Bullous pemphigoid induced by camrelizumab

Discussion

Bullous pemphigoid (BP) is an autoimmune disease categorised by autoantibodies targeting basement membrane band antigens, including BP180 and BP230 antibodies. DIF shows IgG and C3 deposition along the basement membrane bands.² The literature reveals a correlation between the incidence of BP and certain medications; notably, new generation of antidiabetic agents, specifically dipeptidyl peptidase 4 inhibitors (DPP4i), as well as immune checkpoint inhibitors that target the programmed cell death protein 1 (PD-1) and its ligand (PD-L1).³

Upregulated PD-L1 expression in malignant cells will inhibit the immunological responses of peripheral T-cells, thereby facilitating tumour evasion from immune surveillance.⁴ Camrelizumab, a PD-1 inhibitor, is mainly used in treating malignant tumours. A clinical investigation of camrelizumab had documented adverse events, such as reactive cutaneous capillary endothelial proliferation (RCCEP), anaemia and fever, among others.⁵ To date, there have been no documented cases of BP induced by camrelizumab. Existing literature indicates that BP is the most frequent dermatological adverse effect associated with PD-1 inhibitors, typically emerging 6– 8 months post-therapy initiation. In this context, the patient developed skin lesions 6 months following the initiation of PD-1 inhibitor treatment.⁶ Furthermore, a recurrence of the lesions was observed upon re-administration of camrelizumab. The correlation between BP and overall malignancy is quivocal, emerging evidence indicates a potential association with hematologic malignancies.²

Following two separate administrations of camrelizumab, the patient exhibited skin lesions on both occasions, which suggests a potential association between BP and the medication. Upon evaluation using the Naranjo Adverse Drug Reaction Probability Scale, which yielded a score of five, the correlation between bullous pemphigoid (BP) and the administration of camrelizumab is categorised as ‘probable’.

The management of BP triggered by PD-1 inhibitors predominantly involves the application of topical glucocorticoids. Additionally, the administration of omalizumab and rituximab has been documented in instances where BP emerged subsequent to the utilisation of PD-1 inhibitors. Although immune checkpoint inhibitors (ICIs), including PD-1/PD-L1 inhibitors, have improved survival rates for patients with malignant tumours, the immunological adverse effects associated with these therapeutics necessitate vigilant clinical oversight.⁷