Adrenal function may be abnormal in women with polycystic ovary syndro
me (PCOS). This study aims to evaluate adrenal steroid response to the
adrenocorticotropic hormone (ACTH) stimulation test and to find out t
he effect of high serum testosterone levels on adrenal response. We ha
ve also investigated any subtle enzyme deficiency by extending blood s
ampling to 2 h with 30 min intervals following ACTH administration. Tw
enty-eight women with PCOS and 18 healthy controls without hirsutism a
nd oligomenorrhea were included in the study. After determining their
serum basal levels of luteinizing hormone (LH), follicle-stimulating h
ormone (FSH), testosterone, dehydroepiandrosterone sulfate (DHEAS), 17
-hydroxyprogesterone (17-OHP), and progesterone, ACTH stimulation test
was performed. The change in serum 17-OHP and the summed rate of chan
ge in serum 17-OHP and progesterone levels were estimated and 95th per
centile for each value was computed. Women with PCOS were heavier and
move hirsute than controls (p < 0.01, p < 0.001, respectively). Sevum
basal LH, LH: FSH ratio, testosterone (p < 0.001, for all), DHEAS (p <
0.01), and 17-OHP (p < 0.05) were higher in women with PCOS. All of t
he 17-OHP measurements, including basal and each 30 min interval after
the administration of ACTH, were higher in women with PCOS than those
of healthy controls (p < 0.05, p < 0.002, p < 0.001, p < 0.015, p < 0
.018, respectively). However, the incremental changes in serum 17-OHP3
0-0, 17-OHP60-0, 17-OHP90-0, 17-OHP120-0, and the summed rate of chang
e in serum 17-OHP and progesterone in women with PCOS were not differe
nt from those in healthy controls. The incremental response in terms o
f serum progesterone, DHEAS, and testosterone levels to the ACTH stimu
lation test for each 30 min interval was not different in women with P
COS than in healthy controls. We were not able to show any critical va
lue for serum basal testosterone and DHEAS levels that would effect re
sponse to ACTH stimulation in terms of 17-OHP levels. We have conclude
d that extending the duration of blood sampling up to 2h has no advant
age in evaluating adrenal steroid response to ACTH stimulation. Since
serum 17-OHP levels remain within normal limits in response to ACTH st
imulation, the origin of elevated serum basal 17-OHP levels may be pol
ycystic ovaries. Elevated serum testosterone level doer not have any a
dverse effect on adrenal function. Sevum progesterone measurement seem
s to have no place in the diagnosis of 21-hydroxylase deficiency. Adre
nal androgenic response to ACTH stimulation is normal in women with PC
OS.