Lichen Planopilaris Induced by Checkpoint Inhibitors: A Systematic Review

Immune checkpoint inhibitors (ICIs), including anti-CTLA-4, anti–PD–1, and anti–PD–L1 biologics, have transformed cancer treatment by enhancing T–cell–mediated antitumor responses [1]. However, by stimulating immune activity, ICI treatments may also cause immune-related adverse events (irAEs) [2, 3]. Among cutaneous irAEs, lichen planopilaris (LPP) is an uncommon but increasingly recognized condition associated with ICI therapy. This systematic review evaluates the current literature on ICI-induced LPP (ICI-LPP), highlighting implicated ICIs, clinical features, timing, management, and outcomes. We searched PubMed, Embase, and Scopus from inception through March 2025 per PRISMA guidelines (CRD420251056510) (Figure S1 available at doi: 10.17632/ffd4d7s93f.2). Search terms combined “immune checkpoint inhibitor,” “PD-1,” “PD-L1,” “CTLA-4,” with “lichen planopilaris,” “scarring alopecia,” and specific ICI names. Inclusion criteria were: treatment with an ICI, development of LPP or variants temporally linked to ICI use, and English-language manuscripts. Exclusion criteria were: ambiguous cases of LPP, reports of non-scarring alopecia or non-follicular lichenoid reactions, and cases where LPP onset preceded ICI initiation (Table S1 available at doi: 10.17632/5jyn4hsr25.1). In total, 11 cases were identified (Table 1). Diagnosis of LPP was confirmed via scalp biopsy in all cases. Most LPP cases involved the anti–PD-1 agents, nivolumab (n = 5, 45.5%) and pembrolizumab (n = 5, 45.5%). Melanoma was the most common underlying malignancy (n = 8, 72.7%). Time to LPP onset following ICI initiation ranged from 2 months to 2 years (mean 8.7 months, median 16 weeks) (Figure 1). For cases where the time to onset of LPP was reported as a range, the median value was used for consistency. Common clinical findings included scalp pruritus, perifollicular erythema, and progressive hair loss. ICI-LPP was reported in all areas of the scalp; the frontotemporal scalp was the most affected region (n = 9, 81.8%). Eyebrow involvement was noted in 2 cases (18%), with complete loss in 1 case (9%). Body hair loss was noted in 2 cases (18%), and oral mucosal involvement was documented in 2 cases (18%). Ten patients (91%) showed improvement or stabilization with treatment. Topical clobetasol was most common (n = 10, 90.9%), followed by oral tetracyclines (n = 4, 36.4%), and oral corticosteroids (n = 3, 27.3%). Near-complete hair regrowth was observed in a patient with preceding oral lichen planus treated with oral and topical steroids and minocycline. ICIs were discontinued in 1 case (9%), specifically due to the ICI-LPP. One case was notable for diagnostic overlap: initially, lichenoid features evolved into a folliculitis-like pattern after steroid treatment, highlighting ambiguity in ICI-induced cutaneous reactions. This review highlights ICI-induced LPP. The predominance of PD-1 inhibitors in reported cases likely reflects both treatment patterns and biologic differences. PD-1 inhibitors are more widely prescribed than CTLA-4 or PD-L1 agents across melanoma and other solid tumors, which may contribute to over-representation. However, PD-1 blockade elicits stronger peripheral T-cell activation compared with CTLA-4 inhibition, potentially increasing the risk of lichenoid reactions. It remains possible that melanoma patients may harbor immune sensitization pathways that predispose them to this reaction. Misdiagnoses [4], or differences in access to dermatologic evaluation may also play a role, as melanoma patients might undergo earlier assessment for hair loss or scalp pruritus compared with patients receiving ICIs for other cancers. Such factors could also contribute to the overrepresentation of LPP in ICI-treated patients. Further studies are needed to clarify these risks and mechanisms, as well as to define the true incidence of ICI-induced LPP. Proposed mechanisms include ICI-mediated disruption of hair follicle immune privilege and increased presentation of follicular autoantigens, which may trigger a lichenoid inflammatory response leading to scarring alopecia; however, mechanistic evidence remains limited. Limitations of this review included incomplete reporting of outcomes, treatment timelines, and dosages, restricting the depth of analysis. The authors have nothing to report. Dr. Jeffrey Donovan has received honoraria from Pfizer and Vichy, has participated on advisory boards at Pfizer for payment, participates on the Board of Directors for the Scarring Alopecia Foundation, and is the active Director of the Evidence Based Hair Training Program. No other authors have conflicts of interest relevant to this manuscript to disclose. Data supporting the findings of this study are available on Mendeley. Figure S1. PRISMA: ICI-Induced LPP Systematic Review, available at doi: 10.17632/ffd4d7s93f/2. Table S1. ICI-Induced LPP, available at doi: 10.17632/5jyn4hsr25/1.

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