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      Effect of Mitomycin-C Augmented Trabeculectomy on Corneal Endothelial Cells

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          To evaluate the effect of mitomycin-C (MMC) on corneal endothelial cell density (ECD) and morphology after trabeculectomy.


          In this prospective comparative case series, 31 eyes with glaucoma underwent trabeculectomy with (group I), or without (group II) MMC. Specular microscopy was performed pre-, and postoperatively at months 1 and 3. Outcome measures included central corneal endothelial cell count and coefficient of variation (CV) of cell size.


          Overall, mean preoperative ECD was 2,135.8 ± 397.6 cells/mm 2; corresponding values at postoperative months 1 and 3 were 2,019.6 ± 447.2 cells/mm 2, and 1,991.4 ± 425.5 cells/mm 2, respectively ( P > 0.05). Cell loss from month 1 to 3 was 1.3 % ( P > 0.05). Subgroup analysis showed significant differences in endothelial cell loss at month 1 ( P = 0.048) and month 3 ( P = 0.014) between the MMC and control groups with no significant difference between the two groups in terms of cell loss from months 1 to 3, postoperatively ( P = 0.968). Overall, mean pre-and postoperative CVs at months 1 and 3 were 27.38 ± 4.55, 27.96 ± 4.26, and 28.35 ± 4.47, respectively, with no significant difference between the two groups ( P > 0.05). There was no correlation between preoperative central endothelial cell density (CECD) and MMC related cell loss.


          MMC application in trabeculectomy seems to cause a small but significant corneal endothelial loss. Most of the damage occurs intraoperatively, or in the early postoperative period, however progressive endothelial cell loss is not a major concern.

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          Most cited references 28

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          Cell cycle status in human corneal endothelium.

           Jeffrey Joyce (2005)
          Corneal endothelium is the single-cell layer that forms a physical barrier between the corneal stroma and aqueous humour. The barrier and ionic 'pump' functions of corneal endothelium help regulate stromal hydration. Loss of endothelial cells due to increasing age, trauma, disease, dystrophy, or previous corneal transplants can reduce the density of endothelial cells to a critical point below which the stroma becomes edematous and visual acuity is lost. Throughout life, division of endothelial cells either does not occur or occurs at a rate too slow to adequately replace dead cells. Thus, the major means of repairing the monolayer is by cell migration and/or enlargement. The basis for the lack of endothelial cell proliferation is not yet fully understood, although it is clear that cells do retain proliferative capacity. Previous studies from this laboratory have identified certain environmental conditions that may be responsible for maintaining these cells in a non-replicative state in vivo. In addition, corneal endothelial cells exhibit intrinsic, age-related differences in relative proliferative capacity. The studies described below provide evidence to support the hypothesis that, with age, an increasing number of HCEC enter a replicative senescence-like state in which they become increasingly refractive to mitogenic stimulation. This decreasing sensitivity to mitogens appears to be mediated, at least in part, by age-dependent alterations in the relative expression and activity of the cyclin-dependent kinase inhibitors, p27KIP1, p16INK4A, and p21CIP1.
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            Mitomycin as adjunct chemotherapy with trabeculectomy.

             Clovis Palmer (1991)
            Preliminary experience is reported in using mitomycin to improve the prognosis in trabeculectomy operations considered otherwise likely not to succeed. The medication is applied intraoperatively during an otherwise standard trabeculectomy procedure. Surgery was considered successful if the pressure was lowered to a predetermined target level, the only vision reduction was believed to be on the basis of cataract development, and there was no progression of cupping or visual field loss. With a follow-up of 6 to 42 months, the overall success rate is 84%.
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              The corneal endothelium.

               D. Coster,  S Tuft (1989)
              The endothelium is a monolayer of cells on the posterior corneal surface that transports water from the stroma into the anterior chamber. This movement of water counters a natural tendency for the stroma to swell and is necessary to maintain a transparent cornea. Embryologic studies, in particular the demonstration of the derivation of the endothelium from the neural crest, have provided insight into the factors that govern the response of this tissue to disease. In some species the endothelium can regenerate after injury, but in man cellular enlargement is the main mechanism of repair after cell loss. A clinical estimate of endothelial cell density and function is provided by specular microscopy, fluorophotometry and pachymetry. In this paper we review the development, structure and function of the corneal endothelium, and then consider the pathological processes that can affect this tissue.

                Author and article information

                J Ophthalmic Vis Res
                J Ophthalmic Vis Res
                Journal of Ophthalmic & Vision Research
                Medknow Publications & Media Pvt Ltd (India )
                Jul-Sep 2015
                : 10
                : 3
                : 257-262
                Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
                Author notes
                Correspondence to: Ghasem Fakhraie. Farabi Eye Hospital, Qazvin Square, South Kargar Avenue, Tehran 13366, Iran. E-mail: gfakhraie@ 123456gmail.com
                Copyright: © 2015 Journal of Ophthalmic and Vision Research

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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