ABSTRACT.Purpose: To evaluate the specific allergic sensitization and epidemiological characteristics of vernal keratoconjunctivitis (VKC). Methods: This retrospective non-comparative case series included 406 VKC patients. Data included patient and family histories, and results of allergic tests. Annual incidence and prevalence rates were calculated for a cohort of 128 VKC patients from the greater Padua area.

A review of the recent literature allows us to better understand the mechanisms involved in the development of ocular allergy and to guide us toward a more schematic approach, which could possibly be useful in forming a new classification, standardizing clinical phases and individuating new treatment targets.

SummaryThe eye represents an ideal and frequent site for the allergic reactions. The term 'allergic conjunctivitis' refers to a collection of disorders that affect the lid, conjunctiva and/or cornea. Even though the diagnosis is essentially clinical, local tests such as cytology, conjunctival provocation and tear mediator analysis can be performed. The immunoglobulin E (IgE)-mediated mechanism does not explain completely the severity and the clinical course of chronic allergic ocular diseases such as vernal (VKC) and atopic keratoconjunctivitis (AKC), which are probably also related to T cell-mediated responses, massive eosinophil attraction and activation and non-specific hypersensitivity. An altered balance between T helper type 1 (Th1) and Th2 cells and between Th1-and Th2-types of cytokines is thought to be responsible of the development of ocular allergic disorders. New findings suggest that a wide range of cytokines, chemokines, proteases and growth factors are involved by complex interwoven interactions rather than distinct and parallel pathways. In addition, several non-specific enzymatic systems may be activated during acute and chronic allergic inflammation, thus contributing to the complex pathogenesis of the disease. Current drug treatment for ocular allergy targets the key mechanisms involved in the development of clinical disease: mast cells with mast cell stabilizers, histamine with histamine receptor antagonists and inflammation with corticosteroids, severe inflammation with immunomodulators. None of these agents lacks side effects and none abolishes signs and symptoms completely. New therapeutic strategies are still needed to respond to the complex pathogenesis of severe forms of ocular allergy such as VKC and AKC.

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Background: There is growing evidence that autonomic innervation is involved in the pathogenesis of mucus hypersecretion, goblet cell hyperplasia, and conjunctival hyperreactivity.Objective: To determine the expression of neurotransmitters and neurotransmitter receptors in vernal keratoconjunctivitis (VKC) tissues to evaluate whether neurogenic inflammation plays a role in this ocular atopic-related disorder.Methods: Biopsy specimens of upper tarsal conjunctiva from 8 VKC patients with active inflammation and from 4 healthy subjects were processed for immunohistochemistry using anti-M 1 , anti-M 2 , and anti-M 3 muscarinic receptors; ␤ 1 -adrenergic receptor; vasoactive intestinal peptide; nerve growth factor; and protein gene product 9.5, a marker of nerve fibers. Results:In the conjunctival epithelium of VKC pa-tients, M 1 muscarinic receptor, nerve growth factor, and protein gene product 9.5 expression were decreased, whereas M 2 and M 3 muscarinic receptors and ␤ 1adrenergic receptor were irregularly distributed, compared with control subjects. Neurotransmitter receptors and vasoactive intestinal peptide expression were increased in the substantia propria-localized infiltrate of VKC compared with healthy tissue. Nerve growth factor and protein gene product 9.5 staining was also enhanced in the conjunctival stroma of VKC vs healthy conjunctiva. Conclusions:The inflamed conjunctiva of VKC patients demonstrated an obvious alteration in muscarinic and ␤ 1 -adrenergic receptor, vasoactive intestinal peptide, protein gene product 9.5, and nerve growth factor expression. These results substantiate the involvement of an autonomic dysfunction in the pathogenesis of VKC.