May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Plasminogen activator inhibitor in human tears after laser refractive surgery
Author Affiliations & Notes
  • D.M. Silver
    Applied Physics Laboratory, Johns Hopkins University, Laurel, MD
    Ophthalmology,
    University of Debrecen, Medical and Health Science Center, Faculty of Medicine, Debrecen, Hungary
  • A. Csutak
    Ophthalmology,
    University of Debrecen, Medical and Health Science Center, Faculty of Medicine, Debrecen, Hungary
  • Z. Steiber
    Ophthalmology,
    University of Debrecen, Medical and Health Science Center, Faculty of Medicine, Debrecen, Hungary
  • Z. Hassan
    Ophthalmology,
    University of Debrecen, Medical and Health Science Center, Faculty of Medicine, Debrecen, Hungary
  • J. Tőzsér
    Biochemistry & Molecular Biology,
    University of Debrecen, Medical and Health Science Center, Faculty of Medicine, Debrecen, Hungary
  • A. Berta
    Ophthalmology,
    University of Debrecen, Medical and Health Science Center, Faculty of Medicine, Debrecen, Hungary
  • Footnotes
    Commercial Relationships  D.M. Silver, None; A. Csutak, None; Z. Steiber, None; Z. Hassan, None; J. Tőzsér, None; A. Berta, None.
  • Footnotes
    Support  Hungarian Scientific Research Fund OTKA #T038351 & Ministry of Health ETT Grant #185/2001
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 4860. doi:
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      D.M. Silver, A. Csutak, Z. Steiber, Z. Hassan, J. Tőzsér, A. Berta; Plasminogen activator inhibitor in human tears after laser refractive surgery . Invest. Ophthalmol. Vis. Sci. 2004;45(13):4860.

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

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Abstract

Abstract: : Purpose: To observe levels of urokinase–type plasminogen activator inhibitor, PAI–2, in human tears after photorefractive keratectomy (PRK) or laser in situ keratomileusis (LASIK). Methods: Tear samples were collected with glass capillaries from 47 PRK and 13 LASIK patient eyes immediately before and after surgery and on the first (LASIK), third (PRK) and fifth (PRK) post–op days. Enzyme–linked immunoassay (Imubind ELISA) was used for analysis: 148 PRK and 36 LASIK determinations. Haze grading of subepithelial haze was performed using the system of Hanna. Informed consent was obtained from patients in adherence to the Declaration of Helsinki. Results: PRK PAI–2 was found at mean (SD) concentrations of 1.0 (1.2) ng/ml in pre–op tears, 5.5 (3.1) ng/ml at post–op, 0.6 (1.0) ng/ml after 3 days and 0.8 (1.0) ng/ml after 5 days. One PRK patient had an elevated PAI–2 level of 5.7 ng/ml at pre–op, with a depression to 3.8 ng/ml at post–op. This was the only PRK patient to develop haze. All other PRK patients had PAI–2 values less than 3.3 ng/ml at pre–op. LASIK PAI–2 was found at 2.2 (4.6) ng/ml at pre–op, 5.6 (3.5) ng/ml at post–op and 0.8 (0.9) ng/ml after 1 day. Two LASIK patients had high PAI–2 levels (16.6 and 5.1 ng/ml) at pre–op, with a depression at post–op (4.8 and 1.4 ng/ml, respectively). All other LASIK patients had PAI–2 values less than 3.5 ng/ml at pre–op. None of the LASIK patients developed haze. Conclusions: PAI–2 is activated after PRK and LASIK and is expected to influence the plasminogen activator cascade. The similarity in the general time pattern of PAI–2 after PRK and LASIK suggests a common enzymatic wound response to corneal surgical wounding. The unique pattern of elevated pre–op PAI–2 concentration in the one PRK patient that eventually developed haze may be indicative or causative of the eventual haze condition. However, the two LASIK patients that had a similar pre–op elevation of PAI–2 did not develop haze, perhaps due to a difference in the course and position of corneal wound healing between PRK and LASIK.

Keywords: wound healing • enzymes/enzyme inhibitors • cornea: basic science 
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