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      Octreotide Exerts Only Acute, but No Sustained, Effects on MRI Enhancement of Liver Metastases in Carcinoid Syndrome

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          Abstract

          We have investigated the acute and sustained hemodynamic effects of octreotide on hepatic metastases of midgut carcinoids using contrast-enhanced dynamic magnetic resonance imaging (MRI). Seven patients with the carcinoid syndrome and metastasized midgut carcinoid tumors underwent functional dynamic multi-phase gadolinium-enhanced MRI of selected liver metastases at baseline and 60 min after the subcutaneous (s.c.) administration of 100 µg octreotide, and also after 3 months with three times daily (t.i.d.) 100 µg octreotide s.c. Baseline MRIs showed the typical aspect of carcinoid liver metastases with a very bright signal on the T2-weighted sequences and intense enhancement in the arterial phase after injection of gadolinium-diethylenetriaminepentaacetate. MRIs 60 min after the s.c. administration of 100 µg octreotide showed a 34.9 ± 6.2% (mean ± SD) reduction in relative enhancement in the selected liver metastases as compared to baseline. In 2 patients, however, there was no (significant) reduction in the relative enhancement in the selected liver metastases 60 min after the s.c. administration of 100 µg octreotide as compared to baseline. Only in 2 patients did the MRIs at 3 months show a decrease in relative enhancement in one of the selected liver metastases. At 3 months, with 100 µg octreotide s.c. t.i.d., there was no correlation between the change in relative enhancement on MRI and the change in 24-hour 5-HIAA excretion. There is thus only an acute effect of octreotide on the perfusion of liver metastases. This study further shows that contrast-enhanced dynamic MRI can be a very useful tool for studying hemodynamic effects of medical therapies on liver metastases in patients with metastatic midgut carcinoids.

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          Most cited references 27

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          Octreotide.

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            Guidelines for the Diagnosis and Treatment of Neuroendocrine Gastrointestinal Tumours

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              The pathophysiological consequences of somatostatin receptor internalization and resistance.

               L Hofland,  S Lamberts (2003)
              Somatostatin receptors expressed on tumor cells form the rationale for somatostatin analog treatment of patients with somatostatin receptor-positive neuroendocrine tumors. Nevertheless, although somatostatin analogs effectively control hormonal hypersecretion by GH-secreting pituitary adenomas, islet cell tumors, and carcinoid tumors, significant differences are observed among patients with respect to the efficacy of treatment. This may be related to a differential expression of somatostatin receptor subtypes among tumors. In addition, the property of somatostatin receptor subtypes to undergo agonist-induced internalization has important consequences for visualizing, as well as for therapy, of receptor-positive tumors using radioisotope- or chemotherapeutic-compound-coupled somatostatin analogs. This review covers the pathophysiological role of somatostatin receptor subtypes in determining the efficacy of treatment of patients with somatostatin receptor-positive tumors using somatostatin analogs, as well as the preclinical and clinical consequences of agonist-induced receptor internalization for somatostatin receptor-targeted radio- and chemotherapy. Herein, the development and potential role of novel somatostatin analogs is discussed.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2005
                January 2006
                27 January 2006
                : 82
                : 1
                : 41-48
                Affiliations
                aDepartment of Internal Medicine, Section of Endocrinology, and bDepartment of Radiology, Erasmus MC, Rotterdam, The Netherlands
                Article
                90636 Neuroendocrinology 2005;82:41–48
                10.1159/000090636
                16391492
                © 2005 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 2, Tables: 2, References: 37, Pages: 8
                Categories
                Original Paper

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