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Mesenteric Fibrosis in Midgut Neuroendocrine Tumors: Functionality and Radiological Features
Neuroendocrinology
|April 7, 2017
Summary
Mesenteric fibrosis (MF) in midgut neuroendocrine tumors (NETs) is linked to tumor functionality and elevated 5-hydroxyindoleacetic acid (5-HIAA). This suggests a shared mechanism with carcinoid syndrome and carcinoid heart disease (CHD).
Area of Science:
- Oncology
- Radiology
- Pathophysiology
Background:
- Mesenteric fibrosis (MF) is observed in midgut neuroendocrine tumors (NETs) but its cause is unclear.
- MF affects some, but not all, NET patients with lymphatic involvement.
- This study investigated MF's relationship with carcinoid syndrome, 5-hydroxyindoleacetic acid (5-HIAA), and carcinoid heart disease (CHD).
Purpose of the Study:
- To assess the association between mesenteric fibrosis (MF) and clinical/radiological features in midgut neuroendocrine tumors (NETs).
- To identify predictors of MF in patients with midgut NETs.
- To explore the link between MF, tumor functionality, and the development of carcinoid heart disease (CHD).
Main Methods:
- Retrospective analysis of 81 patients with midgut NETs and mesenteric lymphatic metastases.
- Evaluation of imaging characteristics, Ki67 grading, 5-HIAA levels, tumor functionality, and CHD development.
- Multivariate analysis to identify independent predictors of MF.
Main Results:
- Mesenteric fibrosis (MF) was present in 54% of patients.
- MF was significantly associated with mesenteric vessel encasement, hepatic metastases, and tumor functionality.
- Elevated urinary 5-hydroxyindoleacetic acid (5-HIAA) ≥395 µmol/day, age, and largest lymphatic metastasis size were independent predictors of MF.
- MF showed a trend towards association with functionality and CHD, and was linked to decreased time to CHD development in functional midgut NETs.
Conclusions:
- Mesenteric fibrosis (MF) in midgut NETs is significantly associated with metastatic patterns and tumor functionality.
- The link between MF, elevated 5-HIAA, carcinoid syndrome, and potential CHD development suggests a common pathophysiological pathway.
- Further research may elucidate mechanisms similar to endocardial fibrosis.