DELAYED FOLLOW-UP IN PATIENTS WITH NEOVASCULAR AGE-RELATED MACULAR DEGENERATION TREATED UNDER UNIVERSAL HEALTH COVERAGE: Risk Factors and Visual Outcomes.

Background/purpose: To report the rate of delayed follow-up visits (DFU), to identify risk factors of DFU, and to assess the impact of DFU on outcomes in neovascular age-related macular degeneration.

Methods: This retrospective study included all patients with neovascular age-related macular degeneration (n = 1,291) treated with antivascular endothelial growth factor injections between January 2013 and December 2020 in 2 centers in Quebec, Canada. A DFU was defined as a delay of ≥4 weeks than scheduled.

Fear Associated with COVID-19 in Patients with Neovascular Age-Related Macular Degeneration.

Purpose: Since the beginning of the COVID-19 pandemic, news related to the pandemic has created a feeling of fear, particularly among high-risk groups including elderly patients. This study aimed to assess the fear associated with COVID-19 and to evaluate the fear of vision decrease related to the delay of treatment in neovascular age-related macular degeneration patients (nAMD) during the pandemic.

Patients And Methods: This is a prospective cross-sectional study of 160 actively treated patients with nAMD enrolled between September and November 2020 at a tertiary hospital in Québec, Canada.

Transconjunctival suturing of the scleral flap for overfiltration with hypotony maculopathy after trabeculectomy.

Objective: To assess the efficacy of transconjunctival suturing of the scleral flap in improving hypotony maculopathy resulting from overfiltration after trabeculectomy.

Design: Retrospective review.

Participants: 35 eyes of 33 patients.

Functional analysis of the glaucoma-causing TIGR/myocilin protein: integrity of amino-terminal coiled-coil regions and olfactomedin homology domain is essential for extracellular adhesion and secretion.

TIGR/MYOC mutations account for 2-4% of the primary open-angle glaucoma (POAG) patients. More than 90% of the known mutations are located within its carboxy-terminus olfactomedin-homology (Olf) domain (amino acids (aa) 245-504). In vitro and in vivo studies showed that several Olf domain mutations prevented myocilin secretion.