Purpose: To report a case of non-arteritic cilioretinal artery occlusion associated with subcutaneous testosterone pellet therapy in a perimenopausal woman. Methods: A single case was reviewed. Results: A 48-year-old woman presented to the emergency department with an acute central "gray spot" in her left eye that began 6 hours before presentation. Fundus examination revealed intraretinal whitening of the inferior macula along the distribution of the cilioretinal artery, with foveal sparing. Systemic evaluation, including stroke and hypercoagulability work-up, was negative. The patient's history was notable for active treatment with subcutaneous testosterone pellets and prior retinal migraines. Over a 6-week follow-up period, the visual field defect persisted but showed improvement, and the intraretinal whitening resolved completely. Conclusions: This case suggests a possible association between subcutaneous testosterone therapy and non-arteritic cilioretinal artery occlusion in the absence of identifiable thrombophilia or hypofibrinolysis. Clinicians should consider counseling patients and screening before initiating testosterone therapy, given the potential risk of venous and arterial thromboembolism.

We report the case of a 77-year-old woman who presented with progressive, painless bilateral visual loss over three weeks. Ophthalmologic evaluation demonstrated bilateral anterior ischemic optic neuropathy and right central retinal artery occlusion. Notably, she lacked classical systemic features of giant cell arteritis (GCA), including headache, scalp tenderness, or jaw claudication. Laboratory evaluation revealed an elevated erythrocyte sedimentation rate (ESR 64 mm/h). Temporal artery ultrasound demonstrated bilateral halo signs, supporting the diagnosis of GCA. High-dose corticosteroid therapy was promptly initiated; however, visual loss remained irreversible. This case highlights the importance of maintaining a high index of suspicion for GCA in elderly patients presenting with unexplained visual symptoms, even in the absence of typical cranial features. Temporal artery ultrasound is a valuable non-invasive diagnostic tool that can facilitate early diagnosis and prompt treatment, potentially preventing irreversible visual complications.

This report demonstrates the diagnostic evaluation and clinical management of a 16-year-old girl who developed branch retinal artery occlusion secondary to patent foramen ovale. The goal is to increase awareness of this rare presentation in adolescents among clinicians, with a summary of the important clinical features, multimodal imaging findings and therapeutic strategies that allowed for timely reperfusion and subsequent visual recovery.

Ischemia-induced retinopathy is a defining feature of prevalent ocular conditions, including diabetic retinopathy and central retinal artery or vein occlusion. Therapeutic interventions for ischemic retinopathies show limited efficacy and adverse effects, highlighting the need to thoroughly investigate the underlying mechanisms. Histone deacetylase 3 (HDAC3), a member of the histone deacetylase family, plays a central role in regulating gene expression in myeloid cells (microglia and macrophages). We recently showed that myeloid HDAC3 deletion promotes tissue repair and functional recovery after retinal ischemia-reperfusion (IR) injury via efferocytosis, a process by which myeloid cells engulf and clear apoptotic cells. Here, we investigated the mechanism by which myeloid HDAC3 deletion enhances efferocytosis. Employing an in vitro efferocytosis assay coupled with RNA sequencing on HDAC3 KO macrophages revealed that the secreted protein, CD5 molecule-like (CD5L), was the most upregulated among other pro-efferocytic genes. In vivo, we found that CD5L levels markedly increased in the retinas of myeloid HDAC3 KO mice subjected to IR injury, and its expression colocalized with myeloid cells. Co-immunoprecipitation experiments showed that HDAC3 represses CD5L expression in a liver X receptor (LXRα)-dependent manner. Additionally, we found that CD36, a receptor for CD5L that facilitates the clearance of apoptotic cells, was upregulated in retinal myeloid cells after IR. In vitro, CD5L treatment enhanced efferocytosis via CD36. We then evaluated the role of CD5L in retinal IR injury using in vivo neuronal, vascular, structural, and functional endpoints. CD5L KO mice showed worsened outcomes after IR, whereas treatment with recombinant CD5L was protective against retinal ischemic injury. Collectively, our findings suggest that deleting HDAC3 enhances macrophage efferocytosis by upregulating the CD5L/CD36 axis. CD5L may serve as a promising therapeutic target to improve outcomes in ischemic retinopathy.