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      Conjunctival changes and inflammatory aspects in rabbits' conjunctivas induced by fixed combinations of prostaglandin analogues and timolol maleate

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          Abstract

          Background

          The purpose of this research is to compare the histological and immunohistochemical changes induced by fixed combinations of timolol maleate and prostaglandin analogues in the rabbit conjunctiva. Thirty left eyes of rabbits, divided into three groups, were treated for 30 days with the following combinations of drugs: bimatoprost 0.03% + timolol 0.5%, travoprost 0.004% + timolol 0.5% and latanoprost 0.005 + timolol 0.5%. The right eyes served as controls and received no medication. At the end of the experiment, after enucleation, the conjunctivas were assessed through histomorphometry (number of inflammatory and goblet cells, epithelial thickness) and immunohistochemistry (anti-actin antibody to assess the degree of fibrosis).

          Results

          Histomorphometrically, there was infiltration of inflammatory cells in all the treated eyes. An increased number of goblet cells was observed with the use of all fixed combinations of prostaglandin analogues associated with timolol maleate in comparison with the control group. The combination travoprost + timolol resulted in more intense fibrosis. The effect of bimatoprost + timolol caused an intermediate reaction pattern among the other drugs, fostering higher numbers of goblet cells in the conjunctival epithelium, more than the other fixed combinations in this study. There was a difference in the comparison of goblet cells of eyes treated with bimatoprost + timolol (16.11 ± 2.42) and of those treated with latanoprost + timolol (13.18 ± 1.60) ( P = 0.016).

          Conclusion

          It was found that all fixed combinations of prostaglandins analogues + timolol induce a reaction in the conjunctiva, increasing the inflammatory infiltrate.

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          Most cited references23

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          Neuronal death in glaucoma.

          H Quigley (1998)
          Glaucoma is recognized to have its major detrimental effect upon the eye by killing retinal ganglion cells. The process of cell death appears to be initiated at the optic nerve head, though other sites of injury are possible but unsubstantiated. At present the injury at the nerve head seems related to the level of the eye pressure, but its detailed mechanism is as yet unexplained. There is a greater loss of ganglion cells from some areas of the eye, and this feature of glaucoma seems related to the regional structure of the supporting connective tissues of the optic nerve head. Larger retinal ganglion cells have been consistently shown to have somewhat greater susceptibility to injury in glaucoma, though all cells are injured, even early in the process. Ganglion cells die by apoptosis in human and experimental glaucoma, opening several potential areas for future therapies to protect them from dying. Neurotrophin deprivation is one possible cause of cell death and replacement therapy is a potential approach to treatment.
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            Ocular surface inflammatory changes induced by topical antiglaucoma drugs: human and animal studies.

            To investigate conjunctival and trabecular specimens from patients with glaucoma according to the duration and number of drugs received before filtration surgery, and to confirm, in a complementary experimental model, the role of preservative by comparing the effects of preserved and nonpreserved timolol. Experimental animal and human tissue study. Paired specimens of conjunctiva and trabeculum were taken from 61 patients undergoing trabeculectomy. Twenty-six patients were treated with 2 or more drugs for at least 1 year; 30 had received a beta-blocker for more than 1 year and 5 underwent primary surgery. A second study was performed in 25 rats receiving topical solutions in both eyes for 1 month. Immunohistochemistry was performed in all biopsy specimens using 12 different monoclonal antibodies. Ocular structures from rats treated for 1 month with preserved 0.5% timolol, nonpreserved 0.5% timolol, or 0.01% benzalkonium chloride were similarly investigated in an experimental study. Inflammatory cell infiltrates and fibroblasts were evaluated in biopsies, as well as in animal specimens, together with histologic changes induced by the drugs applied. Twenty-four of 26 conjunctivae and 21 of 24 trabecular pieces from multitreated patients were found to be abnormally infiltrated by cells expressing inflammatory or fibroblastic markers or both. Nineteen of 30 conjunctivae and 9 of 22 trabeculums in the monotherapy group and only 1 of 5 specimens from the primary surgery group were abnormal. In rats, preserved timolol and benzalkonium similarly showed infiltrates together with toxic histopathologic changes as compared to the nonpreserved timolol and control groups. These two combined studies confirmed histopathologic effects of antiglaucomatous drugs on the conjunctiva and showed similar effects in the trabecular meshwork. The experimental study showed that benzalkonium chloride is at least, to a large part, responsible for these toxic or immunoinflammatory effects or both on the ocular structures.
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              A comparison of latanoprost, bimatoprost, and travoprost in patients with elevated intraocular pressure: a 12-week, randomized, masked-evaluator multicenter study.

              To Internet Advance publication at ajo.com Feb 13, 2003. compare the intraocular pressure (IOP)-lowering effect and safety of latanoprost, bimatoprost, and travoprost in patients with open-angle glaucoma (OAG) or ocular hypertension (OH). Interventional study. This 12-week, randomized, parallel-group study was conducted at 45 US sites. Previously treated patients with OAG or OH and an IOP > or =23 mm Hg in one or both eyes after washout received either latanoprost 0.005%, bimatoprost 0.03%, or travoprost 0.004% once daily in the evening. At baseline and after 6 and 12 weeks of therapy, masked evaluators measured IOP in triplicate at 8:00 AM, 12 noon, 4:00 PM, and 8:00 PM, and masked investigators graded conjunctival hyperemia before the 8:00 AM IOP measurement. The primary efficacy outcome measure was change between baseline and Week 12 in the 8:00 AM IOP (time of peak drug effect). In all, 410 of 411 randomized patients were included in intent-to-treat analyses (latanoprost, 136; bimatoprost, 136; travoprost, 138). Baseline mean 8:00 AM IOP levels were similar (P =.772); by week 12, reductions were observed in all 3 groups (P <.001 for each). Adjusted (ANCOVA) reductions in mean IOP at 8:00 AM were similar (P =.128) as were those at 12 noon, 4:00 PM, and 8:00 PM. Fewer latanoprost-treated patients reported ocular adverse events (P <.001, latanoprost vs bimatoprost), fewer reported hyperemia (P =.001, latanoprost vs bimatoprost), and average hyperemia scores were lower at week 12 (P =.001, latanoprost vs bimatoprost). Latanoprost, bimatoprost, and travoprost were comparable in their ability to reduce IOP in OAG and OH patients. Latanoprost exhibited greater ocular tolerability.
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                Author and article information

                Contributors
                Journal
                J Ophthalmic Inflamm Infect
                J Ophthalmic Inflamm Infect
                Journal of Ophthalmic Inflammation and Infection
                Springer
                1869-5760
                2013
                28 January 2013
                : 3
                : 22
                Affiliations
                [1 ]Ophthalmology Department, Federal University of Minas Gerais, Av. Alfredo Balena, 190 3rd floor room 3005, Belo Horizonte, Minas Gerais 30130100, Brazil
                [2 ]Graefe Institute of Ophthalmology, Rua Capitão Souza Franco, 95, 80035-050, Curitiba, Parana, Brazil
                [3 ]Veterinary Department, Federal University of Parana, Rua dos Funcionarios 1540, 80035-050, Curitiba, Brazil
                [4 ]Pathology Department, Pontifical Catholic University of Parana, Rua Imaculada Conceição 1155, Prado Velho CEP, 80215-901, Curitiba, Parana, Brazil
                [5 ]Ophthalmology Department, Federal University of São Paulo, Rua Botucatu, 821, 2nd floor, 04023-062, Sao Paulo, Sao Paulo, Brazil
                Article
                1869-5760-3-22
                10.1186/1869-5760-3-22
                3605097
                23514095
                3da869ee-6125-4e66-8e7f-cc7eb0073667
                Copyright ©2013 de Faria et al; licensee Springer.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 October 2012
                : 18 October 2012
                Categories
                Original Research

                Ophthalmology & Optometry
                glaucoma,histology,immunohistochemistry,prostaglandin analogues,timolol, conjunctiva

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