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Ruptured hepatic metastases of cutaneous melanoma during treatment with vemurafenib: an autopsy case report

BACKGROUND: The spontaneous rupture of hepatic metastases is rare compared to that of primary hepatic tumors. In addition, vemurafenib, a selective inhibitor of the mutant BRAF protein or gene product, has been reported to be extremely effective in patients with metastatic melanoma who harbor a BRAF...

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Detalles Bibliográficos
Autores principales: Nosaka, Takuto, Hiramatsu, Katsushi, Nemoto, Tomoyuki, Saito, Yasushi, Ozaki, Yoshihiko, Takahashi, Kazuto, Naito, Tatsushi, Ofuji, Kazuya, Matsuda, Hidetaka, Ohtani, Masahiro, Suto, Hiroyuki, Imamura, Yoshiaki, Nakamoto, Yasunari
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4559873/
https://www.ncbi.nlm.nih.gov/pubmed/26346246
http://dx.doi.org/10.1186/s12907-015-0015-3
Descripción
Sumario:BACKGROUND: The spontaneous rupture of hepatic metastases is rare compared to that of primary hepatic tumors. In addition, vemurafenib, a selective inhibitor of the mutant BRAF protein or gene product, has been reported to be extremely effective in patients with metastatic melanoma who harbor a BRAF V600E mutation. CASE PRESENTATION: A 44-year-old female had previously undergone surgery for resection of a malignant melanoma in the lower right leg. Four years later, hepatic metastases became apparent, and transcatheter arterial embolization (TAE) was performed. Then she underwent treatment with vemurafenib. The size of the hepatic metastases markedly decreased. Two months later, they enlarged rapidly and ruptured, requiring emergency TAE. However, the patient developed hemorrhagic shock and died of renewed intra-abdominal bleeding on the 26th postoperative day. CONCLUSIONS: This is a rare case of ruptured hepatic metastases of malignant melanoma during treatment with vemurafenib. Postmortem examination and immunohistochemical analysis indicated reactivation of the mitogen-activated protein kinase pathway in the metastatic tumor, suggesting secondary resistance to vemurafenib as the possible underlying mechanism.