Jie Li, Mengdie Chen, Lusheng Wang, Kesheng Bo, Ming Chen, Hui Jiang
This case highlights camrelizumab-associated MG-like ocular neuromuscular toxicity after PD-1 inhibitor rechallenge. Its main noteworthy feature is the availability of serial pre-hospitalization biomarker data showing progressive muscle injury-related biomarker abnormalities before overt neurological deterioration. Definite immune-related MG and ICI-associated myocarditis could not be established because confirmatory serological, electrophysiological, and cardiac investigations were incomplete. Longitudinal assessment of muscle injury-related biomarkers may help identify evolving immune-related neuromuscular toxicity in selected patients, although larger studies are needed for validation.
BACKGROUND: Immune checkpoint inhibitors (ICIs) can cause rare but clinically important immune-related neuromuscular adverse events. Early warning signals for ICI-associated neuromuscular toxicity remain poorly defined, particularly after PD-1 inhibitor rechallenge.
CASE PRESENTATION: We report a 71-year-old woman with metastatic hepatocellular carcinoma who developed progressive bilateral ptosis and blurred vision approximately 20 days after camrelizumab rechallenge following a prolonged treatment-free interval. Repetitive nerve stimulation of the left orbicularis oculi muscle showed a 24.8% decremental response, suggesting possible ocular neuromuscular junction involvement. Serial laboratory data showed progressive increases in muscle injury-related biomarkers, including CK, CK-MB, MYO, LDH, and α-HBDH, before hospitalization and before overt neurological deterioration. Cranial MRI and MRA excluded structural central nervous system lesions. Flow cytometric immune profiling showed descriptive changes in CD4+ T-cell parameters and granzyme B-positive CD8+ T-cell proportions, but these findings were not interpreted as evidence of causal immune activation. cTnI was measured using an immunoturbidimetric assay and did not exceed the laboratory-reported reference range; therefore, myocardial injury or ICI-associated myocarditis could not be established with the available data. Based on the temporal association with camrelizumab rechallenge, ocular manifestations, a suggestive RNS finding, serial muscle injury-related biomarker abnormalities, exclusion of structural central nervous system lesions, and clinical improvement after glucocorticoid therapy, camrelizumab-associated immune-related neuromuscular toxicity or an MG-like ocular syndrome was considered.
CONCLUSIONS: This case highlights camrelizumab-associated MG-like ocular neuromuscular toxicity after PD-1 inhibitor rechallenge. Its main noteworthy feature is the availability of serial pre-hospitalization biomarker data showing progressive muscle injury-related biomarker abnormalities before overt neurological deterioration. Definite immune-related MG and ICI-associated myocarditis could not be established because confirmatory serological, electrophysiological, and cardiac investigations were incomplete. Longitudinal assessment of muscle injury-related biomarkers may help identify evolving immune-related neuromuscular toxicity in selected patients, although larger studies are needed for validation.