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Title: Effect of testosterone enanthate on serum lipoproteins in man.
Author: Anderson RA, Wallace EM, Wu FC.
Journal: Contraception; 1995 Aug; 52(2):115-9. PubMed ID: 8536448.
Abstract:
Sixty-three normal Caucasian men were administered intramuscular testosterone enanthate (TE) 200 mg i.m. weekly for 12 months as part of a male contraceptive trial. This dose of TE caused a 2.5-fold increase in trough serum testosterone concentrations. High density lipoprotein cholesterol (HDL-C) was significantly depressed from pretreatment concentration of 1.19 +/- 0.04 nmol/l to 1.03 +/- 0.04 mmol/l after 12 weeks of treatment, and remained suppressed for the duration of treatment (p < 0.001). There were no changes in serum concentration of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) or triglycerides (TG) during treatment, but the concentrations of TC and LDL-C were depressed at three months post-treatment. There was a sustained elevation in LDL-C:HDL-C ratio during TE treatment (p < 0.005), from 3.41 +/- 0.15 pretreatment to 3.88 +/- 0.19 after 12 weeks of TE treatment. Sex hormone binding globulin (SHBG), but not testosterone (T) or estradiol (E2), was significantly associated with HDL-C (r = 0.83, p = 0.001). Lipoprotein (a) (Lp(a)) was measured in a subgroup of 33 men: serum concentration fell from 187 +/- 45 mg/l pretreatment to 140 +/- 35 mg/l after 16 weeks of TE treatment (p < 0.01). 63 normal, healthy Caucasian men 21-42 years old were administered intramuscular testosterone enanthate (TE) 200 mg weekly for 12 months to suppress spermatogenesis for up to 18 months as part of a World Health Organization male contraceptive trial. TE administration caused a sustained increase in serum T concentrations (p 0.001), from 21.9 nmol/l pretreatment to 50.6 nmol/l after 12 weeks. Following cessation of treatment, serum T concentration returned to pretreatment concentrations. Serum estradiol (E2) reached a peak concentration of 163.1 pmol/l at 48 weeks from a pretreatment concentration of 84.2 pmol/l (p 0.001), returning to pretreatment concentrations following cessation of TE treatment. Conversely, sex hormone binding globulin (SHBG) was significantly depressed during treatment (p 0.001), achieving a nadir of 14.8 nmol/l at 36 weeks, but returning to pretreatment concentration (26.0 nmol/l) by the first month. High density lipoprotein cholesterol (HDL-C) was significantly depressed during TE treatment (p 0.001), falling from 1.19 mmol/l pretreatment to 1.03 mmol/l at 12 weeks. This fall was sustained for the duration of treatment. Posttreatment, a significant overcompensation of HDL-C occurred at both 12 and 24 weeks (p 0.01 vs. pretreatment in both cases). There were parallel changes in the low density lipoprotein cholesterol/LDL-C:HDL-C ratio during treatment, with a significant rise (p 0.005) from 3.41 pretreatment to 3.88 after 12 weeks of treatment. There were statistically significant falls in TC and LDL at 12 weeks posttreatment (p 0.05 in both cases vs. pretreatment). Multivariate regression analysis of the hormone and lipid data revealed a significant association between HDL-C and SHBG (p = 0.001), but no significant association between HDL-C and T or E2 once SHBG had been controlled for. In a subgroup of 33 men lipoprotein a (Lp(a)) serum concentration fell from 187 mg/l pretreatment to 140 mg/l after 16 weeks of TE treatment (p 0.001). Lp(a) concentration declined to a similar extent in a group of 8 men from 578 to 416 mg/l; by 28% compared to the whole group (25%), (p 0.005).

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