Background: To measure the anterior and posterior segment structural features of acute primary angle-closure (APAC) eyes.
Methods: A total of 36 subjects with unilateral APAC were recruited in this study. The ocular biometric characteristics were measured by anterior segment optical coherence tomography (AS-OCT) and swept source optical coherence tomography (SS-OCT), respectively at baseline, 2 weeks, and 1 month after surgical intervention.
Results: At baseline, when compared with the fellow eyes, APAC-affected eyes showed significantly greater corneal thickness (P=0.004), shallower anterior chamber depth (ACD) (P<0.001), smaller anterior chamber area (ACA) (P=0.013), angle opening distance at 750 μm from the scleral spur (AOD750) (P=0.002), trabecular–iris space area at 750 μm from the scleral spur (TISA750) (P=0.033), angle recess area (ARA) (P=0.014), and iris area (IARE) (P=0.003), less iris curvature (ICURVE) (P=0.003), and larger lens vault (LV) (P=0.030). After intervention, the corneal thickness was significantly decreased at 1 month (P<0.001), while ACD, ACA, and AOD750 were significantly increased at 2 weeks and 1 month (all P<0.017). Changes in ACD were correlated with decreasing LV (P<0.05). The posterior segment parameters did not change over the 4-week period.
Conclusions: When compared with the fellow eyes, APAC-affected eyes had greater corneal thickness, shallower anterior chamber, narrower angle, less ICURVE, and larger LV. After intervention, the corneal thickness was decreased, while the shallower anterior chamber was relieved to some extent.
Background: To investigate the microstructural features of parapapillary gamma zone and beta zone and their relationship with three-dimensional optic disc shape in non-myopic eyes.
Methods: This cross-sectional study included 62 non-myopic eyes with parapapillary gamma or beta zone and 70 control eyes. On the spectral domain optical coherent tomography (SD-OCT) images, we measured the area of gamma zone and beta zone, the length of border tissue, and related disc parameters. The disc ovality index, disc rotation degrees around three axes, Bruch’s membrane opening (BMO) ovality ratio were calculated based on the SD-OCT images.
Results: The parapapillary gamma zone composed by externally oblique border tissue was found in inferior, nasal and temporal quadrants of the non-myopic eyes. The presence of gamma zone in non-myopic eyes was correlated with smaller disc ovality index, larger rotation degree around vertical and horizontal axes, and larger BMO ovality ratio (P<0.001). Compared with the non-temporal gamma zone group, eyes with temporal gamma zone had a longer axial length and rotated more around vertical axes (P<0.001). Multivariate analysis showed that the area of gamma zone was correlated with the disc ovality index (P<0.001). The presence and area of beta zone was correlated with age (P<0.01).
Conclusions: In non-myopic eyes, the parapapillary gamma zone composed by external oblique border tissue was significantly associated with the disc ovality and disc rotations around vertical and horizontal axes. From a biomechanical perspective, parapapillary gamma zone may contribute to the optic disc stability in association with the structure of BMO.
Abstract: Autoimmune retinopathy (AIR) refers to both paraneoplastic and non-paraneoplastic forms of a rare, acquired retinal degeneration thought to be mediated by the production of antiretinal antibodies. However, the mechanisms underlying AIR pathogenesis are incompletely understood, and it remains a diagnosis of exclusion given the lack of definitive testing as well as its protean clinical presentation. This review summarizes the current literature on the epidemiology, diagnosis, and management of AIR, with a focus on non-paraneoplastic disease and the potential role of immunomodulatory therapy. A recent expert consensus statement on diagnosis and management of non-paraneoplastic AIR served as a framework for interpreting the limited data available, a process that was complicated by the small sample sizes, heterogeneity, and retrospective nature of these studies. Additional work is needed to characterize AIR patients on the basis of cytokine and immunogenetic profiling; to establish the pathogenicity of antiretinal antibodies; and to standardize treatment regimens as well as assessment of clinical outcomes.
Abstract: Acute retinal necrosis (ARN) is a devastating syndrome characterized by panuveitis, retinal necrosis, and a high rate of retinal detachment that may result in poor visual outcomes if not promptly diagnosed and treated. ARN is most commonly caused by viruses within the herpesvirus family. Etiologies include varicella-zoster virus, herpes simplex virus, and cytomegalovirus, and may be promptly diagnosed by polymerase chain reaction testing of aqueous or vitreous fluid. The true incidence of ARN is not known due to its rarity; as a result, clinical treatment is often guided by retrospective case series, case reports, and expert opinion. Standard of care has evolved over time but currently includes a combination of systemic and intravitreal antiviral in conjunction with topical or oral steroids and surgical therapy as needed. Combination therapy may reduce the rate of severe vision loss and increase the rate of visual acuity gain, although further studies are needed in this area. In particular for patients with mild to moderate disease, combination therapy may reduce the rate of retinal detachment. Adjunctive therapies including oral corticosteroid and prophylactic laser barricade are incompletely studied, but corticosteroid in particular, may reduce inflammation, which also is involved in the severe disease pathogenesis observed in ARN. This review discusses the advances in diagnosis and treatment of ARN, including management with combination antiviral medication and surgical interventions.
Abstract: An intestinal dysbiosis is connected to a number of inflammatory diseases through various mechanisms relating to its effect on immune cell function and differentiation. This is a review of the literature summarizing our current understanding of intestinal microbial contributions to non-infectious uveitis and strategies to target the intestinal microbiome to treat uveitis. Several groups have demonstrated an intestinal dysbiosis associated with certain types of non-infectious uveitis. Additionally, approaches to treat uveitis by modifying the intestinal microbiota, such as oral antibiotics or administration of oral short chain fatty acids (SCFAs), which are intestinal bacterial metabolites produced by fermentation of dietary fiber, can successfully treat uveitis in mouse models. This reduction in severity of ocular inflammation occurs via the following mechanisms: enhancement of regulatory T cells, decreasing intestinal permeability, and/or affecting T cell trafficking between the intestines and the spleen. Other strategies that are directed at the intestinal microbiota that might be effective to treat uveitis include dietary changes, probiotics, or fecal microbial transplantation. The commensal gut bacteria are influential in systemic and intestinal mucosal immunity and thus contribute to the development of extraintestinal inflammation like uveitis. Targeting the intestinal microbiome thus has the potential to be a successful strategy to treat non-infectious uveitis.
Abstract: Inherited retinal diseases (IRD) are a leading cause of blindness in the working age population. The advances in ocular genetics, retinal imaging and molecular biology, have conspired to create the ideal environment for establishing treatments for IRD, with the first approved gene therapy and the commencement of multiple therapy trials. The scope of this review is to familiarize clinicians and scientists with the current landscape of retinal imaging in IRD. Herein we present in a comprehensive and concise manner the imaging findings of: (I) macular dystrophies (MD) [Stargardt disease (ABCA4), X-linked retinoschisis (RS1), Best disease (BEST1), pattern dystrophy (PRPH2), Sorsby fundus dystrophy (TIMP3), and autosomal dominant drusen (EFEMP1)], (II) cone and cone-rod dystrophies (GUCA1A, PRPH2, ABCA4 and RPGR), (III) cone dysfunction syndromes [achromatopsia (CNGA3, CNGB3, PDE6C, PDE6H, GNAT2, ATF6], blue-cone monochromatism (OPN1LW/OPN1MW array), oligocone trichromacy, bradyopsia (RGS9/R9AP) and Bornholm eye disease (OPN1LW/OPN1MW), (IV) Leber congenital amaurosis (GUCY2D, CEP290, CRB1, RDH12, RPE65, TULP1, AIPL1 and NMNAT1), (V) rod-cone dystrophies [retinitis pigmentosa, enhanced S-Cone syndrome (NR2E3), Bietti crystalline corneoretinal dystrophy (CYP4V2)], (VI) rod dysfunction syndromes (congenital stationary night blindness, fundus albipunctatus (RDH5), Oguchi disease (SAG, GRK1), and (VII) chorioretinal dystrophies [choroideremia (CHM), gyrate atrophy (OAT)].
