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Accepted Preprint first posted online on 19 September 2008
European Journal of Endocrinology (2008) In press
DOI: 10.1530/EJE-08-0293
Copyright © 2008 by European Society of Endocrinology
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RESEARCH

Retesting the childhood-onset GH deficient patient

Valentina Gasco, Ginevra Corneli, Guglielmo Beccuti, Flavia Prodam, Silvia Rovere, Jaele Bellone, Silvia Grottoli, Gianluca Aimaretti and Ezio Ghigo

V Gasco, Department of Internal Medicine, University of Turin, Division of Endocrinology and Metabolism, Turin, Italy
G Corneli, Amedeo Avogadro University of Novara, Endocrinology Unit, Novara, Italy
G Beccuti, Department of Internal Medicine, University of Turin, Division of Endocrinology and Metabolism, Turin, Italy
F Prodam, Amedeo Avogadro University of Novara, Endocrinology Unit, Novara, Italy
S Rovere, Department of Internal Medicine, University of Turin, Division of Endocrinology and Metabolism, Turin, Italy
J Bellone, Department of Internal Medicine, University of Turin, Division of Endocrinology and Metabolism, Turin, Italy
S Grottoli, Department of Internal Medicine, University of Turin, Division of Endocrinology and Metabolism, Turin, Italy
G Aimaretti, Amedeo Avogadro University of Novara, Endocrinology Unit, Novara, Italy
E Ghigo, Department of Internal Medicine, University of Turin, Division of Endocrinology and Metabolism, Turin, Italy

Correspondence: Valentina Gasco, Email: valentina.gasco{at}unito.it

Abstract

GH deficiency (GHD) in adults has to be shown by a single provocative test, provided that it is validated. ITT has been indicated as the test of choice; now also glucagon test is validated and represents an alternative. The GHRH plus arginine (ARG) test as well as testing with GHRH plus a GH Secretagogue (GHS) are equally reliable diagnostic tools and are now considered as "golden" as ITT. Childhood-onset (CO) GHD needs retesting in late adolescence or young adulthood; this is major clinical challenge and raises questions about the most appropriate method and cut-off value. Appropriate reevaluation of GH status is represented by simple measurement of IGF-I concentration off rhGH treatment. Clearly low IGF-I levels are evidence of persistent severe GHD in subjects with genetic GHD or panhypopituitarism. However, normal IGF-I levels never rule out severe GHD and CO-GHD with normal IGF-I levels must undergo a provocative test. The appropriate GH cut-off limit is specific for each provocative test. As shown by the ROC curve analysis, in late adolescents and young adults the lowest normal GH peak response to ITT is 6.1 µg/l while that to GHRH+ARG test is 19.0 µg/l. These cut-off limits, however, are just indicative as being variable as function of the assay used. No other test is validated for retesting. As GHRH+ARG test mostly explores the GH releasable pool, normal GH response would be verified by a second ITT in order to rule out subtle hypothalamic defect.







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