National Cancer Institute®
Last Modified: March 1, 2002
UI - 11742193
AU - Annibale B; Azzoni C; Corleto VD; di Giulio E; Caruana P; D'Ambra G;
TI - Bordi C; Delle Fave G Atrophic body gastritis patients with enterochromaffin-like cell dysplasia are at increased risk for the development of type I gastric carcinoid.
SO - Eur J Gastroenterol Hepatol 2001 Dec;13(12):1449-56
AD - Digestive and Liver Disease Department, 2nd Medical School, University La Sapienza, Rome, Italy. email@example.com
BACKGROUND/AIMS: In the presence of atrophic body gastritis, gastric carcinoid develops from gastric-body mucosa enterochromaffin-like cells. Few data exist on the prevalence of enterochromaffin-like dysplastic lesions in atrophic body gastritis patients and their presumed risk of evolution to carcinoid has never been assessed prospectively in humans. The aim of the present study was to investigate the prevalence and incidence of dysplastic and neoplastic enterochromaffin-like cell lesions in a consecutive series of patients with atrophic body gastritis. METHODS: A total of 130 atrophic body gastritis patients at diagnosis and 96 atrophic body gastritis patients at follow-up (median 30 months) underwent gastroscopy with multiple biopsies and fasting gastrinaemia evaluation. In patients with enterochromaffin-like cell dysplasia, a more detailed bioptic sampling at follow-up was performed. RESULTS: Of the 130 atrophic body gastritis patients, only one (0.7%) had a gastric carcinoid polyp, whereas enterochromaffin-like cell dysplasia was found in five patients (3.8%). At follow-up only one out of the 96 atrophic body gastritis patients (1%) was diagnosed as having a carcinoid polyp at 41 months. Enterochromaffin-like cell dysplasia was present in four additional patients (4.2%). Two atrophic body gastritis pernicious anaemia patients with enterochromaffin-like cell dysplasia developed a gastric carcinoid in the follow-up. Among nine atrophic body gastritis patients with enterochromaffin-like cell dysplasia, the incidence of carcinoid tumour was 22% compared to 1.1% of atrophic body gastritis patients without dysplasia (odds ratio: 26.00; 95% confidence interval: 2.089-323.52). During the follow-up, fasting gastrin levels increased significantly only in atrophic body gastritis patients with enterochromaffin-like cell dysplasia (mean 677.4 +/- 66.1 vs 1112.2 +/- 185.6; P = 0.0287). CONCLUSION: This study provides the first clinical evidence that, in hypergastrinaemic atrophic body gastritis patients, enterochromaffin-like cell dysplasia carries a markedly increased risk for development of type I gastric carcinoid. This suggests that a more detailed endoscopic/bioptic procedure in this subgroup of atrophic body gastritis patients is able to detect gastric carcinoid at an early stage.
UI - 10848649
AU - Laine L; Ahnen D; McClain C; Solcia E; Walsh JH
TI - Review article: potential gastrointestinal effects of long-term acid suppression with proton pump inhibitors.
SO - Aliment Pharmacol Ther 2000 Jun;14(6):651-68
AD - University of Southern California School of Medicine, Los Angeles, California 90033, USA. firstname.lastname@example.org
This review examines the evidence for the development of adverse effects due to prolonged gastric acid suppression with proton pump inhibitors. Potential areas of concern regarding long-term proton pump inhibitor use have included: carcinoid formation; development of gastric adenocarcinoma (especially in patients with Helicobacter pylori infection); bacterial overgrowth; enteric infections; and malabsorption of fat, minerals, and vitamins. Prolonged proton pump inhibitor use may lead to enterochromaffin-like cell hyperplasia, but has not been demonstrated to increase the risk of carcinoid formation. Long-term proton pump inhibitor treatment has not been documented to hasten the development or the progression of atrophic gastritis to intestinal metaplasia and gastric cancer, although long-term studies are required to allow definitive conclusions. At present, we do not recommend that patients be tested routinely for H. pylori infection when using proton pump inhibitors for prolonged periods. Gastric bacterial overgrowth does increase with acid suppression, but important clinical sequelae, such a higher rate of gastric adenocarcinoma, have not been seen. The risk of enteric infection may increase with acid suppression, although this does not seem to be a common clinical problem with prolonged proton pump inhibitor use. The absorption of fats and minerals does not appear to be significantly impaired with chronic acid suppression. However, vitamin B12 concentration may be decreased when gastric acid is markedly suppressed for prolonged periods (e.g. Zolllinger-Ellison syndrome), and vitamin B12 levels should probably be assessed in patients taking high-dose proton pump inhibitors for many years. Thus, current evidence suggests that prolonged gastric acid suppression with proton pump inhibitors rarely, if ever, produces adverse events. Nevertheless, continued follow-up of patients taking proton pump inhibitors for extended periods will provide greater experience regarding the potential gastrointestinal adverse effects of long-term acid suppression.
UI - 11825129
AU - Pappas S; Diaz L; Talamonti M
TI - Pathologic quiz case: a cystic pancreatic mass discovered in a patient with ileocecal carcinoid.
SO - Arch Pathol Lab Med 2002 Feb;126(2):229-30
AD - Departments of Surgery, Northwestern University Medical School, Northwestern Memorial Hospital, Chicago, IL, USA.
UI - 11870669
AU - Leong WL; Pasieka JL
TI - Regression of metastatic carcinoid tumors with octreotide therapy: two case reports and a review of the literature.
SO - J Surg Oncol 2002 Mar;79(3):180-7
AD - Division of Surgical Oncology, University of Calgary, Calgary, Alberta, Canada.
BACKGROUND: The antiproliferative effect of the somatostatin analogue, octreotide, on metastatic carcinoid tumors is poorly understood. Partial tumor regression seen radiographically has been reported with the use of octreotide therapy for neuroendocrine tumors. Complete regression of carcinoid tumors is rarely reported. RESULTS: Two patients with metastatic midgut carcinoid tumors were treated with subcutaneous octreotide 300 microg/day for symptomatic control of their carcinoid syndrome before debulking palliative surgery. During the laporatomies, both patients were found to have complete macroscopic regression of the metastatic lesions that had been identified radiologically before surgery, including liver metastases in one patient and periportal and retrocaval lymph nodes in the other. After surgery, the patients were evaluated every 3 months, and had no detectable disease at 30 and 43 months, respectively. Thirty cases of partial tumor regression with octreotide administered with or without other treatment modalities have been reported in the literature. Most of the patients involved received other treatment modalities. Only one other case reported in the literature showed complete regression with octreotide monotherapy. CONCLUSIONS: We report two cases of metastatic midgut carcinoid tumors that demonstrated a significant anti-proliferative response to octreotide monotherapy. Review of the literature failed to identify any specific prognostic factors with which the response to octreotide can be predicted. Possible mechanisms for this antiproliferative effect of octreotide on carcinoid tumors are discussed. Copyright 2002 Wiley--Liss, Inc.
UI - 11870673
AU - Yesher J; Herskowitz MM; Ghosh BC
TI - Massive bleeding from duodenal carcinoid treated by gastroduodenal artery embolization.
SO - J Surg Oncol 2002 Mar;79(3):199-200
AD - State University of New York Health Science Center at Brooklyn, New York Harbor Healthcare System-Brooklyn Campus, Brooklyn, New York 11209, USA.
UI - 11740599
AU - Saida Y; Matsueda K; Itai Y
TI - Distal migration of duodenal tumors: simple prolapse or intussusception?
SO - Abdom Imaging 2002 Jan-Feb;27(1):9-14
AD - Department of Radiology, University of Tsukuba, Tennoudai 1-1-1, Tsukuba, Ibaraki 305-8575, Japan.
BACKGROUND: To define radiographically simple prolapse or intussusception in cases of distal migration of duodenal tumors. METHODS: In one pyloric and four duodenal tumors showing distal migration, the findings of gastrointestinal contrast examinations were retrospectively evaluated in relation to CT and operative findings. RESULTS: All lesions were intraluminal growing and well demarcated, and they included two carcinoids, a papillary adenoma, a Brunner's gland adenoma, and a hyperplastic polyp. All lesions were accompanied by long mucosal stalks, and, in three, folding deformity of the proximal jejunum was observed. CT showed no target signs except for one with gastroduodenal intussusception. Intussusception was not verified surgically in any cases. CONCLUSION: Distal migration of duodenal tumors can occur as the result of mucosal elongation and slipping. Duodenojejunal intussusception is not necessarily associated with that phenomenon.
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