National Cancer Institute®
Last Modified: November 21, 2001
UI - 21441830
AU - Abrahams NA; Vesoulis Z; Petras RE
TI - Angiogenic polypoid proliferation adjacent to ileal carcinoid tumors: a nonspecific finding related to mucosal prolapse.
SO - Mod Pathol 2001 Sep;14(9):821-7
AD - Department of Anatomic Pathology, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Case reports have highlighted angiogenic polypoid proliferation in the mucosa adjacent to ileal carcinoid tumors, describing them as granulation tissue polyposis and florid angiogenesis. Some authors have proposed that the ileal carcinoid tumors themselves produce growth factors that cause the change. The purpose of this study was to determine the frequency of angiogenic polypoid proliferation in a large cohort of resected ileal carcinoid tumors compared with control groups. Search of the Cleveland Clinic and Summa Health System pathology files (1985 to 1999) yielded 65 resected ileal carcinoid tumors. Mucosal abnormalities adjacent to the ileal carcinoid tumors were graded 0 to 4+. Twenty ileal resection margins from colonic carcinoma cases served as normal controls. Ileal mucosa adjacent to 22 noncarcinoid neoplasms were also examined. The mucosa adjacent to 54/65 ileal carcinoid tumors (83%) showed mucosal abnormalities (vs. 3/20 normal controls), including mucosal edema, capillary ectasia, muscularis mucosae hypertrophy, fibrosis/smooth muscle proliferation within the lamina propria, club-shaped villi, and intramucosal capillary proliferation. Forty ileal carcinoid tumor cases (61%) showed some degree of angiogenic polypoid proliferation characterized by club-shaped villi and prominent intramucosal capillaries, with 17 (26%) graded as 3+ or 4+. Angiogenic polypoid proliferation was associated with hypertrophy of the muscularis mucosae, lamina proprial fibrosis/smooth muscle proliferation, and capillary ectasia similar to that described with gastrointestinal mucosal trauma/prolapse. This trauma/prolapse change was identified in 45 cases (69%) and was graded 3+ or 4+ in 23 (35%). Seventeen (77%) of the noncarcinoid neoplasms showed trauma/prolapse changes, with 7 (32%) graded as 3+ or 4+. Angiogenic polypoid proliferation also correlated with trauma/prolapse change in the noncarcinoid neoplasm controls. Neither APP (P =.24) nor the prolapse changes (P =.33) were found to be statistically different between the two tumor groups. Angiogenic polypoid proliferation of the adjacent ileal mucosa is common in patients with ileal carcinoid tumors and with noncarcinoid neoplasms. Angiogenic polypoid proliferation almost invariably coexists with fibromuscular change and capillary ectasia within the lamina propria, suggesting that mucosal trauma/prolapse plays a role in the histogenesis. The association of angiogenic polypoid proliferation with a variety of different neoplasms makes it unlikely that the tumors themselves secrete growth factors.
UI - 21443269
AU - Fujimori M; Ikeda S; Shimizu Y; Okajima M; Asahara T
TI - Accumulation of beta-catenin protein and mutations in exon 3 of beta-catenin gene in gastrointestinal carcinoid tumor.
SO - Cancer Res 2001 Sep 15;61(18):6656-9
AD - Second Department of Surgery, Hiroshima University Faculty of Medicine, Hiroshima, Japan 734-8551.
The molecular basis of carcinogenesis in gastrointestinal carcinoid tumors is not well understood. To clarify the contribution of the Wnt/beta-catenin signaling to this type of carcinogenesis, we investigated 72 cases of gastrointestinal carcinoid tumor both immunohistochemically and by direct sequencing of beta-catenin. Accumulation of beta-catenin in the cytoplasm and/or nucleus was observed in 57 cases (79.2%). We also detected mutations in exon 3 of beta-catenin in 27 cases (37.5%) and one mutation in APC (1.4%). Our results suggest that alterations in the Wnt/beta-catenin signaling pathway may be involved in the development of gastrointestinal carcinoid tumors.
UI - 21452938
AU - Kema IP; Meijer WG; Meiborg G; Ooms B; Willemse PH; de Vries EG
TI - Profiling of tryptophan-related plasma indoles in patients with carcinoid tumors by automated, on-line, solid-phase extraction and HPLC with fluorescence detection.
SO - Clin Chem 2001 Oct;47(10):1811-20
AD - Department of Pathology and Laboratory Medicine, University Hospital Groningen, 9700 RB Groningen, The Netherlands. email@example.com
BACKGROUND: Profiling of the plasma indoles tryptophan, 5-hydroxytryptophan (5-HTP), serotonin, and 5-hydroxyindoleacetic acid (5-HIAA) is useful in the diagnosis and follow-up of patients with carcinoid tumors. We describe an automated method for the profiling of these indoles in protein-containing matrices as well as the plasma indole concentrations in healthy controls and patients with carcinoid tumors. METHODS: Plasma, cerebrospinal fluid, and tissue homogenates were prepurified by automated on-line solid-phase extraction (SPE) in Hysphere Resin SH SPE cartridges containing strong hydrophobic polystyrene resin. Analytes were eluted from the SPE cartridge by column switching. Subsequent separation and detection were performed by reversed-phase HPLC combined with fluorometric detection in a total cycle time of 20 min. We obtained samples from 14 healthy controls and 17 patients with metastasized midgut carcinoid tumors for plasma indole analysis. In the patient group, urinary excretion of 5-HIAA and serotonin was compared with concentrations of plasma indoles. RESULTS: Within- and between-series CVs for indoles in platelet-rich plasma were 0.6-6.2% and 3.7-12%, respectively. Results for platelet-rich plasma serotonin compared favorably with those obtained by single-component analysis. Plasma 5-HIAA, but not 5-HTP was detectable in 8 of 17 patients with carcinoid tumors. In the patient group, platelet-rich plasma total tryptophan correlated negatively with platelet-rich plasma serotonin (P = 0.021; r = -0.56), urinary 5-HIAA (P = 0.003; r = -0.68), and urinary serotonin (P <0.0001; r = -0.80). CONCLUSIONS: The present chromatographic approach reduces analytical variation and time needed for analysis and gives more detailed information about metabolic deviations in indole metabolism than do manual, single-component analyses.
UI - 20307241
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 - 21366204
AU - Nojiri T; Ikegami M
TI - Multiple minute carcinoids in type A gastritis: attempt at 3-D reconstruction.
SO - Pathol Int 2001 Jul;51(7):504-10
AD - Department of Pathology, Jikei University School of Medicine, Tokyo, Japan. email@example.com
In type A gastritis, the numbers of endocrine cell micronests (ECM) and carcinoids increase through the trophic action of gastrin. This study examined the characteristics and growth of carcinoids in type A gastritis. A total of 395 lesions in five surgically removed stomachs with type A gastritis were investigated, in terms of number, size, distribution and histological appearance, to clarify the tumorigenesis and progression of carcinoids. 3-D reconstruction using serial paraffin sections was used to study carcinoid progression. Our findings suggest that in type A gastritis, carcinoids arise in areas where minute carcinoids are present at a high density. They also suggest that early stage carcinoids not only become large expansively, but also develop in a very complex manner, by maintaining contact with surrounding minute carcinoids.
UI - 21467940
AU - Danikas D; Sachs R; Dressner RM; Arvanitis ML
TI - Testicular metastasis from ileal carcinoid: report of a case.
SO - Dis Colon Rectum 2001 Sep;44(9):1365-6
AD - Department of Surgery, Monmouth Medical Center, Long Branch, New Jersey, USA.
PURPOSE: This report presents a patient with testicular metastasis from an ileal carcinoid. METHODS: This was a retrospective case review with literature review. RESULTS: The patient underwent right orchiectomy for a solid mass. Pathology revealed carcinoid tumor. Octreotide scan showed increased concentration in the right lower quadrant of the abdomen. Computerized tomography results were negative. Colonoscopy with biopsy revealed carcinoid of the terminal ileum. The patient underwent an elective resection of the terminal ileum and the right colon. Pathology revealed carcinoid tumor with vascular and lymphatic invasion present, and eight lymph nodes were positive. The patient had adjuvant treatment with octreotide. CONCLUSION: Carcinoid tumors have been reported to metastasize to numerous areas. This is the first report of testicular metastasis from ileal carcinoid. Primary carcinoids of the testicle have been reported also. The clinician should be aware of this rare metastatic event. When pathology reveals carcinoid of the testicle, metastatic disease should be excluded before the tumor is identified as primary.
UI - 21289731
AU - Akahoshi K; Fujimaru T; Nakanishi K; Harada N; Nawata H
TI - Endosonography probe-guided endoscopic resection of small flat rectal carcinoid tumor using band ligation technique.
SO - Endoscopy 2001 May;33(5):471
AD - Dept. of Gastroenterology, Aso Iizuka Hospital, Japan. firstname.lastname@example.org
UI - 20576718
AU - Habal N; Sims C; Bilchik AJ
TI - Gastrointestinal carcinoid tumors and second primary malignancies.
SO - J Surg Oncol 2000 Dec;75(4):310-6
AD - Department of Surgical Oncology, John Wayne Cancer Institute, Santa Monica, California, USA.
The development of second primary malignancies (SPM) in patients with gastrointestinal carcinoid tumors is a well-described phenomenon, with reported rates as high as 55%. There is a predilection for gastrointestinal and genitourinary adenocarcinomas, but a variety of other malignancies have been reported as well. The etiology of this malignant predisposition may be rooted in the tumorigenic properties of the various neuroendocrine peptides elaborated and secreted by neuroendocrine cells. Peptides such as secretin, gastrin, bombesin, cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) are believed to promote the growth of tumor cells. As many as 30 peptides and amines identified in neuroendocrine cells may have similar properties. This review of the literature on carcinoid-associated second primary malignancies is accompanied by a case report of metastatic carcinoid identified during surgical exploration for a perforating colon adenocarcinoma. Copyright 2000 Wiley-Liss, Inc.
UI - 21486624
AU - Papotti M; Cassoni P; Volante M; Deghenghi R; Muccioli G; Ghigo E
TI - Ghrelin-producing endocrine tumors of the stomach and intestine.
SO - J Clin Endocrinol Metab 2001 Oct;86(10):5052-9
AD - Department of Biomedical Sciences, University of Turin, Via Santena 7, I-10126 Turin, Italy. email@example.com
Ghrelin is a novel gastrointestinal hormone produced by about 20% of the rat and human gastric neuroendocrine cell population, which possesses strong GH-releasing activity, but also plays other central and peripheral roles, including influence on food intake, gastric motility, and acid secretion. The aim of the present study was to determine whether gastrointestinal endocrine hyperplastic and neoplastic lesions produce ghrelin, at both protein (immunohistochemistry) and mRNA (in situ hybridization and/or RT-PCR) levels, and express the GH secretagogue receptor mRNA by RT-PCR. Sixteen gastric and 20 intestinal carcinoids as well as normal gastrointestinal mucosa and atrophic gastritis-associated neuroendocrine cell hyperplasia were studied. The majority (12 of 16, 75%) of gastric carcinoids and only 5 of 18 (27%) of intestinal endocrine tumors were immunoreactive for ghrelin. In situ hybridization confirmed the immunohistochemical data, but also showed ghrelin mRNA in 1 gastric and 8 intestinal additional tumors. RT-PCR showed ghrelin mRNA in 14 of 14 cases, indicating a low level of ghrelin gene expression in all gastrointestinal endocrine tumors tested. Gastric neuroendocrine hyperplastic cells were also strongly positive for ghrelin. GH secretagogue receptor mRNA was absent in 3 gastric, but present in 7 of 11 intestinal carcinoids studied by RT-PCR. These findings demonstrate that most gastric carcinoids (and related neuroendocrine cell hyperplasias) and some intestinal carcinoids produce ghrelin. These hyperplastic/neoplastic conditions could represent the clinical model to clarify the existence and impact of ghrelin hypersecretion on endocrine and nonendocrine functions.
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