Retrograde Maculopathy in Patients With Glaucoma.

PURPOSE: Macular optical coherence tomography (OCT) analysis can be used for quantitative measures of optic nerve atrophy at a location far from the optic nerve head. This recently led to the finding of microcystic macular edema (MME), that is vacuolar inclusions in the macular inner nuclear layer, in some glaucoma patients. The involvement of individual retinal layers is yet unclear in glaucoma. In this study we systematically investigated glaucoma-induced changes in macular layers to evaluate whether glaucoma-associated damage extends beyond the macular ganglion cell layer. PATIENTS AND METHODS: We included 218 consecutive patients and 282 eyes with confirmed primary open-angle glaucoma or pseudoexfoliation glaucoma, and macular OCT in a cross-sectional observational study. Eyes were screened for presence of MME. Thickness of individual retinal layers was determined using a semiautomatic segmentation algorithm. Peripapillary nerve fiber layer thickness and mean defect in visual field testing were extracted from OCT and medical records, respectively. Results were compared with a small group of eyes with no apparent glaucoma. RESULTS: We found MME in 5 eyes from 5 primary open-angle glaucoma patients and 3 eyes of 3 pseudoexfoliation glaucoma patients (2.8%). MME was confined to the inner nuclear layer in a perifoveal ring and was associated with thinning of the ganglion cell layer and thickening of the macular inner nuclear layer. Glaucoma eyes without MME showed a significant inverse correlation of inner nuclear layer thickness with glaucoma severity. CONCLUSIONS: Glaucomatous damage leads to a gradual thickening of the inner nuclear layer, which leads to MME in more severe glaucoma cases. These changes, along with nerve fiber loss and ganglion cell loss, may be summarized as glaucoma-associated retrograde maculopathy.

No difference in genotype frequencies of polymorphisms of the nitric oxide pathway between Caucasian normal and high tension glaucoma patients.

PURPOSE: Substantial evidence suggests that ocular perfusion is regulated by nitric oxide (NO), and polymorphisms in genes encoding for enzymes involved in NO formation and degradation (endothelial nitric oxide synthase [NOS3] and cytochrome b-235 alpha polypeptide gene [CYBA]) might contribute to vascular dysregulation observed in glaucoma. We therefore assessed the association of glaucoma with polymorphisms of NOS3 and CYBA previously associated with cardiovascular disease. We also compared the distribution of these polymorphisms in patients with high tension glaucoma (HTG) and normal tension glaucoma (NTG) and evaluated its association with vascular dysregulation in a subset of glaucoma patients. METHODS: Three hundred Caucasian patients with HTG and 127 with NTG were enrolled in the study and genotyped for G894T (rs1799983) and T-786C (rs2070744) in NOS3 and C242T (rs4673) in CYBA. RESULTS: None of these polymorphisms had a different allele or genotype distribution between HTG and NTG patients nor had the presence of vasospasms any impact. CONCLUSIONS: We studied the frequencies of a set of relevant polymorphisms of the NO system in a large cohort of glaucoma patients and found no association. These results therefore suggest the absence of a relevant relationship with different glaucoma forms in Caucasians.