Bilateral retrobulbar optic neuropathy as the only sign of zoledronic acid toxicity

• Published in: Journal of clinical neuroscience Vol. 44; pp. 243 - 245
• Main Authors: Lavado, Félix Manco, Prieto, Marta Para, Osorio, María Rosalba Ramoa, Gálvez, María Isabel López, Leal, Lucía Manzanas
• Format: Journal Article
• Language: English
• Published: Scotland Elsevier Ltd 01-10-2017
• Subjects: Aged; Bilateral retrobulbar optic neuropathy; Bone Density Conservation Agents - adverse effects; Diphosphonates - adverse effects; Humans; Imidazoles - adverse effects; Male; Optic nerve; Optic Nerve - physiopathology; Optic Nerve Diseases - diagnosis; Optic Nerve Diseases - etiology; Toxicity; Zoledronic acid; Bilateral retrobulbar optic neuropathy; Zoledronic acid; Optic nerve; Toxicity
• ISSN: 0967-5868; 1532-2653
• DOI: 10.1016/j.jocn.2017.06.048

•Toxic retrobulbar optic neuropathy is an uncommon disease that is generally underdiagnosed.•Zoledronic acid belongs to the class of bisphosphonates and it is increasingly used in the treatment of hypercalcemia, especially patients with cancer.•Bisphosphonates may rarely cause ocular adverse effects like conjunctivitis, epiescleritis, scleritis, uveitis and orbital inflammation.•Ophthalmologists should be consider the possibility of retrobulbar optic neuropathy as a unusual but severe side-effect and the potential vision loss if the drug is not discontinued.
Bisphosphonates may rarely cause ocular adverse effects and retrobulbar optic neuropathy (RON) secondary to zoledronic acid is very rare.
A 67-year-old man was referred because of progressive and painless decrease vision in the left eye. He had been treated with 7 cycles of zoledronic acid infusions because of metastatic prostate cancer. On examination, VA was 20/20 in the right eye (OD) and 20/50 in the left eye (OS). The optic nerve was unremarkable OU. Pattern visual evoked potentials (pVEP) and electroretinography were performed with the result of VEP responses abolished in OS, and the VEP waveform within the normal range amplitude and delayed peak latencies in OD. Due to the high suspicion of bilateral RON secondary to zoledronic acid, we decided to discontinue the treatment. Two months later, VA was 20/20 OD and hand motions OS, with relative afferent pupillary defect and a pallor of the optic disc in OS. The diagnosis of bilateral RON secondary to zoledronic acid infusions was confirmed, and it was only partially reversible.
Zoledronic acid is a potent new generation bisphosphonate increasingly used in oncologic patients and it is usually well tolerated. Optic nerve toxicity is not a side effect recognised by either the Food and Drug Administration or the drug manufacturers, and to our knowledge, this is the first case of zoledronic acid-related bilateral RON with late onset.
In conclusion, patients treated with bisphosphonates should be informed about the possibility of ocular side-effects, and ophthalmologists should be consider discontinuing the drug.