BackgroundΤo perform a molecular epidemiological analysis of viral conjunctivitis among excess conjunctivitis cases recorded at the University Hospital of Patras, Greece, for the period March to June 2012.MethodsA structured questionnaire containing demographic and clinical data was developed in order to collect retrospective data on the cases. Eye swab specimens were collected and molecular detection of adenoviruses was performed by nested PCR. Positive results were confirmed by sequencing. To determine the relatedness between the isolated sequences, a phylogenetic analysis was conducted.ResultsThe epidemiological analysis (including retrospective data) included 231 conjunctivitis cases (47.1% male, and 52.8% female). Based on clinical features 205 of the cases were diagnosed of viral origin (46.3% male and 53.7% female), 4 of bacterial origin (50% male and 50% female) while 22 were undefined conjunctivitis. The outbreak excess cases (included 156 cases) affected all age groups regardless gender predilection. For the positive samples indicated that 29 samples (72.5%) were AdV17, and 5 (12.5%) as AdV54.ConclusionsMolecular analysis could define the cause of viral conjunctivitis, while epidemiological data contributed to the assessment of the risk factors and underlined possible preventive measures. This study is one of the very few on viral conjunctivitis in Greece. This outbreak underscores the need for a national surveillance system for acute infectious conjunctivitis outbreaks. The epidemiological as well as molecular investigation on HAdV ocular infections is rather absent in Greece, which has no surveillance system for viral conjunctivitis.

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Purpose Research has shown that HSPs participates in preserving HIF‐1a function. In this study, HIF‐1a, and HSP90, 70, expression and immunolocalization in ocular pterygium and normal conjunctiva samples was examined. Methods Fifty nine samples of ocular pterygium and twenty samples of normal conjunctiva, surgically removed, were tested with immunohistochemistry, immunofluorecense and western blot analysis. Results Between pterygium specimens and normal conjuctiva specimens, significant differences were observed in the expressions of proteins HSP90 (p=0.002), HIF‐1a (p=0.048). No significant differences were found in the expressions of HSP70 in ocular pterygium when compared to the normal conjunctiva. Conclusion These data provide molecular evidence that Hypoxia‐Inducible Factor‐1a and HSP90 may have a role to play in pterygium pathogenesis.

Cannabinoids, as multi-target mediators, activate cannabinoid receptors and transient receptor potential vanilloid (TRPV) channels. There is evidence to support a functional interaction of cannabinoid receptors and TRPV channels when they are coexpressed. Human conjunctiva demonstrates widespread cannabinoid receptor type 1 (CB1), CB2 and TRPV channel localization. The aim of the present study was to investigate the expression profile for cannabinoid receptors (CB1 and CB2) and TRPV channels in pterygium, an ocular surface lesion originating from the conjunctiva. Semi-serial paraffin-embedded sections from primary and recurrent pterygium samples were immunohistochemically examined with the use of specific antibodies. All of the epithelial layers in 94, 78, 96, 73 and 80% of pterygia cases, exhibited CB1, CB2, TRPV1, TRPV2 and TRPV3 cytoplasmic immunoreactivity, respectively. The epithelium of all pterygia cases (100%) showed strong, mainly nuclear, TRPV4 immunolocalization. In the pterygium stroma, scattered cells demonstrated intense CB2 immunoreactivity, whereas vascular endothelial cells were immunopositive for the cannabinoid receptors and all TRPV channels. Quantitative analyses of the immunohistochemical findings in epithelial cells demonstrated a significantly higher expression level in conjunctiva compared with primary pterygia (P=0.04) for CB1, but not for CB2 (P>0.05). Additionally, CB1 and CB2 were significantly highly expressed in primary pterygia (P=0.01), compared with recurrent pterygia. Furthermore, CB1 expression levels were significantly correlated with CB2 expression levels in primary pterygia (P=0.005), but not in recurrent pterygia (P>0.05). No significant difference was detected for all TRPV channel expression levels between pterygium (primary or recurrent) and conjunctival tissues (P>0.05). A significant correlation between the TRPV1 and TRPV3 expression levels (P<0.001) was detected independently of pterygium recurrence. Finally, TRPV channel expression was identified to be significantly higher than the expression level of cannabinoid receptors in the pterygium samples (P<0.001). The differentiated expression of cannabinoid receptors in combination with the presence of TRPV channels, in primary and recurrent pterygia, imply a potential role of these cannabinoid targets in the underlying mechanisms of pterygium.

Omega-3 fatty acids may effectively improve tear film characteristics, reverse ocular surface features, and alleviate the subjective symptoms associated with dry eye syndrome in patients with type 2 diabetes.

Entecavir is an anti-viral drug commonly used in treatment of hepatitis-B infection but there was no recognised ocular toxicity in its association [1-3]. The mechanism of retinal toxicity remains unclear with lacking histopathological studies. There was a published case report with irreversible blindness when on year(s) of Entecavir complicated by diabetic retinopathy at the time of suspected retinal toxicity [4]. Our case shared similar clinical features as their reported second eye. Notably, Entecavir drug toxicity is causing sequential rather than bilateral simultaneous eye manifestations. Our patient's left eye was profoundly involved but his right eye had not progressed more than the minimal peripheral vascular staining in late fundus photographs and fluorescein angiography phase (Fig. 1: 2A). Our case confirmed short-term Entecavir use could cause reversible retinal toxicity upon drug cessation. Prescribing physicians and ophthalmologists should be aware of the potential retinal toxicity of Entecavir. We reported this adverse drug reaction to the UK Medicines and Health Products Regulatory Agency.

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