Saksens et al1 reported the clinical characteristics and long-term follow-up of dominant cystoid macular dystrophy (DCMD). They identified the association of high axial hyperopia with intraretinal cystoid macular fluid collections (CFC) and implicated a primary dysfunction of Muller cells and/or the retinal pigment epithelium as the cause of CFC. An alternate explanation of the pathophysiology may involve a thick choroid that may occur in hyperopia.2 Increased choroidal thickness may result in increased osmotic pressure causing secondary leakage into the retina via the relatively weak blood–retinal barrier at the optic disc margin.

Watanabe y otros (p. 2103) investigaron el efecto de la severidad de la córnea guttae en la calidad de visión en pacientes con distrofia corneal de Fuchs leve. Encontraron que la córnea guttae — aún sin edema visible en la lámpara de hendidura — tiene un impacto negativo en la en la calidad de visión de los pacientes y que la dispersión frontal de la luz intraocular producida por la guttae puede resultar en problemas visuales. Este estudio de corte transversal incluyó 23 ojos de 14 pacientes con distrofia de Fuchs sin evidencia de edema.

This report by Chew et al1 claims to refute our analyses2,3 showing a relationship among zinc supplementation, genotype, and age-related macular degeneration (AMD) progression. The report includes inaccurate and misleading statements, which we address below.

Watanabe (p. 2103) 等在轻度Fuchs’角膜营养不良患者中就角膜滴状赘疣严重程度对视觉质量的影响进行研究。他们发现即使在裂隙灯检查未见角膜水肿的患者, 角膜滴状赘疣仍对其视觉质量产生不良影响, 由滴状赘疣向前的眼内光散射将引起视觉障碍。该横断面研究包括14名Fuchs’角膜营养不良患者的23例眼, 患眼均未见明显水肿。研究人员评估滴状赘疣面积比例及其与矫正远视力 (corrected distance visual acuity, CDVA)、字母对比敏感度 (letter contrast sensitivity, LCS) 以及眼内散射光之间的相关性。结果显示滴状赘疣严重程度与以上3项视觉指标均呈负相关关系。此外, 散射光程度较重患者CDVA及LCS较差。

We thank Dr Pearlman for his comments regarding the controversy of whether we need to conduct genetic testing prior to administering the Age-Related Eye Disease Study (AREDS) supplements or not. He expressed his concern regarding the following: (1) whether we did a “pooled” analysis of our “residual cohort”1 with that of the cohort of Awh et al,2 (2) whether there was comparability in the residual cohort with the cohort of Awh et al, and (3) whether this residual cohort was large enough and truly independent to provide us with clinically meaningful information.