American Journal of Ophthalmology
Volume 125, Issue 6 , Pages 844-851, June 1998

Gelatinase B in proliferative vitreoretinal disorders☆

  • Ahmed M. Abu El-Asrar, MD

      Affiliations

    • Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia (Dr Abu El-Asrar)
    • Corresponding Author InformationCorrespondence to Ahmed M. Abu El-Asrar, MD, Department of Ophthalmology, King Abdulaziz University Hospital, Airport Rd, PO Box 245, Riyadh 11411, Saudi Arabia; fax: 966-1-477-5741
    • ,
  • Lieve Dralands, MD

      Affiliations

    • Department of Ophthalmology Leuven, Belgium (Drs Dralands, Veckeneer, and Missotten)
    • ,
  • Marc Veckeneer, MD

      Affiliations

    • Department of Ophthalmology Leuven, Belgium (Drs Dralands, Veckeneer, and Missotten)
    • ,
  • Karel Geboes, MD

      Affiliations

    • Laboratory of Histochemistry and Cytochemistry Leuven, Belgium (Dr Geboes), University Hospital St Rafael, Leuven, Belgium
    • ,
  • Luc Missotten, MD

      Affiliations

    • Department of Ophthalmology Leuven, Belgium (Drs Dralands, Veckeneer, and Missotten)
    • ,
  • Ilse Van Aelst

      Affiliations

    • Rega Institute for Medical Research, Laboratory of Molecular Immunology (Ms Van Aelst and Dr Opdenakker), University of Leuven, Leuven, Belgium
    • ,
  • Ghislain Opdenakker, MD, PhD

      Affiliations

    • Rega Institute for Medical Research, Laboratory of Molecular Immunology (Ms Van Aelst and Dr Opdenakker), University of Leuven, Leuven, Belgium

Accepted 23 September 1997.

Abstract 

Purpose: To investigate whether gelatinases A and B are involved in the pathogenesis of proliferative vitreoretinal disorders.

Methods: In a prospective study of 101 consecutive patients, vitreous and paired serum samples were obtained from 38 patients with rhegmatogenous retinal detachment complicated by proliferative vitreoretinopathy, 25 patients with rhegmatogenous retinal detachment with no proliferative vitreoretinopathy, and 38 patients with proliferative diabetic retinopathy. Gelatinase activities were determined by quantitative zymography.

Results: All vitreous samples contained comparable levels of the constitutive gelatinase A. Inducible gelatinase B was detected in eight (32%) of 25 vitreous samples from patients with rhegmatogenous retinal detachment with no proliferative vitreoretinopathy (mean ± SD, 319.5 ± 521.0 scanning units), in 17 (44.7%) of 38 vitreous samples from patients with proliferative vitreoretinopathy (560.6 ± 718.9 scanning units), and in 34 (89.5%) of 38 vitreous samples from patients with proliferative diabetic retinopathy (1,707.2 ± 1,220.3 scanning units). The incidence of detection of gelatinase B in proliferative diabetic retinopathy cases was significantly higher than it was in rhegmatogenous retinal detachment with no proliferative vitreoretinopathy and proliferative vitreoretinopathy cases (P < .001). Gelatinase B levels in the vitreous samples of patients with proliferative diabetic retinopathy were higher than the levels found in patients with rhegmatogenous retinal detachment with no proliferative vitreoretinopathy and in patients with proliferative vitreoretinopathy (P = .0152). Gelatinase A was detected in all the tested sera, whereas none of the tested paired serum samples contained detectable gelatinase B activity.

Conclusions: Gelatinase B may play an important role in extracellular matrix degradation associated with neovascularization in proliferative diabetic retinopathy.

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☆ This study was supported by the Geconcerteerde OnderzoeksActies (Dr Opdenakker) and by the Fonds voor Wetenschappelijk Onderzoek-Vlaanderen (Dr Opdenakker).

PII: S0002-9394(98)00041-5

American Journal of Ophthalmology
Volume 125, Issue 6 , Pages 844-851, June 1998

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