Alopecia areata as an immune-related adverse event of immune checkpoint inhibitors: A review

Dermatol Ther. 2020 Nov;33(6):e14171. doi: 10.1111/dth.14171. Epub 2020 Sep 7.

Abstract

Immune checkpoint inhibitors (ICI) improve the ability of the immune system to target cancer cells by blocking signaling through either the cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), programmed cell death (PD-1) receptor, or its ligand (PD-L1). They have been found to cause a variety of immune-related adverse events (irAEs) including a form of nonscarring alopecia that resembles alopecia areata (AA) in presentation and histology. Clinical features of ICI-induced AA are poorly described. We queried the Pubmed database for cases of AA secondary to ICI use reporting on extent of hair loss, treatments attempted, alopecia outcome, and time of follow-up with 13 cases identified. Although most patients had localized hair loss with subsequent regrowth, four of them experienced extensive and persistent AA, lasting up to a year. All but one patient continued ICI after the onset of hair loss. Many used topical corticosteroids with varying outcomes. Possible prognostic factors for severe and persistent disease may include young age and male sex. However, the low number of reported cases limits the generalizability of these findings. Tumor response was positive in every case of immune-induced AA where it was reported. Further investigation will be needed to better characterize clinical features of this irAE, risk factors for persistent disease, and determine its optimal management.

Keywords: alopecia areata; atezolizumab; immune checkpoint inhibitor; immune-related adverse event; ipilimumab; irAE; nivolumab; pembrolizumab.

Publication types

  • Review

MeSH terms

  • Alopecia Areata* / chemically induced
  • Alopecia Areata* / diagnosis
  • Databases, Factual
  • Humans
  • Immune Checkpoint Inhibitors
  • Male
  • Neoplasms* / drug therapy
  • Programmed Cell Death 1 Receptor

Substances

  • Immune Checkpoint Inhibitors
  • Programmed Cell Death 1 Receptor