July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
The role of prostaglandins in floppy eyelid syndrome.
Author Affiliations & Notes
  • Brittany Simmons
    Ophthalmology, University of Rochester Medical Center, Rochester, New York, United States
  • Tailun Zhao
    Associates in Ophthalmology, West Mifflin, Pennsylvania, United States
  • Collynn Woeller
    Environmental Medicine, University of Rochester Medical Center, Rochester, New York, United States
    Ophthalmology, University of Rochester Medical Center, Rochester, New York, United States
  • Mithra Gonzalez
    Ophthalmology, University of Rochester Medical Center, Rochester, New York, United States
    Dentistry, University of Rochester Medical Center, Rochester, New York, United States
  • Footnotes
    Commercial Relationships   Brittany Simmons, None; Tailun Zhao, None; Collynn Woeller, None; Mithra Gonzalez, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 335. doi:https://doi.org/
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      Brittany Simmons, Tailun Zhao, Collynn Woeller, Mithra Gonzalez; The role of prostaglandins in floppy eyelid syndrome.. Invest. Ophthalmol. Vis. Sci. 2018;59(9):335. doi: https://doi.org/.

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

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Abstract

Purpose : Floppy Eyelid Syndrome (FES) causes significant ocular symptoms and morbidity. It is characterized by an easily everted upper eyelid, papillary conjunctivitis and eye irritation, and is often underdiagnosed. The pathogenesis and molecular etiology of the disease are unclear, though excess fatty tissue behind the eyelid is thought to drive FES. Lipid-derived mediators such as arachidonic acid-derived prostaglandins play key signaling roles in inflammation and adipogenesis, and patients on prostaglandin therapies have exhibited features similar to FES. We hypothesize that altered prostaglandin metabolism is involved in the pathogenesis of FES.

Methods : Excess tissue normally classified as surgical waste was collected from 2 sets of patients: 1) those with a diagnosis of FES undergoing horizontal tightening procedures (n=10), and 2) non-FES control patients receiving pentagonal wedge lid lesion biopsies or those requiring horizontal shortening not associated with FES (n=10). Patients with active inflammation or cancerous lesions were excluded, as were those on topical prostaglandin therapy. Tissue was flash frozen, after which quantitative real-time polymerase chain reaction (RT-PCR) was performed for microsomal prostaglandin E2 synthase (PGE2S) and prostaglandin F2α synthase (PGF2αS/AKR1C3).

Results : Normalized PGE2S mRNA levels were nearly 200% higher in FES patients compared to control patients. Normalized PGF2αS mRNA levels were roughly 30% lower in FES patients compared to controls. Interestingly, in several FES patients PGF2αS mRNA was undetectable.

Conclusions : Prostaglandins and prostaglandin-derived molecules are employed for a number of clinical therapies, and patients on prostaglandins can exhibit changes similar to those found in FES. To explore the role of prostaglandins in FES, human data derived from patient samples was used to measure expression levels of enzymes in the prostaglandin metabolic pathway. This study supports the concept that FES patients have altered prostaglandin metabolism. PGE2S and PGF2αS have a role in acute and chronic inflammatory disease. In addition, PGE2S generally promotes lipid production, whereas PGF2αS blocks adipogenesis. To further establish the roles for prostaglandin-associated pathologic changes in eyelid tissue at the structural and molecular level, additional work will include increased sample size, broader RT-PCR targets, ELISA testing for prostaglandin levels, and immunohistochemistry.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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