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Vernal Keratoconjunctivitis

Journal

SURVEY OF OPHTHALMOLOGY
Volume 64, Issue 3, Pages 289-311

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.survophthal.2018.12.001

Keywords

vernal keratoconjunctivitis; eosinophil; papillae; limbal stem cell deficiency; keratoconus; topography; steroid; shield ulcer; cyclosporine; tacrolimus

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Vernal keratoconjunctivitis, a chronic bilateral seasonal allergic inflammatory disease of the eye, is an important cause of visual debilitation and impairment of quality of life in children and young adults in certain parts of the world such as the Mediterranean areas, Central and West Africa, the Middle East, Japan, the Indian subcontinent, and South America. It usually has a self-limiting course; however, in a few cases, the disease is recurrent and leads to long-term visual disabling complications such as keratoconus and limbal stem cell deficiency. The main pathogenic mechanism is immunoglobulin E mediated; however, there may be non-immunoglobulin E and certain nonspecific hypersensitivity mechanisms. The predominant cell types involved are CD4 T cells and eosinophils. The management of vernal keratoconjunctivitis is challenging. Although an acute episode can be well managed with the help of currently available topical agents, the major challenge lies in preventing recurrences and their consequences. Steroids are highly effective in controlling both an acute episode and chronic disease; however, the long-term complications of steroid use often prevent their continued use. Immunomodulators such as tacrolimus and cyclosporine may be used as steroid-sparing agents; however, the dosing and duration of use still need to be clearly defined. Surgery is required for the management of complications such as shield ulcer and corneal ectasia or opacity; however, the disease process and management are largely well defined, and genetic predisposition factors responsible for chronicity and an effective albeit safe treatment modality for the chronic form of the disease need further research. (C) 2018 Elsevier Inc. All rights reserved.

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