Possible role of the vitamin E solubilizer in topical diclofenac on matrix metalloproteinase expression in corneal melting: An analysis of postoperative keratolysis

Sylvia L. Hargrave, Jae Chang Jung, M. Elizabeth Fini, Henry Gelender, Christian Cather, Anne Guidera, Ira Udell, Stephen Fisher, James V. Jester, Robert W Bowman, James P McCulley, Harrison D Cavanagh

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Abstract

Objective: To analyze tissue matrix metalloproteinase (MMP) expression in three patients who developed postoperative corneal melts after treatment with topical diclofenac sodium 0.1% (Falcon; Fort Worth, TX) ophthalmic solution. Design: Retrospective noncomparative interventional case series with tissue analysis. Main Outcome Measures: Three patients were examined in this study. We report two patients from the same center with acute corneal melts after uncomplicated photorefractive keratectomy (PRK). Prior to these cases, 1500 patients were treated at the Zale Lipshy University Laser Center for Vision with no adverse effects. All 1500 patients were treated with the same postoperative regimen of ciprofloxacin, rimexolone, and suprofen ([Profenal, (CIBA, Duluth, GA]). The next 27 cases were treated postoperatively with ciprofloxacin and rimexolone. However, diclofenac sodium 0.1% was used instead of Profenal. A third case was also discussed. This melt occurred at another center in a postoperative cataract patient who developed cystoid macular edema after cataract extraction with intraocular lens placement. He was initially treated with diclofenac sodium 0.1% (Ciba Vision, Duluth, GA) then with diclofenac sodium 0.1%. He subsequently developed a corneal perforation requiring penetrating keratoplasty. All tissue specimens were examined by light microscopy. Microbiologic cultures and stains were also performed. Immunolocalization and in situ hybridization were performed on all keratoplasty specimens to detect expression and localization of MMPs. All patients had a complete diagnostic evaluation for systemic autoimmune diseases. Results: Postoperatively, all patients developed corneal perforations requiring surgical intervention while being treated with diclofenac sodium 0.1%. Microbiologic cultures and special stains were negative for microorganisms. Induced expression of specific tissue degrading enzymes of the matrix metalloproteinase family was demonstrated within corneal epithelial cells, stromal keratocytes, and at the level of Descemet's membrane. The uniform distribution pattern of expression was not consistent with the localization expected of a repair response, suggesting the involvement of some outside agent. Conclusions: Whereas MMP expression is a normal component of repair, excessive or inappropriate MMP activity is associated with corneal keratolysis. Our study provides preliminary evidence that topical application of diclofenac sodium 0.1% may be associated with aberrant MMP expression in the cornea.

Original languageEnglish (US)
Pages (from-to)343-350
Number of pages8
JournalOphthalmology
Volume109
Issue number2
DOIs
StatePublished - 2002

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Diclofenac
Matrix Metalloproteinases
Vitamin E
Freezing
Corneal Perforation
Ciprofloxacin
Suprofen
Coloring Agents
Descemet Membrane
Photorefractive Keratectomy
Penetrating Keratoplasty
Corneal Transplantation
Macular Edema
Cataract Extraction
Ophthalmic Solutions
Intraocular Lenses
Cornea
Cataract
Autoimmune Diseases
In Situ Hybridization

ASJC Scopus subject areas

  • Ophthalmology

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Possible role of the vitamin E solubilizer in topical diclofenac on matrix metalloproteinase expression in corneal melting : An analysis of postoperative keratolysis. / Hargrave, Sylvia L.; Jung, Jae Chang; Fini, M. Elizabeth; Gelender, Henry; Cather, Christian; Guidera, Anne; Udell, Ira; Fisher, Stephen; Jester, James V.; Bowman, Robert W; McCulley, James P; Cavanagh, Harrison D.

In: Ophthalmology, Vol. 109, No. 2, 2002, p. 343-350.

Research output: Contribution to journalArticle

Hargrave, Sylvia L. ; Jung, Jae Chang ; Fini, M. Elizabeth ; Gelender, Henry ; Cather, Christian ; Guidera, Anne ; Udell, Ira ; Fisher, Stephen ; Jester, James V. ; Bowman, Robert W ; McCulley, James P ; Cavanagh, Harrison D. / Possible role of the vitamin E solubilizer in topical diclofenac on matrix metalloproteinase expression in corneal melting : An analysis of postoperative keratolysis. In: Ophthalmology. 2002 ; Vol. 109, No. 2. pp. 343-350.
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abstract = "Objective: To analyze tissue matrix metalloproteinase (MMP) expression in three patients who developed postoperative corneal melts after treatment with topical diclofenac sodium 0.1{\%} (Falcon; Fort Worth, TX) ophthalmic solution. Design: Retrospective noncomparative interventional case series with tissue analysis. Main Outcome Measures: Three patients were examined in this study. We report two patients from the same center with acute corneal melts after uncomplicated photorefractive keratectomy (PRK). Prior to these cases, 1500 patients were treated at the Zale Lipshy University Laser Center for Vision with no adverse effects. All 1500 patients were treated with the same postoperative regimen of ciprofloxacin, rimexolone, and suprofen ([Profenal, (CIBA, Duluth, GA]). The next 27 cases were treated postoperatively with ciprofloxacin and rimexolone. However, diclofenac sodium 0.1{\%} was used instead of Profenal. A third case was also discussed. This melt occurred at another center in a postoperative cataract patient who developed cystoid macular edema after cataract extraction with intraocular lens placement. He was initially treated with diclofenac sodium 0.1{\%} (Ciba Vision, Duluth, GA) then with diclofenac sodium 0.1{\%}. He subsequently developed a corneal perforation requiring penetrating keratoplasty. All tissue specimens were examined by light microscopy. Microbiologic cultures and stains were also performed. Immunolocalization and in situ hybridization were performed on all keratoplasty specimens to detect expression and localization of MMPs. All patients had a complete diagnostic evaluation for systemic autoimmune diseases. Results: Postoperatively, all patients developed corneal perforations requiring surgical intervention while being treated with diclofenac sodium 0.1{\%}. Microbiologic cultures and special stains were negative for microorganisms. Induced expression of specific tissue degrading enzymes of the matrix metalloproteinase family was demonstrated within corneal epithelial cells, stromal keratocytes, and at the level of Descemet's membrane. The uniform distribution pattern of expression was not consistent with the localization expected of a repair response, suggesting the involvement of some outside agent. Conclusions: Whereas MMP expression is a normal component of repair, excessive or inappropriate MMP activity is associated with corneal keratolysis. Our study provides preliminary evidence that topical application of diclofenac sodium 0.1{\%} may be associated with aberrant MMP expression in the cornea.",
author = "Hargrave, {Sylvia L.} and Jung, {Jae Chang} and Fini, {M. Elizabeth} and Henry Gelender and Christian Cather and Anne Guidera and Ira Udell and Stephen Fisher and Jester, {James V.} and Bowman, {Robert W} and McCulley, {James P} and Cavanagh, {Harrison D}",
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T1 - Possible role of the vitamin E solubilizer in topical diclofenac on matrix metalloproteinase expression in corneal melting

T2 - An analysis of postoperative keratolysis

AU - Hargrave, Sylvia L.

AU - Jung, Jae Chang

AU - Fini, M. Elizabeth

AU - Gelender, Henry

AU - Cather, Christian

AU - Guidera, Anne

AU - Udell, Ira

AU - Fisher, Stephen

AU - Jester, James V.

AU - Bowman, Robert W

AU - McCulley, James P

AU - Cavanagh, Harrison D

PY - 2002

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N2 - Objective: To analyze tissue matrix metalloproteinase (MMP) expression in three patients who developed postoperative corneal melts after treatment with topical diclofenac sodium 0.1% (Falcon; Fort Worth, TX) ophthalmic solution. Design: Retrospective noncomparative interventional case series with tissue analysis. Main Outcome Measures: Three patients were examined in this study. We report two patients from the same center with acute corneal melts after uncomplicated photorefractive keratectomy (PRK). Prior to these cases, 1500 patients were treated at the Zale Lipshy University Laser Center for Vision with no adverse effects. All 1500 patients were treated with the same postoperative regimen of ciprofloxacin, rimexolone, and suprofen ([Profenal, (CIBA, Duluth, GA]). The next 27 cases were treated postoperatively with ciprofloxacin and rimexolone. However, diclofenac sodium 0.1% was used instead of Profenal. A third case was also discussed. This melt occurred at another center in a postoperative cataract patient who developed cystoid macular edema after cataract extraction with intraocular lens placement. He was initially treated with diclofenac sodium 0.1% (Ciba Vision, Duluth, GA) then with diclofenac sodium 0.1%. He subsequently developed a corneal perforation requiring penetrating keratoplasty. All tissue specimens were examined by light microscopy. Microbiologic cultures and stains were also performed. Immunolocalization and in situ hybridization were performed on all keratoplasty specimens to detect expression and localization of MMPs. All patients had a complete diagnostic evaluation for systemic autoimmune diseases. Results: Postoperatively, all patients developed corneal perforations requiring surgical intervention while being treated with diclofenac sodium 0.1%. Microbiologic cultures and special stains were negative for microorganisms. Induced expression of specific tissue degrading enzymes of the matrix metalloproteinase family was demonstrated within corneal epithelial cells, stromal keratocytes, and at the level of Descemet's membrane. The uniform distribution pattern of expression was not consistent with the localization expected of a repair response, suggesting the involvement of some outside agent. Conclusions: Whereas MMP expression is a normal component of repair, excessive or inappropriate MMP activity is associated with corneal keratolysis. Our study provides preliminary evidence that topical application of diclofenac sodium 0.1% may be associated with aberrant MMP expression in the cornea.

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