Eur J Endocrinol
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DOI: 10.1530/eje.0.1470165
European Journal of Endocrinology, Vol 147, Issue 2, 165-171
Copyright © 2002 by European Society of Endocrinology
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Articles

Growth hormone deficiency in pituitary disease: relationship to depression, apathy and somatic complaints

S Zenker, F Haverkamp, and D Klingmuller

Department of Clinical Biochemistry, University of Bonn, 53105 Bonn, Germany.

OBJECTIVE: Adults with GH deficiency (GHD) have been reported to suffer from increased levels of depression and apathy, which are thought to contribute to the reduced quality of life observed in these patients when compared with healthy controls. Recent studies, however, cast doubt on the attribution of these impairments to GHD as opposed to an unspecific stress response to the chronic medical condition. DESIGN: To further clarify this relationship, we used psychometric tests to quantify depression, apathy and typical psychosomatic complaints in patients with different types of pituitary disease and compared the results with measurements of the patients' widely varying GH status. SUBJECTS AND METHODS: In 98 patients, serum IGF-I was measured and at least one provocative test of the somatotrope pituitary axis was performed (GH-releasing hormone test (GHRHT) and/or insulin tolerance test (ITT)). All patients completed a set of well-established psychometric instruments (Beck Depression Inventory (BDI), Apathy Evaluation Scale (AS) and List of Somatic Complaints (LSC)). In addition, AS was administered in an informant report version for completion by a close relative or friend to verify the validity of the patient's self assessment. RESULTS: No relationship between measures of GHD (IGF-I, GHRHT and ITT) and psychometrically measured depression, apathy or psychosomatic well-being was found. A highly significant linear correlation between scores of all psychometric instruments (BDI, AS and LSC) was found. CONCLUSIONS: The absence of any relationship between the severity of GHD and the level of depression/apathy/psychosomatic complaints suggests that these impairments are not specific symptoms of GHD. The reported improvement of these symptoms under GH substitution therapy might thus be interpreted as a secondary effect of somatic effects of GH substitution. Consequently, indication for GH substitution therapy should not be based on psychological impairments alone without the presence of somatic symptoms of GHD.





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