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D Huebler

Publications and source records attributed to D Huebler.

7 recordsLinked to original sources

Testosterone undecanoate maintains spermatogenic suppression induced by cyproterone acetate plus testosterone undecanoate in normal men.

In this study we evaluated whether testosterone undecanoate (TU), alone or combined with low dose cyproterone acetate (CPA), can maintain spermatogenic suppression induced by higher doses of CPA plus TU. Twenty-four men received for 12 wk 20 mg/d CPA plus 1000 mg/6 wk TU and then 1000 mg/8 wk TU plus 20 mg/d CPA (n = 8), 2 mg/d CPA (n = 8), or plus placebo (n = 8) for 32 wk. Blood samples, physical examinations, hormones, chemistry, hematology, semen analysis, and sexual/behavioral assessments were performed throughout the study. Sperm counts decreased to less than 1 million/ml in all subjects by wk 12, and 54% of them achieved azoospermia. Suppression of sperm counts was maintained until wk 44. Serum LH and FSH levels were suppressed by wk 12 of hormone administration and remained suppressed until wk 44. No significant changes in any biochemical parameters were detected at wk 44 in any group. There was a slight increase in total prostate volume to within the normal range at wk 44 that returned to baseline 1 yr after stopping hormone administration. In conclusion, TU alone or combined with lower doses of CPA maintains sperm suppression induced by higher dose CPA plus TU for 32 wk. This prototype regimen represents a promising male contraceptive regimen.

Adult↗

Dehydroepiandrosterone supplementation in healthy men with an age-related decline of dehydroepiandrosterone secretion.

Serum dehydroepiandrosterone declines with age. Whether this represents a harmful deficiency or an age-related adaptation is not known. Dehydroepiandrosterone replacement in adrenal insufficiency, a state of pathological loss of dehydroepiandrosterone production, improves well-being, mood, and sexuality. To determine the effects of dehydroepiandrosterone in healthy men with a physiological, age-related decline in serum dehydroepiandrosterone sulfate, we conducted a double blind cross-over study in 22 healthy male volunteers (age range, 50-69 yr) with endogenous dehydroepiandrosterone sulfate levels below 4.1 micromol/liter (1500 ng/ml) receiving 4 months of dehydroepiandrosterone (50 mg/d) and 4 months of placebo treatment in random order, with a 1-month washout period. Dehydroepiandrosterone treatment increased serum dehydroepiandrosterone and dehydroepiandrosterone sulfate to concentrations usually found in young men. Circulating androgen levels did not change; however, androgen metabolites increased, indicating enhanced peripheral androgen synthesis. At baseline, psychometric assessment revealed normal well-being and sexuality scores. After 4 months of dehydroepiandrosterone, no effect on sexuality was observed, whereas some mood scores improved slightly, but were not significantly different from scores after placebo. Compared with placebo, dehydroepiandrosterone had no effect on serum lipids, bone markers, body composition, or exercise capacity. Thus, in contrast to previous findings in adrenal insufficiency, we found no obvious benefit of 4 months of dehydroepiandrosterone supplementation in healthy men with a physiological decline of dehydroepiandrosterone production.

Affect↗

Dehydroepiandrosterone replacement in women with adrenal insufficiency: effects on body composition, serum leptin, bone turnover, and exercise capacity.

Studies in animals and humans using supraphysiological doses of dehydroepiandrosterone (DHEA) reported significant changes in body composition and carbohydrate metabolism. To investigate the metabolic action of a physiological DHEA replacement dose, we studied 24 women with adrenal insufficiency (AI; mean +/- SD age, 42.3 +/- 9.3 yr; duration of disease, 9.2 +/- 8.4 yr; body mass index, 23.4 +/- 4.0 kg/m(2)) in a double blind, placebo-controlled, randomized, cross-over design. They received 50 mg DHEA/day and placebo orally for 4 months each, with a 1 -month washout period. Measurements included fasting serum glucose, insulin, leptin, bone markers, anthropometric parameters determined by bioimpedance analysis, and exercise capacity as assessed by an incremental cycling test. DHEA did not induce any change in body mass index (placebo vs. DHEA, 23.3 +/- 4.1 vs. 23.2 +/- 3.9 kg/m(2); P = 0.39), parameters of body composition, or exercise capacity. However, compared with placebo, DHEA replacement led to a significant decrease in serum leptin (absolute change after 4 months, DHEA vs. placebo, -5.3 +/- 8.0 vs. 1.1 +/- 5.7 ng/mL; P = 0.01). This is most likely the result of the DHEA-induced normalization of circulating androgens. DHEA had no effect on fasting glucose, insulin, or the glucose/insulin ratio. Compared with placebo, serum osteocalcin increased slightly, but significantly, during DHEA treatment (absolute change after 4 months DHEA vs. placebo, +1.6 +/- 5.3 vs. -1.2 +/- 6.2 ng/mL; P = 0.02). However, urinary cross-links excretion did not change. In conclusion, replacement of DHEA in a physiological dose in patients with pathological DHEA deficiency does not have a significant effect on carbohydrate metabolism, body composition, or exercise capacity. The biological relevance of the changes in leptin and osteocalcin levels remains to be determined.

Adrenal Insufficiency↗

Dehydroepiandrosterone replacement in women with adrenal insufficiency.

BACKGROUND: The physiologic role of dehydroepiandrosterone in humans is still unclear. Adrenal insufficiency leads to a deficiency of dehydroepiandrosterone; we therefore, investigated the effects of dehydroepiandrosterone replacement, in patients with adrenal insufficiency. METHODS: In a double-blind study, 24 women with adrenal insufficiency received in random order 50 mg of dehydroepiandrosterone orally each morning for four months and placebo daily for four months, with a one-month washout period. We measured serum steroid hormones, insulin-like growth factor I, lipids, and sex hormone-binding globulin, and we evaluated well-being and sexuality with the use of validated psychological questionnaires and visual-analogue scales, respectively. The women were assessed before treatment, after one and four months of treatment with dehydroepiandrosterone, after one and four months of placebo, and one month after the end of the second treatment period. RESULTS: Treatment with dehydroepiandrosterone raised the initially low serum concentrations of dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, and testosterone into the normal range; serum concentrations of sex hormone-binding globulin, total cholesterol, and high-density lipoprotein cholesterol decreased significantly. Dehydroepiandrosterone significantly improved overall well-being as well as scores for depression and anxiety. For the global severity index, the mean (+/-SD) change from base line was -0.18+/-0.29 after four months of dehydroepiandrosterone therapy, as compared with 0.03+/-0.29 after four months of placebo (P=0.02). As compared with placebo, dehydroepiandrosterone significantly increased the frequency of sexual thoughts (P=0.006), sexual interest (P=0.002), and satisfaction with both mental and physical aspects of sexuality (P=0.009 and P=0.02, respectively). CONCLUSIONS: Dehydroepiandrosterone improves well-being and sexuality in women with adrenal insufficiency.

Adrenal Insufficiency↗

Pharmacokinetics of ethynyl estradiolsulfonate in minipigs.

The pharmacokinetics of ethynyl estradiolsulfonate labelled with 3H in the steroid nucleus and with 14C in the isopropylsulfonic acid side chain was investigated in male minipigs. The plasma level after intravenous administration was interpreted according to a three-compartment model. After oral administration the first two phases were overlapped by the absorption period. The renal and fecal excretion of the two labellings were investigated. In urine the majority of the 3H-labelled steroid was excreted in the unconjugated and in the glucuronide fractions. More than 70% of 14C in urine was unextractable.

Administration, Oral↗