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Presentation

Managing Immune Checkpoint Inhibitor Skin Toxicities in Dermatology

Description

The talk reviewed how immune checkpoint inhibitors, especially PD-1 and CTLA-4 agents, work by disinhibiting T cells to improve cancer control, and why they commonly cause skin immune-related adverse events. The speaker emphasized that dermatologists play a key role in identifying and managing these eruptions, which can range from morbilliform rash, eczema, psoriasis, lichenoid dermatitis, prurigo, and bullous pemphigoid to less common entities like cutaneous lupus. A major theme was how to communicate severity using CTCAE grading while recognizing that body surface area alone can be misleading: some widespread rashes are tolerable, while small-area oral or genital disease can be highly morbid. Management depends on timing, phenotype, and quality-of-life impact; morbilliform eruptions often occur early and may allow rechallenge, while bullous pemphigoid is typically late and often needs more aggressive treatment such as dupilumab. The speaker stressed avoiding reflexive long-term steroids when possible, being cautious about restarting immunotherapy if disease remains active, and remembering that stopping the checkpoint inhibitor does not always make the rash resolve. Another key point was to avoid tunnel vision and consider alternative diagnoses or contributing medications, as some eruptions initially blamed on immunotherapy may actually be infections or drug reactions such as tinea or SCLE triggered by another medication. Overall, the talk encouraged dermatologists to confidently lead on diagnosis, grading, and treatment decisions in collaboration with oncology.

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Conclusions

Immune checkpoint inhibitors have transformed cancer care but frequently cause dermatologic immune-related adverse events that dermatologists are well positioned to diagnose and manage.
Cutaneous toxicities are common, can be severe, and often require individualized treatment rather than automatic assumptions based on CTCAE grade alone.
The timing of checkpoint inhibitor skin reactions is highly variable, so eruptions cannot be excluded simply because therapy started long ago or has already been stopped.
Many patients can continue or restart immunotherapy if their skin disease is controlled, but severe mucosal, bullous, or life-altering reactions may warrant treatment interruption or escalation of therapy.
Long-term systemic corticosteroid use should be minimized when possible because it may undermine cancer treatment benefit, but short-term prednisone is sometimes necessary for severe flares.
Dermatologists should lead management decisions for these eruptions because accurate morphologic diagnosis is essential and “rash” is too nonspecific for oncologic decision-making.
Pre-existing inflammatory skin disease does not automatically preclude checkpoint inhibitor therapy, but it may worsen unpredictably and should be monitored closely.
Th2-skewed reactions such as prurigo and bullous pemphigoid often need earlier, more aggressive intervention than many morbilliform or some Th1-mediated eruptions.
Not every rash in a patient receiving immunotherapy is caused by the checkpoint inhibitor, so alternative diagnoses and concomitant medications must always be considered.
Collaborative, case-by-case decision-making that balances cancer control, skin disease severity, and quality of life is the best approach to managing checkpoint inhibitor toxicities.

Chang et al. Oncologist. 2021.
CTCAE skin and subcutaneous tissue disorder grading table referenced on slide.
Academic reference text printed along the bottom of slides on managing timing and interventions.