Triple Trouble with Triple Solutions: A Unique Case Report of a Severe Exudative Retinal Detachment Accompanied by Retinal Traction and Two Retinal Holes in Coats Disease.

Introduction: Coats disease is a rare vasculature pathology that usually presents as retinal telangiectasia with possible progression to exudative retinal detachment (RD). Intravitreal anti-VEGF injections, cryotherapy, laser photocoagulation, and surgery are commonly used to control the disease and prevent its progression. Although iatrogenic tractional RDs secondary to anti-VEGF injections have been reported in patients with Coats disease, RDs in Coats disease are exudative, secondary to retinal exudation and vascular abnormalities. In this article, we present the first reported case of a severe exudative RD accompanied by retinal traction and two retinal holes in a patient with Coats disease. Case Presentation: A 32-year-old male initially presented with Coats disease stage 2A, which then progressed to 3A1 within a month of close follow-ups, finally leading to exudative RD. Following cryotherapy and bevacizumab injections, the exudative RD progressed, with the emergence of retinal traction and two retinal holes. This complex case was successfully treated with a scleral buckle vitrectomy accompanied by radial elements to support the RD, pars plana vitrectomy, silicon oil tamponade, and post-surgical bevacizumab injections. Six months following the surgical intervention, the patient's vision is restored at 20/30, and retinal imaging shows a totally flattened retina. Conclusion: We present the first reported case of a severe exudative RD accompanied by retinal traction and two retinal holes in a patient with Coats disease. The combination of surgical treatment and bevacizumab injections is thought to have collectively contributed to our patient's favorable outcome.

Oxidative stress facilitates exogenous mitochondria internalization and survival in retinal ganglion precursor-like cells.

Ocular cells are highly dependent on mitochondrial function due to their high demand of energy supply and their constant exposure to oxidative stress. Indeed, mitochondrial dysfunction is highly implicated in various acute, chronic, and genetic disorders of the visual system. It has recently been shown that mitochondrial transplantation (MitoPlant) temporarily protects retinal ganglion cells (RGCs) from cell death during ocular ischemia. Here, we characterized MitoPlant dynamics in retinal ganglion precursor-like cells, in steady state and under oxidative stress. We developed a new method for detection of transplanted mitochondria using qPCR, based on a difference in the mtDNA sequence of C57BL/6 and BALB/c mouse strains. Using this approach, we show internalization of exogenous mitochondria already three hours after transplantation, and a decline in mitochondrial content after twenty four hours. Interestingly, exposure of target cells to moderate oxidative stress prior to MitoPlant dramatically enhanced mitochondrial uptake and extended the survival of mitochondria in recipient cells by more than three fold. Understanding the factors that regulate the exogenous mitochondrial uptake and their survival may promote the application of MitoPlant for treatment of chronic and genetic mitochondrial diseases.