No abstract

Purpose The severe acute respiratory syndrome coronavirus-2 and its associated infection known as COVID-19 have resulted in a global pandemic. Ocular manifestations of COVID-19 are nonspecific and include hyperemia, chemosis, epiphora, secretions, and eyelid edema. There is a paucity in the literature regarding COVID-19 related inflammatory syndromes which may also include ocular manifestations. Observations In pediatric patients, conjunctivitis has been recently reported in association with a multisystem inflammatory condition related to COVID-19 that shares features with Kawasaki disease and toxic shock syndrome. We describe the clinical course of an adult patient with symptoms and signs consistent with a Kawasaki-like syndrome. Conclusions and Importance To our knowledge, this report may be the first case of a Kawasaki-like syndrome in an adult with COVID-19 infection.

Recent studies have shown that constitutive activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in Schwann cells (SCs) increases myelin thickness in transgenic mice. In this secondary analysis, we report that these transgenic mice develop a postnatal corneal neurofibroma with loss of corneal transparency by age 6 months. We show that expansion of nonmyelinating SCs, under the control of activated ERK1/2, also drive myofibroblast differentiation that derive from both SC precursors and resident corneal keratocytes. Further, these mice also harbor activated mast cells in the central cornea, which contributes to pathological corneal neovascularization and fibrosis. This breach of corneal avascularity and immune status is associated with the growth of the tumor pannus, resulting in a corneal stroma that is nearly 4 times its normal size. In corneas with advanced disease some axons became ectopically myelinated and the disruption of Remak bundles is evident. To determine whether myofibroblast differentiation was linked to vimentin, we examined the levels and phosphorylation status of this fibrotic biomarker. Concomitant with the early upregulation of vimentin, a serine 38-phosphorylated isoform of vimentin (pSer38vim) increased in SCs, which was attributed primarily to the soluble fraction of protein—not the cytoskeletal portion. However, the overexpressed pSer38vim became predominantly cytoskeletal with growth of the corneal tumor. Our findings demonstrate an unrecognized function of ERK1/2 in the maintenance of corneal homeostasis, wherein its overactivation in SCs promotes corneal neurofibromas. This study is also the first report of a genetically engineered mouse that spontaneously develops a corneal tumor.

Purpose of reviewThe prevalence of diabetic retinopathy continues to rise. This review highlights advances in imaging, medical, and surgical management of proliferative diabetic retinopathy (PDR) in recent years. Recent findingsUltra-widefield fluorescein angiography has been shown to better characterize which patients have predominantly peripheral lesions and who may advance to more advanced forms of diabetic retinopathy. This was well demonstrated in DRCR Retina Network's Protocol AA. Protocol S demonstrated that antivascular endothelial growth factor (VEGF) treatment alone can be useful in the management of select PDR patients --particularly those without high-risk features. However, a growing body of literature highlights how lapse in care is a significant concern in PDR patients, and tailoring one's approach to treatment based on patient needs is recommended. In patients with high-risk features or where there is concern for lost-to-follow-up, incorporation of panretinal photocoagulation in the treatment paradigm is recommended. Protocol AB highlighted how patients with more advanced disease may benefit from earlier surgical intervention for earlier visual recovery but that continued anti-VEGF treatment may result in similar visual outcomes over a longer period. Finally, earlier surgical intervention for PDR without vitreous hemorrhage (VH) or retinal detachment is being considered a potential option to minimize treatment burden.