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      Modulation by Glucocorticoids of Growth Hormone Secretion in Patients with Different Pituitary Tumors

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          Abstract

          The acute administration of glucocorticoids is a new stimulus of growth hormone (GH) secretion in man. In order to ascertain its point of action, and also the suitability of this new test as a diagnostic tool in GH pathological states, 33 subjects were studied. Eight of them were normal controls, and 25 were patients with tumors affecting the hypothalamopituitary area. A glucocorticoid stimulus, dexamethasone 4 mg i.v. was administered at 0 min and GH levels (means ± SEM, µg/l) were measured during the following 5 h. In addition, GH-releasing hormone (GHRH) and clonidine were employed as either pituitary or hypothalamic GH stimuli. Dexamethasone administration to normal subjects did not alter GH levels in the first 2 h of the test. Afterwards, a GH peak was observed around the third hour, GH levels returning to basal ones thereafter. The dexamethasone-induced GH peak (6.7 ± 1.5) and area under the curve (526 ± 137) were lower than after GHRH (14.0 ± 4.5 and 1,070 ± 369, respectively). In the 14 acromegalic patients studied, the GHRH-induced GH net increase was similar to that observed in controls, while the placebo did not alter GH basal levels. An absence of hypothalamic control was evident because clonidine did not stimulate GH release. On the other hand, and contrary to normal subjects, dexamethasone strongly inhibited GH secretion, the values being significantly lower when calculated either as mean GH peak, or maximum GH increment (Δ). The Δ GH was -2.5 ± 3.1 after placebo, +3.7 ± 4.5 after clonidine, +17.0 ± 3.3 after GHRH and -13.4 ± 4.5 following dexamethasone administration. In 4 patients harboring pituitary prolactinomas, dexamethasone stimulated GH secretion in 1 subject with a microadenoma but was devoid of action in the 3 marcoprolactinoma patients, which had suprasellar extension and absent clonidine-induced GH secretion. Similarly, in 4 out of 5 patients with nonsecreting pituitary adenomas that had a functional pituitary stalk section (suprasellar extension, mild prolactin levels and no GH response to hypothalamic stimulus), dexamethasone was ineffective, while it stimulated GH secretion in the other patient of this group with a normal hypothalamopituitary connection. In addition, in 2 other patients with hypothalamic germinoma and well-preserved GH response to GHRH, dexamethasone was devoid of action. These results indicate that GH stimulation by glucocorticoid is only observed in normal subjects and requires a normal hypothalamopituitary connection. On the contrary, in acromegaly, glucocorticoids induced, instead, an inhibition of GH secretion. In conclusion, glucocorticoid stimulatory action over GH secretion seems to be exerted at the hypothalamic level. On the contrary, in acromegalic patients a ‘paradoxical’ inhibition of GH secretion is observed after glucocorticoid injection. Acute administration of glucocorticoids may be a suitable test in the diagnosis and follow-up of GH pathological states.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1993
          1993
          08 April 2008
          : 58
          : 4
          : 465-472
          Affiliations
          Institute of Endocrinology, University Clinical Center, Belgrade, Serbia; Department of Medicine, Endocrine Section Faculty of Medicine and Hospital General de Galicia, Santiago de Compostela, Spain
          Article
          126577 Neuroendocrinology 1993;58:465–472
          10.1159/000126577
          8284031
          © 1993 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
          Pages: 8
          Categories
          Clinical Neuroendocrinology

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