Photosensitive Lichenoid Drug Eruption Due to Pembrolizumab in a Patient with Non-Small Cell Lung Cancer

초록

Pembrolizumab is a highly selective anti-programmed death ligand 1 (PD-L1) humanized monoclonal antibody that binds to the programmed death-1 (PD-1) receptor and increases T-cell immune response against malignant cells. Pembrolizumab shows efficacy in the treatment of melanoma and non-small cell lung cancer (NSCLC); however, it can have adverse cutaneous effects, including maculopapular eruption, pigmentary change, psoriasiform reaction, and lichenoid reaction1 . A 78-year-old male presented with pruritic, erythematouspapules and patches on his scalp, face, nape, upper chest, buttocks, and dorsum of hands for 10 days. One year prior to presentation, he had been diagnosed with NSCLC (T3N1M1a stage IVA), and he had started 200 mg of pembrolizumab every 3 weeks. Sixteen courses after the initiation of pembrolizumab, skin lesions were observed mainly on photo-exposed areas (Fig. 1). There had been no changes in other drugs. Histopathologic findings of the chest revealed localized dyskeratotic cells, interface dermatitis, and lichenoid infiltration consisting of lymphocytes and eosinophils in the upper dermis (Fig. 2). Considering the development of cutaneous lesions during pembrolizumab treatment and lack of evidence to support other etiological contributors, the patient was diagnosed with pembrolizumab-induced lichenoid drug eruption. The administration of pembrolizumab was discontinued, and the skin lesions improved after treatment with systemic corticosteroid and topical corticosteroid. Cutaneous lichenoid drug eruption is a rare form of adverse drug reaction (ADR). In contrast to other cutaneous ADR, late onset of skin lesions after exposure is characteristic. The time interval between initiation of the drug and manifestation of lichenoid drug eruption varies from months to years, depending on the type of drug, dosage, and host predisposition1,2. Various clinical presentations range from typical lichen planus to vesiculobullous lesions1,3. The immunologic mechanism of lichenoid drug reactions is thought to be a T-cell mediated response. Blocking PD-L1 causes not only an escalation in the immune function of tumor-specific T cells but also incremental antigenic immune response or self-immunity, which leads to widespread nonspecific T-cell activation, resulting in ADR in the skin1 . In one analysis of lichenoid drug eruption, checkpoint inhibitors, including PD-1 inhibitor, were the most frequently reported culprit drugs2 . Most patients were treated with topical (42.1%) or systemic steroids (16.7%), and the culprit drug was discontinued in only 26.3%, which is low compared with other types of ADR2 . This is probably due to the benefit-risk ratio favoring the drug, as is often the case in cancer therapy2 . Some studies showed that the development of cutaneous ADR could be a positive prognostic factor for 62 Korean Journal of Dermatology: Vol. 62 No. 1 2024 cancer treatment. Such cutaneous manifestations could be the product of more potent immune system activation4 . In some patients with lichenoid drug eruptions, as in our case, lesions are localized to photo-exposed areas and exhibit photoaggravation5 . Several studies classified lichenoid drug eruption into photoallergy subtypes. Clinicians should be aware of the possibility of skin complications, and patients should be informed about proper sunscreen use and other protective measures during treatment with pembrolizumab. Herein, we report a case of photosensitive lichenoid drug eruption due to pembrolizumab in a patient with NSCLC.

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