Background/Objectives: to report a novel KRT3 Meesmann corneal dystrophy (MECD) mutation and its clinical findings in a Spanish family, thus completing the international database. Case series study. Methods: Two generations of three family members were studied. The clinical ophthalmologic evaluation was made including best-corrected visual acuity (BCVA), biomicroscopy with and without fluorescein, fundoscopy, Schirmer test I, non-invasive break-up time (NiBUT), and esthesiometry. In vivo confocal microscopy (IVCM), anterior segment optical coherence tomography (AS-OCT) with an epithelial map, and genetic analysis were also performed. Results: A novel heterozygous mutation in the KRT3 gene c.1527G>T (p. Glu509Asp) was identified. Biomicroscopy revealed bilateral multiple corneal intraepithelial cysts. IVCM showed numerous and relatively small microcysts (12–32 µm), hyperreflective materials, subepithelial nerve and Bowman’s layer alterations. AS-OCT scan revealed diffuse hyperreflectivity and the epithelial map displayed thickening of the corneal epithelium in the interpalpebral zone (proband: 52–68 µm and father’s proband: 55–71 µm) with a slightly thinned cornea. Conclusions: We identified a new mutation in the KRT3 gene–c.1527G>T (p. Glu509Asp) in a Spanish family with MECD. A comprehensive characterization of the clinical signs, using different techniques, especially an epithelial map, could be useful to diagnose and monitor epithelial changes by quantitative measures. Epithelial map changes provide better understanding of MECD differential epithelial behavior and its progression changes. Larger studies will be necessary to better understand these specific patterns and clinically evaluate new therapies.

Purpose: The aim of this study was to describe the clinical features and endothelial involvement in a case of Mpox virus keratitis by in vivo confocal microscopy (IVCM). Methods: This is a case report. Results: A 35-year-old man presented with redness, photophobia, pain, tearing, and a low visual acuity of 0.09 (decimal) in the left eye with a 6-week history of Mpox and corneal trauma. Previous testing of blood, interdigital skin lesions, and conjunctival and eyelid margin swabs confirmed the presence of Mpox by polymerase chain reaction. Biomicroscopy displayed superficial stromal infiltrates with a continuous but irregular epithelium. IVCM revealed the presence of pseudoguttata, loss of defined cell boundaries, infiltration of inflammatory cells in the endothelial layer, endothelial ridges, and precipitated pigmented granules, consistent with endotheliitis. After this episode, the patient had 4 reactivations, also treated with topical corticoids and oral tecovirimat 600 mg twice a day for 2 weeks. On the fourth reactivation, this treatment was extended to 4 weeks. On the last visit, the patient presented a visual acuity of 0.5 with disciform keratitis and reduced endotheliitis signs. The endothelial cell density remained normal during the follow-up (2763 ± 376 cell/mm² at baseline and 2795 ± 238 cell/mm² at the last visit). Polymegathism and pleomorphism showed altered values during the follow-up. Conclusions: Patients with an altered corneal epithelial barrier could suffer Mpox endotheliitis, like other DNA viruses, before disciform keratitis appears. IVCM is a useful tool for the early detection of endotheliitis and for describing its evolution, improving patient care.

This study describes the clinical and genetic features of Meesmann epithelial corneal dystrophy (MECD) in two unrelated families and reports new genotype–phenotype associations. Ten patients from a Lebanese family (n = 4) (Family 1) and a Spanish family (n = 6) (Family 2) underwent ophthalmologic evaluation, in vivo confocal microscopy (IVCM), anterior segment optical coherence tomography (AS-OCT) with epithelial thickness mapping (ET-map), and targeted next-generation sequencing (NGS) using a custom-designed 133-gene panel associated with anterior segment dystrophies. In Family 1, a novel homozygous KRT12 c.1181T>C (p.Leu394Pro) variant was identified in the symptomatic proband and his clinically asymptomatic brother, while both parents, who were first cousins, were heterozygous for this nucleotide variant. The proband also carried the heterozygous KRT3 c.250C>T (p.Arg84Trp) variant, which has been previously reported but, to our knowledge, has not been described in co-occurrence until now. In addition, the proband showed a complex phenotype with signs of MECD and epithelial basal membrane alterations consistent with epithelial basement membrane dystrophy (EBMD). In Family 2, four affected members carried the KRT3 c.1492G>A (p.Glu498Lys) variant in heterozygosity, which has been previously described. The elderly members affected showed typical signs of MECD and EBMD. To our knowledge, these concomitant alterations have not been previously described with genetical confirmation. In conclusion, this study provides the first evidence that the co-occurrence of variants in two Meesmann corneal dystrophy-associated genes (KRT3 and KRT12) can jointly account for the disease phenotype. We also highlight the association of MECD with EBMD in both families. Characterization using IVCM and AS-OCT ET-Map provides a deeper understanding of the morphological changes and phenotypic variability in MECD, confirming the utility of this multimodal imaging approach for diagnosis and management.

Background: To assess intraocular pressure (IOP) changes and complications after XEN45 implants in medically controlled eyes (MCE) vs. medically uncontrolled eyes (MUE). Methods: A retrospective study, in a tertiary referral hospital, on mild-to-moderate primary open-angle glaucoma (POAG) cases under topical medication, including 32 eyes with IOP < 21 mmHg (MCE group) and 30 eyes with IOP ≥ 21 mmHg (MUE group). The success criteria using Kaplan–Meier analysis was IOP < 21 mmHg without medications (complete success) or fewer drugs than preoperatively (qualified success) at the last visit, without new surgery or unresolved hypotony. Results: No significant preoperative differences were found between the groups. The mean IOP was 15.6 ± 3.8 mmHg in MCE and 15.1 ± 4.1 mmHg in the MUE group (p > 0.05; Mann–Whitney test) at the end of the follow-up (mean of 26.1 ± 15.6 months and 28.3 ± 15.3 months, respectively) (p = 0.414, Mann–Whitney Test). The device caused a significant IOP reduction at 24 h in both groups. Thereafter, the MCE group significantly tended to increase IOP, recovering baseline values at 1 month and maintaining them until the end of the follow-up. In contrast, in the MUE group, the IOP values tended to be similar after the first reduction. No relevant complications and no significant differences between the groups in the survival analysis were found. Conclusions: XEN45 provided stable IOP control in both the MCE and MUE group without important complications in the medium term. The IOP increasing in the MCE group, after a prior decrease, led to restored baseline values 1 month after surgery. The homeostatic mechanism that causes the rise in the IOP to baseline values and its relationship with failure cases remains to be clarified.