P14.126 radiation-induced optic neuropathy

Abstract

Abstract BACKGROUND Optic neuropathy is an inflammation of the optic nerve leading to a rapidly progressive visual loss. Most frequent etiologies are multiple sclerosis, vasculitides, and infections. In the context of tumorous pathology, optic neuropathy can occur due to meningeal infiltration, tumoral compression, or antitumor therapeutics (radiation therapy, some targeted cancer therapies, and checkpoint inhibitors). In the current study, we examine radiation-induced optic neuropathy (RION), which is the most frequent among optic neuropathies caused by antitumor therapeutics. MATERIAL AND METHODS We present the cases of 3 patients who experienced RION. For each patient, we collected data on age, type of tumor, date and modalities of radiation-therapy, starting date of visual loss, ophthalmologic description, MRI images, treatment, and clinical and radiological evolution. RESULTS The three patients were aged 57 to 68 years old at the time of NORI. They had irradiation between 2013 and 2018. Two patients had proton therapy and one had whole brain irradiation. The visual loss occurred between seven and twelve months after the end of radiation therapy. In all patients the symptoms were bilateral and the loss of vision was rapidly worsened until culminating in almost total blindness. The MRI abnormalities were consistent with retrobulbar optic neuritis. The visual loss remained severe despite the treatment administered. High dose steroids had no clinical effect. Bevacizumab enabled a discrete subjective visual improvement in one patient, but a worsening of visual loss in another. Hyperbaric oxygen therapy had no clinical effect but was undertaken three months after the starting date of visual loss which is probably too late for efficiency. Interestingly one patient was treated with an anti-IL6 antibody (tocilizumab). It was administered in order to avoid fibrosis formation, which is the ultimate condition of the inflammatory process. The rationale is that radiation-induced opening of the bood-brain-barrier and destruction of endothelial and glial cells lead to reparation process through microglia activation. In-vitro studies showed an increased secretion of IL-6 (and other pro-inflammatory cytokines) by the activated microglia. Our patient could not experience benefit from tocilizumab, but the treatment was administered four months after the starting date of visual loss and fibrosis was probably already formed. CONCLUSION These cases are consistent with existing literature. The risk is mostly due to the total dose and dose per fraction of the irradiation and the prognosis is very poor with no efficient treatment at the present time. Anti-IL6 antibody could be an interesting treatment if administered at an early stage, but a future prospective clinical trial would be needed to clinically validate this hypothesis.