Prevalence of Cystoid Macular Edema After Cataract Surgery in Eyes with Previous Macular Surgery.

OBJECTIVE: To determine the prevalence and risk factors for cystoid macular edema (CME) after cataract surgery in eyes that have previously undergone macular surgery. STUDY DESIGN AND METHODS: Retrospective consecutive interventional case series. Patient medical records and Spectral Domain Optical Coherence Tomography (SD-OCT) were reviewed for eyes that underwent vitrectomy for full thickness macular hole (FTMH), lamellar macular hole (LMH) or epiretinal membrane (ERM) and subsequent cataract surgery at a large private retina practice between 2016 and 2018. RESULTS: Around 9.1% of eyes (22/243) developed CME post cataract surgery. The mean time from macular surgery to cataract surgery was 273 days (range: 87-797) in eyes with CME and 289 days (range: 22-897) in eyes without CME (p = 0.67). There was no difference in final visual acuity between eyes with CME (20/40, logMAR 0.312) and without CME (20/30, logMAR 0.206) (p = 0.101). Compared with patients with FTMH or LMH, patients with epiretinal membrane were more likely to develop post cataract CME (OR = 2.97, p = 0.031, Chi square test). CONCLUSION: In eyes with history of macular surgery, the prevalence of post cataract surgery CME was around 9.1%. The development of CME is not dependent on timing of cataract surgery but is more common in eyes with history of epiretinal membrane.

Characteristics of Pentosan Polysulfate Sodium-Associated Maculopathy and Similarities With Other Maculopathies Commonly Managed in a Retina Practice.

Purpose: This work describes characteristics of pentosan polysulfate sodium (PPS)-associated maculopathy and its similarities with common maculopathies in a retina practice cohort. Methods: Thirty-two patients were identified through electronic medical record query who were exposed to PPS. One patient was excluded for lack of retinal imaging. Thirty-one patients (62 eyes) were included. A retrospective review was used to obtain patient characteristics, examination findings, and retinal imaging of the study patients. Classification into "likely," "unlikely," or "possible" to have PPS-associated maculopathy groups was based on the fundus photography and retinal imaging. Main outcome measures were best-corrected visual acuity, age, sex, diagnosis of reason for referral, allocation into designated maculopathy group, and presence of choroidal neovascularization. Results: Of 31 patients (62 eyes), the median age was 70 years (range, 24-104 years) and the majority were women (87%). Mean best-corrected visual acuity was 0.3 ± 0.4 logMAR at presentation. The most common reason for referral was age-related macular degeneration (29%). Maculopathy grades were "likely" (29%, 9 total patients), "possible" (26%, 8 total patients), or "unlikely" (45%, 14 total patients). Choroidal neovascularization was noted in 9.7% of all eyes and 11% of eyes in the "likely" group. The "possible" and "likely" groups had older ages of presentation (P < .05) compared with the "unlikely" group. Conclusions: A high percentage (55%) of patients with a history of chronic PPS exposure showed features of "likely" or "possible" maculopathy. Similarities with common maculopathies such as age-related macular degeneration and the importance of screening and recognizing at-risk patients are highlighted.

Spontaneous resolution of unilateral Behcet's associated neuroretinitis.

PURPOSE: Behcet's disease is an immune-mediated condition which can commonly have ocular involvement. We present a case of Behcet's associated neuroretinitis, which is a rare ocular manifestation of Behcet's disease. OBSERVATIONS: The patient experienced significant improvement in her neuroretinitis without initiation of treatment. After 28 days of observation there was spontaneous resolution of exam findings and return of Snellen visual acuity to 20/20. CONCLUSIONAND IMPORTANCE: There are only two other cases reported in the literature of Behcet's associated neuroretinitis. Both cases report bilateral involvement with concomitant frosted branch angiitis. This is also the only reported case with spontaneous resolution of abnormal exam findings with return to 20/20 visual acuity. This case highlights the complexity of ocular involvement in Behcet's disease.

A role for the circadian clock protein Per1 in the regulation of aldosterone levels and renal Na+ retention.

The circadian clock plays an important role in the regulation of physiological processes, including renal function and blood pressure. We have previously shown that the circadian protein period (Per)1 regulates the expression of multiple Na(+) transport genes in the collecting duct, including the α-subunit of the renal epithelial Na(+) channel. Consistent with this finding, Per1 knockout mice exhibit dramatically lower blood pressure than wild-type mice. We have also recently demonstrated the potential opposing actions of cryptochrome (Cry)2 on Per1 target genes. Recent work by others has demonstrated that Cry1/2 regulates aldosterone production through increased expression of the adrenal gland-specific rate-limiting enzyme 3ß-dehydrogenase isomerase (3ß-HSD). Therefore, we tested the hypothesis that Per1 plays a role in the regulation of aldosterone levels and renal Na(+) retention. Using RNA silencing and pharmacological blockade of Per1 nuclear entry in the NCI-H295R human adrenal cell line, we showed that Per1 regulates 3ß-HSD expression in vitro. These results were confirmed in vivo: mice with reduced levels of Per1 had decreased levels of plasma aldosterone and decreased mRNA expression of 3ß-HSD. We postulated that mice with reduced Per1 would have a renal Na(+)-retaining defect. Indeed, metabolic cage experiments demonstrated that Per1 heterozygotes excreted more urinary Na(+) compared with wild-type mice. Taken together, these data support the hypothesis that Per1 regulates aldosterone levels and that Per1 plays an integral role in the regulation of Na(+) retention.

Opposing actions of Per1 and Cry2 in the regulation of Per1 target gene expression in the liver and kidney.

Mounting evidence suggests that the circadian clock plays an integral role in the regulation of many physiological processes including blood pressure, renal function, and metabolism. The canonical molecular clock functions via activation of circadian target genes by Clock/Bmal1 and repression of Clock/Bmal1 activity by Per1-3 and Cry1/2. However, we have previously shown that Per1 activates genes important for renal sodium reabsorption, which contradicts the canonical role of Per1 as a repressor. Moreover, Per1 knockout (KO) mice exhibit a lowered blood pressure and heavier body weight phenotype similar to Clock KO mice, and opposite that of Cry1/2 KO mice. Recent work has highlighted the potential role of Per1 in repression of Cry2. Therefore, we postulated that Per1 potentially activates target genes through a Cry2-Clock/Bmal1-dependent mechanism, in which Per1 antagonizes Cry2, preventing its repression of Clock/Bmal1. This hypothesis was tested in vitro and in vivo. The Per1 target genes αENaC and Fxyd5 were identified as Clock targets in mpkCCDc14 cells, a model of the renal cortical collecting duct. We identified PPARα and DEC1 as novel Per1 targets in the mouse hepatocyte cell line, AML12, and in the liver in vivo. Per1 knockdown resulted in upregulation of Cry2 in vitro, and this result was confirmed in vivo in mice with reduced expression of Per1. Importantly, siRNA-mediated knockdown of Cry2 and Per1 demonstrated opposing actions for Cry2 and Per1 on Per1 target genes, supporting the potential Cry2-Clock/Bmal1-dependent mechanism underlying Per1 action in the liver and kidney.