Riboflavin‐ultraviolet light induced cross‐linking in endothelial decompensation

Purpose: To evaluate the potential of collagen cross‐linking in the treatment of corneal oedema caused by endothelial decompensation. Methods: Riboflavin‐ultraviolet (UV) treatment induces cross‐linking and reduces stromal swelling. Eleven patients with corneal oedema were treated. The technique comprised: epithelial abrasion; instillation of 0.1% riboflavin in saline, and 5.4 J/cm² illumination with 365 nm UV‐A light over approximately 30 mins (3 mW/cm²). Results: A reduction in corneal thickness was observed in 10 patients. The majority also experienced improvement in vision. The effect occurred over weeks and lasted for months. Conclusions: The study shows a potential application of collagen cross‐linking in the management of patients with corneal oedema. Experimental and additional clinical studies are necessary in order to define the precise indications for this type of treatment.     

Pterygium‐induced corneal astigmatism

A significant degree of corneal astigmatism can be induced by the encroachment of a pterygium onto a cornea. The pterygium generally causes with‐the‐rule corneal astigmatism that is hemimeridional on the side of the pterygium. There is a significant correlation between the extension of the pterygium onto the cornea and the amount of induced astigmatism. However, there is a poor correlation between pterygium‐induced astigmatism measured topographically and that measured by manifest refraction. Successful pterygium surgery will reduce pterygium‐induced refractive astigmatism and improve visual acuity. This paper outlines the management of a patient with an advanced pterygium, in whom a large degree of corneal astigmatism was induced by the encroachment of a pterygium onto the cornea. Subsequent excision of the pterygium brought about a reversal of the pterygium‐induced corneal astigmatism.     

Delayed neovascularization in inflammation‐induced corneal neovascularization in interleukin‐10‐deficient mice

Purpose: To investigate the potential modulatory role of interleukin‐10 (IL‐10) in the suture model for corneal neovascularization. Methods: Neovascularized areas were measured on corneal flat‐mounts in IL‐10^?/? and wild‐type C57BL6 mice. The inflammatory cellular response was characterized with immunohistochemistry. Gene expression was measured by real‐time polymerase chain reaction. Results: IL‐10^?/? mice showed a delayed neovascular response compared to wild‐type animals at day 6 after suture, when approximately half of the cornea was neovascularized. No apparent differences in inflammatory responses or in messenger RNA (mRNA) expression for proangiogenic factors were detected in IL‐10^?/? versus wild‐type mice. Conclusion: IL‐10 appears to have a proangiogenic effect in the suture model for corneal neovascularization that cannot be explained by either IL‐10’s anti‐inflammatory effect or apparent cross‐talk with the angiogenic factors vascular endothelial growth factor (VEGF)‐A, metalloproteinase (MMP)‐2 and MMP‐9, angiopoietin (Ang)‐1 and Ang‐2.     

Contrast‐induced transient cortical blindness

We present a case of transient cortical blindness secondary to contrast medium toxicity. A 58‐year‐old man had successful endovascular coiling of a right posterior inferior cerebellar artery aneurysm but became confused and unable to see after the procedure. His visual acuity was no light perception bilaterally. Clinically, there was no new intra‐ocular pathology. An urgent non‐contrast computed tomography scan of the brain showed cortical hyperdensity in both parieto‐occipital cortices, consistent with contrast medium leakage through the blood–brain barrier from the coiling procedure. The man remained completely blind for 72 hours, after which his visual acuity improved gradually back to his baseline level.     

Neuroprotective effect of epigallocatechin‐3‐gallate against N‐methyl‐D‐aspartate‐induced excitotoxicity in the adult rat retina

Purpose: Epigallocatechin‐3‐gallate (EGCG), the major polyphenol of green tea, has been suggested to reduce glutamate excitotoxicity. We therefore investigated the potentially protective effects of EGCG against N‐methyl‐d ‐aspartate (NMDA)‐induced excitotoxicity in the retina. Methods: Female Wistar rats (n = 171) were divided into a normal control group (n = 9); saline control group with intravitreal saline injections (n = 54); NMDA control group with an intravitreal NMDA injection and intraperitoneal saline injections (n = 54); and NMDA study group (n = 54) receiving an intravitreal NMDA injection plus intraperitoneal EGCG (25 mg/kg) injections. Starting at 2 days prior to the intravitreal NMDA injection, the intraperitoneal injections were performed daily for the whole study period. At 12 hr, 1, 2, 3 days, 1 and 2 weeks after the intravitreal NMDA injection, the animals were killed. We counted the neurons in the retinal ganglion cell layer (GCL) on histological sections, measured the thickness of Thy‐1 immunoreactivity and assessed the expression of Thy‐1 mRNA by real‐time polymerase chain reaction. Results: At all time‐points, GCL cell density, thickness of Thy‐1 immunoreactivity and expression of Thy‐1 mRNA were significantly (all p < 0.05) lower in the NMDA control group than in the NMDA study group, in which the parameters were significantly (all p < 0.05) lower than in the saline control group and the normal control group. In both groups with an intravitreal NMDA injection, GCL cell density, thickness of Thy‐1 immunoreactivity and expression of Thy‐1 mRNA decreased significantly with increasing follow‐up time. Conclusions: Intraperitoneal application of EGCG resulted in a significantly less marked NMDA‐associated loss of retinal ganglion cells.     

Inhibition of selenite‐induced cataract by caffeine

Purpose: The objective of the investigation was to study possible inhibition of oxidative stress and cataract formation by caffeine in vivo. Methods: Oxidative stress and consequent cataract formation was induced by intraperitoneal administration of a single dose of sodium selenite (1.16 μmol) to Sprague–Dawley rat pups on day 9 postnatally. In experiments designed to inhibit such cataract formation, the pups were pretreated intraperitoneally with caffeine (5.15 μmol), starting 2 days prior to the administration of selenite and continuing such treatment till day 21, when the experiments were terminated. The extent of tissue damage caused by the selenite was assessed biochemically by measurements of the levels of GSH and ATP in the isolated lenses. Cataract formation and its prevention were monitored by examining the eye with pen light illumination and subsequent photography of the isolated lenses. Results: Injection of selenite led to a significant loss of lens clarity because of cataract formation. In the group treated with caffeine, the formation of cataract was significantly prevented. In the caffeine‐untreated group, the levels of lens GSH and ATP were substantially lower than in the caffeine‐treated group. The levels of GSH decreased from a value of ～ 8.2 μmol to ～ 2 μmol/g wet weight of the lens. The content of ATP decreased from ～ 2.5 μmol to about ～ 1 μmol. In the case of caffeine‐treated group, these decreases were significantly prevented from taking place, the corresponding values of GSH and ATP being ～ 5.8 and ～ 1.6 μmol/g, respectively. Conclusion: Over all, the results suggest that caffeine can exert a significant preventive effect against cataract formation induced by agents generating reactive oxygen species such as sodium selenite.