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Vernal keratoconjunctivitis: an update
  1. Stefan De Smedt1,
  2. Gerhild Wildner2,
  3. Philippe Kestelyn3
  1. 1Ophthalmology Department, Kabgayi Hospital, Muhanga, Rwanda
  2. 2Section of Immunobiology, Department of Ophthalmology, Klinikum der Universität, Munich, Germany
  3. 3Ophthalmology Department, Ghent University Hospital, Ghent, Belgium
  1. Correspondence to Dr Stefan De Smedt, Leopoldstraat 36 2800 Mechelen, Belgium; dr.stefan.desmedt{at}gmail.com

Abstract

Vernal keratoconjunctivitis (VKC) is a bilateral, usually seasonally recurrent, allergic inflammation of the conjunctiva, characterised by limbal gelatinous hypertrophy and/or upper tarsal giant conjunctival papillae. Although rare in temperate regions, it represents an important cause of hospital referral in many parts of Africa and Asia. Clinical and immunohistochemical studies suggest that IgE-dependent (type I allergic) and IgE-independent (type IV allergic) mechanisms are involved in the immunopathogenesis of VKC, in which various inflammatory cells, including different T cell subpopulations play an active role via a cascade of chemical mediators. Endocrine, genetic, neurogenic, environmental and socioeconomic risk factors have been identified. However, its aetiology and pathophysiology remain unclear. The clinical course of this disease is usually benign and self-limiting, but a minority of patients will face very debilitating and sight threatening complications. Topical corticosteroids are often used during flare-ups in combination with mast cell stabilizers as maintenance treatment for VKC. However this management is unsatisfactory in controlling severe cases and avoiding recurrences. Non-steroidal immune modulators such as ciclosporin A and tacrolimus are promising alternatives, but tolerance to these agents needs to be improved and production costs reduced. The purpose of this review is to give an update on its epidemiology, immunopathogenesis and management.

  • Drugs
  • Ocular surface
  • Treatment Medical
  • Conjunctiva
  • Cornea

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