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Prolactin responses in dexamethasone suppression test in patients with anorexia nervosa
Author(s) -
Tamai H.,
Takii M.,
Nozaki T.,
Kiyohara K.,
Kobayashi N.,
Nakagawa T.,
Benbarka M. M.,
Jr R. M. Walter,
Kumagai L. F.
Publication year - 1990
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.1990.tb01388.x
Subject(s) - medicine , endocrinology , prolactin , basal (medicine) , dexamethasone suppression test , dexamethasone , anorexia nervosa , hypothalamic–pituitary–adrenal axis , hydrocortisone , glucocorticoid , hormone , psychology , eating disorders , psychiatry , insulin
ABSTRACT In anorexia nervosa (AN), abnormalities are present in the hypothalamic‐pituitary‐adrenal axis, but the prolactin (PRL) response to dexamethasone suppression test (DST) has not yet been studied. In order to study the interrelationships between the various endocrine abnormalities, we investigated the responses of PRL and cortisol to DST (1 mg of dexamethasone at 2300) in AN patients. The subjects were 12 female inpatients with AN and 8 age‐ and sex‐matched healthy controls. The percentage suppression and absolute change in PRL levels before and after dexamethasone administration were significantly different in the 2 groups. In the control group PRL levels suppressed to 36.5 ± 3.7% of basal, while AN levels declined to 79.4 ± 8.9% of basal. When the percentage suppression of PRL was compared between patients with and without cortisol suppression, the mean PRL level was 68.9 ± 7.8% of the basal level for the cortisol‐suppressed patients and 100.4 ± 19.1% for the nonsuppressed patients. Hence in both groups, the percentage PRL suppression was significantly reduced compared with the control group, and indeed nonexistent in cortisol‐nonsuppressed patients. The finding that there was less PRL suppression in the cortisol‐suppressed patients than in the controls suggests that, in AN, there may be an abnormality in PRL secretion not related to the hypothalamic‐pituitary‐adrenal axis. Further work is needed to distinguish between the PRL response to stress and potential hypothalamic abnormality.