Contact Lenses and Ocular Allergy

Allergies and contact lenses can wreak havoc on the ocular surface. Find out how to give your patients relief.


Contact Lenses and Ocular Allergy

Allergies and contact lenses can wreak havoc on the ocular surface. Find out how to give your patients relief.

By William Townsend, OD, FAAO

Dr. Townsend practices in Canyon, Texas and is an adjunct faculty member at UHCO. E-mail him at

More than half (54.6 percent) of all U.S. citizens test positive to one or more allergens, and up to 50 percent of these individuals will exhibit some degree of ocular allergy. Approximately 35 million people in the United States wear contact lenses. Both ocular allergy and contact lens wear can profoundly impact the anterior surface of the eye, and when they occur in combination, those effects may become compounded.

To clearly understand the potential impact of concomitant ocular allergy and contact lens wear, we should understand how each of these factors independently affects the ocular surface. This article will review the anatomy and physiology of the ocular surface as well as the independent effects of contact lenses and allergy on the eye and how they interact when both are present. Finally, it will discuss management and treatment of these conditions.

Tears and the Ocular Surface

Tears bring nutrition and oxygen to the cornea and conjunctiva; they serve as the substrate on which a contact lens rests and through which allergens reach the surface of the eye. The outermost layer of corneal and conjunctival squamous cells is covered with microscopic folds (microplicae) and microvilli. The function of microplicae and microvilli is not well established, but it has been suggested that they anchor a layer of lubricating and cushioning mucin that protects the underlying tissue from abrasion. Others suggest that they increase the surface area of the superficial epithelial cells, enhance the absorption of oxygen and other nutrients, and promote the elimination of metabolic products from the cells.

Corneal microplicae and microvilli are covered with glycocalyx, i.e., membrane-associated mucins (MUC1, MUC4, and MUC16) secreted by the epithelial cells of the cornea and conjunctiva. The glycocalyx allows the relatively hydrophobic surface of the cornea to become hydrophilic, and it couples tears to the underlying corneal epithelium. Mucins are critical to the health of the ocular surface; they are believed to facilitate the spreading of tears across the cornea and conjunctiva.

The aqueous layer of tears, which overlies the corneal glycocalyx, is a complex solution that contains electrolytes, proteins, growth factors, and other components. Secreted mucins are a critical component in the aqueous layer. They are primarily secreted mucins that are produced by goblet cells; there is evidence that the main and accessory lacrimal glands also contribute gel-forming mucins to the aqueous layer. Gel-forming mucins dispersed within the aqueous phase may help stabilize the tear film and also serve as a substrate between glycocalyx and the aqueous layer of the tear film. Gel-forming mucins may also adhere to debris that reaches the eye (i.e., dirt, dust, and microbes) and remove them via the nasolacrimal duct.

More than 400 different proteins have been identified in human tears. Lysozyme comprises 20 percent to 40 percent of tear proteins. Other major proteins include lactoferrin, which is secreted mainly from the acini of the lacrimal gland and possesses antibacterial functions; epidermal growth factor, which is important in wound healing and maintenance of the ocular surface; and lipocalin, which may contribute to tear viscosity. IgA, the most abundant immunoglobulin in the tears, has been proposed as the first line of the host defense mechanism on the ocular surface.

Allergy and the Ocular Surface

Allergic eye disease is an abnormal immune hypersensitivity response to harmless substances called allergens. It is characterized by IgE-mediated and/or T-lymphocyte-mediated immune hypersensitivity reactions that ultimately result in the clinical manifestations of ocular allergy. It is beyond the scope of this article to extensively detail the pathophysiology of allergy, but a brief review might be helpful.

Allergic diseases have an unmistakable genetic predisposition, but are not inherited in a classic Mendelian pattern. Studies show that in humans, genes on chromosomes 5, 11, 16, and 12 may contribute to development of asthma and allergy.

The moniker "allergy" refers to a type I hypersensitivity reaction. Sensitization to an allergen occurs in one of two ways. An allergen may encounter a naive B-lymphocyte, which processes it and eventually induces activated B-lymphocytes to produce antibodies. The second path involves dendritic cells — dedicated antigen-presenting cells (APCs) — which play a key role in sensing danger and initiating both innate and adaptive responses. APCs encounter an antigen, process it and present it to a CD4+ T-lymphocyte. The lymphocyte then differentiates into a helper 1 or a t-helper 2 lymphocyte. T-1 helper cells participate in cell-mediated inflammation. T-2 helper cells present the processed allergen to an activated B-cell that produces antibodies specific to the allergen. IgE antibodies bind to the surfaces of mast cells and basophils. If the same allergen later contacts a sensitized cell, it interacts with the surface IgE and stimulates degranulation of the mast cell. This results in the release of preformed mediators (histamine, tryptase, chymase, and heparin), chemotactic factors (eosinophil chemotactic factor, neutrophil chemotactic factor), and arachidonic acid from phospholipid membranes. Release of these substances causes the classic signs and symptoms of ocular allergy, which may include itching, redness, edema of the lids and conjunctiva, papillary hypertrophy (Figure 1), and a watery mucoid discharge. Histamine is quickly taken up by the H1 receptors or is metabolized by N-methlytransferase (70 percent) or histaminase (30 percent).

Figure 1. Papillary hypertrophy in seasonal allergic conjunctivitis.

The duration of the "allergy season" for affected individuals depends to some extent on the specific allergens to which they are sensitized. Seasonal allergic conjunctivitis (SAC) is limited to times during which specific pollens are released, typically in the spring and fall when various grasses, trees, and other vegetation pollinate. Histamine concentration in tears of allergic conjunctivitis patients can reach values greater than 100 ng/mL, as compared with values of five-to-15 ng/mL in controlled patients. Perennial allergic conjunctivitis (PAC) clinically appears very similar to SAC; however, signs and symptoms are present during most of the year. The offending allergens in this condition are typically animal dander, dust mite droppings, and molds. Despite the fact that these conditions can negatively affect quality of life, they are self limiting and pose no threat to vision.

Atopic keratoconjunctivitis (AKC) and vernal keratoconjunctivitis (VKC) are rare conditions comprising less than 5 percent of all allergic conditions. In the strictest sense they are not purely allergic conditions; both are characterized by more chronic inflammatory cellular infiltrates, the development of giant papillae on the upper tarsus (Figure 2), and, in some cases, potentially sight-threatening corneal involvement.

Figure 2. Giant papillae in patient who has AKC.

VKC is a relatively rare bilateral disease of young people. Onset of the disease typically occurs during childhood and the early teens; in most cases it "burns out" by the late teens and early 20s. As its name implies, VKC is seasonal with peak incidence of signs and symptoms occurring from early spring until autumn. In warmer climates it may be perennial. In younger populations, males are approximately three times more likely to be affected, but after the age of 16, there is no difference in occurrence between genders. Characteristic clinical signs and symptoms of this disease include intense itching, severe photophobia, foreign body sensation, papillary and giant papillary hypertrophy of the upper tarsus, inflammatory cell infiltration of the limbus, and excessive mucin secretion. Some degree of corneal involvement in VKC has been reported in 50 percent of cases. These changes manifest as increased risk for keratoconus, keratoglobus, marginal corneal degeneration, astigmatism, corneal plaques, and shield ulcers.

AKC is a disease of adults. It is invariably bilateral, but may be asymmetrical. AKC occurs in 25-to-40 percent of patients who have atopic dermatitis, a general term for exudative dermatitis for one of the eczemas. The onset of the dermatitis frequently occurs during the early childhood years. It is familial in nature and rarely found in individuals who are not genetically susceptible. Asthma occurs in 87 percent of individuals who suffer from AKC. Triggering factors include irritants, allergens, heat, low humidity, rough clothing, scratching and stress. Studies show that it is possibly related to a stem cell defect in the bone marrow.

AKC onset typically occurs after age 30 and, unlike VKC, it is usually not self-limiting. Adult onset dermatitis is typified by skin lesions on the periocular area, the face and trunk, and the popliteal and antecubital flexures of the knees and elbows, respectively (Figure 3). Lid lesions show indurated skin with lesions that are often exudative; dermal thickening from chronic inflammation and edema results in the appearance of Dennie-Morgan folds. Intense itching of the skin is frequently reported, and repeated scratching may result in secondary infection or maceration of the surface. Other lid changes associated with AKC include meibomian gland dysfunction, dry eyes, and blepharitis. Cataracts occur in 8 percent to 12 percent of patients who have severe dermatitis. Onset of cataracts typically occurs 10 years after the onset of atopic dermatitis. They may progress rapidly and require surgery as little as six months after detection.

Figure 3. Dermatitis at antecubital space in AKC.

Corneal changes associated with AKC, which occur in up to 75 percent of cases, are similar to those found in VKC and include keratoconus, keratoglobus, punctate keratitis, and pannus. Other findings associated with AKC include gelatinous infiltrates of the limbus (Trantas spots) and shield ulcers (Figure 4). Herpes simplex virus, which is found in 13 percent to 22 percent of patients who have AKC, is more difficult to treat than herpetic disease in non-atopic individuals.

Figure 4. Shield ulcer in AKC.

Patients who have VKC and AKC develop significant ocular surface changes including reduced tear film breakup time (TBUT), reduced corneal sensitivity, increased squamous metaplasia, and reduced goblet cell density. Brush cytology samples reveal elevated levels of neutrophils, eosinophils, and lymphocytes in the tissue.

Contact Lenses and the Ocular Surface

Applying a contact lens to the ocular surface alters the environment in a number of ways. A contact lens divides the tears into a pre-lens tear film (PLTF) and a pre-corneal tear film (PCTF). Nichols et al (2005) used interferometry to measure the thickness of these layers and found that in the presence of a contact lens, the PLTF showed faster thinning than did the PCTF.

Yasueda and coworkers (2005) used sophisticated analytic methods such as high-performance liquid chromatography and gel electrophoresis to evaluate the effect of contact lens wear on tear film mucins. They found that contact lens wear led to lowered mucin levels in the tear film but, interestingly, did not cause a detectable loss of goblet cells. They attributed this to low-grade chronic inflammation that was significant enough to reduce mucin production, but mild enough to not affect the goblet cell population of the conjunctiva.

Evaporation is a significant factor in the loss of tears from the eye. In a study aimed at evaluating the impact of contact lens wear on tear film evaporation, Guillon and Maissa (2008) divided 379 subjects into non-contact lens wearers, contact lens wearers not wearing lenses on the day of the testing, and contact lens wearers. They determined the rate of evaporation for each group and found it was highest for contact lens wearers, lower for contact lens patients not wearing lenses that day, and lowest for non-contact lens wearers. There was a significant difference between the evaporation rates in the last two groups, suggesting that lens wear affects evaporation rates even when the patients are not wearing their lenses.

Nichols and Sinnot (2006) used a battery of tests to assess the impact of medical history, tear film, lens characteristics, and social history on a group of 415 contact lens patients who self-reported dry eye symptoms. They concluded that contact lens-related dry eye may be attributed to multiple factors including tear film thinning, increased tear film osmolarity, use of high-water-content lenses, surface changes, use of over-the-counter (OTC) pain medications, and female gender. Their study confirmed previous results from others; individuals wearing low-water-content lenses are less likely to report dry eye symptoms.

Glasson et al (2006) conducted a study to determine the effect of contact lens wear on the tear film and ocular surface of individuals who were either tolerant to or intolerant to contact lens wear. They obtained baseline findings and then repeated them at the end of six hours of contact lens wear. They found that both tolerant and intolerant subjects demonstrated statistically significant increases in bulbar and overall conjunctival hyperemia after six hours of lens wear. Intolerant contact lens wearers showed lower baseline TBUTs and tear flow prior to wear. After six hours of wear, TBUTs for the two groups were essentially the same, but tolerant wearers continued to have higher tear flow values.

These studies demonstrate that contact lenses can clearly impact the surface of the eye. The important question to address is: What happens when a contact lens wearer also suffers from ocular allergy?

Contact Lenses, Allergy, and the Ocular Surface

It may be more difficult than you would expect to determine whether a patient is suffering from allergy, dry eye, or both. Fujishima et al (1996) stated that ideally we should diagnose ocular allergy based on a history of confirmed allergy, symptoms of itching, papillae on the conjunctival surface, and the presence of IgE in serum. But this is not the norm in clinical practice. They found that individuals positive for IgE in tears had normal Schirmer tests (ST) and tear clearance tests (TCC). Individuals lacking IgE in tears showed reduced ST and TCC. They also found that ocular itching may occur in individuals who do not have allergy, but suffer solely from dry eye.

Allergy as a separate entity exerts several effects on the ocular surface. It causes tear film instability. Tears normally contain nanomolar concentrations of mediators such as cytokines, growth factors, enzymes, and compliment. The concentration of some of these components may increase significantly in the presence of injury, infection, or stress such as allergy. In both the allergic and non-allergic eye, biofilms form on the surface of a contact lens within minutes of application. While benign and an expected finding, they may serve as a substrate for adherence to the lens surface of denatured proteins, mucins, calcium, and lipids as well as bacteria. Biofilms may also contribute to inflammation of the ocular surface.

Managing Contact Lens Patients Who Have Ocular Allergy

There are three primary approaches to managing contact lens wearers who suffer from ocular allergy: lens selection, care solution regimen, and pharmacologic management.

Lens Selection Lemp, Bielory, and others have advocated the use of daily disposable lenses to minimize the untoward effects of the lens-allergy combination. Heys et al (2003) found that 67 percent of ocular allergy sufferers who switched to one-day lenses reported improved comfort while only 18 percent of those who simply replaced their habitual lenses reported improvement. This study demonstrates the potential benefits of one-day lenses for patients who have ocular allergy. When this approach is not feasible, instruct patients on the daily vigorous cleaning of traditional hydrogel or silicone hydrogel contact lenses.

Jones and Sack (1990) evaluated the presence of inflammatory markers on the surface of low- and high-water contact lenses. They found a marked increase in immunoglobulin deposition on high-water-content lenses (especially of non-ionic composition) when contrasted with low-water-content lenses. They also observed marked levels of immunoglobulins on extended wear lenses as compared to lenses worn on a daily wear basis. They concluded that use of high-water-content lenses or extended lens wear results in a greater degree of inflammatory and/or immune stress. This would suggest that in patients who have seasonal allergy, extended wear should be limited to periods when the patient's allergy is minimally active.

Instruct patients who have seasonal allergy to discontinue lens wear during those periods when their allergies are most active. This, of course, necessitates their having back-up spectacles available during those periods when lens wear is contraindicated.

Based on findings by Bielory (2008) and others, I would recommend the following:

• Limit extended wear of contact lenses in ocular allergy patients.

• Patients who have SAC should avoid or limit contact lens use during peak periods of allergy.

• Patients who have ocular allergy should rub and rinse contact lenses daily to minimize deposit buildup (Figure 5).

Figure 5. Heavily coated contact lens surface.

• Prescribe one-day disposable lenses for patients who have significant allergy and do not do well with daily wear lenses; alternatively, prescribe two-week replacement lenses on a daily wear regimen.

• Instruct patients to never instill OTC allergy drops while contact lenses are on the eye. They should instill topical medications five or more minutes before applying contact lenses.

• Contact lenses are contraindicated in patients who have VKC.

Care Solution Regimen Contact lens solutions and materials can profoundly affect the wettability and deposition characteristics of a contact lens surface. Emch and Nichols (2009) evaluated silicone hydrogel lens materials and solutions with regard to protein deposits. They determined that Opti-Free Express (Alcon) consistently removed more protein from the silicone hydrogels than did ReNu with MoistureLoc (Bausch & Lomb) or Complete MoisturePlus (Advanced Medical Optics). In all patients wearing contact lenses, it is important to determine which lens materials and solutions have the lowest potential for presenting antigens to the immune system.

Pharmacologic Management of Allergy in Contact Lens Wearers In 2001, Solomon et al stated that, "The most common topical drugs invariably used by ophthalmologists for all forms of allergic conjunctivitis are the mast cell stabilizing agents." Much has changed since that time; the advent of topical combination antihistamine-mast cell stabilizers such as Patanol (olopatadine 0.1%, Alcon), Elestat (epinastine 0.05%, Inspire Pharmaceuticals), Optivar (azelastine 0.05%, Meda Pharmaceuticals), and Zaditor (ketotifen 0.025% Novartis) has afforded us with efficacious medications to treat SAC and PAC. All of these products possess high affinity for H1 receptors and have assumed a major market share in the ocular allergy segment. They are prescribed on a twice-per-day basis and hence require contact lens patients to remove their lenses after 12 hours. Ketotifen 0.025% is now available OTC as Alaway (Bausch & Lomb).

The introduction of olopatadine 0.2% (Pataday, Alcon) marked a milestone in ocular allergy management. Abelson et al (2008) demonstrated superiority of this formulation over placebo and epinastine. Because it is approved by the Food and Drug Administration (FDA) for once-a-day dosing, daily contact lens wearers can instill a single dose in the morning before contact lens application and experience significant relief from itching and redness for their entire wearing period. Instruct patients who wear soft contact lenses to wait at least 10 minutes after instilling Pataday before applying their contact lenses.

Topical corticosteroids produce their effect on responsive cells by activating glucorticoid receptors to directly or indirectly regulate the transcription of target genes. The major effect of corticosteroids is to inhibit the synthesis of multiple inflammatory proteins through suppression of the genes that encode them. Steroids are useful in managing inflammatory conditions of the eye, but are not without side effects. Site-specific steroids such as rimexolone and loteprednol are highly effective in the acute and prophylactic treatment of allergic conjunctivitis, but long-term use may lead to posterior subcapsular cataracts, elevations of intraocular pressure, dilatation of the pupil, and variable ptosis. The use of steroids for ocular immune conditions should be reserved for sight-threatening conditions such as VKC and AKC. Steroid preparations are effective therapy for moderate-to-severe forms of VKC and AKC, but may cause the aforementioned complications. Cyclosporine A has been used successfully for managing the more severe presentations of these conditions and has fewer potential complications compared to topical steroid preparations.


Allergic eye diseases and contact lens wear have potential impact on the ocular surface. These common conditions may co-exist in a patient presenting for care. It is vital for clinicians to understand the pathophysiology of these conditions, to correctly diagnose them, and to deal with them appropriately to prevent permanent sequelae. We must use our knowledge, skills, and clinical expertise to provide the safest, most practical mode of vision correction and therapeutic intervention for this important subset of patients. CLS

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