RESUMO
Radiation-induced morphea (RIM) is a rare but recognized late complication of radiotherapy. It was first described in 1905, not long after the initial discovery of X-rays by Roentgen. Characterized by the deposition of excess collagen in the dermis, it results in thickening of the skin. Its frequency is approximately 2 in 1000. We present a series of three cases involving patients receiving radiotherapy treatment for breast cancer, each of which subsequently developed RIM. Because of its rarity, RIM is often misdiagnosed as infection or metastatic disease. This can lead to delayed diagnosis and treatment, leading to poorer outcomes such as chronic pain issues. Early dermatological involvement and tissue sampling to examine histopathological features can avoid this, leading to better care and improved results. A variety of treatment options are available, ranging from topical to systemic, with early induction more likely to result in a positive response.
Assuntos
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/imunologia , Mediadores da Inflamação/metabolismo , Interleucina-17/metabolismo , Psoríase/imunologia , Pele/patologia , Células Th17/imunologia , Inibidores do Fator de Necrose Tumoral/efeitos adversos , Adulto , Idoso , Proliferação de Células , Feminino , Humanos , Ativação Linfocitária , Masculino , Pessoa de Meia-Idade , Psoríase/etiologia , Inibidores do Fator de Necrose Tumoral/uso terapêutico , Adulto JovemRESUMO
Colonic polyps may arise from BRAF inhibitor treatment of melanoma, possibly due to paradoxical activation of the mitogen-activated protein (MAP)-kinase pathway. In an alternative evidence based scenario, tubular colonic adenomas with APC gene mutations have also been identified in the context of BRAF inhibitor treatment, in the absence of mutations of MAPK genes. A minority of colorectal cancers develop by an alternative "serrated polyp pathway". This article postulates a novel hypothesis, that the established phenotypic and molecular characteristics of serrated colonic polyps/CRC offer an intriguing insight into the pathobiology of BRAF inhibitor induced colonic polyps. Serrated polyps are characterized by a CpG island methylation phenotype, MLH1 silencing and cellular senescence. They also have BRAF mutations. The contention is that BRAF inhibitor induced polyps mimic the afore-described histology and molecular features of serrated polyps with the exception that instead of the presence of BRAF mutations they induce C-RAF homodimers and B-RAF: C-RAF heterodimers.
