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Midgut carcinoid tumors: CT findings and biochemical profiles
P K Woodard1, J M Feldman, S S Paine
1Department of Radiology, Cleveland Clinic Foundation, OH 44195-5103, USA.
Objective:
Our goal was to describe the abdominal CT findings in 52 patients with midgut carcinoid tumors and correlate these findings with their biochemical profiles.
Materials And Methods:
Abdominal/pelvic CTs of 52 patients with midgut carcinoid tumors were reviewed retrospectively for the presence of liver metastases, mesenteric and peritoneal disease, bowel changes, lymphadenopathy, and the presence of the primary tumor. Logistic regression models were used to evaluate the association between these findings and the serum and platelet serotonin and urine 5-hydroxyindolacetic acid levels.
Results:
The most common finding was hepatic metastases (34/52). Nonspecific mesenteric soft tissue stranding was present in 26 of 52 and a discrete mesenteric mass was present in 25 of 52. These masses had linear, radiating soft tissue spokes in 16 of 25 and contained calcification in 10 of 25. Retroperitoneal and mesenteric lymphadenopathy was present in 14 of 52 and 11 of 52 cases, respectively. Carcinomatosis was present in 11 of 52. Bowel wall thickening was seen in 9 of 52. Six patients had a small bowel obstruction. Elevated serum serotonin, platelet serotonin, and urine 5-hydroxyindolacetic acid levels were significantly associated with the presence of liver metastases (p = 0.0032, 0.0098, and 0.0450, respectively). Elevated platelet serotonin levels were also significantly associated with the presence of a mesenteric mass (p = 0.0101).
Conclusion:
In our population, the most common findings of a midgut carcinoid tumor are liver metastases, nonspecific mesenteric soft tissue changes, a discrete mesenteric mass with radiating soft tissue spokes, often containing calcification, and lymphadenopathy. As expected, liver metastases correlate strongly with the presence of elevated biochemical levels. A new observation is the correlation of elevated platelet serotonin levels and mesenteric masses. We hypothesize that platelet serotonin may be the factor that stimulates stromal cells to produce mesenteric fibrosis and mass formation.