Abstract 569P
Background
Survival of patients with metastatic digestive neuroendocrine tumours (NETs) is often prolonged and has improved over the last decades. The causes of death (COD) in this setting have been poorly described.
Methods
We identified all deceased patients from the prospectively collected cohort of all patients (n=1250) treated in one expert centre from January 2000 to December 2019. All consecutive dead patients with metastatic, histologically proven well-differentiated NET from pancreatic (p) or small-intestine (si) origin were included. We centrally determined the main/secondary CODs and related mechanisms and explored their associations with disease characteristics using logistic regression analyses.
Results
We included 196 patients (female gender 46%, median age 59 years) with metastatic pNET (55%) or siNET (45%), functioning in 49% and classified as G1, G2 or G3 NETs in 25%, 64% and 12% of cases, respectively. Tumour invasion was responsible for 69% of CODs, which were mainly hepatobiliary (liver failure, biliary obstruction; 24% of all patients) or digestive (occlusion, ischemia, bleeding; 13%). Hormone hypersecretion was responsible for 13% of CODs, mainly cardio-respiratory (carcinoid heart disease; 10%). Iatrogenic mechanism was related to 13% of CODs, mainly cardio-respiratory and sepsis (5% and 4%, respectively). On multivariate analysis (mechanisms related to primary or secondary CODs), death by tumour invasion was associated with pNET (p=0.03), sporadic setting (p<0.01) and higher number of systemic treatments (p<0.01). Death by hormone secretion was associated with carcinoid heart disease (p<0.01), more metastatic sites (p=0.02) and higher number of systemic treatments (p<0.01). Death by iatrogenic mechanism was associated with liver-directed therapies (p=0.02), older age (p=0.11) and the absence of targeted therapies (p=0.037).
Conclusions
This is the first study with precise description of CODs and related mechanisms in a large real-life cohort. It provides meaningful insights on of the natural history of these neoplasms and its evolution over the past two decades.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Department of Pancreatology, Beaujon Hospital, Clichy, APHP, France.
Funding
ARCAD Fondation.
Disclosure
O. Hentic: Financial Interests, Personal, Advisory Role: AAA; Financial Interests, Personal, Advisory Role: Ipsen; Financial Interests, Personal, Advisory Role: Keocyt; Financial Interests, Personal, Advisory Role: Novartis; Financial Interests, Personal, Advisory Role: Pfizer. V. Rebours: Financial Interests, Personal, Advisory Role: AAA. P. Ruszniewski: Financial Interests, Personal, Invited Speaker: AAA; Financial Interests, Personal, Invited Speaker: Ipsen; Financial Interests, Personal, Invited Speaker: Keocyt; Financial Interests, Personal, Invited Speaker: Novartis. L. de Mestier: Financial Interests, Personal, Invited Speaker: AAA; Financial Interests, Personal, Invited Speaker: Ipsen; Financial Interests, Personal, Invited Speaker: Keocyt; Financial Interests, Personal, Invited Speaker: Novartis; Financial Interests, Personal, Invited Speaker: Pfizer; Financial Interests, Personal, Invited Speaker: Sirtex. All other authors have declared no conflicts of interest.