Outcomes of corneal transplantation: a corneal surgeon vs the general ophthalmologist.

AIMS: The aim of this study was to examine the outcomes of corneal transplantation in cases performed by a group of general ophthalmologists and those performed by an ophthalmologist with a subspecialist interest in corneal surgery. METHODS: A retrospective analysis of the outcomes in corneal transplantation was carried out for a 4-year period in three separate units in South Wales. In addition to patient demographic details, the primary diagnosis, type of keratoplasty performed, and outcome of surgery were noted. The data were analysed statistically by the Mann-Whitney U-test (one-tailed). RESULTS: Group A (n=35) was defined as those patients whose surgery was performed by a general ophthalmologist. There were seven surgeons in this group with a mean of five procedures each over the study period. Group B (n=54) were all operated on by the same surgeon. The mean age in both groups was similar with group A comprising of 66% males with 50% males in group B. The commonest indication for surgery in both groups was endothelial cell failure In group A, graft clarity at 1 year was 83% for all aetiologies and 73% at 2 years. In group B, the results were 97 and 92%, respectively. In group A, overall 56% achieved 6/18 or better compared with 68% in group B. In group A 73% had an improvement of one or more lines compared with 84% in group B (P=0.085). Reasons for graft failure in both groups were similar. CONCLUSION: The success rate of corneal transplantation carried out by general ophthalmologists in this study is reduced when compared with cases performed by a corneal surgeon. The explanation for this is not clear, but is undoubtedly multifactorial.

Ultrastructural morphology and expression of proteoglycans, betaig-h3, tenascin-C, fibrillin-1, and fibronectin in bullous keratopathy.

AIMS: To investigate the ultrastructural localisation of proteoglycans (PG), betaig-h3 (keratoepithelin), tenascin-C (TN-C)), fibrillin, and fibronectin in bullous keratopathy (BK) corneas. METHODS: Five corneas from cases of pseudophakic bullous keratopathy (BK) were examined by electron microscopy. PG were demonstrated using cuprolinic blue, and the proteins betaig-h3, TN-C, fibrillin, and fibronectin were immunolocalised with rabbit anti-betaig-h3, mouse anti-TN-C (BC10 and TN2), mouse anti-fibrillin-1 (MAB2502), mouse anti-fibrillin (MAB1919), and rabbit anti-fibronectin by using a standard immunogold technique. RESULTS: Epithelial cells contained numerous vacuoles. Epithelial folds and large, electron lucent subepithelial bullae were present. Basal lamina was thickened and traversed by disrupted anchoring filaments. In the stroma, interfibrillar collagen spacing was increased and abnormally large PG were present. Descemet's membrane (DM) contained lucent spaces in which there were small filaments. Keratocyte and endothelial cells contained melanin granules. A posterior collagenous layer (PCL) contained numerous microfilaments and wide spacing collagen fibres with a periodicity of 100 nm. Large quantities of abnormal PG were observed at the endothelial face of the PCL. Very strong labelling with betaig-h3 antibody was observed in the basement membrane, Bowman's layer, stroma, DM, and PCL, but not in keratocytes and endothelial cells. Strong labelling with BC10 and TN2 was seen below the epithelium, in electron lucent spaces where the hemidesmosomes were absent, in the fibrotic pannus, in parts of Bowman's layer, the stroma, and Descemet's membrane. Labelling with BC10 was stronger and more evenly distributed than with TN2. Fibrillin-1 (MAB2502) and fibrillin (MAB1919) labelling was similar to TN-C labelling. Fibrillin (MAB1919) labelling was stronger than fibrillin-1 (MAB2502) labelling. CONCLUSIONS: Immunoelectron microscopy showed precise labelling of proteins at both the cellular and the subcellular level. Expression of proteins betaig-h3, TN-C, fibrillin, and fibronectin was highly increased compared with normal cornea. In the oedematous stroma, increased collagen fibril separation may facilitate a wider distribution of some soluble proteins, such as betaig-h3, throughout stroma. The modified expression of the proteins studied in these cases of BK may be regarded as part of an injury response.

Tarantula keratouveitis.

PURPOSE: To report a case of chronic bilateral keratouveitis, which was initiated after contact with a pet tarantula. METHODS: A 16-year-old male presented with a photophobia and redness of his eyes two days after handling a tarantula. He was found to have a number of linear corneal foreign bodies with subepithelial infiltrates. The infiltrates were found at varying levels of the corneal stroma with deposits on the endothelium. The anterior chamber had a mild cellular reaction. RESULTS: He was treated with topical steroid drops, which made him asymptomatic. However, he continued to have a mild persistent keratitis and iritis four months after the onset. CONCLUSION: Tarantula hairs may be associated with a chronic keratouveitis, which is usually self-limiting and responds well to treatment with topical steroids. Tarantula pet owners should be forewarned of the ocular dangers associated with handling these spiders.

Aland island eye disease: clinical and electrophysiological studies of a Welsh family.

Clinical and molecular genetic studies were performed on a single, large, white family, in which congenital nystagmus and moderate to high refractive error segregated as a sex linked trait with manifestation in some female carriers. In this family, affected males demonstrate myopia, but a high proportion of female carriers, and some of the possibly affected males, show hypermetropia. Clinical ophthalmic examination and electrodiagnostic studies of retinal function were fully compatible with a diagnosis of either incomplete congenital stationary night blindness or of Aland island eye disease. Previous studies have mapped both disorders to the proximal short arm of the X chromosome: our molecular studies support this localisation. Incomplete congenital stationary nightblindness and Aland Island eye disease could be considered as a single entity.