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

Abstract

Background: Recent immune therapy with checkpoint inhibitors (CPIs) has demonstrated remarkable antitumor effects on specific tumors, such as malignant lymphoma and non-small cell lung carcinoma. By contrast, CPIs cause an imbalance in the immune system, triggering a wide range of immunological side effects termed immune-related adverse effects (irAEs). Here, we report a rare case of optic neuritis and hypopituitarism during anti-programmed death-ligand 1 (PD-L1) antibody treatment.

Case presentation: A patient with non-small cell lung carcinoma received anti-PD-L1 antibody treatment every 3 weeks; however, the patient started experiencing headaches, general fatigue, anorexia, and diarrhea approximately 1 year after the initiation of the treatment. Moreover, sudden visual loss of the right eye occurred 1 week after the interruption of the anti-PD-L1 antibody treatment. MRI findings showed gadolinium enhancement in the left optic nerve, but no enlargement of the pituitary gland and stalk. Laboratory data showed decreased serum adrenocorticotropic hormone (ACTH), cortisol, and free T₄ levels, and a hormone tolerance test indicated hypopituitarism, hypothyroidism, and hypoadrenocorticism. The central scotoma caused by optic neuritis completely disappeared immediately after a course of steroid pulse therapy, and no recurrence occurred up to 2 years after initiation of the steroid pulse therapy while replacement therapy for hypothyroidism and hypoadrenocorticism was continued.

Conclusions: The patient presented with optic neuritis and hypopituitarism, possibly due to irAEs of the anti-PD-L1 antibody treatment. Steroid pulse therapy was effective for optic neuritis, suggesting underlying immunological mechanisms. Neurological complications including optic neuritis should be considered when examining patients with cancer undergoing CPI treatment.

Keywords: Anti-PD-L1 antibody; Hypopituitarism; Immune-related adverse effects; Optic neuritis.

Fig. 1

Change in visual field before and after steroid pulse therapy. a The Goldmann kinetic visual field test demonstrating a defect in the nasal visual field and enlarged blind spot. b No visual defects were observed in the right eye. c After steroid pulse therapy, the visual field recovered completely.

Fig. 2

Fundus photograph and fluorescein angiography of the optic disk. a A fundus photograph of the right eye showing large cupping of optic disk without visual field defect. b The optic disk of the left eye was swollen and retinal venous vessels demonstrated mild congestion without bleeding. c Fluorescent angiography showing optic disk leakage without a choroidal filling defect or other retinal abnormalities. The time after initiation was 39 s.

Fig. 3

Gadolinium-enhanced magnetic resonance imaging (MRI) before and after steroid pulse therapy. Gadolinium-enhanced MRI showed enhancement in the left optic neuritis on coronal (a) and sagittal (b) fat-suppressed T1-weighted imaging. c No abnormalities were detected in the pituitary body and stalks. d After steroid pulse therapy, the high-intensity area in the left optic nerve markedly decreased.