

Epinastine is another H1 antihistamine and mast cell stabilizer. As with azelastine, the usual dose is 1 drop in the affected eye(s) twice daily.

Azelastine hydrochloride 0.05% (Optivar)

 

Azelastine is both an antihistamine and mast cell stabilizer. The usual dose is 1 drop in the affected eye(s) twice daily.

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Corticosteroids

Class Summary

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

Loteprednol etabonate 0.5%, 0.2% (Lotemax, Alrex)

 

Loteprednol is structurally similar to other corticosteroids, but the number 20 position ketone group is absent. This agent is highly lipid soluble, which enhances cell penetration, and undergoes a predictable transformation to an inactive carboxylic acid metabolite.

Loteprednol was shown to be less effective than prednisolone acetate 1% in two 28-day controlled clinical studies in acute anterior uveitis; 72% of patients treated with Lotemax experienced resolution of anterior chamber cells compared with 87% of patients treated with prednisolone acetate 1%. The incidence of patients with clinically significant increases in intraocular pressure (>10 mm Hg) was 1% with Lotemax and 6% with prednisolone acetate 1%.

Fluorometholone 0.1%, 0.25% (FML, FML Forte)

 

Fluorometholone inhibits edema, fibrin deposition, capillary dilatation, and phagocytic migration of acute inflammatory response and capillary proliferation, collagen deposition, and scar formation. Used topically, this agent can elevate intraocular pressure (IOP) and cause steroid-response glaucoma. However, in clinical studies of documented steroid responders, fluorometholone demonstrated a significantly longer average time to produce a rise in IOP than dexamethasone phosphate. In a small percentage of individuals, a significant rise in IOP occurred within 1 week. The ultimate magnitude of the rise was equivalent.

Prednisolone acetate 1%, 0.12% (Pred Forte, Pred Mild)

 

On the basis of weight, prednisolone has 3-5 times the anti-inflammatory potency of hydrocortisone. Glucocorticoids inhibit edema, fibrin deposition, capillary dilatation and proliferation, phagocytic migration of the acute inflammatory response, deposition of collagen, and scar formation.

Difluprednate ophthalmic (Durezol)

 

Difluprednate ophthalmic is an ophthalmic corticosteroid indicated for inflammation and pain associated with ocular surgery. It is available as a 0.05% ophthalmic emulsion.

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Immunosuppressants

Class Summary

Immunosuppressant agents are used as adjunctive or alternative treatment in situations in which steroid use is ineffective or requires minimization.

Cyclosporine (Restasis)

 

The exact mechanism of the immunosuppressive activity of cyclosporine is unknown, but preferential and reversible inhibition of T lymphocytes in the G0 or G1 phase of the cell cycle has been suggested.

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Contributor Information and Disclosures
Author

Anne Chang-Godinich, MD, FACS Clinical Associate Professor, Department of Ophthalmology, Baylor College of Medicine; Physician, 1960 Eye Surgeons, PA; Attending Surgeon, Veterans Affairs Medical Center of Houston

Anne Chang-Godinich, MD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Society of Cataract and Refractive Surgery, Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Michael B Raizman, MD Associate Professor, Department of Ophthalmology, Tufts School of Medicine; Consulting Staff, Ophthalmic Consultants of Boston, Inc

Michael B Raizman, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, Phi Beta Kappa, Pan-American Association of Ophthalmology, American Uveitis Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Hospital

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Ophthalmological Society, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, International Society of Refractive Surgery, Cornea Society, Eye Bank Association of America

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cornea Society, Allergan, Bausch & Lomb, Bio-Tissue, Shire, TearScience, TearLab<br/>Serve(d) as a speaker or a member of a speakers bureau for: Allergan, Bausch & Lomb, Bio-Tissue, TearScience.

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, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Andrew W Lawton, MD Neuro-Ophthalmology, Ochsner Health Services

Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, Southern Medical Association

Disclosure: Nothing to disclose.

References
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  2. Power WJ, Tugal-Tutkun I, Foster CS. Long-term follow-up of patients with atopic keratoconjunctivitis. Ophthalmology. 1998 Apr. 105(4):637-42. [Medline].

  3. Hu Y, Matsumoto Y, Adan ES, Dogru M, Fukagawa K, Tsubota K, et al. Corneal in vivo confocal scanning laser microscopy in patients with atopic keratoconjunctivitis. Ophthalmology. 2008 Nov. 115(11):2004-12. [Medline].

  4. Casey R, Abelson MB. Atopic keratoconjunctivitis. Int Ophthalmol Clin. 1997 Spring. 37(2):111-7. [Medline].

  5. Akpek EK, Dart JK, Watson S, et al. A randomized trial of topical cyclosporin 0.05% in topical steroid-resistant atopic keratoconjunctivitis. Ophthalmology. 2004 Mar. 111(3):476-82. [Medline].

  6. Hingorani M, Moodaley L, Calder VL, Buckley RJ, Lightman S. A randomized, placebo-controlled trial of topical cyclosporin A in steroid-dependent atopic keratoconjunctivitis. Ophthalmology. 1998 Sep. 105(9):1715-20. [Medline].

  7. Donnenfeld E, Pflugfelder SC. Topical ophthalmic cyclosporine: pharmacology and clinical uses. Surv Ophthalmol. 2009 May-Jun. 54(3):321-38. [Medline].

  8. Hoang-Xuan T, Prisant O, Hannouche D, Robin H. Systemic cyclosporine A in severe atopic keratoconjunctivitis. Ophthalmology. 1997 Aug. 104(8):1300-5. [Medline].

  9. Anzaar F, Gallagher MJ, Bhat P, Arif M, Farooqui S, Foster CS. Use of systemic T-lymphocyte signal transduction inhibitors in the treatment of atopic keratoconjunctivitis. Cornea. 2008 Sep. 27(8):884-8. [Medline].

  10. Miyazaki D, Tominaga T, Kakimaru-Hasegawa A, Nagata Y, Hasegawa J, Inoue Y. Therapeutic effects of tacrolimus ointment for refractory ocular surface inflammatory diseases. Ophthalmology. 2008 Jun. 115(6):988-992.e5. [Medline].

  11. Labcharoenwongs P, Jirapongsananuruk O, Visitsunthorn N, Kosrirukvongs P, Saengin P, Vichyanond P. A double-masked comparison of 0.1% tacrolimus ointment and 2% cyclosporine eye drops in the treatment of vernal keratoconjunctivitis in children. Asian Pac J Allergy Immunol. 2012 Sep. 30(3):177-84. [Medline].

  12. Al-Amri AM. Long-term follow-up of tacrolimus ointment for treatment of atopic keratoconjunctivitis. Am J Ophthalmol. 2014 Feb. 157(2):280-6. [Medline].

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Atopic keratoconjunctivitis. Limbal Trantas dots can be seen in this image.
Atopic keratoconjunctivitis. A corneal shield ulcer is illustrated in this image.
Atopic keratoconjunctivitis. This image depicts a symblepharon.
 
 
 
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