Histopathological Changes in Corneal Ectasia. / Histopathologische Veränderungen bei kornealen Ektasien.

Corneal ectasia comprises keratoconus, keratoglobus, pellucid marginal degeneration, and iatrogenic keratectasia. In all forms of corneal ectasia, there is a thinning of the cornea, usually accompanied by steepening of the cornea, leading to irregular astigmatism. Here, we provide an overview of histopathologic alterations of the various corneal ectasias. Furthermore, histologic changes after surgical procedures that are performed in severe cases of corneal ectasia, such as corneal cross-linking and penetrating keratoplasty (pKPL), as well as refractive surgical procedures that may lead to postsurgical ectasia are presented. In addition to a literature review, histopathologic archival material was reviewed and examined to illustrate the specific histologic changes.

Spatial and temporal immunoreaction of nestin, CD44, collagen IX and GFAP in human retinal Müller cells in the developing fetal eye.

The purpose of this study was to investigate Müller cells during the fetal development of the human eye. Müller cells in eyes of 39 human fetuses (11-38 weeks of gestation, WOG) and 6 infants (5 died of abusive head trauma, AHT, aged 1-9 months) were immunohistochemically stained and investigated for spatial and temporal immunoreaction of nestin, CD44, collagen IX and GFAP, which are stem cell markers or markers of intermediate filaments, respectively, in one of the hitherto largest cohorts of fetal eyes. Müller cells could be detected immunohistochemically as early as 12 WOG by immunohistochemical staining with nestin. Nestin was more strongly expressed in Müller cells of the peripheral retina and a centroperipheral gradient of immunoreaction over time was observed. CD44 was predominantly expressed in fetal eyes of the late second and early third trimester between (23 and 27 WOG) and significantly stronger in the infant eyes. Collagen IX labeling in the central retina was significantly stronger than in more peripheral sectors and increased with fetal age. GFAP staining in Müller cells was seen in the eye of a fetus of 38 WOG who died postnatally and in the infant eyes with and without history of AHT. Additionally, GFAP staining was present in the astrocytes of fetal and infant eyes. All examined markers were expressed by Müller cells at different developmental stages highlighting the plasticity of Müller cells during the development of the human eye. GFAP should be cautiously used as a marker for AHT as it was also expressed in fetal astrocytes and Müller cells in eyes without history of AHT.

[Histological changes in keratoconus and wound healing after corneal cross-linking]. / Histologische Veränderungen beim Keratokonus und Wundheilung nach kornealem Crosslinking.

BACKGROUND: Keratoconus is classified as a corneal ectasia and is a multifactorial disease. In those affected, mostly adolescent patients visual deterioration occurs due to the development of irregular astigmatism. Treatment by corneal cross-linking (CXL) has been indicated in progressive disease for several years. OBJECTIVE: To present the pathophysiology and histological changes in keratoconus as well as wound healing processes after CXL and their potential complications. MATERIAL AND METHODS: Histological changes in keratoconus as well as wound healing processes after CXL and their potential complications are presented based on histological examination of corneal specimens with keratoconus with and without a condition after CXL. Relevant literature and own data are analyzed and discussed. RESULTS: Besides inflammatory processes, atopic and genetic dispositions play a role in the development of keratoconus. The histological characteristics of keratoconus include changes in the epithelium, Bowman's layer and stroma. Wound healing processes after CXL include healing of the surface epithelium and transient loss of keratocytes and nerve fibers. CONCLUSION: Keratoconus shows characteristic histopathological changes, such as epithelial irregularities, stromal thinning and breaks of Bowman's layer, whereas the endothelium and Descemet's membrane remain unchanged (apart from cases of corneal hydrops). After CXL wound healing processes can be followed primarily in vivo by confocal microscopy. Complications after CXL are rare. Persistent loss of keratocytes can be clinically manifested as a visually relevant scar.

Short-term real-world outcomes following intravitreal brolucizumab for neovascular AMD: SHIFT study.

BACKGROUND: Brolucizumab has recently been approved in Europe as a novel treatment for patients with neovascular age-related macular degeneration (nAMD). We report on early experiences with real-world outcomes of switch to brolucizumab therapy in previously anti-vascular endothelial growth factor (anti-VEGF)-treated patients. METHODS: Patients with recalcitrant nAMD were switched to brolucizumab therapy. Functional and structural parameters 4 weeks after first brolucizumab injection were evaluated including best-corrected visual acuity (BCVA (logMAR)), foveal centre point (FCP (µm)), central subfield retinal thickness (CSRT (µm)) and macular volume (mm³). RESULTS: Sixty-three eyes of 57 patients with nAMD (52.6% females) with a mean (±SD) age of 79.5±6.7 years were included. Mean change of BCVA was 0.03±0.14 logMAR (p=0.115). Significant reductions were recorded for FCP with a mean (±SD) change of -66.81±72.63 µm, -66.76±60.71 µm for CSRT and -0.27±0.24 mm³ for macular volume (all p<0.001). Intraocular inflammation was observed in seven eyes of seven patients, including one case of retinal vasculitis. CONCLUSIONS: The results of the SHIFT study indicate that switch to brolucizumab may represent a treatment option in patients with nAMD poorly responsive to other anti-VEGF agents. Further long-term analyses appear prudent to assess efficacy and safety of brolucizumab in a routine clinical setting.