[Pubmed] Case Report: Probable toripalimab-associated ocular myasthenia gravis-like presentation after chemoimmunotherap

[RSS-Bot]

Front Neurol. 2026 Aug 31;17:1897436. doi: 10.3389/fneur.2026.1897436. eCollection 2026.

ABSTRACT

Toripalimab, an anti-programmed cell death protein 1 (PD-1) monoclonal antibody developed in China, is increasingly used in the treatment of solid tumors. Although immune checkpoint inhibitors improve antitumor immunity, they may also cause immune-related adverse events involving the nervous system. We report a 60-year-old woman with triple-negative right breast cancer who developed bilateral ptosis and mild limitation of horizontal eye movements approximately 2 weeks after receiving nab-paclitaxel, carboplatin, and toripalimab. Serological testing showed positivity for anti-ryanodine receptor antibody (RYR-IgG, 1:100) and anti-titin antibody (Titin-IgG, 1:320), whereas acetylcholine receptor, muscle-specific kinase, and low-density lipoprotein receptor-related protein 4 antibodies were negative. The neostigmine test was negative. Routine nerve conduction studies were largely normal, and repetitive nerve stimulation showed no low-frequency decrement. After symptom onset, CK-MB mass was markedly elevated despite a normal hs-cTnI level, and AST and ALT were also increased. Because simultaneous total CK and myoglobin measurements were unavailable, the tissue source of the CK-MB elevation could not be determined, and the result was considered uninterpretable in isolation. Possible skeletal-muscle involvement, including ocular myositis, therefore remained in the differential diagnosis. Brain MRI showed chronic ischemic changes without an acute explanatory lesion. No bulbar, respiratory, limb, or cardiac symptoms were documented. After differential assessment, a probable toripalimab-associated ocular myasthenia gravis-like presentation was considered. Toripalimab was discontinued, and oral methylprednisolone 20 mg once daily was administered for 6 days from January 17 to January 22, 2026, beginning the day after discharge. Ptosis improved during early follow-up and remained improved at the subsequent visit. This case illustrates that ocular symptoms after PD-1 inhibitor therapy may represent a neuromuscular immune-related adverse event even when conventional myasthenia gravis antibodies and repetitive nerve stimulation are negative. The significance of RYR-IgG and Titin-IgG positivity in this patient remains uncertain because the assay platform and laboratory cut-offs were unavailable. Their detection should not be regarded as confirmation of ocular myasthenia gravis.

PMID:42741200 | PMC:PMC13572282 | DOI:10.3389/fneur.2026.1897436


Source: https://pubmed.ncbi.nlm.nih.gov/4274120 ... 7&v=2.20.1