Faculty Bibliography

PURPOSE/OBJECTIVE:To evaluate the efficacy of ultraviolet-corneal cross-linking (CXL) for treating infectious melting keratitis. METHODS:Five patients with infectious keratitis associated with corneal melting were treated with CXL at the outpatient departments of the Institut für Refraktive und Ophthalmo-Chirurgie and the eye hospital at the University of Zurich. CXL was performed when the infection did not respond to systemic and topical antibiotic therapy. Follow-up after cross-linking ranged from 1 to 9 months. RESULTS:In all cases, the progression of corneal melting was halted after CXL treatment. Emergency keratoplasty was not necessary in any of the 5 cases presented. CONCLUSIONS:CXL is a promising option for treating patients with therapy-refractory infectious keratitis to avoid emergency keratoplasty.

Glaucoma, frequently associated with high IOP (intra-ocular pressure), is a leading cause of blindness, characterized by a loss of retinal ganglion cells and the corresponding optic nerve fibres. In the present study, acutely and transiently elevated IOP, characteristic of acute angle-closure glaucoma in humans, was observed in CLR (calcitonin receptor-like receptor) transgenic mice between 1 and 3 months of age. Expression of CLR under the control of a smooth muscle alpha-actin promoter in these mice augmented signalling of the smooth-muscle-relaxing peptide adrenomedullin in the pupillary sphincter muscle and resulted in pupillary palsy. Elevated IOP was prevented in CLR transgenic mice when mated with hemizygote adrenomedullin-deficient mice with up to 50% lower plasma and organ adrenomedullin concentrations. This indicates that endogenous adrenomedullin of iris ciliary body origin causes pupillary palsy and angle closure in CLR transgenic mice overexpressing adrenomedullin receptors in the pupillary sphincter muscle. In human eyes, immunoreactive adrenomedullin has also been detected in the ciliary body. Furthermore, the CLR and RAMP2 (receptor-activity-modifying protein 2), constituting adrenomedullin receptor heterodimers, were identified in the human pupillary sphincter muscle. Thus, in humans, defective regulation of adrenomedullin action in the pupillary sphincter muscle, provoked in the present study in CLR transgenic mice, may cause acute and chronic atony and, thereby, contribute to the development of angle-closure glaucoma. The CLR transgenic mice used in the present study provide a model for acute angle-closure glaucoma.

PURPOSE/OBJECTIVE:To present early visual and keratometric results for corneal cross-linking with riboflavin and UV irradiation in patients with progressive keratoconus. METHODS:Twenty-five eyes of twenty patients (15 males and 5 females) with a progressive keratoconus in the previous 6 months were followed. Unaided visual acuity (UVA), best spectacle corrected visual acuity (BSCVA), spherical equivalent (SEQ), manifest cylinder, and maximal corneal curvature (max K) values were followed at 1, 3 and 6 months. All patients were submitted to corneal cross-linking using riboflavin (vitamin B2) as the photosensitizer and ultraviolet light (UV, wavelength 370 nm). Epithelium was removed with 20% alcohol, cornea was soaked with vitamin B2 for 15 min, and then irradiated with UV light for 30 min, after which a bandage contact lens (BCL) was placed. RESULTS:UVA increased after one month (from 0.15 +/- 0.15 to 0.23 +/- 0.20), and went on increasing at 3 and 6 months, reaching statistical significance (p=0.025 e p=0.037, respectively). BSCVA increased from 0.41 +/- 0.27 to 0.49 +/- 0.29 at month six, without reaching statistical significance at any time point. Progression of keratoconus stopped in all patients, in contrast with progression in all of them in the six-month period prior to the surgery. Max K decreased by more than 2 D (from 53.02 +/- 8.42 to 50.88 +/- 6.05 D), SEQ less that 1 D (from -3.27 +/- 4.08 to -2.68 +/- 3.02 D), while refractive cylinder decreased less than 0.5 D (from -2.29 +/- 1.77 to -1.86 +/- 0.92 D), without reaching a statistically significant difference. None of the eyes lost any line of BSCVA, 12 maintained the preoperative BSCVA, 7 gained one line, 5 gained two lines, and 1 patient gained three lines of BSCVA. CONCLUSIONS:Corneal cross-linking with riboflavin and UV light seems to be a safe (no loss of BSCVA) and effective (anatomical and optical properties maintained) procedure, which has shown to stop the progression of the keratoconus: a reduction, although not statistically significant, of the corneal curvature, spherical equivalent and refractive cylinder took place in patients where previous progression of keratoconus had been described.

PURPOSE: To determine whether riboflavin and ultraviolet-A (UVA) corneal crosslinking can be used as an alternative therapy to prevent the progression of keratectasia. SETTING: Institute for Refractive and Ophthalmic Surgery, Zurich, Switzerland, and a private clinic, Athens, Greece. METHODS: Corneal crosslinking was performed in 10 patients with formerly undiagnosed forme fruste keratoconus or pellucid marginal corneal degeneration who had laser in situ keratomileusis (LASIK) for myopic astigmatism and subsequently developed iatrogenic keratectasia. Surgery was performed in 1 eye per patient. RESULTS: Crosslinking induced by riboflavin and UVA arrested and/or partially reversed keratectasia over a postoperative follow-up of up to 25 months as demonstrated by preoperative and postoperative corneal topography and a reduction in maximum keratometric readings. CONCLUSION: Riboflavin-UVA corneal crosslinking increased the biomechanical stability of the cornea and may thus be a therapeutic means to arrest and partially reverse the progression of LASIK-induced iatrogenic keratectasia.

Adenoid cystic carcinoma (ACC) is a rare epithelial malignancy, which tends to grow slowly. ACC is an intractable neoplasm due to its ability to invade perineural spaces. Local recurrence after excision is not unusual. ACC most commonly arises in the lacrimal gland. Very rarely, ACC originates from accessory lacrimal gland tissue. Here, we present a patient with a large ACC of the central upper eyelid, which had been misdiagnosed and treated as a chalazion without histological examination. Its origin most likely is an accessory lacrimal gland.

BACKGROUND:Transconjunctival orbital decompression ("swinging eyelid technique") nowadays is the technique of choice for the reduction of proptosis in Graves' orbitopathy. Here, we present the first report of two patients who developed corneal dellen secondary to conjunctival chemosis following swinging eyelid decompression. CASE REPORTS/METHODS:Two female patients, 38 and 52 years old, underwent transconjunctival orbital decompression in 2006. Postoperatively, they developped corneal dellen secondary to conjunctival chemosis. The dellen and the chemosis completely regressed after intensive topical and oral therapy. CONCLUSION/CONCLUSIONS:Corneal dellen represent a potential cause of postoperative pain following transconjunctival orbital decompression.

PURPOSE/OBJECTIVE:In the past few years, the essential role of the homeobox gene Pax6 for eye development has been demonstrated unambiguously in a variety of species including humans. In humans, Pax6 mutations lead to a variety of ocular malformations of the anterior and posterior segment. However, little is known about PAX6 expression in the adult human retina. We have therefore investigated PAX6 levels and localization in the human retina at various ages. METHODS:Adult human eyes of various ages (17-79 years) were obtained from the Zurich Eye Bank. PAX6 expression levels and patterns were analysed by Western blot analysis of total retinal protein and by immunohistochemistry on paraffin sections, respectively. RESULTS:PAX6 expression in the retina was detected up to 79 years of donor age and was predominantly localized to the ganglion cell layer and the inner part of the inner nuclear layer. CONCLUSIONS:PAX6 remains distinctly expressed throughout the lifespan of the human retina suggesting a role for PAX6 in the retina after completion of eye morphogenesis.