The hypothalamo-pituitary-adrenal axis across the normal menstrual cycle and in polycystic ovary syndrome.
OBJECTIVE
We explored the hypothesis that activation of the hypothalamo-pituitary-adrenal axis is involved in the pathogenesis of hyperandrogenism in the polycystic ovary syndrome.


METHODS
Seven women with polycystic ovary syndrome (mean age 27.6 +/- 1.6 (SEM) years) (hirsutism, oligo/amenorrhoea and elevated serum testosterone and dehydroepiandrosterone sulphate) and nine normal female controls (mean age 24.6 +/- 1.5 years) were studied. To exclude anovulation as a confounding factor, four of these normal women were studied in both the follicular and luteal phase of the menstrual cycle.


METHODS
Plasma ACTH and cortisol levels were measured at 15-minute intervals between 0600 h and 1800 h. ACTH and cortisol mean levels, pulse number and amplitude were calculated using established computer software, programmed to identify ACTH and cortisol peaks.


RESULTS
With the exception of mean plasma levels of ACTH over the 12-hour period, which were reduced in the luteal phase of the menstrual cycle (1.8 +/- 0.3 pmol/l) compared to the follicular phase (2.3 +/- 0.2 pmol/l, P < 0.05), there were no differences in the pattern of ACTH or cortisol secretion across the normal cycle. In polycystic ovary syndrome, 12-hour ACTH pulse frequency was reduced (3.6 +/- 0.7) compared with controls (5.9 +/- 0.6, P < 0.05), but cortisol pulsatility and ACTH and cortisol mean levels were similar in both groups.


CONCLUSIONS
The hyperandrogenism of polycystic ovary syndrome cannot be explained by enhanced ACTH secretion. Normal circulating cortisol levels, yet elevated dehydroepiandrosterone sulphate levels, suggests that polycystic ovary syndrome is yet another example of discrepant adrenal glucocorticoid and androgen secretion, and provides further evidence for a putative adrenal androgen stimulating factor.
Department of Medicine, University of Birmingham, Queen Elizabeth Hospital, UK.
P M
PM
Stewart
R
R
Penn
R
R
Holder
A
A
Parton
J G
JG
Ratcliffe
D R
DR
London
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D003687:Dehydroepiandrosterone / Q000031:analogs & derivatives / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate; D005260:Female; D005498:Follicular Phase / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D008183:Luteal Phase / Q000097:blood; D008598:Menstruation / Q000502:physiology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D012636:Secretory Rate / Q000502:physiology
D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone