RESUMO
BACKGROUND: The appearance of solid tumors und lymphomas during treatment with fingolimod was observed in studies and has been described in case reports. OBJECTIVE: To report a case of primary cutaneous CD30(+) anaplastic large-cell T-cell lymphoma during treatment of multiple sclerosis (MS) with fingolimod. METHODS: Case study. RESULTS: Our patient developed a lymphoma a few weeks after initialization of therapy with fingolimod; 5 weeks after discontinuation of treatment the lesions resolved. CONCLUSION: Causality of fingolimod is indicated by the fact that the skin lesions appeared after commencement of treatment and resolved after discontinuation of therapy. This case serves as a reminder of the potential side effects of fingolimod.
Assuntos
Cloridrato de Fingolimode/efeitos adversos , Imunossupressores/efeitos adversos , Antígeno Ki-1 , Linfoma Anaplásico de Células Grandes/induzido quimicamente , Esclerose Múltipla/tratamento farmacológico , Neoplasias Cutâneas/induzido quimicamente , Feminino , Humanos , Pessoa de Meia-IdadeAssuntos
Eritema/diagnóstico , Eritema/etiologia , Neoplasias Cutâneas/patologia , Neoplasias Cutâneas/secundário , Telangiectasia/diagnóstico , Telangiectasia/etiologia , Idoso , Antineoplásicos/uso terapêutico , Diagnóstico Diferencial , Eritema/prevenção & controle , Feminino , Humanos , Neoplasias Cutâneas/tratamento farmacológico , Telangiectasia/prevenção & controle , Resultado do TratamentoRESUMO
Pathogenetic pathways of gastrointestinal stromal tumors (GIST) lacking mutations in KIT and PDGFRA (â¼15%) are still poorly studied. Nearly nothing is known about PI3K alterations in GISTs and only a few GISTs with BRAF mutations have been reported. BRAF mutations (V600E) were found in 3/87 tumors (3.5%) concomitantly were wild type for KIT and PDGFRA. No mutations were detected in KRAS, NRAS, and FGFR3. For the first-time we demonstrated a PIK3CA mutation (H1047L) simultaneously occurring with a 15-bp deletion in KIT exon 11 in one tumor. We suggest that BRAF mutations are of pathogenetic significance in wild type GISTs. The PI3K pathway should be assessed in future studies.
Assuntos
Tumores do Estroma Gastrointestinal/enzimologia , Tumores do Estroma Gastrointestinal/genética , Mutação , Fosfatidilinositol 3-Quinases/genética , Proteínas Proto-Oncogênicas B-raf/genética , Proteínas Proto-Oncogênicas c-kit/genética , Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , Sequência de Aminoácidos , Classe I de Fosfatidilinositol 3-Quinases , Análise Mutacional de DNA , Feminino , Tumores do Estroma Gastrointestinal/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Dados de Sequência Molecular , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas B-raf/metabolismo , Proteínas Proto-Oncogênicas c-kit/metabolismo , Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo , Transdução de SinaisRESUMO
According to current statistics of the WHO, tuberculosis is the infectious disease that causes the most deaths worldwide. Its most common cutaneous manifestation is lupus vulgaris which is seldom diagnosed today. A 69-year old immunocompetent woman complained of a partly elevated, partly sclerotic plaque on her left thigh which had been present for more than 55 years before slowly becoming ulcerated. After biopsy and subsequent excision of the 13 cm ulcer, the diagnosis of carcinoma in lupo with lymph node metastasis was made. Cutaneous and additional nodal metastases appeared rapidly. Tuberculostatic therapy was initiated. Despite systemic chemotherapy the tumor subsequently progressed and the patient died of metastatic carcinoma in lupo 15 months after the initial diagnosis. Early diagnosis and treatment of lupus vulgaris might have prevented the development of carcinoma in lupo and ensuing metastatic death of the patient.
