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This Article Accepted manuscript (PDF) All Versions of this Article: EJE-08-0420v1 159/4/475    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Grozinsky-Glasberg, S. Articles by Gross, D. PubMed PubMed Citation Articles by Grozinsky-Glasberg, S. Articles by Gross, D.

Long acting somatostatin analogues are an effective treatment for type 1 gastric carcinoid tumours

S Grozinsky-Glasberg, Endocrine Institute, Beilinson Hospital, Petah Tikva, Israel
G Kaltsas, Laiko Hospital, School of Medicine, National & Kapodistrian University of Athens, Department of Endocrinology, Athens, Greece
C Gur, Endocrinology and Metabolism Service, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
E Gal, Gastroenterology, Beilinson Hospital, Petah Tikva, Israel
D Thomas, Laiko Hospital, School of Medicine, National & Kapodistrian University of Athens, Department of Endocrinology, Athens, Greece
S Fichman, Pathology, Beilinson Hospital, Petah Tikva, Israel
D Barak, Endocrinology and Metabolism Service, BarakHadassah-Hebrew University Medical Center, Jerusalem, Israel
B Glaser, Endocrinology and Metabolism, BarakHadassah-Hebrew University Medical Center, Jerusalem, Israel
I Shimon, Endocrinology, Beilinson Institute, Petah Tikva, Israel
D Gross, Department of Medicine, Hadassah University Hospital, Jerusalem, Israel

Correspondence: Simona Grozinsky-Glasberg, Email: s.grozinsky{at}qmul.ac.uk

Abstract

Background: Gastric carcinoid tumours type 1 (GCA1) originate from hyperplastic enterochromaffin like (ECL) cells secondary to hypergastrinemia. Treatment with somatostatin analogues might impede ECL-cell hyperplasia by suppressing gastrin secretion and/or by a direct anti-proliferative effect on ECL cells. We conducted a multicenter prospective study to assess the effects of long-acting somatostatin analogues (SSA) on hypergastrinemia and ECL-cell proliferation in patients with GCA1.

Methods: We studied 15 patients with GCA1 treated with monthly long acting octreotide LAR (20 to 30 mg) (n=14) or Lanreotide 90 mg (n=1) for at least 6 months. Patients had serum gastrin and chromogranin A (CgA) measurements performed and biopsies taken from both tumours and surrounding mucosa before, and every 6-12 months following treatment. Sections were immunostained for neuroendocrine markers. The cell proliferation index Ki-67, intensity of immunohistochemistry staining and the gastric wall invasion were also assessed.

Results: All patients tolerated treatment well (mean follow-up of 18 months). In 11 patients (73%), a complete disappearance of the tumours at one year of treatment was observed on endoscopy, while in 3 patients (20%), the tumours decreased significantly in number and size. Gastrin levels normalized in 25% of patients, and were reduced by more than 80% in the remaining 75%.

Conclusions: Treatment with SSAs in GCA1 leads to a substantial tumour load reduction, with a concomitant decrease of serum gastrin levels. Our data indicate an important anti-proliferative effect of somatostatin analogues on ECL cells, providing clinical benefit and obviating, at least temporarily, the need for invasive therapies for GCA1.