title: Androgen deficiency in women with hypopituitarism.
abstract: Androgen deficiency in men is associated with severe osteopenia, alterations in body composition including an increase in fat mass, and decreased libido. Little is known about the pathophysiology, metabolic consequences, or gender-specific effects of androgen deficiency in women. Acquired hypopituitarism in women is characterized by central hypogonadism and/or hypoadrenalism and therefore may affect critical sources of androgen production in women. We hypothesized that serum androgen levels would be decreased in women with hypopituitarism. We therefore determined serum androgen levels in 55 women with hypopituitarism and 92 controls. This included 4 subsets of hypopituitary women: 1) women less than 50 yr old not receiving estrogen, 2) women less than 50 yr old receiving estrogen, 3) women more than 50 yr old not receiving estrogen, and 4) women more than 50 yr old receiving estrogen. Premenopausal controls with regular menstrual cycles were studied in the early follicular phase, midcycle, and luteal phase during one cycle. All other subjects were studied 3 times during the month at comparable intervals to mimic these 3 time points of the normal menstrual cycle. Serum testosterone, free testosterone, androstenedione, and dehydroepiandrosterone sulfate levels were markedly reduced in all 4 groups of women with hypopituitarism compared with controls (P < 0.0001). Moreover, serum testosterone, free testosterone, and androstenedione levels were lower in women with central hypoadrenalism and hypogonadism than in subjects with hypoadrenalism or hypogonadism alone (P < 0.025). Mean DHEAS levels were decreased in hypopituitary women with both hypogonadism and hypoadrenalism compared with those in women with hypogonadism alone (P < 0.0001). These data demonstrate hypoandrogenemia in women with hypopituitarism. The physiological consequences of low androgen levels in this population remain to be determined.
authors.affiliation: Neuroendocrine Unit, Department of Medicine, Clinical Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
authors.forename: K K
authors.initials: KK
authors.lastname: Miller
authors.forename: G
authors.initials: G
authors.lastname: Sesmilo
authors.forename: A
authors.initials: A
authors.lastname: Schiller
authors.forename: D
authors.initials: D
authors.lastname: Schoenfeld
authors.forename: S
authors.initials: S
authors.lastname: Burton
authors.forename: A
authors.initials: A
authors.lastname: Klibanski
mesh_terms: D000236:Adenoma / Q000097:blood; D000309:Adrenal Insufficiency / Q000097:blood / Q000150:complications; D000735:Androstenedione / Q000097:blood*; D001932:Brain Neoplasms / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood*; D015914:Estrogen Replacement Therapy; D005260:Female; D006801:Humans; D007006:Hypogonadism / Q000097:blood* / Q000150:complications; D007018:Hypopituitarism / Q000097:blood* / Q000145:classification; D008597:Menstrual Cycle; D008875:Middle Aged; D010911:Pituitary Neoplasms / Q000097:blood; D017698:Postmenopause; D017697:Premenopause; D012016:Reference Values; D013739:Testosterone / Q000097:blood*
chemical_list: D013739:Testosterone; D000735:Androstenedione; D019314:Dehydroepiandrosterone Sulfate