June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Analysis of Inflammatory Markers and Clinical Inflammation After Cataract Surgery in Glaucoma
Author Affiliations & Notes
  • Mazeyar Saboori
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Sonia Rana
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Pawan Kumar Singh
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Saya Nagori
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Justin Tannir
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Aman Shukairy
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Mark S Juzych
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Bret A Hughes
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Ashok Kumar
    Ophthalmology, Kresge Eye Inst/Wayne State Univ, Royal Oak, MI
  • Footnotes
    Commercial Relationships Mazeyar Saboori, None; Sonia Rana, None; Pawan Kumar Singh, None; Saya Nagori, None; Justin Tannir, None; Aman Shukairy, None; Mark Juzych, None; Bret Hughes, None; Ashok Kumar, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 1994. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Mazeyar Saboori, Sonia Rana, Pawan Kumar Singh, Saya Nagori, Justin Tannir, Aman Shukairy, Mark S Juzych, Bret A Hughes, Ashok Kumar; Analysis of Inflammatory Markers and Clinical Inflammation After Cataract Surgery in Glaucoma. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1994.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Inflammation is reported as one of the underlying mechanisms of ganglion cell death. Glaucoma patients undergoing cataract surgery exhibit increased inflammation in the postoperative period than those without glaucoma. Our aim is to assess the levels of inflammatory mediators in these two groups and identify markers for diagnosis or treatment, and to correlate these findings with an experimental glaucoma model.

Methods: Aqueous humor of 15 patients were collected prior to cataract surgery using a cannula via anterior chamber paracentesis and then stored in liquid nitrogen. Clinical inflammation was graded over a 1 month course postoperatively using the Standardization of Uveitis Nomenclature (SUN) grading scheme. Of the 15 samples, only 12 with adequate sample quantity were subject to cytokine/chemokine assays. Following protein estimation, equal amounts of protein were mixed with beads coated with antibodies against IL-6, IL-8, IL1b, IL 10, and TNF-α. Stained samples were analyzed using Flowcytometry. Our secondary aim in the experimental model used C57BL/6 mice injected with microbeads in the anterior chamber. IOP was measured on alternate days. The expression of inflammatory cytokines was assessed by RT-PCR and ELISA and retinal ganglion cell death was determined by TUNEL staining in retinal cryosections.

Results: Of the patients, 50% had Primary Open Angle Glaucoma (POAG), 17% were Glaucoma Suspects (GS) and 33% did not have either (controls). The average amount of IL6 was 227.7 femtograms/ml (fg/ml) in POAG patients, markedly higher compared to normal. The average levels of IL-1β, IL8, TNF-α, and IL10 varied among the groups ranging from 0.03 fg/ml to 227.7 fg/ml. The average level of postoperative inflammation showed an increased trend in POAG patients over one month. The experimental model showed increased intraocular pressure (IOP) within one week which remained elevated up to 3 weeks. Increased levels of cytokines were detected in the mouse tissue coinciding with increased ganglion cell death.

Conclusions: Our pilot study showed a trend of increased postoperative inflammation and inflammatory cytokines in POAG patients. Higher IOP resulted in higher levels of inflammatory mediators and ganglion cell death in the glaucoma mouse model. Further studies with increased patient sample size are needed to draw a conclusion and determine the mechanism of increased inflammation in POAG patients.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×