- •Dedication
- •Foreword
- •Preface
- •Ocular Allergy Overview
- •The ocular surface
- •Clinical examination
- •Immunopathophysiology of ocular allergy
- •Acute allergic conjunctivitis
- •Vernal keratoconjunctivitis
- •Atopic keratoconjunctivitis
- •Giant papillary conjunctivitis
- •Contact dermatitis of the eyelids
- •Blepharoconjunctivitis
- •Bacterial conjunctivitis
- •Viral conjunctivitis
- •Vasomotor conjunctivitis
- •Ocular examination
- •Ophthalmic procedures and testing
- •Summary
- •References
- •Ocular Mast Cells and Mediators
- •Mast cell mediators
- •Preformed granule-associated mediators
- •Biogenic amines
- •Proteoglycans
- •Neutral proteases
- •Newly generated mediators
- •Lipid mediators
- •Cytokines
- •Mast cell heterogeneity
- •Phenotypic heterogeneity
- •Functional heterogeneity
- •Pharmacologic heterogeneity
- •Ocular mast cells
- •The normal eye
- •Mast cells in diseases of the eye
- •Allergic conjunctivitis
- •Vernal conjunctivitis
- •Giant papillary conjunctivitis
- •Experimental autoimmune uveitis
- •Summary
- •References
- •Allergic Conjunctivitis
- •History
- •Examination
- •Seasonal and perennial allergic conjunctivitis
- •Seasonal allergic conjunctivitis
- •Perennial allergic conjunctivitis
- •Procedures
- •Late-phase reaction
- •Treatment
- •Antihistamines
- •Mast cell stabilizers
- •Lodoxamide tromethamine 0.1% (Alomide)
- •Ketorolac tromethamine (Acular)
- •Olopatadine (Patanol, Pataday)
- •Ketotifen (Zaditor)
- •Nedocromil (Alocril)
- •Pemirolast (Alamast)
- •Azelastine (Optivar)
- •Epinastine (Elestat)
- •Corticosteroids (Vexol, Lotemax)
- •Summary
- •References
- •Vernal Conjunctivitis
- •History
- •Epidemiology
- •Clinical manifestation
- •Conjunctival signs
- •Limbal signs
- •Corneal signs
- •Pathogenesis
- •Laboratory evaluation
- •Allergy testing
- •Conjunctival examination
- •Tear evaluation
- •Ocular challenge test
- •Treatment
- •Mast cell stabilizers
- •Antihistamines
- •Corticosteroids
- •Immunosuppressive agents
- •Other medical therapies
- •Surgical therapy
- •Treatment of secondary infections
- •Hyposensitization and immunotherapy
- •Prognosis
- •References
- •Giant Papillary Conjunctivitis
- •Signs and symptoms
- •Stages of giant papillary conjunctivitis
- •Stage 1: preclinical giant papillary conjunctivitis
- •Stage 2: mild giant papillary conjunctivitis
- •Stage 3: moderate giant papillary conjunctivitis
- •Stage 4: severe giant papillary conjunctivitis
- •Epidemiology
- •Histopathology
- •Coated contact lenses
- •Pathophysiology
- •Treatment
- •Treatment for stage 1: preclinical giant papillary conjunctivitis
- •Treatment for stage 2: mild giant papillary conjunctivitis
- •Treatment for stage 3: moderate giant papillary conjunctivitis
- •Treatment for stage 4: severe giant papillary conjunctivitis
- •Summary
- •References
- •Recognizing marginal dry eye disease
- •Contact lens wear in patients with dry eye
- •The use of therapeutic contact lenses in dry eye
- •The use of contact lenses in a patient with ocular allergy
- •Contact lenses and allergic reactions
- •Managing contact lens wear in the patient with ocular allergy
- •Summary of contact lens use in patient with ocular allergy
- •References
- •Mucous membrane pemphigoid
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Linear immunoglobulin A disease
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Epidermolysis bullosa acquisita
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Ocular pemphigus vulgaris
- •Clinical features
- •Diagnostic studies
- •Disease course and treatment
- •Summary
- •References
- •Seborrheic dermatitis
- •Treatment
- •Vitiligo
- •Heliotrope rash
- •Port-wine stains
- •Xanthelasmas and plane xanthomas
- •Seborrheic keratosis
- •Skin tags
- •Warts
- •Comedones
- •Syringoma
- •Rosacea
- •Lipoid proteinosis
- •Angioedema
- •Contact urticaria
- •Erysipelas
- •Trichinosis
- •Chalazion
- •Hordeolum
- •Nevi
- •Sarcoid
- •Hemangioma
- •Basal cell carcinoma
- •Squamous cell carcinoma
- •Sebaceous carcinoma
- •Malignant melanoma
- •Eyelid dermatitis
- •Atopic dermatitis
- •Contact dermatitis
- •Acute, subacute, and chronic
- •Epidemiology
- •Irritant versus allergic
- •Etiologies
- •Irritation due to mascara and eye cosmetic preservatives
- •Fragrance
- •Irritation due to conjunctival deposition
- •Nail polish
- •Metals
- •Aeroallergens
- •Medications/eyedrops/contact lens solution
- •Paper
- •Plants
- •Histology
- •Diagnosis
- •Herpes simplex
- •Herpes zoster
- •Treatment considerations for the eyelids
- •Eyelid dermatitis
- •Infections
- •Urticaria and angiodema
- •Benign tumors and growths
- •Malignant tumors
- •‘‘Cosmetic’’ lesions of the eyelids
- •Vascular lesions
- •Vitiligo
- •Others
- •References
- •Bacterial conjunctivitis
- •Viral conjunctivitis/herpes simplex virus infections
- •Treatment of infectious conjunctivitis
- •Nasolacrimal duct obstruction
- •Allergic conjunctivitis
- •Neonatal conjunctivitis
- •Congenital glaucoma
- •Uveitis
- •References
- •Ocular Allergy Treatment
- •Ocular allergy treatment algorithm
- •Advisory nonprescription interventions
- •Environmental control
- •Cold compresses
- •Lubrication
- •Contact lenses
- •Decongestants
- •Antihistamines
- •Oral antihistamines
- •Topical antihistamines
- •Topical antihistamines
- •Levocabastine
- •Emedastine
- •Cromoglycate
- •Lodoxamide
- •Pemirolast
- •Ketorolac
- •Multiple action agents
- •Olopatadine
- •Ketotifen
- •Nedocromil
- •Azelastine
- •Epinastine
- •Mizolastine
- •Picumast
- •Amlexanox
- •Topical antihistamines and dry eye
- •Steroids
- •Ophthalmic steroids
- •Intranasal steroids
- •Immunomodulatory agents
- •Cyclosporine
- •Immunotherapy
- •Summary
- •References
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mediators including vasoactive amines, which are responsible for initiating the complex of symptoms. The increased proteins in the tear film result in further coating on the contact lenses, perpetuating the cycle of events. Lactoferrin, a potent inhibitor of C3a, has been found to be decreased in the tears of patients with GPC; this results in an increased formation of C3a, also found to be elevated in the tears of patients with GPC. This cascade of events is shown graphically in Fig. 10. In addition, tear film clearance is delayed, and this delay in tear clearance can prolong the presence of inflammatory mediators and may aggravate the coating of the contact lens [63].
It is possible that in localized GPC secondary to silicone hydrogels, the sti er modulus of the contact lens itself, the edge design, or the fitting characteristics of these lenses may induce trauma to the conjunctiva, resulting in the release of NCF, which in itself may be important in the development of the clinical picture seen in the localized form of GPC. The generalized form is associated with a reaction to the coated contact lens similar to that occuring with HEMA-based contact lenses.
Treatment
On the basis of the authors’ hypothesis, a rational approach to the treatment of GPC can be undertaken. Therapy can either be directed at decreasing the coating on the contact lens, which decreases the antigen load and trauma to the conjunctival surface, or it can involve modulation
Fig. 10. Flow chart outlining pathophysiology of giant papillary conjunctivitis. (From Donshik PC. Giant papillary conjunctivitis. Trans Am Ophthalmol Soc 1994;92:687–744; with permission.)
GIANT PAPILLARY CONJUNCTIVITIS |
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of the immune reaction. The modalities that are available to decrease the coating of contact lenses are improved cleaning, decreased wearing time, or a change in the contact lens material or design [64–71]. Methods that are available to modulate the immune response are the use of topical corticosteroids, topical nonsteroidal anti-inflammatory agents, and mast cell stabilizers.
In a study of 221 patients with GPC [22], the authors found that if contact lens wear was not discontinued, but the cleaning regimen was changed, only 50% were able to continue wearing their contact lenses. If the patients decreased their wearing time, only 20% were able to continue wearing their lenses, and if they just replaced their contact lenses, 78% of patients could continue wearing their lenses. If patients discontinued wearing their contact lenses for 3 to 4 weeks and then were refitted with a new contact lens, however, 94% were able to continue wearing their lenses. If one looked at the di erent types of lenses used in refitting patients after a period of discontinuing contact lens wear, refitting the patients with the same type of lens only resulted in a success rate of 68%. Refitting to a rigid gas-permeable lens resulted in a success rate of 82%, and changing to a glyceryl methylmethacrylate resulted in an 81% success rate; however, using a frequent replacement or disposable lens resulted in a 91% success rate. It seems that the most successful lens modality to refit patients with GPC is the use of a frequent replacement or a disposable contact lens worn on a daily wear basis.
Studies reported in the literature on modulating the immune response have consisted mainly of the use of mast cell stabilizers [72–74]. Kruger and colleagues [75] reported that 14 (70%) of 20 patients with moderate to severe GPC who had a return of symptoms after changing their contact lens (patients first treated with a combination of improved lens care and refitting with a contact lens of a di erent design or polymer) were able to continue wearing their contact lenses when treated with topical cromolyn sodium. There have also been reports of nonsteroidal anti-inflammatory agents being e ective in the management of GPC [76]. The use of topical steroids has not been widely advocated because the potential complications of glaucoma and cataracts outweigh the potential benefits of keeping individuals in contact lenses. Loteprednol etabonate (a soft steroid) has been reported to be beneficial in treating the signs and symptoms of GPC over a 4-week period; however, the long-term beneficial e ects of this drug have not been investigated [77,78]. On the basis of these studies, the following regimen for the management of GPC is suggested.
Treatment for stage 1: preclinical giant papillary conjunctivitis
Patients who have minimal lens changes with minimal or no symptoms can often be managed by decreasing the replacement interval of their contact lenses. If the patient wears conventional hydrogel contact lenses they
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should be replaced at least twice a year. Another alternative is to use frequent replacement or disposable lenses, with replacement intervals of 2 weeks to 3 months. In addition to daily lens cleaning and disinfection, preferably with hydrogen peroxide and unpreserved saline solution, enzymatic cleaning once or twice a week should be used if lenses are replaced at intervals greater than 2 weeks. Because they are at higher risk, these patients should be followed two to three times a year and instructed to consult their physician at the initiation of any of the symptoms associated with GPC.
Treatment for stage 2: mild giant papillary conjunctivitis
Patients with early lens changes and mild symptoms are best managed by the use of frequent replacement daily wear lenses with a replacement cycle of 2 to 4 weeks. For patients wearing soft HEMA lenses, another alternative is to change to a lens of a non-HEMA material. The use of an enzymatic cleaner once or twice a week is then required, and these lenses can be replaced every 4 to 6 months. These patients are at high risk and should be followed four times a year.
Treatment for stage 3: moderate giant papillary conjunctivitis
Patients with moderate signs and symptoms should stop wearing their contact lenses for approximately 4 weeks. At that time, patients should be re-evaluated to ascertain that there is no evidence of keratitis and to ensure that the apical staining of the tarsal papules has resolved. In the authors’ experience, these patients do well with frequent replacement or disposable contact lenses worn on a daily wear basis and replaced every 1 to 2 weeks. These lenses require daily cleaning and disinfection, preferably with hydrogen peroxide and unpreserved saline. Newly introduced daily disposable contact lenses should be e ective in the management of patients in stage 3. Another option is to refit these patients with rigid gas-permeable lenses. They should be followed at 3-month intervals.
Treatment for stage 4: severe giant papillary conjunctivitis
Patients with severe GPC require discontinuation of their contact lenses for a minimum of 4 weeks. During this time, the inflammatory reaction should resolve; however, if apical staining of the papules was noted at the time of diagnosis, the tarsal plate must be re-examined to ensure that staining has resolved. The cornea also has to be free of punctate staining noted with fluorescein instillation. The papillary reaction of the tarsal plate will probably be unchanged. Injection and inflammation of the tarsal conjunctiva often diminishes, but may not totally be eliminated during this time. In the authors’ experience, these patients are best managed by fitting them with frequent replacement or disposable contact lenses worn on a daily
