Eight-Year Outcomes of Implantation of Posterior Chamber Phakic Intraocular Lens With a Central Port for Moderate to High Ametropia

Purpose: To assess the 8-year clinical outcomes of implantation of an implantable collamer lens (ICL) with a central port (KS-Aquaport; EVO-ICL) for moderate to high myopia and myopic astigmatism.Methods: This retrospective study comprised a total of 177 eyes of 106 patients with spherical equivalents of −7.99 ± 3.33 D [mean ± standard deviation], who underwent EVO-ICL implantation. We evaluated the safety, efficacy, predictability, stability, and adverse events of the surgery, at 1 month, and 1, 2, 4, 6, and 8 years postoperatively.Results: The logarithm of the minimal angle of resolution (LogMAR) uncorrected distance visual acuity (UDVA) and corrected distance visual acuity (CDVA) were −0.07 ± 0.17 and −0.20 ± 0.09, respectively, at 8 years postoperatively. The safety and efficacy indices were 1.18 ± 0.24 and 0.89 ± 0.28, respectively. At 8 years, 83 and 93% eyes were within ± 0.5 D and ± 1.0 D of the targeted correction, respectively. Change in manifest refraction from 1 month to 8 years postoperatively was −0.13 ± 0.30 D. Three eyes (1.7%) that developed cataracts had a slight pre-existing peripheral anterior subcapsular cataract formation required simultaneous ICL extraction and cataract surgery at 2 or 3 years or ICL size change (1 size up) at 7 years postoperatively. We found that neither significant intraocular pressure (IOP) rise (including pupillary block) nor significant endothelial cell loss occurred in any case throughout the 8-year observation period.Conclusions: Current ICL implantation with central port technology offered good continuous outcomes for all measures of safety, efficacy, predictability, and stability for correcting moderate to high myopic errors over a long period, thereby suggesting its long-term viability as a surgical approach for the treatment of such eyes.

A Case of Implantable Collamer Lens (ICL) with Reverse Orientation for 10 Years

Background. Implantable collamer lens (ICL) might rarely cause complications that warrant explantation. Here, we presented a case of inverted ICL that has undergone explantation after a 10-year duration. Case Presentation. A 49-year-old male with past ocular history of ICL implantation 10 years ago presented complaining of progressive decrease of visual acuity in the left eye for a long time. On examination, decreased visual acuity, anterior subcapsular cataract, and low ICL vault were noted. The anterior segment optical coherence tomography (AS OCT) showed inverted ICL. The ICL was explanted, and cataract surgery was done. Conclusion. Inverted ICL should be kept in mind as a rare cause of long-term poor visual acuity in patient with a history of ICL surgery.

Unilateral Toxic Anterior Segment Syndrome Resulting in Cataract and Urrets-Zavalia Syndrome after Sequential Uneventful Implantation of a Posterior Chamber Phakic Toric Intraocular Lens at Two Different Surgical Facilities: A Series of Unfortunate Events

Background. Phakic Intraocular Lens (P-IOL) implantation is a safe, easy, predictable intervention designed to manage moderate to high refractive errors. Complications are relatively uncommon and include mainly cataract and intraocular pressure spikes. Toxic Anterior Segment Syndrome (TASS) is a rather unusual sterile anterior segment inflammation after uneventful intraocular surgery, extremely rarely reported after P-IOL implantation. Urrets-Zavalia Syndrome (UZS) is also very rarely described after P-IOL. To date, to the best of the authors’ knowledge, no article has ever described the simultaneous occurrence of TASS and UZS in a patient after P-IOL implantation. Objective. In this article, the authors present the case of a female patient with moderate myopic astigmatism, who underwent sequential P-IOL implantation at two different facilities. The postoperative course of the first eye was uneventful, but she developed complications associated to the intervention in the second eye. Materials. The article describes the case of a young patient who underwent a sequential Phakic Intraocular Lens (P-IOL) implantation at two different institutions. The postoperative course of the first eye (left eye) was uneventful; however, the second eye (right eye) initially developed Toxic Anterior Segment Syndrome (TASS). Although timely and correct management was instituted, upon resolution of TASS, the patient developed Urrets-Zavalia Syndrome, anterior subcapsular cataract, and significant endothelial damage in the same eye. Results. The patient was followed closely and managed accordingly; corneal edema and anterior segment inflammation of the right eye eventually resolved. Nevertheless, an anterior subcapsular cataract and a fixed dilated pupil remained; with normal intraocular pressure (IOP). Specular microscopy confirmed an endothelial cell loss in the TASS eye (right eye). Pupil size showed no reaction to repeated doses of Pilocarpine 2%. A month after surgery, refraction on her right eye was + 0.25 + 0.75 × 93 , which resulted in a 20/50 vision. Conclusions. TASS and UZS are both extremely rare complications after uneventful P-IOL implantation, with only a handful of cases having been reported of each of them. To date, this is the very first case where UZS ensued after and potentially as a consequence of TASS in a patient who had undergone P-IOL implantation. Although a direct causative element could not be pinpointed, the fact that the complication ensued after being operated in one surgical institution and not the other, could suggest some role of different sterilization and handling procedures, but no direct conclusion can be made on this case.

Long Noncoding RNA NEAT1 Regulates TGF-β2-Induced Epithelial-Mesenchymal Transition of Lens Epithelial Cells through the miR-34a/Snail1 and miR-204/Zeb1 Pathways

The aim of this study was to explore whether the long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1)/miR-34a/Snail1 and NEAT1/miR-204/Zeb1 pathways are involved in epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Primary human LECs (HLECs) were separated and cultured. Our results identified that TGF-β2 induces NEAT1 overexpression in a dose-dependent manner and a time-dependent manner. Additionally, TGF-β2 induced downregulation of E-cadherin and upregulation of fibronectin in primary HLECs through a NEAT1-dependent mechanism. Microarray analysis showed that NEAT1 overexpression inhibited the miR-34a and miR-204 levels in the LECs. The expression of miR-34a and miR-204 was decreased, and the levels of Snail1 and Zeb1 were elevated in human posterior capsule opacification- (PCO-) attached LECs and the LECs obtained from anterior subcapsular cataract (ASC) by quantitative RT-PCR (qRT-PCR). Mechanistic studies revealed that NEAT1 negatively regulates miR-34a or miR-204, and miR-34a or miR-204 directly targets Snail1 or Zeb1 by luciferase assay and RNA-binding protein immunoprecipitation assay, respectively. Overall, the NEAT1/miR-34a/Snail1 and NEAT1/miR-204/Zeb1 pathways are involved in TGF-β2-induced EMT of HLECs. In summary, TGF-β2 induces NEAT1 overexpression, which in turn suggests that NEAT1 acts as a ceRNA targeting Snail1 or Zeb1 by binding miR-34a or miR-204, and promotes the progression of EMT of LECs.

Amiodarone-associated optic neuropathy in the treatment of cardiovascular diseases

An increase in the growth of cardiovascular diseases has been observed in the last few years. Cardiac rhythm disturbances, especially atrial fibrillation, in absence of cardioversion and proper prophylaxis lead to thromboembolic complications. Drug therapy in rhythm disorders consists of the many antiarrhythmic drugs, prescribed for a long period of time. This fact can result to the ocular toxicy, which have insidious and slow progression. First and foremost, there is a risk of amiodarone-associated toxicity. Amiodarone affects as anterior segment structures (photosensitivity, corneal and conjunctiva deposits, anterior subcapsular cataract) as posterior segment structures (optic neuropathy). Fibers of the papillomacular bundle are the most vulnerable structures in optic nerve to the toxic effect of amiodarone due to the absence of myelination and salutatory conduction, their small size and high-energy requirements. The difficulties in diagnosis of amiodarone-associated optic neuropathy are related to slow progression (patients don’t notice symptoms until the late stages) and clinical similarity to ischemic optic neuropathy.