作者: Nerea Fernandez-Ros , Mercedes Iñarrairaegui , Jose A. Paramo , Carmen Berasain , Matias A. Avila
DOI: 10.1111/LIV.12592
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摘要: Background & Aims Radioembolization may rarely induce liver disease resulting in a syndrome that is similar to veno-occlusive complicating bone marrow transplantation where inflammation, endothelial cell activation and thrombosis are likely involved. We hypothesized mechanisms could be implicated radioembolization-induced (REILD). Moreover, lobar radioembolization hypertrophy of the non-treated hemiliver most probably by inducing regeneration. Methods In patients with hepatocellular carcinoma, we prospectively studied serum levels markers regeneration, oxidative stress, pro-inflammatory pathways, coagulation parameters over 2 months after radioembolization. Results Although REILD did not occur among 14 treated patients, decrease effective blood flow was observed. Radioembolization followed persistent increase (interleukin 6 8) stress (malondyaldehide) markers, an induction injury (vW factor PAI-1) cascade (factor VIII, PAI-1, D-Dimer) as well significant factors related regeneration (FGF-19 HGF). Conclusion Radioembolization activates produces inflammatory cytokines induces partial cascade. These findings have implications pathogenesis, prevention therapy development new therapies enhance surgical perspective.