May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Loteprednol Etabonate (Lotemax, 0.5%) Reduces Inflammatory Response Associated With Pterygium Progression
Author Affiliations & Notes
  • H. T. Nguyen
    Eastern Virginia Medical School, Norfolk, Virginia
    Physiological Sciences,
  • S. S. Samudre
    Eastern Virginia Medical School, Norfolk, Virginia
    Physiological Sciences,
  • F. A. Lattanzio, Jr.
    Eastern Virginia Medical School, Norfolk, Virginia
    Physiological Sciences,
  • P. B. Williams
    Eastern Virginia Medical School, Norfolk, Virginia
    Physiological Sciences,
  • J. D. Sheppard, Jr.
    Eastern Virginia Medical School, Norfolk, Virginia
    Ophthalmology,
  • Footnotes
    Commercial Relationships  H.T. Nguyen, None; S.S. Samudre, None; F.A. Lattanzio, None; P.B. Williams, None; J.D. Sheppard, Bausch and Lomb, C.
  • Footnotes
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Investigative Ophthalmology & Visual Science May 2008, Vol.49, 6027. doi:https://doi.org/
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      H. T. Nguyen, S. S. Samudre, F. A. Lattanzio, Jr., P. B. Williams, J. D. Sheppard, Jr.; Loteprednol Etabonate (Lotemax, 0.5%) Reduces Inflammatory Response Associated With Pterygium Progression. Invest. Ophthalmol. Vis. Sci. 2008;49(13):6027. doi: https://doi.org/.

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

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Abstract

Purpose: : Pterygium is a fibrovascular tissue growth onto the cornea that is continuous with the conjunctiva. It is associated with ultraviolet light exposure. When pterygia encroach upon the visual axis, they induce significant astigmatism and irritation. Pterygia are commonly treated surgically but have a recurrence rate of greater than 40%. Treatment with corticosteroids is hypothesized to delay pterygium progression. The objective of this study is to evaluate the efficacy of loteprednol etabonate (0.5%) by evaluating glucocorticoid receptor migration.

Methods: : In this study, 5 patients with mild to severe pterygium were enrolled. Patients were treated with loteprednol etabonate (0.5%) twice daily for 2 wks, after which the pterygia were excised surgically. In addition to the pterygium tissue, conjunctival tissues were excised from the corneal, posterior, limbal area of the pterygia. A normal conjunctival sample was also excised form the affected eye. Samples were then homogenized in RIPA Buffer, supernatant was collected, and protein and Western blots analysis were performed. The glucocorticoid receptor activation was measured as a function of glucocorticoid migration from the cytosol into the nucleus.

Results: : Control conjunctival protein concentration was 0.95±0.5 ug/ul. Pterygium protein concentration was elevated to 1.2±0.9 ug/ul (n=4). Posterior and limbal pterygium protein concentration was not markedly different. The GCR migration was greatest at the corneal site > limbal = posterior > control. This may reflect selective steroid uptake by inflamed conjunctival tissues.

Conclusions: : GCR activation and migration were readily measured for the first time in human conjunctival tissues, correlating well with our animal model. The absence of GCR in the cytosol reflects an activated receptor that has migrated to the nucleus. Receptor migration activity increased significantly following treatment with loteprednol. Loteprednol had the greatest effect on pterygium tissues, with lesser effect on normal tissues. Additional study of untreated conjunctiva and other ocular surface diseases is warranted.

Keywords: pterygium • inflammation • corticosteroids 
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