To compare anterior segment measurements and morphology of 2 optical coherence tomography (OCT) systems. Department of Ophthalmology, District Railway Hospital, and the Nursing Department and Social Medical Issues, Health Care Division, Silesian Medical University, Katowice, Poland. In normal eyes and in eyes with corneal and trabecular-iris angle disorders, the central corneal thickness (CCT), trabecular-iris angle, and angle-opening distance at the nasal and temporal angles were measured 3 times during 1 visit using the Visante time-domain OCT system and the RTVue-100 Fourier-domain corneal anterior module OCT system. Anterior segment morphology was assessed and compared. Fifty-four eyes were evaluated. The mean values (+/-SD) by time-domain OCT and Fourier-domain OCT were, respectively, automatic CCT, 535 +/- 33.07 microm and 538 +/- 31.82 microm; manual CCT, 545 +/- 30.91 microm and 542 +/- 30.57 microm; nasal trabecular-iris angle, 34.7 +/- 9.5 degrees and 35.2 +/- 8.9 degrees; temporal trabecular-iris angle, 35.3 +/- 8.5 degrees and 35.5 +/- 9 degrees; nasal angle-opening distance, 435 +/- 95 microm and 444 +/- 98 microm; and temporal angle-opening distance, 443 +/- 103 microm and 452 +/- 99 microm. There was no significant difference between mean values, and they were highly correlated. On morphologic analysis, time-domain OCT had lower resolution; however, all anterior chamber structures were visible on 1 image. Fourier-domain OCT provided precise information about small areas of the anterior chamber. Fourier-domain OCT provided accurate anterior eye segment measurements that agreed with those obtained with time-domain OCT.

SUMMARY: Human alphaherpesvirus 1 (HSV-1) is a highly successful neurotropic pathogen that primarily infects the epithelial cells lining the orofacial mucosa. After primary lytic replication in the oral, ocular, and nasal mucosal epithelial cells, HSV-1 establishes life-long latency in neurons within the trigeminal ganglion. Patients with compromised immune systems experience frequent reactivation of HSV-1 from latency, leading to virus entry in the sensory neurons, followed by anterograde transport and lytic replication at the innervated mucosal epithelial surface. Although recurrent infection of the corneal mucosal surface is rare, it can result in a chronic immuno-inflammatory condition called herpetic stromal keratitis (HSK). HSK leads to gradual vision loss and can cause permanent blindness in severe untreated cases. Currently, there is no cure or successful vaccine to prevent latent or recurrent HSV-1 infections, posing a significant clinical challenge to managing HSK and preventing vision loss. The conventional clinical management of HSK primarily relies on anti-virals to suppress HSV-1 replication, anti-inflammatory drugs (such as corticosteroids) to provide symptomatic relief from pain and inflammation, and surgical interventions in more severe cases to replace damaged cornea. However, each clinical treatment strategy has limitations, such as local and systemic drug toxicities and the emergence of anti-viral-resistant HSV-1 strains. In this review, we summarize the factors and immune cells involved in HSK pathogenesis and highlight alternate therapeutic strategies for successful clinical management of HSK. We also discuss the therapeutic potential of immunoregulatory cytokines and immunometabolism modulators as promising HSK therapies against emerging anti-viral-resistant HSV-1 strains.

The aim of this study was to analyze the corneal morphology features and define mutations in the UbiA prenyltransferase domain-containing 1 (UBIAD1) gene in patients with Schnyder corneal dystrophy from a Polish population. Five affected and 15 unaffected members originating from 3 families with Schnyder corneal dystrophy were included in the study. Phenotype analysis consisted of visual acuity, slit-lamp biomicroscopy with photography, time domain optical coherence tomography, spectral domain optical coherence tomography, and confocal microscopy. Three patients underwent a penetrating keratoplasty. Corneal buttons obtained from the penetrating keratoplasty were processed for light microscopy. A novel mutation I245N of the UBIAD1 gene was revealed in 1 proband and associated with the phenotype without central corneal opacities. The analysis of the other patients showed the N102S mutation. In vivo corneal morphology analysis using optical coherence tomography and confocal microscopy confirmed the presence of multiple crystalline corneal deposits in all affected corneas. The histological examination revealed multiple empty widenings of the corneal lamellae that could represent lipids removed from the specimen. N102S may also be a mutation hotspot in the Polish population, as in other previously reported populations. Corneal crystals formed a characteristic pattern on optical coherence tomography scans.

The purpose of this study was to assess the effect of environmental working conditions on the symptoms and signs of dry eye disease and to examine whether and how those conditions impact the ocular surface. Methods: This single-center, prospective clinical study with a 1-year follow-up included 150 patients. The following parameters were evaluated: non-invasive keratograph break-up time (NIKBUT), tear meniscus height (TMH), and conjunctival and limbal hyperemia. We also performed staining of the surface of the eye for simulated fluorescein images, Schirmer’s test I, assessment of Meibomian gland dysfunction (MGD), and an Ocular Surface Disease Index (OSDI) questionnaire. Results: In the OW (office workers) group, in people working >4 h at the computer, the NIKBUT before work and the Schirmer test results were statistically significantly lower than in people working 4 h at a computer in both groups and after work in the MW (medical workers) group. Low relative air humidity in the building and air-conditioned rooms negatively affects the tear film, causing the symptoms of dry eye disease. At the 1-year follow-up, there was a statistically significant reduction in conjunctival and limbal hyperemia in the OW group as well as a statistically significant reduction in TMH at the first examination before and after work, and in the second examination after 1 year in both groups. Conclusions: Environmental factors such as reduced relative air humidity, increased air temperature, and decreased illumination have a negative impact on the ocular surface.