Hypergastrinemia as a cause of chromogranin A increase in blood in patients suspected to have neuroendocrine tumor

Citation
A. Kleveland et al., Hypergastrinemia as a cause of chromogranin A increase in blood in patients suspected to have neuroendocrine tumor, DIGESTION, 64(2), 2001, pp. 71-74
Citations number
24
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTION
ISSN journal
00122823 → ACNP
Volume
64
Issue
2
Year of publication
2001
Pages
71 - 74
Database
ISI
SICI code
0012-2823(2001)64:2<71:HAACOC>2.0.ZU;2-0
Abstract
Background. Chromogranin A (CgA) is a sensitive marker for neuroendocrine n eoplasia. Enterochromaffin-like cell hyperplasia secondary to hypergastrine mia also leads to CgA increase in blood. Treatment with inhibitors of acid secretion, atrophic gastritis and infection with Helicobacter pylori are pr evalent conditions leading to hypergastrinemia. We therefore wanted to stud y whether concomitant determination of gastrin could increase the utility o f CgA as a marker of neuroendocrine neoplasia. Methods: CgA and gastrin con centrations were determined by radioimmunoassay methods, while pepsinogen I (used to diagnose severe atrophic gastritis) was determined by a commercia l immunoenzymatic assay. Results: Among 100 patients with elevated CgA, we found that 29% had hypergastrinemia. Vice versa, CgA was elevated in 23 out of 26 (88.5%) in a population of patients with hypergastrinemia. By determ ining pepsinogen I in blood in patients with hypergastrinemia, a proportion of them was diagnosed as having severe atrophic gastritis. Conclusion: We conclude that determination of gastrin in blood in patients with CgA elevat ion will increase the utility of CgA in the diagnosis of neuroendocrine tum ors. Copyright (C) 2001 S. Karger AG, Basel.