Adrenal response to adrenocorticotropic hormone stimulation in patients with premenstrual syndrome.
Several studies have been performed during recent years to investigate the existence of a possible endocrine cause for premenstrual syndrome (PMS); the results reported are often discordant. Great interest has been raised around allopregnanolone, which could be involved in the determination of mood disorders reported by PMS patients. During the luteal phase, lower levels of this hormone have been detected in PMS patients. The aim of our study was to evaluate estradiol, progesterone, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), androstenedione, total and free testosterone, cortisol, pregnenolone and allopregnanolone levels in 20 patients suffering from PMS and to compare them with those found in 20 fertile healthy women in the follicular and the luteal phases. Adrenocorticotropic hormone (ACTH) tests after dexamethasone suppression were performed in 10 patients of each group during the follicular and the luteal phases. In the PMS group, significantly lower allopregnolone levels were found in the luteal phase, while progesterone was lower in the PMS group in both phases. In the PMS group, higher free testosterone levels were found during the luteal phase and higher DHEA levels in both the follicular and the luteal phases. The present data confirm reduced allopregnanolone levels in the luteal phase in PMS patients, together with higher levels of DHEA and free testosterone. It is possible to conclude that, in addition to the previously described reduced luteal secretion of allopregnanolone, the adrenal gland production of this steroid in PMS sufferers is also impaired in the luteal phase. Considering the specific actions of these hormones on the control of mood and behavior, this specific hormonal milieu may contribute to the cyclic occurrence of anxiety, aggressiveness and irritability reported by PMS patients.
Lombardi
I
I
Department of Reproductive Medicine and Child Development, Division of Obstetrics and Gynecology, University of Pisa, Pisa, Italy.
Luisi
S
S
Quirici
B
B
Monteleone
P
P
Bernardi
F
F
Liut
M
M
Casarosa
E
E
Palumbo
M
M
Petraglia
F
F
Genazzani
A R
AR
D000293:Adolescent; D000302:Adrenal Cortex / Q000187:drug effects* / Q000378:metabolism; D000304:Adrenal Cortex Function Tests; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000328:Adult; D000735:Androstenedione / Q000097:blood; D016022:Case-Control Studies; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology*; D004958:Estradiol / Q000097:blood; D005260:Female; D005498:Follicular Phase / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008183:Luteal Phase / Q000097:blood; D011280:Pregnanolone / Q000097:blood*; D011284:Pregnenolone / Q000097:blood; D011293:Premenstrual Syndrome / Q000097:blood*; D011374:Progesterone / Q000097:blood; D013739:Testosterone / Q000097:blood
D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D011374:Progesterone; D004958:Estradiol; D019314:Dehydroepiandrosterone Sulfate; D011284:Pregnenolone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D011280:Pregnanolone; D006854:Hydrocortisone