Use of Topical Insulin to Treat Refractory Neurotrophic Corneal Ulcers.

Purpose: To report the clinical course of 6 patients with refractory neurotrophic corneal ulcers that were treated with topical insulin drops.

Methods: Retrospective chart review of patients who had neurotrophic corneal ulcers or epithelial defects refractory to standard medical and surgical treatment. Insulin drops, prepared by mixing regular insulin in artificial tears with a polyethylene glycol and propylene glycol base at a concentration of 1 unit per milliliter, were prescribed 2 to 3 times daily.

Rheumatoid arthritis and the prevalence of diabetic retinopathy.

Objective: RA increases vascular disease and angiogenesis, yet a 1964 Lancet report paradoxically linked RA to lower diabetic retinopathy. Our objective was to examine RA as a risk factor for diabetic retinopathy compared with other vascular risk factors.

Methods: This cohort study compared the prevalence of diabetic retinopathy in diabetes patients with and without RA in a 5% Medicare sample.

Conjunctivitis: a systematic review of diagnosis and treatment.

Importance: Conjunctivitis is a common problem.

Objective: To examine the diagnosis, management, and treatment of conjunctivitis, including various antibiotics and alternatives to antibiotic use in infectious conjunctivitis and use of antihistamines and mast cell stabilizers in allergic conjunctivitis.

Evidence Review: A search of the literature published through March 2013, using PubMed, the ISI Web of Knowledge database, and the Cochrane Library was performed.

Regulation of the receptor for TNFalpha, TNFR1, in human conjunctival epithelial cells.

Purpose: Previous studies demonstrated that mast cell-derived TNFalpha stimulation is critical to the upregulation of intercellular adhesion molecule (ICAM)-1 on human conjunctival epithelial cells (HCECs), which is an important feature of ocular allergic inflammation. Shedding of TNFR1 by TNFalpha-converting enzyme (TACE) is a primary mechanism for the regulation of TNFalpha-mediated events. This process has not been examined in HCECs.

Allergic tears promote upregulation of eosinophil adhesion to conjunctival epithelial cells in an ex vivo model: inhibition with olopatadine treatment.

Purpose: The mechanism by which eosinophils adhere to the ocular surface during allergic inflammation is unknown. This study examined whether the incubation of human conjunctival epithelial cells (HCEs) with tears from allergic subjects promotes eosinophil adhesion, and it examined the effect of treatment with olopatadine on this process.

Methods: Allergic subjects (n = 6) and nonallergic subjects (n = 4) were treated in season for 1 week with olopatadine in one eye while the other eye remained untreated.

Toll-like receptor 2 expression on human conjunctival epithelial cells: a pathway for Staphylococcus aureus involvement in chronic ocular proinflammatory responses.

Background: Staphylococcus aureus colonization is common in atopic keratoconjunctivitis, potentially activating epithelial cells via toll-like receptor 2 (TLR-2) and the receptor for platelet-activating factor (PAFR).

Objectives: To examine human conjunctival epithelial cells for the expression of TLR-2 in vitro and in vivo and to evaluate the role of TLR-2 in S aureus-mediated activation of these cells.

Methods: Conjunctival epithelial cells isolated from cadaveric tissues were stimulated with interferon gamma (IFN-gamma) or a commercial S aureus cell wall extract (Staphylococcus aureus-CWE) (with or without anti-TLR-2 blocking antibody or PAFR antagonist) and were analyzed for tumor necrosis factor alpha (TNF-alpha) and interleukin 8 (IL-8) release; surface expression of TLR-2, intercellular adhesion molecule-1, HLA, and CD14; and TLR-2 messenger RNA expression.

Ocular allergic disease.

Purpose Of Review: This review will focus on recent advances in our understanding of the pathogenesis of allergic eye diseases. Common findings in acute allergic conjunctivitis (seasonal and perennial) and chronic allergic conjunctivitis (vernal keratoconjunctivitis, atopic keratoconjunctivitis, and giant papillary conjunctivitis) include evidence of mast cell activation and eosinophil attraction and activation. Cytokine levels found in tears, conjunctival impression cytology and biopsy specimens, and serum have been evaluated as markers of disease, and as targets of therapeutic intervention.

The promotion of eosinophil degranulation and adhesion to conjunctival epithelial cells by IgE-activated conjunctival mast cells.

Background: Allergen-mediated mast cell activation is a key feature of ocular allergic diseases. Evidence of eosinophil-derived mediators in tears and conjunctival biopsy specimens has been associated with chronic ocular allergic inflammation.

Objective: To examine the role of conjunctival mast cell mediators in eosinophil adhesion to conjunctival epithelial cells and eosinophil degranulation.

Differential and cooperative effects of TNFalpha, IL-1beta, and IFNgamma on human conjunctival epithelial cell receptor expression and chemokine release.

Purpose: To gain better understanding of conjunctival epithelial cell responses to proinflammatory cytokines, the individual and combined effects of TNFalpha, IL-1beta, and IFNgamma on chemokine release (IL-8, regulated on activation normal T-cell expressed and secreted [RANTES]) and surface receptor expression (intercellular adhesion molecule [ICAM]-1, and HLA-DR, -DP, and -DQ) were examined.

Methods: Conjunctival epithelial cells were isolated from cadaveric conjunctival tissues and cultured in 24-well plates until almost confluent. Recombinant cytokines (0.

Pathophysiology of ocular allergy: the roles of conjunctival mast cells and epithelial cells.

Allergic eye disease is associated with IgE-mediated conjunctival inflammation leading to signs of immediate hypersensitivity, including redness, itching, and tearing. Pathologic studies using conjunctival mast cells demonstrate that these cells, when sensitized with IgE antibody and exposed to environmental allergens, release mediators involved with allergic inflammation. The type, release kinetics, and concentration of these mediators in the conjunctiva have not been completely characterized.