Treatment of anorchia with oral testosterone undecanoate: pharmacodynamics and clinical effectiveness

Weil, Jordan; Bidlingmaier, F.; Butenandt, O; Sippell, Wolfgang G.; Baumgärtner, Wolfgang; Knorr, D

doi:10.1530/acta.0.0950244

Cited by 16 publications

(9 citation statements)

References 12 publications

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“…We had the opportunity to study such patients and to treat them with long-acting testosterone [ 14], Most of them received 100 mg per month during the first 1-1.5 years, and 250 mg per month thereafter. All grew normally before and after treatment, as observed by others [ 15]. Replace ment caused a normal pubertal growth spurt, and mea surements of body proportion showed no eunuchoid val ues at a prepubertal or pubertal age.…”

supporting

confidence: 77%

Therapeutic Indications for Delayed Puberty and Hypogonadism in Adolescent Boys

Zachmann¹

1991

Horm Res

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Testosterone and synthetic androgens have formerly been used indiscriminately, but are now applied more selectively. They are the only treatment of primary hypogonadism, but are also useful in gonadotropin deficiency and constitutional delay. 17-Alkylated androgens are no longer used. Oral testosterone undecanoate is not suitable for adolescents because of unreliable absorption. The prototype disorder where replacement is necessary is congenital anorchia. As a physiological replacement, an initial dose of 35 mg/m₂ per month for 6 months, followed by 70 mg/m2 for 1 year, and 150 mg/m² thereafter, is recommended. No general rules can be given for other types of primary hypogonadism. In testicular atrophy after cryptorchidism, defects of testosterone biosynthesis, galactosemia or other causes, it is advisable to carry out periodic testosterone determinations and to wait until the levels drop below normal. Progress has been made in the treatment of gonadotropin deficiency, and pulsatile gonadotropin-releasing hormone (GnRH) has been shown to be effective in the hypothalamic type. Nevertheless, androgens still have a temporary place in this condition. In constitutional delay of growth and adolescence, treatment is not necessary somatically, but there are often psychosocial reasons. Gonadotropins, GnRH or growth hormone (GH)- releasing hormone have been used. Also treatment with human GH is successful in accelerating height velocity. The most simple and economic treatment is still testosterone in a physiological dose for 3–6 months. Oxandrolone or other synthetic androgens have no advantages.

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supporting

confidence: 77%

Therapeutic Indications for Delayed Puberty and Hypogonadism in Adolescent Boys

Zachmann¹

1991

Horm Res

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“…These androgen-induced effects on hepatic biochemical function must be distinguished from the hepatotoxicity, which was not observed in this trial nor after up to 6 years of treatment with oral testosterone undecanoate (Gooren, 1986). The lack of gonadotrophin suppression by a fixed dose oral testosterone undecanoate regime (Weil et al, 1980;Skakkebaek et a!., 198l), together with the patients' subjective evaluation of poor androgenic effects, may be a reflection of poor peripheral (i.e. post-hepatic) androgenization achieved by this regime despite the high doses used and prominent androgenic effects on the liver.…”

Section: Discussionmentioning

confidence: 66%

Randomized clinical trial of testosterone replacement therapy in hypogonadal men

et al. 1988

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We have compared the pharmacokinetics and pharmacodynamics of the three commonly used testosterone formulations in a prospective, randomized cross-over clinical trial. Plasma free and total testosterone and their ratio (proportion of unbound testosterone), sex hormone-binding globulin (SHBG), oestradiol, LH and FSH were measured in 15 hypogonadal men (nine hyper- and six hypogonadotrophic) who underwent, in a randomized sequence, three treatment periods each separated by an intervening washout period. The treatments were: (i) intramuscular injection of 250 mg mixed testosterone esters at 2-weekly intervals, (ii) oral testosterone undecanoate 120 mg bd, and (iii) subcutaneous testosterone pellets (6 x 100 mg). Pellet implantation gave the most prolonged effect with free and total testosterone levels being elevated for up to 4 months. This was accompanied by prompt and sustained suppression of plasma LH and FSH, an increase in plasma levels of oestradiol but no change in SHBG levels. In contrast, intramuscular injections induced marked but reproducible week-to-week fluctuations in free and total testosterone, which resulted in a small decrease in plasma SHBG levels, less marked suppression of LH and FSH and a smaller increase in plasma levels of oestradiol. Oral testosterone undecanoate produced the most variable plasma levels of free and total testosterone with a peak in the first treatment week and a fall thereafter and, despite maintenance of testosterone levels within the physiological range, there was no significant suppression of plasma levels of LH and FSH, and oestradiol levels were unchanged but levels of SHBG and total cholesterol were decreased. Free testosterone levels were increased disproportionately during testosterone treatment as the proportion of unbound testosterone was increased by all three treatments. All three testosterone preparations lowered plasma levels of urea and all were without biochemical or haematological toxicity. Reported sexual function was better maintained and side-effects were fewer with parenteral compared with oral treatments. The marked decrease in SHBG and cholesterol levels during oral testosterone undecanoate, when compared with parenteral treatments, occurred despite lesser androgenic effects (suppression of gonadotrophin levels and reported sexual function), which suggests that the liver is exposed to excessive androgenic load via the portal vein during oral treatment with testosterone esters. It is concluded that testosterone pellets give the closest approximation to zero-order (steady-state) delivery conditions for up to 4 months after a single insertion.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…It has been convincingly demonstrated that this preparation is orally active and that it results in biologically meaningful levels of androgen in the bloodstream (Franchimont et al 1978;Weil et al 1980).…”

mentioning

confidence: 98%

Prolactin secretion in the human male is increased by endogenous oestrogens and decreased by exogenous/endogenous androgens

et al. 1984

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There is evidence that prolactin may be involved in testicular steroidogenesis, and we have therefore investigated whether there is feedback regulation of androgens/oestrogens on prolactin secretion in the human male. To assess this we have measured basal and TRH-stimulated prolactin levels in: Six eugonadal men before and after 2 weeks' administration of the aromatase inhibitor delta'-testolactone, which led to a fall in oestradiol levels with unchanged levels of testosterone. In these patients, prolactin levels decreased. Six eugonadal subjects before and after 6 weeks' administration of dihydrotestosterone undecanoate. In these subjects, prolactin levels decreased. Six agonadal subjects, tested after 12 weeks' treatment with dihydrotestosterone undecanoate and compared to: Six agonadal subjects who received no sex steroid treatment. Again, it was found that dihydrotestosterone treatment decreased prolactin levels in patients from Group C. Six eugonadal subjects were also studied before and after 6 weeks' administration of the androgen receptor antagonist, spironolactone, and this treatment increased Prl secretion. It is concluded that in the human male, endogenous oestrogens increase prolactin secretion whilst exogenous/endogenous androgens decrease prolactin secretion.

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Treatment of anorchia with oral testosterone undecanoate: pharmacodynamics and clinical effectiveness

Cited by 16 publications

References 12 publications

Therapeutic Indications for Delayed Puberty and Hypogonadism in Adolescent Boys

Therapeutic Indications for Delayed Puberty and Hypogonadism in Adolescent Boys

Randomized clinical trial of testosterone replacement therapy in hypogonadal men

Prolactin secretion in the human male is increased by endogenous oestrogens and decreased by exogenous/endogenous androgens

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