Table of Contents
1
UI - 11807677
AU - Schmittenbecher PP
TI -
Carcinoid tumours of the appendix in children--epidemiology, clinical
aspects and procedures.
SO - Eur J Pediatr Surg 2001 Dec;11(6):428
2
UI - 11561765
AU - Waldum HL; Qvigstad G; Falkmer S
TI -
Indications for a neuroendocrine tumor-carcinoma sequence.
SO - Virchows Arch 2001 Aug;439(2):215-7
3
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. bruno.annibale@uniroma1.it
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.
4
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. llaine@usc.edu
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.
5
UI - 11328270
AU - Waldum HL
TI -
The safety of proton pump inhibitors.
SO - Aliment Pharmacol Ther 2001 May;15(5):729-30
6
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.
7
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.
8
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.
9
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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