EFFECTS OF GONADOTROPIN AND TESTOSTERONE TREATMENTS ON LIPOPROTEIN(A), HIGH-DENSITY-LIPOPROTEIN PARTICLES, AND OTHER LIPOPROTEIN LEVELS IN MALE HYPOGONADISM

Citation
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
Citations number
70
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
81
Issue
9
Year of publication
1996
Pages
3372 - 3378
Database
ISI
SICI code
0021-972X(1996)81:9<3372:EOGATT>2.0.ZU;2-3
Abstract
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.