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This Article Full Text Full Text (PDF) All Versions of this Article: 288/1/E63    most recent 00317.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by van Aken, M. O. Articles by Roelfsema, F. Search for Related Content PubMed PubMed Citation Articles by van Aken, M. O. Articles by Roelfsema, F.

Growth hormone secretion in primary adrenal Cushing's syndrome is disorderly and inversely correlated with body mass index

¹Department of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands; and ²Division of Endocrinology and Metabolism, Mayo Medical and Graduate Schools of Medicine, Mayo Clinic, Rochester, Minnesota

Submitted 19 July 2004 ; accepted in final form 21 August 2004

To evaluate the impact on the somatotropic axis of endogenous cortisol excess in the absence of primary pituitary disease, we investigated spontaneous 24-h growth hormone (GH) secretion in 12 adult patients with ACTH-independent hypercortisolism. Plasma GH concentration profiles (10-min samples) were analyzed by deconvolution to reconstruct secretion and approximate entropy to quantitate orderliness of the release process. Comparisons were made with a body mass index (BMI)-, age-, and gender-matched control group and an age- and gender-matched lean control group. GH secretion rates did not differ from BMI-matched controls but were twofold lower compared with lean subjects, mainly due to a 2.5-fold attenuation of the mean secretory burst mass (P = 0.001). In hypercortisolemic patients, GH secretion was negatively correlated with BMI (R = –0.55, P = 0.005) but not cortisol secretion. Total serum IGF-I concentrations were similar in the three groups. Approximate entropy (ApEn) was increased in patients with Cushing's syndrome compared with both control groups (vs. BMI-matched, P = 0.04; vs. lean, P = 0.001), denoting more irregular GH secretion patterns. ApEn in patients correlated directly with cortisol secretion (R = 0.77, P = 0.003). Synchrony between cortisol and GH concentration series was analyzed by cross-correlation, cross-ApEn, and copulsatility analyses. Patients showed loss of pattern synchrony compared with BMI-matched controls, but copulsatility was unchanged. We conclude that hyposomatotropism in primary adrenal hypercortisolism is only partly explained (30%) by increased body weight and that increased GH secretory irregularity and loss of synchrony suggest altered coordinate regulation of GH release.

cortisol; entropy; adrenal adenoma