May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Secondary Corneal Amyloidosis Proving an Association with Lactoferrin
Author Affiliations & Notes
  • K. Kitagawa
    Ophthalmology, Kanazawa Medical University, Uchinada, Japan
  • T. Nakamura
    Ophthalmology, Kanazawa Medical University, Uchinada, Japan
  • T. Nojima
    Pathology, Kanazawa Medical University Hospital, Uchinada, Japan
  • Y. Ando
    Laboratory Medecine, Kumamoto University School of Medecine, Kumamoto, Japan
  • N. Takahashi
    Laboratory Medecine, Kumamoto University School of Medecine, Kumamoto, Japan
  • Footnotes
    Commercial Relationships  K. Kitagawa, None; T. Nakamura, None; T. Nojima, None; Y. Ando, None; N. Takahashi, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1401. doi:
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      K. Kitagawa, T. Nakamura, T. Nojima, Y. Ando, N. Takahashi; Secondary Corneal Amyloidosis Proving an Association with Lactoferrin . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1401.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Secondary corneal amyloidosis rarely appears after chronic irritation from trichiasis. The origin of the amyloid protein localized in the cornea has not yet been sufficiently proven, although the precursor protein in lattice corneal dystrophy has been revealed to be mutant gelsolin. Lactoferrin is an iron-binding glycoprotein found in lacrimal fluid. We studied the association of lactoferrin with secondary corneal amyloidosis. Methods: Subepithelial nodular excrescent lesions in the lower center of the cornea were therapeutically taken from a young female patient who was clinically diagnosed with secondary corneal amyloidosis in the right eye due to trichiasis. Ocular and systemic examinations were performed. Histochemical studies and lactoferrin gene analysis were performed of the taken samples after obtaining informed consent. Results: The samples were confirmed as being amyloid with positive Congo red stain which emitted green light under polarized light, with the existence of amyloid fibrils noted under an electron microscope. No abnormalities were noted in the ocular examinations except for hyperopic astigmatism in the right eye, and there was no evidence of systemic amyloidosis either. Immunoreactivity of antibodies against human lactoferrin and serum amyloid P component was recognized. Lactoferrin gene analysis also revealed a Glu561Asp mutation. Conclusions: These results indicate that lactoferrin forms amyloid in the cornea especially in patients with lactoferrin gene mutation.

Keywords: degenerations/dystrophies • immunohistochemistry • gene/expression 
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