Keratoconus unmasked by unilateral ptosis repair.

Astigmatic changes have been shown to occur after ptosis repair due to the altered vector forces on the underlying cornea from the repositioned upper eyelid. The astigmatic change is usually transient, but it may affect a patient's vision for at least the first few months after surgery. The authors present a case of a patient who underwent ptosis repair and subsequently developed postoperative decline in best-corrected visual acuity due to previously undiagnosed keratoconus. The patient's irregular astigmatism seems to have been masked by the ptotic upper eyelid, which we postulate to have acted similar to a stenopaic slit. Correction of the upper eyelid ptosis unveiled previously asymptomatic irregular astigmatism including vertical coma, leading to alteration in the optical wavefront and resultant image degradation.

Soluble vascular endothelial growth factor receptor-1 contributes to the corneal antiangiogenic barrier.

PURPOSE: Pathological neovascularisation within the normally avascular cornea is a serious event that can interfere with normal vision. Upregulation of vascular endothelial growth factor (VEGF) has been associated with neovascularisation in the eye, suggesting that maintaining low levels of VEGF is important for corneal avascularity and intact vision. This study aims to determine the expression profile and possible contribution of sVEGFR-1 to the corneal avascular barrier. DESIGN: Experimental case series investigating VEGF and soluble fms-like tyrosine kinase (sFlt) levels in normal and neovascularised human corneas. PARTICIPANTS: Four normal human corneas, five human corneas with alkali burns, three human corneas with aniridia, one with ocular cicatricial pemphigoid and two with interstitial keratitis were examined. METHODS: Western blot and immunohistochemical analyses were performed to determine sFlt and VEGF levels in normal and neovascularised human corneas. Immunoprecipitation was utilised to demonstrate sFlt-VEGF binding. RESULTS: Normal human corneas strongly express sFlt in the corneal epithelium and weakly in the corneal stroma close to the limbus. VEGF is bound by sFlt in the normal human cornea. Neovascularised human corneas have greatly reduced expression of sFlt and significantly less VEGF bound by sFlt. CONCLUSIONS: sFlt is highly expressed in the human cornea and normally sequesters VEGF.