To report the utility of tacrolimus 0.03% dermatologic ointment (Protopic) in a case of refractory atopic keratoconjunctivitis with giant papillae. A review of the medical literature is presented. A 32-year-old man with a long-standing history of severe atopic disease was referred to our department because of bilateral intense eye pain, itching, photophobia, and epiphora. Biomicroscopy examination showed conjunctival hyperemia, superficial punctata keratitis, and tarsal giant papillae. This patient had undergone previous treatment with systemic and topical steroids, antihistamines, topical antihistamine/mast cell stabilizer drops, cyclosporine A, and even surgical resection-cryopexy of giant papillae-without success. The patient was started on tacrolimus 0.03% ointment treatment of the conjunctival fornix twice daily. After 2 months, the patient experienced resolution of his clinical symptoms with a significant decrease in papillae size. No side effects were reported. Treatment was continued for 1 month and gradually reduced with increasingly wide intervals between applications. Eight months after treatment, there were no signs of reactivation, and the patient remains asymptomatic. Application of tacrolimus 0.03% dermatologic ointment into the lower fornix seems to constitute an interesting alternative treatment for atopic keratoconjunctivitis that is refractory to traditional treatment.

This article presents three cases of Descemet’s membrane detachment (DMD) occurring during ‘ab externo’ phacocanaloplasty procedures in three patients with uncontrolled primary open-angle glaucoma (OAG) and discusses the management of this condition by reviewing the available literature. Following a successful 360° cannulation of Schlemm’s canal (SC), the microcatheter was withdrawn while an ophthalmic viscosurgical device (OVD) was injected into the canal. During passage through the inferonasal quadrant, a spontaneous separation of the posterior layer of the cornea was observed. Each case was managed differently after diagnosis, with the third case being drained intraoperatively based on experience gained from the previous cases. On the first postoperative day, slit-lamp biomicroscopy (BMC) revealed multiple DMDs in case one and a hyphema in the lower third of a deep anterior chamber. In the other two cases, a single DMD was observed. The second case developed hemorrhagic Descemet membrane detachment (HDMD), while the other two were non-hemorrhagic. In all three cases, anterior segment optical coherence tomography (AS-OCT) revealed the presence of retrocorneal hyperreflective membranes indicative of DMDs. These membranes were located in the periphery of the cornea and did not impact the visual axis. After evaluation, a small incision was made in the inferotemporal DMD of the first case. However, for the two remaining cases, a strategy of watchful waiting was deemed appropriate due to the location and size of the DMDs, as they did not affect the best-corrected visual acuity (BCVA). Over time, the patients demonstrated progressive improvement with a gradual reduction in the size of the DMDs.

Changes in the cornea can influence outcomes in patients with primary open-angle glaucoma (POAG). We aimed to evaluate the relevance of changes in corneal biomechanics and intraocular pressure (IOP) in patients undergoing non-penetrating deep sclerectomy (NPDS) with the Esnoper V2000 implant^® (AJL Ophthalmic S.A., Gasteiz, Spain). We included 42 eyes of 42 patients with POAG scheduled for NPDS with the Esnoper V2000 implant. Biomechanical properties were measured by Ocular Response Analyzer^® G3 (ORA; Reichert Inc., Depew, NY, USA). Corneal hysteresis (CH), corneal resistance factor (CRF), corneal compensated IOP (IOPcc), and Goldmann-correlated IOP (IOPg) were measured the day before surgery and on day 1, 7, and 30 and 2 and 3 months after surgery. CH initially increased, fell below the presurgical value at 30 days after the surgery, and increased again at 2 and 3 months. CRF, IOPcc, and IOPg decreased on the first day after surgery, then followed a trend of increasing but stayed below pre-surgery levels. All values reached statistical significance. While observed changes in corneal biomechanics after NPDS and Esnoper V2000 implant were significant, more studies are needed if we are to understand their influence on corneal biomechanics and their clinical relevance in POAG.

Background and Clinical Significance: Biallelic pathogenic variants in the PCARE gene (photoreceptor cilium actin regulator), also known as C2orf71 (chromosome 2 open reading frame 71), are typically associated with retinitis pigmentosa type 54 (RP54) and, less frequently, with cone–rod dystrophy (CORD23). Case Presentation: A 52-year-old man presented with an eight-year history of progressive visual loss, without photophobia or nyctalopia. He underwent a comprehensive ophthalmological evaluation, including multimodal retinal imaging, automated perimetry, and full electrophysiological testing, in accordance with International Society for Clinical Electrophysiology of Vision (ISCEV)’s standards. Genetic testing was performed using next-generation sequencing (NGS) with an inherited retinal dystrophy gene panel, and findings were confirmed by Sanger sequencing. Clinical examination revealed bilateral macular atrophy with minimal foveal sparing and a central scotoma. Optical coherence tomography (OCT) showed disruption of the outer retinal layers and retinal pigment epithelium (RPE) abnormalities. Fundus autofluorescence (FAF) demonstrated central hypoautofluorescence surrounded by a hyperautofluorescent ring. Electrophysiological testing revealed severely reduced rod- and cone- mediated responses on full-field electroretinography (ERG), absent pattern ERG responses, and markedly reduced multifocal ERG responses, indicating widespread retinal dysfunction with significant macular involvement. Genetic analysis identified a homozygous pathogenic nonsense variant in PCARE [c.3289C>T; p.(Gln1097*)], confirming the diagnosis of an autosomal recessive inherited retinal dystrophy. Conclusions: Biallelic PCARE variants can cause late-onset severe retinal dystrophy, with predominant macular involvement and cone–rod dysfunction. Given its phenotypic overlap with other inherited retinal diseases, accurate diagnosis requires the integration of multimodal retinal imaging, electrophysiological testing, and comprehensive genetic analysis.