Vernal and Atopic Keratoconjunctivitis

VKC and AKC are the most severe atopic disorders because of their chronic-ity and their potential to involve the cornea and subsequently impair vision. The role of genetic and environmental factors remains unclear. Vernal disease is commonly seen in pediatric patients and it is characterized by intense pruritus and copious mucus secretion, giant papillae in the upper tarsus and the presence of gelatinous nodules around the limbus, with or without Trantas dots [1].

Although the pathogenesis of this disorder remains unknown, there is a contribution of both type I and type IV hypersensitivity reactions [33]. There is a genetic predisposition to this disease leading to an imbalance between Th2 and Th1 cells, which favors IgE synthesis [34].

AKC is found in atopic dermatitis patients and is the most severe of the allergic conjunctival diseases [34, 35]. Occasionally, these patients may have episcleritis, scleritis and even uveitis - whether these disorders are related to atopy or are just chance associations remains unknown. Individuals suffering from generalized allergic disorders are at a greater risk of contact lens-induced allergy.

Fig. 1. a Upper tarsal conjunctiva in a contact lens-wearing patient showing giant papillary reaction. b Upper fornix (double eversion of upper lid) showing giant papillary con-junctival reaction.

Local Contact Lens-Induced Allergic Conjunctivitis

Contact lens-induced papillary conjunctivitis (GPC) appears to be an allergic response to the contact lens, to the preservatives in the contact lens solution or to deposits on the contact lens [36].

Giant Papillary Conjunctivitis

GPC is a chronic inflammatory process leading to the production of giant papillae (>0.3 mm) on the tarsal conjunctiva lining the upper eye lids (fig. 1). The condition occurs in patients who wear soft contact lenses, an ocular prosthesis or have unburied sutures after surgery [37]. The etiology is uncertain and probably multifactorial, but the clinical picture resembles that of VKC [38]. It seems to be a delayed-type hypersensitivity reaction. The symptoms are pseudoptosis, redness, irritation, mucoid discharge, blurring of vision, tearing and photophobia. The eye is dry and the upper eye lid will show the characteristic giant papillae on the tarsal, and sometimes in the forniceal, conjunctiva (fig. 1). Mucous, cell debris and microorganisms are frequently found on the lenses and play a pathogenic role in GPC [39]. The immune privilege of the eye may reduce the incidence of intraocular inflammation. However, the lens produces a continuous antigenic stimulus evoking a localized allergic reaction in the upper tarsal conjunctiva [40]. Hard contact lenses wearers are rarely affected and GPC appears to occur after longer periods, up to 8 years [38]. Allergic and dry eye symptoms improve by switching to a disposable form of soft contact lenses [41]. The condition is more common in patients with a history of asthma, rhinitis or hay fever-type allergic reaction (SAC).

Pathogenesis of Giant Papillary Conjunctivitis

GPC is due to a combination of mechanical irritation and hypersensitivity [42]. A history of generalized allergy and/or allergy to disinfectant solutions is relatively frequent [43]. The allergy correlates with high levels of IgE and IgG in tears, IgM deposits on lenses and conjunctival infiltration by eosinophils. An increase in eotaxin levels in tears also correlates with GPC [44]. A high level of mucosal mast cells and a significant increase in tear concentrations of leukotriene C4 levels have been found in patients with contact lens-associated GPC [45]. Thus, leukotriene-inhibitory therapy may be beneficial to patients. The presence of neutrophil chemotactic factors in the tears of patients with GPC is also important, as the release of these factors from the injured conjunctiva may play an important role [46]. The reduction in lactoferrin levels in tears would favor microbial deposition on the contact lens [47].

The lens coatings from GPC patients induced a tear IgE response and cellular infiltration at the epithelial-stromal junction in tarsal conjunctival biopsy specimens [48]. Such allergic responses in the eye are late phase reactions, and increased levels of IL-1 have been found [49]. Contact lens wear can cause a change in corneal physiology which can lead to epithelial, stromal and endothe-lial compromise [50].

The inflammatory response in allergic disease is caused by the recruitment of leukocytes by chemokines and the upregulation of adhesion factors. IL-1 increases chemokine production, adhesion factors, macrophage infiltration and activity, and lymphocyte proliferation [50]. The presence of eosinophils at the site of allergic reactions is due to increased levels of RANTES, eotaxin and macrophage inflammatory protein-1a. These chemokines are also chemotactic for activated T cells, eosinophils, basophils and monocytes/macrophages [51, 52]. Eotaxin has a potent and selective chemotactic effect for eosinophils. All of these soluble factors are known to interact through a CC chemokine receptor (CCR3), which is mainly expressed on eosinophils, basophils and Th2 cells [53].

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