Acute visual loss after ipilimumab treatment for metastatic melanoma

Abstract

BackgroundIpilimumab, a humanized CLTA-4 antibody is a standard therapy in the treatment of advanced melanoma. While ipilimumab provides an overall survival benefit to patients, it can be associated with immune related adverse events (IrAEs).Case presentationHere we describe a patient treated with ipilimumab who experienced known IrAEs, including hypophysitis, as well as a profound vision loss due to optic neuritis. There are rare reports of optic neuritis occurring as an adverse event associated with ipilimumab treatment. Furthermore, the patient experienced multiple complications from high dose steroids used to manage his IrAEs.ConclusionsThis case highlights the need for recognition of atypical immune mediated processes associated with newer checkpoint inhibitor therapies including ipilimumab.

Ipilimumab-induced hypophysitis involving the optic tracts and tuber cinereum evaluated using 3D fluid-attenuated inversion recovery

“…Those findings are not typically seen in patients with pituitary mass, but the characteristic visual field defect caused by pituitary mass with suprasellar extension is bitemporal hemianopsia. Ophthalmologic complications from ipilimumab therapy are rare, occurring in less than 1% of patients, but generally manifest as uveitis [6] . In our case, 3D FLAIR clearly showed high-signal lesions in optic tracts and tuber cinereum, which were considered related to her visual symptoms.…”

“…Recent studies suggest that approximately 10%-15% of patients receiving ipilimumab may develop hypophysitis [2] , [3] . Symptoms affecting vision are rarely observed in ipilimumab-induced hypophysitis [4] , [5] , [6] , because it is thought that pituitary lesions due to ipilimumab are not large enough to compress the optic chiasma, in contrast to lesions of autoimmune lymphocytic hypophysitis. Here we report a case of ipilimumab-induced hypophysitis with involvement of the optic tracts and tuber cinereum.…”

Optic Neuritis Possibly Induced by Anti-PD-L1 Antibody Treatment in a Patient with Non-Small Cell Lung Carcinoma

“…A variety of ocular complications, such as peripheral ulcerative keratitis, uveitis, Vogt-Koyanagi-Harada disease, inflammatory orbital disease, choroid neovascularization, melanoma-associated retinopathy, and polymyalgia rheumatoid giant cell arteritis, have been previously reported, predominately in cases treated with anti-CTLA-4 antibodies. Of these, optic neuritis is a rare complication, with only 2 cases reported to be caused by anti-CTLA-4 and 1 case caused by anti-PD-L1 antibody treatment [ 6 , 8 , 9 ]. Wilson et al [ 6 ] reported a case of metastatic melanoma accompanied by bilateral optic neuritis and hypophysitis, in which the patient became blind in the right eye despite combination therapy with steroid pulse, intravenous immunoglobulin, and plasma exchanges.…”

“…Among patients experiencing irAEs, 1–5% show neurological dysfunction and < 1% have ophthalmic complications [ 4 , 5 ]. Optic neuritis has been recently reported in association with anti-CTLA-4 antibody treatment [ 6 , 7 , 8 ]; however, a detailed description of optic neuritis associated with anti-PD-1 or anti-PD-L1 antibody treatment has not yet been published [ 9 ]. Here, we report the rare case of a patient with optic neuritis as an irAE, which occurred 1 year after the initiation of anti-PD-L1 antibody (MPDL3280A) treatment, and was accompanied by hypopituitarism due to the decreased release of adrenocorticotropic hormone (ACTH) and thyroid-stimulating hormone (TSH).…”

Neuro-ophthalmic side effects of molecularly targeted cancer drugs

“…54,66 Wilson et al described a patient on ipilimumab who despite systemic corticosteroids developed recurrent visual loss due to optic neuritis requiring plasma exchange and mycophenolate mofetil. 68 In a case report of autoimmune encephalitis, the patient received rituximab in addition to corticosteroids and IVIg. 69 Occasionally, immune checkpoint inhibitor induced myasthenia gravis may spontaneously resolve but in most cases require an antiacetylcholinesterase and/or corticosteroids and in severe cases IVIg or plasma exchange.…”