The effects of a dopamine antagonist on luteinizing hormone and prolactin release in women with anorexia nervosa and in normal controls

• Published in: Journal of adolescent health Vol. 13; no. 2; pp. 155 - 160
• Main Authors: Golden, Neville H., Pepper, Gary M., Sacker, Ira, Avruskin, Theodore W.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.1992
• Subjects: Adolescent; Adult; Amenorrhea - etiology; Anorexia Nervosa; Anorexia nervosa Dopamine Luteinizing hormone Prolactin; Dopamine Agents - administration & dosage; Estradiol - physiology; Female; Humans; Luteinizing Hormone - drug effects; Luteinizing Hormone - secretion; Metoclopramide - administration & dosage; Prolactin - drug effects; Prolactin - secretion; Anorexia nervosa Dopamine Luteinizing hormone Prolactin
• ISSN: 1054-139X; 1879-1972
• DOI: 10.1016/1054-139X(92)90083-N

To evaluate the possible role of central dopaminergic suppression of gonadotropin secretion in the genesis of amenorrhea associated with anorexia nervosa (A.N.), a central D-2 dopamine receptor blocker was administered to 10 women with A.N. and 10 regularly menstruating age-matched controls. Serum prolactin and luteinizing hormone (LH) levels were measured at − 15, 0, 30, 60, 120, and 180 min after administration of metoclopramide (10 mg orally). Mean basal prolactin ( p < 0.001) and estradiol levels ( p < 0.02) were significantly lower in women with A.N. The prolactin response to metoclopramide was significantly impaired in women with anorexia nervosa. No correlation was found between the prolactin response and percentage ideal body weight. Basal and post-stimulation prolactin levels were correlated with estradiol levels. After adjusting for the effects of estradiol, significant differences between patients with A.N. and controls remained in prolactin levels at baseline ( p < 0.01), 120 min ( p < 0.02) and 180 min ( p < 0.05). Metoclopramide did not induce a significant rise in LH levels in either the A.N. or control groups. These data are consistent with central dopaminergic inhibition of prolactin secretion in anorexia nervosa but do not support the hypothesis that central dopaminergic inhibition is related to diminished LH release in this state.