Cyclosporine eyedrops 2% have been used for treatment of corticosteroid-resistant vernal keratoconjunctivitis (VKC) cases. The purpose of our study was to verify the efficacy of 1.25% vs. 1% topical cyclosporine in improving severe form of VKC in childhood. Twenty children with severe VKC, were enrolled in a double-blind, placebo-controlled study and received cyclosporine 1.25% in one eye for 2 wk. Then an open trial was conducted during the next 3 months and 2 wk. Thirty-two more patients were recruited the next year into a new open trial and they received cyclosporine 1% for 4 months. Ocular subjective symptoms and objective signs were scored in all children at entry, 2 wk and 4 months. Skin prick tests and conjunctival scraping tests were also performed; serum immunological and biochemical markers were assessed. The mean score values for severity of subjective symptoms and objective signs were significantly decreased after 2 wk, and 4 months, compared with those at entry (p < 0.001), in both groups of children who received cyclosporine eyedrops 1.25% and 1%, respectively. Serum markers did not differ from the beginning to the end of treatment. Conjunctival eosinophils and cyclosporine serum levels were not detectable at the end of therapy, nor were endothelial corneal cells damaged. Our findings suggest that 1% cyclosporine concentration might be the minimal effective treatment regimen to control symptoms and local inflammation in severe forms of VKC.

The purpose of our study was to verify the efficacy of prolonged cycles of 1% topical cyclosporine in improving severe form of vernal keratoconjunctivitis (VKC) in childhood and investigate for factors affecting the response to therapy. We conducted an open trial involving 197 children with severe VKC, who received topical cyclosporine 1% for 4 months. Ocular subjective symptoms (SS) and objective signs (OS) were scored in all children at entry, 2 wks and 4 months. Skin prick tests and microscope endothelial cells evaluation were also performed; serum immunoglobulin E and cyclosporine levels were assessed. The mean score values for severity of SS and OS were significantly decreased after 2 wks and 4 months, compared with those at entry (p < 0.001) in all children. Cyclosporine serum levels were neither detectable at the end of therapy, nor were endothelial corneal cells damaged. Patients who started the therapy at the beginning of the disease and/or received long-term regimen of treatment with cyclosporine had a faster improvement of ocular signs and symptoms, compared with all other patients. Our findings suggest that 1% cyclosporine concentration administrated topically at the beginning of the disease and for a long-term period might be the most effective treatment to control symptoms and local inflammation in severe forms of VKC in childhood.

The purpose of this study was to test for detectable serum levels of antibodies usually associated with immune-related diseases in children with Vernal keratoconjunctivitis (VKC) and seek for their family history of allergies and autoimmune disorders. The association of human leukocyte antigens (HLA) with VKC was also investigated. We enrolled 181 VKC children and assessed total and specific IgE, antithyroglobulin (AbTG), antithyroidperoxidase (AbTPO), antitransglutaminase (tTG), and antinuclear antibodies (ANA) by standard procedures. Class I and II HLA typing was also carried out following standard protocols, and it was compared with that of healthy subjects. Patients were positive for AbTG (22%), AbTPO (14.6%), and ANA (15.8%), and AbTG positivity was associated with VKC severity (mean ocular score ± SD positive vs. negative: 6.56 ± 2.1 vs. 4.82 ± 2.1; p = 0.03). We found that 12.2% of VKC cases had a positive family history for psoriasis, 6.4% for other cases of VKC, and 5.2% for thyroiditis, while 50.2% of them were atopic. The expression of HLA class I B37 was significantly higher in VKC patients than in controls (7.1% vs. 2.1%, p = 0.04), although not confirmed after multiple antigens testing analysis. Our study suggests a role of common components associated with immune-based diseases in the clinical expression of VKC.

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