OBJECTIVE Acne is one of the most common skin disorders. Androgens are
known to play an important and possibly central role. Androgens secre
ted from ovaries and adrenal glands (androstenedione, dehydroepiandros
terone and its sulphate, testosterone) and target tissue-produced andr
ogens (testosterone and its 5alpha-reduced metabolite, dihydrotestoste
rone) have been implicated. Although the sebaceous gland and the hair
follicle form a single morphological entity, the pilosebaceous unit, a
cne and hirsutism do not always appear concomitantly, thus leading to
the supposition that these two structures may have different degrees o
f sensitivity to similar androgenic stimulation. DESIGN AND PATIENTs T
o determine whether acne and hirsutism are the clinical expression of
a different androgen metabolism at target tissue levels we studied 90
randomly selected patients who came to our Out-patient Department for
diagnosis and treatment during the last 2 years with isolated acne of
mild to severe degree and 52 patients with idiopathic hirsutism withou
t acne or history of acne. Twenty-four women without acne or hirsutism
and without a history of endocrine disease were studied as controls.
MEASUREMENTS in both groups of patients, plasma levels of sex hormone
binding globulin, of dihydrotestosterone, and of 3alpha-androstanediol
and of its glucuronide were evaluated. In all patients the percentage
of free testosterone and the testosterone/sex hormone binding globuli
n ratio were also calculated. RESULTS Patients with acne and those wit
h isolated hirsutism showed significantly decreased sex hormone bindin
g globulin plasma levels. The values of the percentage free testostero
ne and those of the testosterone/sex hormone binding globulin ratio we
re, on the contrary, higher with respect to the controls, although the
re were no statistically significant differences between the two group
s. Significantly increased plasma levels of dihydrotestosterone with r
espect to the controls were observed in patients with acne or in those
with hirsutism. However, while all patients with hirsutism showed inc
reased plasma values of 3alpha-androstanediol and its glucuronide, all
patients with acne showed plasma levels within the normal range, inde
pendently of the precursor plasma levels. CONCLUSIONS Our results demo
nstrate that dihydrotestosterone is further reduced to 3alpha-androsta
nediol and its glucuronide only in hirsute patients but not in acne pa
tients. These results suggest that dihydrotestosterone may undergo dif
ferent metabolic pathways at skin levels and support the hypothesis th
at the two clinical manifestations may be the expression of the differ
ent metabolic fate of dihydrotesterone itself. Moreover, our results d
emonstrate that 3alpha-androstanediol and its glucuronide cannot be us
ed as plasma markers of target-tissue produced androgens in all hypera
ndrogenic conditions.