Diffuse dermal mucinosis secondary to colony‐stimulating factor 1 receptor monoclonal antibody treatment: A novel and peculiar drug‐induced diffuse cutaneous mucinosis. Issue 3 (20th November 2020)

• Record Type: Journal Article
• Authors: Olmos‐Alpiste, Ferran; Segura, Sonia; Tomás‐Velázquez, Alejandra; Aguado, Leyre; España, Agustín; Arriola, Edurne; Martín‐Algarra, Salvador; Barranco, Carlos; Lloreta, Josep; Pujol, Ramon M.
• Is Part Of: Journal of dermatology. Volume 48:Issue 3(2021)
• Page Start: 380
• Page End: 384
• Publication Date: 2020-11-20
• Subjects: anti‐programmed death ligand 1 -- colony‐stimulating factor 1 receptor inhibitor -- dermal mucinosis -- drug reaction -- skin toxicity; Dermatology -- Periodicals; Dermatology -- Japan -- Periodicals; Skin -- Diseases -- Periodicals; 616.5005
• DOI: 10.1111/1346-8138.15662
• Languages: English
• ISSNs: 0385-2407

Abstract

Abstract: Colony‐stimulating factor 1 receptor (CSF1R) inhibitors represent a new class of immune‐modulatory drugs, mostly investigated in clinical trials in different malignant neoplasms. Four patients, diagnosed with recurrent or advanced malignant neoplasm and treated with a combination of anti‐programmed death ligand 1 and anti‐CSF1R monoclonal antibodies, developed an asymptomatic cutaneous eruption characterized by an ill‐defined pseudoedematous to waxy diffuse infiltration with a reticular cobblestone‐like pattern. Histopathological examination revealed diffuse mucin deposition involving the superficial and mid‐dermis with fragmented and scattered elastic fibers. The exact pathogenic mechanisms implicated in the development of mucin deposits in patients treated with CSF1R inhibitors remain to be elucidated. A reduced degradation and clearance of components of the extracellular matrix by macrophages secondary to CSF1 pathway inhibition may be hypothesized. Shredding and fragmentation of elastic fibers may be a result of the increased accumulation of mucopolysaccharides. This observation illustrates the new spectrum of skin‐related toxicities secondary to new targeting therapies. This may contribute to a better understanding of the underlying pathogenic mechanisms in skin diseases characterized by a persistent dermal glycosaminoglycan deposition.