Exp Clin Endocrinol Diabetes 1983; 82(5): 160-172
DOI: 10.1055/s-0029-1210272
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Endocrine Study of Anorexia Nervosa

G. de Rosa, S. M. Corsello, E. de Rosa1 , S. Della Casa, M. P. Ruffilli, P. Grasso, E. Pasargiklian
  • Institute of Endocrinology (Head: Prof. E. Pasargiklian), Catholic University School of Medicine, Rome/Italy
  • 1Institute of Psychiatry (Head: Prof. L. Ancona), Catholic University School of Medicine, Rome/Italy
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Publikationsverlauf

82

Publikationsdatum:
17. Juli 2009 (online)

Summary

The main objective of the study was to evaluate the endocrinological picture of anorexia. The sample consisted of 23 anorectic patients (20 females, 3 males) with a control group of 10 normal females and 5 normal males. All participants underwent a work-up which included testing for hypothalamic, hypophyseal, thyroidal, adrenal, gonadal functioning and glucose metabolism.

Our results revealed a reduced urinary output and low serum levels of gonadotropins with different responses to LHRH correlating with the stage of the illness. We found reduced urinary estrogens and elevated testosterone levels in females. Males demonstrated a reduction of testosterone. While basal prolactinemia was normal in both sexes, males showed an exaggerated response to TRH. The thyroid function study in anorectic patients revealed a decrease in T3 and in free T3 and an increase in reverse T3. Free T4 was slightly increased with normal T4 levels. Basal TSH was normal with a delayed peak after TRH. We also noticed in the anorectic population reduced basal glucose levels with a flat glucose curve; reduced insulin levels with a slight increase after glucose administration; elevated basal GH with a fair response to L-Dopa; elevated serum cortisol with loss of circadian rhythm and slightly inhibited by dexamethasone. In addition, both noradrenalin and VMA were reduced.

We concluded that the multiple endocrine abnormalities found are consistent with hypothalamic dysfunction. The etiology of this dysfunction remains for the endocrinologist highly controversial.

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