Abstract

To evaluate possible risk factors contributing to biliary toxicity after drug-eluting bead transarterial chemoembolization (DEB-TACE) treatment of neuroendocrine tumor (NET) hepatic metastases. 13 patients (mean age: 65.8, 55% males) who underwent 23 DEB-TACE treatments between 2011-2015 for hepatic NET metastases from gut (n = 4), pancreas (n = 6), lung (n = 2) & unidentified (n = 1) primary sites were reviewed retrospectively. Tumor characteristics (grade, burden, arterial supply), previous therapeutic history (systemic chemotherapy and targeted therapies, peptide radiotherapy, resection of primary tumor), and clinical outcomes were evaluated. Because of recent published warnings, special emphasis was placed on biliary toxicity, including biliary ductal dilatation, biloma and/or abscess formation, and biochemical toxicity. 7 patients developed biloma or abscess but only 1 required hospitalization and percutaneous drainage. 10 patients developed focal intrahepatic ductal dilatation. Biliary complications were associated with lower tumor burden (P = 0.036), and prior biliary/pancreatic surgical interventions (P = 0.021). 3 patients demonstrated grade 3/4 alkaline phosphatase elevation, but none had severe elevations of serum bilirubin. No relationship was found with catheterization or treatment selectivity (segmental/lobar) or tumor grade. Large tumor burden and its covariables of large administered dose of doxorubicin (>75 mg) and necessity for supplemental bland embolization, were found to reduce risk of biliary complications (P = 0.033). Prior systemic treatment with antiangiogenic drugs also decreased the risk of biliary complications (P = 0.037). DEB-TACE showed median time to progression (TTP) of 13.7 months and overall survival (OS) of 56.7 months. DEB-TACE is an effective option for treatment of NET hepatic metastases, but is associated with a high incidence of biliary complications. It appears to be safest for patients with large tumor burdens who have undergone previous treatment by systemic antiangiogenic drugs, perhaps due to minimized nontarget deposition.

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