It is known that
lipoprotein(a) [Lp(a) is an independent risk factor for developing
atherosclerosis, whereas the LpA-I particle of
high density lipoprotein (HDL) is an antiatherogenic factor. The effects of
androgen replacement
therapy on
lipid and
lipoproteins have previously been reported in male
hypogonadism. However, no study reported the effect of
gonadotropin or
testosterone treatment on Lp(a), LpA-I, or LpA-I;A-II levels in make
hypogonadism. We, therefore, determined Lp(a), LpA-I, LpA-I:A-II, and other
lipoprotein levels before and 3 months
after treatment in 22 patients with
idiopathic hypogonadotropic hypogonadism (IHH) and in 9 patients with
Klinefelter's syndrome. All patients had been previously untreated for
androgen deficiency. Plasma FSH, LH, PRL,
testosterone (T),
estradiol, and
dehydroepiandrosterone sulfate levels were also determined before and 3 months
after treatment. Patients with IHH were treated with hCG/
human menopausal gonadotropin, whereas patients with
Klinefelter's syndrome received T treatment. Three months
after treatment, mean T levels role to low normal levels in both groups.
Triglyceride, LpA-I:A-II, Lp(a),
HDL cholesterol,
HDL3 cholesterol, and
apolipoprotein (
apo) A-I concentrations did not change significantly
after treatment, whereas total
cholesterol,
low density lipoprotein cholesterol, LpA-I, and HDL2 concentrations were significantly increased 3 months
after treatment in both groups. The
apo B concentration significantly increased in patients with
klinefelter's syndrome, whereas no change was observed in the IHH group. Lp(a) concentrations were not related to all hormonal and clinical parameters in both groups. LpA-I concentrations were significantly and negatively correlated with free T (r = -0.80; P = 0.010) in patients with
Klinefelter's syndrome and were not correlated with all hormonal and clinical parameters in the IHH group. The LpA-I:A-II concentration was only correlated with body mass index (r = -0.83; P = 0.005) in patients with
Klinefelter's syndrome, whereas it was correlated negatively with
dehydroepiandrosterone sulfate (r = -0.57; P = 0.005) in the IHH group.2 Overall, our study demonstrates that
gonadotropin or T treatment has a complex effect on
lipids and
lipoproteins. This complexity will be resolved when sufficient large scale
androgen treatment data are available for assessment of the long term outcome of
androgen treatment. The increases in total
cholesterol and
low density lipoprotein cholesterol concentrations
after treatments are the adverse effects of these treatments, whereas the increases in HDL2 and LpA-I concentrations and the lack of changes in Lp(a) are the beneficial effects.
Gonadotropin or T treatment did not modify the Lp(a) concentration, indicating that it is not affected by the hormonal milieu in male
hypogonadism. Our study also showed that LpA-I, but not LpA-I:A-II, particles could be modified by
androgen replacement
therapy.