Overview and Management of EGFR Inhibitor–Induced Skin Toxicities

Conclusions

• EGFR inhibitor skin toxicities are extremely common, affecting most treated patients and sometimes nearly all of them.
• The most common and clinically important eruption is an early papulopustular/acneiform rash that usually begins within 1 to 2 weeks and peaks by 3 to 5 weeks.
• Later toxicities such as xerosis, eczematous dermatitis, paronychia, and hair/nail changes can emerge or worsen over time, so long-term monitoring is necessary.
• Preventive regimens started at treatment onset, especially tetracycline antibiotics plus topical steroids, moisturizers, and sun protection, reduce rash severity, rescue treatments, and cancer therapy interruptions.
• Dermatologic management can help patients stay on effective cancer therapy by decreasing unnecessary dose holds and changes.
• More severe or late papulopustular eruptions may reflect bacterial superinfection, especially with Staphylococcus aureus, and culture-guided antibiotic treatment can be important.
• Oral retinoids can help refractory acneiform eruptions and erosive pustular scalp disease, but they should be used cautiously because they can worsen dryness.
• Topical beta blockers appear useful for paronychia and pyogenic granuloma-like lesions and may be a practical low-risk adjunct.
• Dupilumab has promising evidence for EGFRi- or TKI-associated eczematous dermatitis and may reduce the need for systemic steroids.
• Nutritional deficiencies, especially zinc deficiency, appear to contribute to some EGFRi skin toxicities and may respond to supplementation.
• Zinc repletion at modest doses can improve cutaneous toxicity, but excessive zinc should be avoided because of the risk of copper deficiency.
• Overall, EGFRi toxicities are predictable and manageable, and proactive dermatologic care can improve both skin outcomes and continuation of cancer therapy.