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1 General aspects (0)   1.1 Epidemiology (3)   1.2 Population genetics (1)   1.3 Pathogenesis (3)   1.4 Quality of life (4)   1.5 Glaucomas as cause of blindness (2)   1.6 Prevention and screening (4) 2 Anatomical structures in glaucoma (1)   2.1 Conjunctiva (1)   2.2 Cornea (8)   2.3 Sclera (1)   2.4 Anterior chamber angle (0)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (12)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (3)     2.6.1 Production (0)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (2)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (3)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (0)   2.13 Retina and retinal nerve fibre layer (11)   2.14 Optic disc (5)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (2)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (8)   3.1 Microscopy (2)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (13)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (10)     3.4.2 Gene studies (4)   3.5 Molecular biology incl. 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with intraocular tumors (0)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (0)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (1)       9.4.11.2 Glaucomas in aphakia and pseudophakia (1)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (0)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (2)     9.4.15 Glaucoma in relation to systemic disease (5)     9.4.20 Other (0) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (6) 11 Medical treatment (0)   11.1 General management, indication (8)   11.2 Cholinergic drugs (1)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (0)     11.3.4 Betablocker (12)     11.3.5 Other (0)   11.4 Prostaglandins (31)   11.5 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Without tube implant (9)     12.8.2 With tube implant or other drainage devices (12)     12.8.3 Non-perforating (6)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (10)     12.8.11 Complications, endophthalmitis (8)   12.9 Trabeculotomy, goniotomy (1)   12.10 Cyclodestruction (3)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (12)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (1)     12.14.3 Phacoemulsification (7)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (0)   12.20 Other (6) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (5) 15 Miscellaneous (10)

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Abstract #12511 Published in IGR 7-2

Prolonged antiscarring effects of ilomastat and MMC after experimental glaucoma filtration surgery

Wong TT; Mead AL; Khaw PT
Investigative Ophthalmology and Visual Science 2005; 46: 2018-2022

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PURPOSE: To determine the long-term antiscarring effect of ilomastat treatment after experimental glaucoma filtration surgery (GFS). METHODS: In a randomized, prospective, masked-observer study, 21 New Zealand White rabbits underwent modified GFS. The animals were allocated to receive either intraoperative mitomycin-C (MMC) at a concentration of 0.2 mg/mL or postoperative subconjunctival injections of either ilomastat or phosphate-buffered saline (PBS). Fifteen injections were given to each animal during the study period. The animals were killed 60 days after surgery. Bleb morphology and intraocular pressures were recorded. Tissue sections were immunohistochemically stained for signs of scarring. RESULTS: Ilomastat significantly improved surgical outcome compared with vehicle (P < 0.0163) and length of bleb survival was similar to the MMC group. The mean day of failure was 46.2 (range, 42-60) with ilomastat, 51.3 (range, 49-60) with MMC, and 16 (range, 15-21) with vehicle. IOP maintenance with ilomastat was similar to that in the MMC group. Histologically, minimal scar tissue was seen with MMC and ilomastat. MMC-treated tissue demonstrated subconjunctival hypocellularity associated with peripheral fibrosis. Ilomastat resulted in normal-appearing conjunctival morphology. CONCLUSIONS: Ilomastat successfully prolongs bleb survival. MMP inhibition may provide an additional, potentially safer method of controlling intraocular pressure, thus preventing failure of glaucoma surgery, and may also act as a potential adjuvant treatment when MMC alone is inadequate.

Dr. T.T. Wong, Ocular Repair and Regeneration Biology Unit, Institute of Ophthalmology, London, UK. tina.wong@ucl.ac.uk

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Classification:

12.8.10 Woundhealing antifibrosis (Part of: 12 Surgical treatment > 12.8 Filtering surgery)

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