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The T-lymphocyte proliferative response to phytohemoagglutinin (PHA) stimulation was the same in 11 anorexic women, 6 restricted (AN-R) and 5 bulimic (AN-B), and in 11 sex- and age-matched controls, in basal conditions and after acute administration of corticotropin-releasing hormone (CRH). Basal plasma levels of ACTH and cortisol were higher in patients than in controls, while beta-endorphin (beta-EP), growth hormone (GH) and prolactin (PRL) concentrations did not differ in the two groups. ACTH and beta-EP responses to CRH stimulation were blunted in patients, while those of cortisol did not differ in the two groups. ACTH, beta-EP and cortisol responses to the dexamethasone suppression test were impaired in 55% of the patients. Baseline T-lymphocyte concentrations of cholecystokinin-8 (CCK-8) and beta-EP were measured in another group of 56 anorexics, 33 restricted and 23 bulimic, and in 24 controls. CCK-8 values were significantly lower and beta-EP values significantly higher in patients than in controls.

Baseline concentrations of cholecystokinin-8 (CCK-8) and beta-endorphin (beta-EP) were measured in T-lymphocytes from 33 restricting patients with anorexia nervosa (AN-R), 23 binging/purging patients with anorexia nervosa (AN-BP), and 24 healthy volunteers. CCK-8 basal values were significantly lower and beta-EP values significantly higher in AN-R and AN-BP patients than in normal volunteers. Levels of the peptides were measured three more times during a 4-month combined cognitive-behavioral/psychopharmacological treatment (nortriptyline or fluoxetine in AN-R, fluoxetine or amineptine in AN-BP). CCK-8 values fluctuated (nonsignificantly) during each treatment, while beta-EP values decreased (to a significant degree only in fluoxetine-treated AN-R patients).

Concentrations of cholecystokinin-8 (CCK-8) and beta-endorphin (beta-EP) in T-lymphocytes of 26 women with bulimia nervosa (BN) and in 26 age- and sex-matched healthy comparison subjects were measured. Ten patients were then treated with 300 mg/day of fluvoxamine, p.o., and five patients were treated with 300 mg/day of amineptine, p.o., for 4 months. Concentrations of the two peptides were measured again after 1, 2, and 4 months of therapy. Basal CCK-8 values were significantly lower in patients than in healthy subjects. During fluvoxamine therapy, CCK-8 values increased, reaching normal levels by month 4 of treatment. No such increase occurred during amineptine therapy. Baseline beta-EP values were normal in the bulimic patients but had declined by month 4 of fluvoxamine therapy.