Effect of Smoking on Retinal Thickness and Vascular Density in Thyroid Eye Disease.

PURPOSE: To evaluate the effect of smoking on retinal thickness and macular and peripapillary vascular density in thyroid eye disease (TED). METHODS: In this cross-sectional study, subjects diagnosed with TED were analyzed in three groups: smokers, passive smokers, and non-smokers. Ganglion cell complex thickness, total retinal thickness, macular superficial vascular plexus densities, deep vascular plexus densities, optic nerve head, and radial peripapillary capillary density were measured in each group. RESULTS: Twenty-two eyes (21.6%) of active smokers, 11 eyes (10.8%) of passive smokers, and 69 eyes (67.6%) of non-smokers constitute the study subjects. Twenty-one eyes (12.6%) had active status (clinical activity score ≥3), 77 eyes (46.1%) were neither active nor compressive, four eyes (2.4%) of two patients constituted the compressive group. Age and disease activity adjusted analysis was performed. Ganglion cell complex thickness of smokers was significantly higher than non-smokers in the inferior hemi-parafoveal sector (p = 0.04). Active smokers had significantly higher (p < 0.01) retinal thickness in all sectors compared to non-smokers, except the foveal sector. Smokers had lower superficial vessel density in the superior parafoveal sector compared to non-smokers (p = 0.04). Considering deep vessel densities between smokers and non-smokers, no significant difference was observed. Radial peripapillary capillary densities (significant difference was observed in the whole image and infranasal peripapillary sector), Macular vascular densities (significant difference was observed in parafoveal sectors), and optic nerve head (not reaching statistical significance level in any sectors) were highest in passive smokers. CONCLUSIONS: Smoking is associated with increased total retinal thickness. Macular vascular densities were not different between smokers and non-smokers in TED.

Culture-proven endogenous endophthalmitis: microbiological and clinical survey.

PURPOSE: To report causative organisms, visual outcomes, and associated medical conditions in endogenous endophthalmitis (EE). METHODS: Microbiological and medical reports of patients with culture-proven EE referred to Farabi Eye Hospital, Tehran, Iran, from January 2008 to January 2018 were reviewed. RESULTS: A total of 144 cases (171 eyes) were included in the present study. Candida albicans (30.6%) and Staphylococcus aureus (27.1%) were the most prevalent microbial causes. Diabetes mellitus (43.8%) and IV drug abuse (10.4%) were the leading associated systemic conditions. Age of the patients (P = 0.002) and presenting corrected distance visual acuity (CDVA) (P < 0.001) were correlated with postoperative CDVA. Patients with bilateral involvement had significantly lower mean logMAR (P = 0.002), and patients with hypopyon had significantly higher mean logMAR (P = 0.006). Eyes with gram-negative bacillus cultures had a significantly worse logMAR than eyes with gram-positive cocci (P = 0.009). CONCLUSION: Candida albicans and S. aureus were the most common causes of EE, and diabetes mellitus was the most common associated medical condition. EE is associated with poor visual outcome, especially in older patients, those with worse visual acuity at presentation, and those with positive cultures for gram-negative bacilli.

Nitric oxide mediates the anticonvulsant effects of thalidomide on pentylenetetrazole-induced clonic seizures in mice.

Thalidomide is an old glutamic acid derivative which was initially used as a sedative medication but withdrawn from the market due to the high incidence of teratogenicity. Recently, it has reemerged because of its potential for counteracting number of diseases, including neurodegenerative disorders. Other than the antiemetic and hypnotic aspects, thalidomide exerts some anticonvulsant properties in experimental settings. However, the underlying mechanisms of thalidomide actions are not fully realized yet. Some investigations revealed that thalidomide could elicit immunomodulatory or neuromodulatory properties by affecting different targets, including cytokines (such as TNF α), neurotransmitters, and nitric oxide (NO). In this regard, we used a model of clonic seizure induced by pentylenetetrazole (PTZ) in male NMRI mice to investigate whether the anticonvulsant effect of thalidomide is affected through modulation of the l-arginine-nitric oxide pathway or not. Injection of a single effective dose of thalidomide (10 mg/kg, i.p. or higher) significantly increased the seizure threshold (P<0.05). On the one hand, pretreatment with low and per se noneffective dose of l-arginine [NO precursor] (10, 30 and 60 mg/kg) prevented the anticonvulsant effect of thalidomide. On the other hand, NOS inhibitors [l-NAME and 7-NI] augmented the anticonvulsant effect of a subeffective dose of thalidomide (1 and 5 mg/kg, i.p.) at relatively low doses. Meanwhile, several doses of aminoguanidine [an inducible NOS inhibitor] (20, 50 and 100 mg/kg) failed to alter the anticonvulsant effect of thalidomide significantly. In summary, our findings demonstrated that the l-arginine-nitric oxide pathway can be involved in the anticonvulsant properties of thalidomide, and the role of constitutive nNOS is prominent in the reported neuroprotective feature.