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Effects of dexamethasone on selective lymphocyte subpopulations in hypercortisolemic patients with anorexia nervosa and with bulimia nervosa: Preliminary report
Author(s) -
Chiappelli Francesco,
Gwirtsman Harry E.,
Cormley Glenn J.,
Lowy Martin T.,
Esmail Imu,
Dan Nguyen Linn,
Nguyen Ly,
Strober Michael,
Weiner Herbert
Publication year - 1992
Publication title -
international journal of eating disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.785
H-Index - 138
eISSN - 1098-108X
pISSN - 0276-3478
DOI - 10.1002/1098-108x(199207)12:1<37::aid-eat2260120106>3.0.co;2-j
Subject(s) - anorexia nervosa , endocrinology , medicine , glucocorticoid , dexamethasone , cd8 , bulimia nervosa , lymphocyte , population , adrenocorticotropic hormone , immune system , hormone , glucocorticoid receptor , immunology , eating disorders , psychiatry , environmental health
The studies reported here describe the effects of intravenous (IV) administration of the synthetic glucocorticoid dexamethasone (DEX) on certain neuroendocrine and immunological measures in hypercortisoiemic patients with anorexia nervosa (AN) and with bulimia nervosa (BN). The results demonstrate that failure to suppress cortisol levels after DEX administration in patients with AN is associated with failure to reduce the level of adrenocorticotropic hormone (ACTH), the ratio of CD4‐to‐CD8 lymphocytes, the percent and number of circulating CD4 lymphocytes, and the percent and number of virgin CD4 cells (CD4+CD45RA+). Administration of DEX to patients with BN suppressed plasma ACTH and cortisol levels, reduced the CD4/CD8 ratio and the percent and number of CD4 and of CD4 + CD45RA+ lymphocytes, and increased the percent and number of circulating CD8 lymphocytes. Administration of DEX failed to alter other immune measures in either patient population, including circulating populations of B and natural killer cells, the proliferative response to T‐cell mitogen, and the number of glucocorticoid receptors in circulating lymphocytes.