To evaluate tear levels of neuromediators in patients with dry eye disease and to identify statistical correlations with the clinical findings.Methods: Nineteen patients with dry eye disease (Sjö gren syndrome, n=5 patients; non-Sjö gren syndrome, n=10; and ocular cicatricial pemphigoid, n = 4) and 12 healthy volunteers were enrolled. The eyes of all participants were evaluated by slitlamp examination, Schirmer testing, fluorescein staining, and tear film break-up time. Grading of dry eye severity was recorded. Tear samples were collected, and substance P, calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY), vasoactive intestinal peptide, and nerve growth factor (NGF) concentrations were evaluated by enzyme-linked immunoassay and correlated with the clinical findings.Results: Nerve growth factor tear levels were significantly increased in participants with dry eye disease; CGRP and NPY concentrations were significantly decreased when compared with those in healthy participants. Dry eye severity showed a direct correlation with NGF and an inverse correlation with CGRP and NPY tear levels. Nerve growth factor tear levels showed a direct correlation with conjunctival hyperemia and fluorescein staining results, CGRP directly correlated with Schirmer test values, and NPY inversely correlated with tear film break-up time. Subgroup analysis showed that CGRP and NPY but not NGF were changed in autoimmune (ie, Sjö gren syndrome and ocular cicatricial pemphigoid) dry eye disease. Conclusions:The decreased tear levels of NPY and CGRP in dry eye disease are related to impaired lacrimal function, and tear levels of NGF are more closely related to corneal epithelial damage. Our findings suggest that NPY, CGRP, and NGF could become useful markers of dry eye severity.

This study confirmed the importance of cytological tests in the diagnosis of LSCD. Furthermore, the absence of goblet cells may not exclude corneal conjunctivalisation as demonstrated by cytokeratin 19 immunostaining. Lastly, corneal conjunctivalisation was associated with zone-specific impairment in corneal sensitivity.

BackgroundThe purpose of this study was to evaluate the long-term postoperative incidence of and key factors in the genesis of corneal ectasia after myopic laser-assisted in situ keratomileusis (LASIK) in a large number of cases.MethodsA retrospective review of one surgeon’s myopic LASIK database was performed. Patients were stratified into two groups based on date of surgery, ie, group 1 (1313 eyes) from 1999 to 2001 and group 2 (2714 eyes) from 2001 to 2003. Visual acuity, refraction, pachymetry, and corneal topography data were available for each patient from examinations performed both before and after the refractive procedures.ResultsOf the 4027 surgically treated eyes, 23 (0.57%) developed keratectasia during the follow-up period, which was a minimum seven years; nine eyes (0.69%) were from group 1 and 14 eyes (0.51%) were from group 2. The onset of corneal ectasia was at 2.57 ± 1.04 (range 1–4) years and 2.64 ± 1.29 (range 0.5–5) years, respectively, for groups 1 and 2. The most important preoperative risk factors using the Randleman Ectasia Risk Score System were manifest refractive spherical error in group 1 and a thin residual stromal bed in group 2. Each of the cases that developed corneal ectasia had risk factors that were identified.ConclusionEctasia was an uncommon outcome after an otherwise uncomplicated laser in situ keratomileusis procedure. The variables present in eyes developing postoperative LASIK ectasia can be better understood using the Randleman Ectasia Risk Score System.

Aims: The aim of this study was to assess the efficacy of currently available topical drugs for vernal keratoconjunctivitis (VKC) through a meta-analysis of randomised clinical trials (RCTs). Methods: Twenty-seven RCTs (n = 2184 eyes) that had evaluated the efficacy of topical drugs for the treatment of VKC were selected according to the set criteria; 10 of these trials were suitable for statistical analysis and were enrolled in the meta-analysis. Articles published up to December 2005 were identified from the following data sources: Medline, Embase, Lilacs, the Cochrane Controlled Trials Register, and references from relevant articles. Articles in any language published with an English abstract, were screened, and those selected for inclusion were written in English, French, German, Italian, Portuguese or Spanish. The quality of the trials was assessed by the Delphi list. Statistical analysis was performed using STATAH software. Results: A significant improvement in all signs and symptoms, except photophobia, was observed after topical treatment for active VKC, independent of the type of treatment. Comparison of the efficacy of different drugs was not possible due to a lack of standardised criteria among studies. Conclusion:The currently available topical drugs are effective in treating acute phases of VKC. However, there is a lack of evidence to support the recommendation of one specific type of medication for treating this disorder. There is a need for standard criteria to assess diagnosis and therapy based on severity. There is also a need for RCTs assessing long-term effects of single drugs to control the disease and to prevent complications. V ernal keratoconjunctivitis (VKC) is a recurrent bilateral chronic allergic inflammatory disease of the ocular surface affecting mainly young males in the first decade of life. Diagnosis is based on signs and symptoms including itching, photophobia, sticky mucous discharge, giant papillae on the upper tarsal conjunctiva or at the limbus, superficial keratopathy and corneal shield ulcer. An immunopathogenic mechanism has been proposed for this disease on the basis of personal or familial history of atopy, increased serum levels of total and specific IgE, the response to antiallergic therapy and the presence of several immune cells and mediators in the conjunctiva. [1][2][3] At present, the exact pathogenic mechanism has not been completely identified. In spite of its generally benign and selflimited presentation, therapeutic measures are required to control signs and symptoms of the disease and to avoid the longstanding permanent inflammatory sequelae that may lead to fibrovascular reaction, new collagen deposition, tissue remodelling and permanent visual damage. 1-3Several reports indicate that topical anti-inflammatory and antiallergic eye-drops are the mainstay of treatment for VKC, but a gold-standard treatment has not yet been established for this disease. In the present report, we systematically reviewed RCTs and conducted a meta-analysis of the combined results ...

VKC is a chronic disease that requires prolonged treatment to control the inflammatory process. Our preliminary study demonstrates the efficacy and safety of preservative-free diclofenac sodium 0.1% eye drops in controlling the signs and symptoms of VKC in prolonged treatment.