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Y. Kaji, S. Amano, R. Nagai, Y. Takazawa, M. Fukayama, T. Oshika; Deposition of Advanced Glycation End Products in Climatic Droplet Keratopathy . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1649.
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© ARVO (1962-2015); The Authors (2016-present)
Climatic droplet keratopathy (CDK) is a common disease especially in equatoward and subarctic areas. However, the nature of the depositions in CDK is still unclear. To reveal the mechanism of the development of CDK, we investigated the immunohistochemical localization of advanced glycation end products (AGEs) in the surgical specimens of CDK.
We investigated corneas with CDK (n = 3), bullous keratopathy (n = 4), band keratopathy (n = 3), and corneas without any diseases (n = 4). Monoclonal antibodies to Nε–(carboxy)methyl–L–lysine (CML), pentosidine, and pyrraline were prepared. Immunohistochemical localization of AGEs was investigated using the above antibodies and streptavidin–biotin method. The immunohistochemistry was carried out triplicate.
Strong immunoreactivities to CML and pentosidine and weak immunoreactivity to pyrraline were detected in the subepithelial deposits in all specimens with CDK. In contrast, no immunoreactivities to CML, pentosidine, or pyrraline were detected in corneas with bullous keratopathy, spheroid degeneration, and control corneas.
Deposition of advanced glycation end products is a cause of climatic droplet keratopathy. In this sense, protection against ultraviolet ray, one of the accelerators of AGEs formation, would be an effective measure to prevent CDK.
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