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Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor
Sarcoidosis is a non‐infective granulomatous disorder of unknown aetiology, with cutaneous involvement affecting up to 30% of patients. Drug‐induced sarcoidosis has been reported secondary to modern melanoma therapies including immune‐checkpoint inhibitors and first generation BRAF inhibitors such a...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9060087/ https://www.ncbi.nlm.nih.gov/pubmed/35663773 http://dx.doi.org/10.1002/ski2.71 |
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author | Pham, J. P. Star, P. Wong, S. Damian, D. L. Saw, R. P. M. Whitfeld, M. J. Menzies, A. M. Joshua, A. M. Smith, A. |
author_facet | Pham, J. P. Star, P. Wong, S. Damian, D. L. Saw, R. P. M. Whitfeld, M. J. Menzies, A. M. Joshua, A. M. Smith, A. |
author_sort | Pham, J. P. |
collection | PubMed |
description | Sarcoidosis is a non‐infective granulomatous disorder of unknown aetiology, with cutaneous involvement affecting up to 30% of patients. Drug‐induced sarcoidosis has been reported secondary to modern melanoma therapies including immune‐checkpoint inhibitors and first generation BRAF inhibitors such as vemurafenib and dabrafenib. Herein, we report a case of cutaneous micropapular sarcoidosis that first developed on immune‐checkpoint inhibition with ipilimumab and nivolumab for metastatic melanoma, which was exacerbated and further complicated by pityriasis rubra pilaris‐like palmar plaques upon transition to a next‐generation BRAF‐dimerisation inhibitor. Both the micropapular eruption and palmar plaques rapidly resolved after cessation of the novel BRAF‐inhibitor and concurrent commencement of hydroxychloroquine. It is unclear how inhibition of BRAF‐dimerisation results in granuloma formation, though upregulation of T(H)1/T(H)17 T‐cells and impairment of T‐reg cells may be responsible. Clinicians should be aware of the potential for exacerbation of sarcoidosis when transitioning from immune‐checkpoint inhibitors to these novel BRAF‐dimerisation inhibitors, particularly as their uptake in treating cancers increases beyond clinical trials. Further studies are required to assess whether these next‐generation agents can trigger sarcoidosis de‐novo, or simply exacerbate pre‐existing sarcoidosis. |
format | Online Article Text |
id | pubmed-9060087 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-90600872022-06-04 Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor Pham, J. P. Star, P. Wong, S. Damian, D. L. Saw, R. P. M. Whitfeld, M. J. Menzies, A. M. Joshua, A. M. Smith, A. Skin Health Dis Case Reports Sarcoidosis is a non‐infective granulomatous disorder of unknown aetiology, with cutaneous involvement affecting up to 30% of patients. Drug‐induced sarcoidosis has been reported secondary to modern melanoma therapies including immune‐checkpoint inhibitors and first generation BRAF inhibitors such as vemurafenib and dabrafenib. Herein, we report a case of cutaneous micropapular sarcoidosis that first developed on immune‐checkpoint inhibition with ipilimumab and nivolumab for metastatic melanoma, which was exacerbated and further complicated by pityriasis rubra pilaris‐like palmar plaques upon transition to a next‐generation BRAF‐dimerisation inhibitor. Both the micropapular eruption and palmar plaques rapidly resolved after cessation of the novel BRAF‐inhibitor and concurrent commencement of hydroxychloroquine. It is unclear how inhibition of BRAF‐dimerisation results in granuloma formation, though upregulation of T(H)1/T(H)17 T‐cells and impairment of T‐reg cells may be responsible. Clinicians should be aware of the potential for exacerbation of sarcoidosis when transitioning from immune‐checkpoint inhibitors to these novel BRAF‐dimerisation inhibitors, particularly as their uptake in treating cancers increases beyond clinical trials. Further studies are required to assess whether these next‐generation agents can trigger sarcoidosis de‐novo, or simply exacerbate pre‐existing sarcoidosis. John Wiley and Sons Inc. 2021-10-20 /pmc/articles/PMC9060087/ /pubmed/35663773 http://dx.doi.org/10.1002/ski2.71 Text en © 2021 The Authors. Skin Health and Disease published by John Wiley & Sons Ltd on behalf of British Association of Dermatologists. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Reports Pham, J. P. Star, P. Wong, S. Damian, D. L. Saw, R. P. M. Whitfeld, M. J. Menzies, A. M. Joshua, A. M. Smith, A. Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor |
title | Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor |
title_full | Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor |
title_fullStr | Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor |
title_full_unstemmed | Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor |
title_short | Cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel BRAF dimerization inhibitor |
title_sort | cutaneous sarcoidosis due to immune‐checkpoint inhibition and exacerbated by a novel braf dimerization inhibitor |
topic | Case Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9060087/ https://www.ncbi.nlm.nih.gov/pubmed/35663773 http://dx.doi.org/10.1002/ski2.71 |
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