Preventive and Therapeutic Interventions for Anticancer Drug-induced Dermatologic Toxicities: a Scoping Review

Yohei Iimura1, Seiichiro Kuroda2

  • 1Department of Pharmacy, The IMSUT Hospital, The Institute of Medical Science, The University of Tokyo, 4-6-1, Shirokanedai, Minato-Ku, Tokyo, 108-8639, Japan. youhei0519@g.ecc.u-tokyo.ac.jp.

Abstract

Insights

Anticancer drug toxicities like EGFR inhibitor rash and hand-foot syndrome (HFS) require specific management. This review shows mechanism-driven, toxicity-specific strategies are most effective, moving beyond a one-size-fits-all approach.

Area of Science:

  • Oncology
  • Dermatology
  • Pharmacology

Background:

  • Anticancer drug-induced dermatologic toxicities significantly impact patient quality of life and treatment adherence.
  • Current management strategies lack clear evidence patterns across different drug classes.
  • Understanding the mechanisms of these toxicities is crucial for developing effective interventions.

Purpose of the Study:

  • To systematically map clinical studies on preventive and therapeutic interventions for specific anticancer drug-induced dermatologic toxicities.
  • To analyze evidence patterns for EGFR inhibitor-associated rash, capecitabine-induced hand-foot syndrome (HFS), and multikinase inhibitor-associated hand-foot skin reaction (HFSR).
  • To utilize a mechanism- and outcome-based framework for evaluating interventions.

Main Methods:

  • Conducted a scoping review of 51 clinical studies.
  • Analyzed interventions for EGFR inhibitor rash, capecitabine-induced HFS, and multikinase inhibitor-associated HFSR.
  • Mapped interventions based on underlying pathophysiological mechanisms and clinical outcomes.

Main Results:

  • Prophylactic antibiotics and topical corticosteroids effectively reduced EGFR inhibitor rash.
  • COX-2 inhibition and methylcobalamin showed efficacy in preventing capecitabine-induced HFS.
  • Barrier reinforcement, COX-2 inhibition, and corticosteroids were effective for HFSR.
  • Identified distinct pathophysiological profiles: inflammatory-epithelial (EGFR rash), inflammatory-neuropathic (HFS), and mechanical-vascular-inflammatory (HFSR).

Conclusions:

  • Dermatologic toxicities from anticancer therapies exhibit clear mechanistic divergence.
  • Toxicity-specific preventive strategies are necessary, challenging a one-size-fits-all approach.
  • Mechanism-driven, toxicity-specific supportive care is the most rational and effective management strategy.

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