Hepatic embolization for Cushing syndrome from metastatic tumors: a single-center case series

Cushing syndrome (CS) from metastatic adrenocortical carcinoma (ACC) or neuroendocrine tumors (NETs) presents a therapeutic challenge when surgery is not feasible. Liver-directed embolization, including bland transarterial embolization (TAE) and yttrium-90 (Y-90) radioembolization, may palliate hypercortisolism arising from hormonally active hepatic metastases.

We conducted a retrospective single-center case series of 4 adult patients (≥18 years) with CS and liver-dominant metastatic ACC or NET who underwent hepatic embolization between 2015 and 2025. Inclusion criteria were: (1) confirmed CS based on standard biochemical testing, and (2) receipt of liver-directed embolization (TAE or Y-90) for hypercortisolism. Exclusion criteria were absence of pre- and postembolization hormonal data preventing biochemical assessment. The primary outcome was biochemical response within 14 days (≥50% reduction or normalization of morning cortisol). Secondary outcomes included duration of biochemical control, radiographic response (RECIST 1.1), and adverse events (CTCAE v5.0).

Four patients (2 ACC, 2 NET) underwent Y-90 (n = 1) or TAE (n = 3). All achieved significant cortisol; 2/4 normalized cortisol with transient adrenal insufficiency. The Y-90 patient had sustained remission, while 2 TAE patients achieved partial hormonal control enabling tapering of medical therapy. Radiographically, tumor burden stabilized or improved in most treated lesions. Embolization was well tolerated, with only 1 case of post-embolization syndrome and no procedure-related mortality. One patient died from disease progression; 3 remain alive with controlled or improving disease.

Hepatic embolization is a viable palliative option for CS due to unresectable liver-dominant metastases, providing meaningful biochemical improvement with acceptable safety and supporting integration into multidisciplinary CS management.