The iridocorneal endothelial (ICE) syndrome is a rare ocular disorder that includes a group of conditions characterized by structural and proliferative abnormalities of the corneal endothelium, the anterior chamber angle, and the iris. Common clinical features include corneal edema, secondary glaucoma, iris atrophy, and pupillary anomalies, ranging from distortion to polycoria. The main subtypes of this syndrome are the progressive iris atrophy, the Cogan-Reese syndrome, and the Chandler syndrome. ICE syndrome is usually diagnosed in women in the adult age. Clinical history and complete eye examination including tonometry and gonioscopy are necessary to reach a diagnosis. Imaging techniques, such as in vivo confocal microscopy and ultrasound biomicroscopy, are used to confirm the diagnosis by revealing the presence of “ICE-cells” on the corneal endothelium and the structural changes of the anterior chamber angle. An early diagnosis is helpful to better manage the most challenging complications such as secondary glaucoma and corneal edema. Treatment of ICE-related glaucoma often requires glaucoma filtering surgery with antifibrotic agents and the use of glaucoma drainage implants should be considered early in the management of these patients. Visual impairment and pain associated with corneal edema can be successfully managed with endothelial keratoplasty.

Congenital ptosis is a rare condition characterized by lower positioning of the upper eyelid that is present at birth and is a clinical condition that is persistent if not treated. It may be unilateral or bilateral and may be associated with other ocular disorders or systemic conditions, including Marcus Gunn, Horner, and Duane syndromes. It is a benign condition but causes functional, cosmetic, and psychological problems in children. However, not all patients need to undergo surgery, and usually only patients at risk of amblyopia need a prompt surgical correction, while in other cases, surgery can be postponed. The grade of ptosis, the eyelid function, and the amblyopic risk are the parameters that affect the ophthalmologist’s decision on timing of surgery and the surgical technique to be used. In fact, there are several types of surgical techniques to correct a congenital ptosis, although very often more than one is needed to obtain an acceptable result. This paper reviews the causes of congenital ptosis and associated diseases. Particular emphasis is given to surgical management and different procedures available to correct the upper eyelid anomaly and avoid permanent damage to visual function.

A retrospective chart review of patients with persistent subretinal and/or intraretinal fluid, despite previous treatment with intravitreal ranibizumab (0.5 mg), who were switched to aflibercept injections, was performed. Treatment was three monthly aflibercept (2 mg) injections followed by dosing on pro re nata basis. Main outcome measures included changes in best corrected visual acuity (BCVA), 1 mm central subfield (CSF) retinal thickness, the height of the pigment epithelial detachment (PED), and subfoveal choroidal thickness on optical coherence tomography at 6 months. Thirty-one eyes of 30 patients were analyzed. The mean number of injections before aflibercept conversion was 34.4 ± 11.9. After an average of 4.5 aflibercept injections (range 3 to 6) over 6 months, no significant change in BCVA was observed (P>0.05). Compared with baseline, there was a significant reduction of the CSF retinal thickness (449 ± 179 versus 269 ± 145 μm,P<0.001), maximum PED height (262 ± 134 versus 183 ± 100 μm,P<0.001), and choroidal thickness (192 ± 67 versus 167 ± 51 μm,P<0.01). Stable visual acuity and anatomical improvement were obtained for up to 6 months after aflibercept conversion. However, choroidal thinning related to treatment was observed.

Ocular fibrosis leads to severe visual impairment and blindness worldwide, being a major area of unmet need in ophthalmology and medicine. To date, the only available treatments are antimetabolite drugs that have significant potentially blinding side effects, such as tissue damage and infection. There is thus an urgent need to identify novel targets to prevent/treat scarring and postsurgical fibrosis in the eye. In this review, the latest progress in biological mechanisms underlying ocular fibrosis are discussed. We also summarize the current knowledge on preclinical studies based on viral and non-viral gene therapy, as well as chemical inhibitors, for targeting TGFβ or downstream effectors in fibrotic disorders of the eye. Moreover, the role of angiogenetic and biomechanical factors in ocular fibrosis is discussed, focusing on related preclinical treatment approaches. Moreover, we describe available evidence on clinical studies investigating the use of therapies targeting TGFβ-dependent pathways, angiogenetic factors, and biomechanical factors, alone or in combination with other strategies, in ocular tissue fibrosis. Finally, the recent progress in cell-based therapies for treating fibrotic eye disorders is discussed. The increasing knowledge of these disorders in the eye and the promising results from testing of novel targeted therapies could offer viable perspectives for translation into clinical use.

Purpose: To compare the changes in subfoveal choroidal thickness (CT) in eyes with neovascular age-related macular degeneration (nAMD) treated with intravitreal ranibizumab or aflibercept. Methods: In this retrospective case series, the medical records of 28 patients with nAMD treated with at least 3 consecutive monthly injections of ranibizumab (0.5 mg/0.05 mL) or aflibercept (2 mg/0.05 mL) between December 2013 and June 2014 and who were followed up for at least 3 months were reviewed. Subfoveal choroidal thickness was measured using enhanced depth imaging optical coherence tomography. Results: Choroidal thickness decreased over time in the aflibercept group, but was unchanged throughout the study in the ranibizumab group. At each time point, the decrease was significantly greater in aflibercept-treated eyes compared with ranibizumab-treated eyes ( P <0.05). No significant change in best-corrected visual acuity (BCVA) was seen in either group during follow-up. There was no correlation between change in choroidal thickness and age, sex, duration of previous antivascular endothelial growth factor treatment, number of previous injections, spherical equivalent, baseline choroidal thickness, and the BCVA outcome in either group. Conclusions: Subfoveal choroidal thickness appeared to decrease significantly in eyes with nAMD during 3 months of aflibercept treatment. No corresponding decrease in choroidal thickness occurred in ranibizumab-treated eyes.