Antiviral treatment following penetrating keratoplasty for herpetic keratitis.

PURPOSE: To assess the effect of antiviral treatment on corneal graft survival following penetrating keratoplasty for herpetic keratitis. METHODS: Retrospective cohort study of 454 patients receiving primary penetrating keratoplasties (PKs) for viral infection reported to NHS Blood and Transplant (NHSBT) between April 1999 and June 2005. Follow-up data were available on 403 PKs. Kaplan-Meier survival estimates were used to determine graft survival for the three treatment groups: no medication, topical antiviral, and oral antiviral medication. A Cox regression model was used to investigate the combined effects of all additional factors on graft failure. The model was fitted using all pre-operative factors first and then post-operative factors including type of antiviral medication were included. RESULTS: Patients who received oral antiviral medication post-operatively had consistently better graft survival than those receiving no medication or only topical medication. Patients receiving oral antivirals were less than a third as likely to have a failed graft at 5 years compared with those on no antiviral medication (relative risk (RR) 0.3, CI: 0.2-0.7, P=0.002). Other factors that were found to influence the risk of graft failure were the presence of deep corneal vascularisation (P=0.009), PK performed for therapeutic reasons (P=0.03), large diameter grafts (P=0.04), and experiencing a rejection episode (P=0.003). CONCLUSION: Oral antiviral treatment reduces the risk of graft failure in patients undergoing primary PK for herpetic keratitis and should be routinely used in this group of patients post-operatively unless contra-indicated.

Mutational screening of VSX1 in keratoconus patients from the European population.

PURPOSE: To perform mutational screening of the visual system homeobox gene 1 (VSX1; MIM#605020) in patients with sporadic and familial keratoconus (MIM#148300) in a European population and, for the first time, report the mutational analysis of the two newly identified VSX1exons. METHODS: VSX1sequence variants in patients with keratoconus were evaluated by direct sequencing of the entire coding region, including two novel exons. In familial keratoconus cases, segregation of potentially pathogenic VSX1variants was assessed to determine pathogenicity. Transcript analysis was carried out on splice site and synonymous sequence variants not detected in controls. RESULTS: A total of 66 unrelated patients with keratoconus from the European population (27 with familial keratoconus; 39 with sporadic keratoconus) were analysed for VSX1 mutations. Four sequence variants were not observed in 100 healthy control individuals: c.432C>G (p.D144E), c.479G>A (p.G160D), c.789C>T (p.S263S), and an intronic change c.844-13T>A (numbered with respect to NM_014588). Segregation was not detected for p.D144E and c.844-13T>A. The change in p.G160D was observed in two patients with sporadic keratoconus. Although predicted to alter VSX1 splicing, p.S263S had no effect on transcript processing. Four known SNPs were detected and the following polymorphic variants were observed in keratoconus patients and controls: c.711T>A (NM_199425; p.P237P), c.844-5_-6insT (NM_014588), c.*28G>T (DQ854811/DQ854812), and c.*50G>A (DQ854809/DQ854810). CONCLUSIONS: VSX1has a minor role in keratoconus pathogenesis. The pathogenicity of p.G160D remains controversial and this change may represent a rare polymorphism or genetic modifier. Further evidence is provided that the previously reported variant, p.D144E, is a polymorphism.

The ophthalmo-meningeal foramen masquerading as an intraocular foreign body.

Although the diagnosis of intraocular foreign body is primarily a clinical one, radiographic imaging is often used to clarify the diagnosis and to localise the foreign body. For this case the radiographic findings served to confuse the diagnosis.

Trans-scleral diode laser cyclophoto-coagulation in the treatment of diabetic neovascular glaucoma.

AIMS: To assess efficacy of trans-scleral diode laser cyclophotocoagulation in the treatment of diabetic neovascular glaucoma refractory to medical therapy. METHODS: Case notes of 20 eyes of 20 patients who had the treatment were analysed. The mean follow-up after initial treatment was 22.5 months (range of 18-24). RESULTS: Mean (SD) pretreatment intraocular pressure (IOP) for the 20 eyes was 34.4 mmHg (9.5) reducing to 18.2 mmHg (12.4) at the final index visit (P = 0.0001). The mean (SD) number of topical antiglaucoma medication was significantly lowered from 3.9 (0.3) to 1.2 (1.3). Four patients had visual acuity of 6/60 or better before the treatment. Two of them maintained the same level of vision and the other two had their vision reduced over the course of study; however, none of them deteriorated beyond 6/60. Six out of the remaining 16 patients who had vision of counting fingers or worse before treatment progressed to no perception of light at the final index visit. The mean (SD) number of treatment sessions was 1.45 (0.68). A total of 10 patients had previous pars plana vitrectomy (PPV). Patients with two or more PPVs developed hypotony (IOP

The response of trout and zebrafish embryos to low and high boron concentrations is U-shaped.

Fish in the embryo-larval stage of development have been shown to be sensitive to boron (B) at both ends of the dose-response curve (1,2). The present study evaluated the health effects of low and high B concentrations on rainbow trout (Oncorhynchus mykiss), a cold water species, and zebrafish (Danio rerio), a warm water species. Rainbow trout embryos were incubated from day 1 until 2 wk posthatch in Type 1 ASTM ultrapure-grade water (12.5 degrees C) supplemented with only B (0-500 microM) as boric acid, or together with CaCO3 (0-2 mM) to increase water hardness. Embryonic growth was stimulated by B in a dose-dependent manner at all Ca concentrations (p < 0.001). Chronic exposures below 9 micromol B/L impaired embryonic growth and above 10 mmol B/L caused death (p < 0.001). Thus, the safe range of exposure for the rainbow trout was between the adverse effect concentrations of 9 micromol B/L and 10 mmol B/L. Zebrafish were maintained for 6 mo in ultrapure water containing <0.2 micromol B/L to determine the effect of low-level exposure. High-level exposure was assessed by exposing zygotes, derived from parents maintained at 46 micromol B/L, to graded concentrations of boric acid up to a concentration of 75 mmol B/L from fertilization until they were free feeding (96 h). Fertilization occurred, but zygotes failed to survive when water contained <0.2 micromol B/L (p < 0.001). Death occurred at and above 9.2 mmol B/L. Thus, the safe range of B exposure for zebrafish was between the adverse effect concentrations of 0.2 micromol B/L and 9.2 mmol B/L. The dose-response for both species was thus U-shaped.