Purpose to compare tear cytokine and chemokine concentrations in asymptomatic control and dysfunctional tear syndrome (DTS) patients and determine the correlations between tear inflammatory mediators and clinical severity. Design Prospective observational cohort study Methods Concentrations of epidermal growth factor (EGF), interleukin (IL) - 1α, 1β, 6, 10, 12 and 13, interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α) and chemokines: IL-8 (CXC), MIP-1α (CCL3) and RANTES (CCL5) were measured by a multiplex immunobead assay in an asymptomatic control group and DTS patients with and without MGD. Spearman correlations between tear cytokines and severity of irritation symptoms and ocular surface signs were calculated. Results Tear concentrations of IL-6, IL-8 and TNF-α were significantly higher in DTS with and without MGD and EGF was significantly reduced in the DTS without MGD group compared to the control group. MIP-1α was greater in entire DTS and DTS without MGD groups than the control group and RANTES was greater in DTS with MGD than the control and DTS without MGD groups. IL-12 was significantly higher in the DTS with MGD than the DTS without MGD subgroup. Significant correlations were observed between IL-6 and irritation symptoms and between a number of cytokines and chemokines and clinical parameters. Conclusions As predicted, patients with DTS have higher levels of inflammatory mediators in their tears that show correlation with clinical disease parameters. Furthermore, different tear cytokine/chemokine profiles were observed in DTS patients with and without MGD groups.

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PURPOSE To report an unusual presentation of posterior polymorphous corneal dystrophy (PPCD) associated with band keratopathy, iridocorneal adhesions, heterochromia, keratoconus, and confocal microscopic findings suggestive of iridocorneal endothelial syndrome (ICE). METHODS Confocal microscopy, corneal topography, electroretinography and genetic analysis were performed in the proband and his siblings. RESULTS A 23 year old man presented with decreased vision in both eyes over 9 months. Examination revealed bilateral alterations in corneal endothelial mosaic with corneal edema and beaten metal appearance in the right eye, and cystoid endothelial opacities in the left eye. Marked heterochromia, band keratopathy, and broad peripheral anterior synechiae were present in both eyes. Topographic features of keratoconus were noted. Electroretinography did not detect abnormal retinal function, as has been described with PPCD associated with VSX1 mutations. Diagnosis of PPCD was postulated based on the examination of the three proband's brothers by confocal microscopy. Genetic analysis of three known PPCD genes, VSX1, COL8A2, and TCF8, did not detect any mutations. CONCLUSIONS In severe cases, PPCD can resemble iridocorneal endothelial syndromes (ICE) in both clinical appearance and imaging studies (confocal microscopy). There was a strong genetic phenotypic penetrance in the family which was essential in the diagnostic decision-making. A yet undetermined genotype is contributing to this unusual PPCD phenotype.