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Are enterochromaffinlike cell tumours reversible? An experimental study on gastric carcinoids induced in Mastomys by histamine2-receptor blockade.

Artikel i vetenskaplig tidskrift
Författare Bo Wängberg
Ola Nilsson
E Theodorsson
I M Modlin
A Dahlström
Håkan Ahlman
Publicerad i Regulatory peptides
Volym 56
Nummer/häfte 1
Sidor 19-33
ISSN 0167-0115
Publiceringsår 1995
Publicerad vid Institutionen för de kirurgiska disciplinerna, Avdelningen för kirurgi
Sidor 19-33
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Carcinoid Tumor, drug therapy, etiology, pathology, Cell Count, Cell Division, Cell Transformation, Neoplastic, Enterochromaffin Cells, drug effects, metabolism, pathology, Female, Gastrins, blood, Histamine, metabolism, Histamine H2 Antagonists, pharmacology, Hyperplasia, Male, Muridae, Parietal Cells, Gastric, drug effects, metabolism, pathology, Stomach Neoplasms, drug therapy, etiology, pathology, Triazoles, pharmacology
Ämneskategorier Cancer och onkologi, Gastroenterologi

Sammanfattning

A rapid induction of enterochromaffinlike (ECL) cell tumours has been shown in Praomys (Mastomys) natalensis subjected to histamine2-receptor blockade. In the present study the reversibility of ECL cell proliferation induced by acid inhibition was investigated. Short-term treatment (8 weeks) with the histamine2-receptor antagonist loxtidine caused a moderate hypergastrinemia, accompanied by a minor increase in histamine contents and a 2-fold increased volume density of the endocrine cells in gastric oxyntic mucosa. Eight weeks after withdrawal of treatment the volume density of endocrine cells was normalised as were the tissue levels of histamine, indicating a total reversibility of ECL cell hyperplasia. Long-term treatment (24 weeks) caused severe changes in the endocrine cell population of the oxyntic mucosa with neoplasia (5/21), dysplasia (11/21) and nodular hyperplasia (5/21). The endocrine cell density increased twofold and tissue histamine levels fourfold. 24 weeks after cessation of treatment, the endocrine cell density had decreased to 136% of controls, while histamine concentrations were normalised. The frequency of invasive carcinoids after recovery (4/23) differed only slightly from that seen after treatment for 24 weeks (5/21). Dysplastic lesions were only seen in 1/23 and hyperplastic lesions were of less severe type after recovery. The results demonstrate that ECL cell hyperplasia and dysplasia, induced by acid inhibition, are reversible after cessation of treatment. However, ECL cell tumours did not disappear, within the given observation period. One may therefore speculate that ECL cell proliferation is no longer reversible once the neoplastic (transformed) phenotype has developed.

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