EFFECTS OF GONADOTROPIN AND TESTOSTERONE TREATMENTS ON LIPOPROTEIN(A), HIGH-DENSITY-LIPOPROTEIN PARTICLES, AND OTHER LIPOPROTEIN LEVELS IN MALE HYPOGONADISM
M. Ozata et al., EFFECTS OF GONADOTROPIN AND TESTOSTERONE TREATMENTS ON LIPOPROTEIN(A), HIGH-DENSITY-LIPOPROTEIN PARTICLES, AND OTHER LIPOPROTEIN LEVELS IN MALE HYPOGONADISM, The Journal of clinical endocrinology and metabolism, 81(9), 1996, pp. 3372-3378
It is known that lipoprotein(a) [Lp(a)] is an independent risk factor
for developing atherosclerosis, whereas the LpA-I particle of high den
sity lipoprotein (HDL) is an antiatherogenic factor. The effects of an
drogen replacement therapy on lipid and lipoproteins have previously b
een reported in male hypogonadism. However, no study reported the effe
ct of gonadotropin or testosterone treatment on Lp(a), LpA-I, or LpA-I
:A-II levels in male hypogonadism. We, therefore, determined Lp(a), Lp
A-I, LpA-I:A-II, and other lipoprotein levels before and 3 months afte
r treatment in 22 patients with idiopathic hypogonadotropic hypogonadi
sm (IHH) and in 9 patients with Klinefelter's syndrome. All patients h
ad been previously untreated for androgen deficiency. Plasma FSH, LH,
PRL, testosterone (T), estradiol, and dehydroepiandrosterone sulfate l
evels were also determined before and 3 months after treatment. Patien
ts with IHH were treated with hCG/human menopausal gonadotropin, where
as patients with Klinefelter's syndrome received T treatment. Three mo
nths after treatment, mean T levels rose to low normal levels in both
groups. Triglyceride, LpA-I:A-II, Lp(a), HDL cholesterol, HDL(3) chole
sterol, and apolipoprotein (ape) A-I concentrations did not change sig
nificantly after treatment, whereas total cholesterol, low density lip
oprotein cholesterol, LpA-I, and HDL(2) concentrations were significan
tly increased 3 months after treatment in both groups. The apo B conce
ntration significantly increased in patients with Klinefelter's syndro
me, whereas no change was observed in the IHH group. Lp(a) concentrati
ons were not related to all hormonal and clinical param eters in both
groups. LpA-I concentrations were significantly and negatively correla
ted with Gee T (r = -0.80; P = 0.010) in patients with Klinefelter's s
yndrome and were not correlated with all hormonal and clinical paramet
ers in the IHH group. The LBA-I:A-II concentration was only correlated
with body mass index (r = -0.83; P = 0.005) in patients with Klinefel
ter's syndrome, whereas it was correlated negatively with dehydroepian
drosterone sulfate (r = -0.57; P = 0.005) in the IHH group. Overall, o
ur study demonstrates that gonadotropin or T treatment has a complex e
ffect on lipids and lipoproteins. This complexity will be resolved whe
n sufficient large scale androgen treatment data are available for ass
essment of the long term outcome of androgen treatment. The increases
in total cholesterol and low density lipoprotein cholesterol concentra
tions after treatments are the adverse effects of these treatments, wh
ereas the increases in HDL(2) and LpA-I concentrations and the lack of
changes in Lp(a) are the beneficial effects. Gonadotropin or T treatm
ent did not modify the Lp(a) concentration, indicating that it is not
affected by the hormonal milieu in male hypogonadism. Our study also s
howed that LBA-I, but not LpA-I:A-II, particles could be modified by a
ndrogen replacement therapy.