Carcinoma of prostate: response of plasma luteinizing hormone and testosterone to oestrogen therapy.

Alder, A; Burger, Henry G.; Davis, Jennifer; Dulmanis, Ausma; Hudson, Bryan; Sarfaty, Gordon; Straffon, W.G.E.

doi:10.1136/bmj.1.5583.28

Cited by 73 publications

(32 citation statements)

References 9 publications

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“…(24,25) established the efficacy of estrogen therapy in androgen-dependent prostatic cancer. Although it has been shown that estrogen depresses blood testosterone levels (26), estrogen also is a potent stimulator of pituitary PRL release (27,28). Since PRL appears to increase the affinity of the prostate for testosterone (22), it is possible that prostatic tissue exposed to high circulating prolactin can more effectively concentrate the lower serum levels of androgen.…”

Section: Discussionmentioning

confidence: 99%

Effects of Castration, Testosterone, Estradiol, and Prolactin on Specific Prolactin-Binding Activity in Ventral Prostate of Male Rats

et al. 1976

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Lactoperoxidase-catalyzed 125I-labeled ovine prolactin (PRL) was found to bind specifically to particulate membrane fractions of rat ventral prostate. Unlabeled PRL readily displaced the labeled PRL, whereas ovine GH, LH, FSH, or TSH showed no such competition. Castration reduced the binding of 125I-labeled PRL to about 1/6 of that in intact rats, and injections of testosterone propionate (TP) increased PRL binding to values as great or greater than those in intact controls. Injections of TP into intact immature and mature rats also increased PRL binding. In vitro binding of labeled PRL was inhibited in prostatic tissue removed from intact immature rats 2 h after injecting unlabeled PRL, but not in ventral prostates from rats killed 26 or 74 h after injecting unlabeled prolactin. PRL injected together with TP in castrated rats produced no greater increase in prolactin binding than TP alone, while estrogen appeared to decrease PRL binding beyond that produced by castration alone.

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Section: Discussionmentioning

confidence: 99%

Effects of Castration, Testosterone, Estradiol, and Prolactin on Specific Prolactin-Binding Activity in Ventral Prostate of Male Rats

et al. 1976

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“…Testicular atrophy and low scrum concentrations of testosterone are consequences of estrogen treatment in patients with prostatic carcinoma [11]. Since there is a concomitant reduction of both LH and FSH, it has been suggested that the testosterone decrease is secondary to estrogen effects upon the hypothalamus-pituitary axis [3], Jones at al. [12], who administered 2 mg of estrogen i.m.…”

Section: Discussionmentioning

confidence: 99%

“…Estrogen therapy and orchidectomy are accepted methods for the treatment of patients with prostatic car cinoma [1], Both methods reduce serum testosterone concentrations to similar levels [2], To suppress serum testosterone levels in patients treated with estrogen, a high dose of estrogen is required [2], It is generally believed that the reduction in testosterone concentration is a result of a direct estrogen action at the hypothala mus-pituitary level [3]. It has also been suggested that estrogen has a direct effect upon the testis [4], Recently, it was reported that testosterone concentration may re main low after cessation of previous long-term estrogen therapy but not after short-term therapy [5].…”

Section: Introductionmentioning

confidence: 99%

Effect of Orchidectomy Performed after Cessation of Estrogen Therapy on Serum Testosterone Concentrations in Patients with Prostatic Carcinoma

Tomić¹,

Damber²

1987

Urol Int

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Serum concentrations of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were determined before and after orchidectomy performed at different intervals (2–29 months) after withdrawal of estrogen therapy in patients with prostatic carcinoma. Patients previously treated with estrogen for more than 3 years had low testosterone concentrations after estrogen withdrawal and the values were not significantly changed by orchidectomy. In contrast, in patients treated with estrogen for less than 3 years, the testosterone concentrations were below or within the normal values after estrogen cessation and following orchidectomy, the values were significantly decreased. In both groups of patients the LH and FSH values were within or above the normal range both before and after orchidectomy, but FSH was significantly lower in patients previously treated with estrogen for more than 3 years. In conclusion, orchidectomy performed after cessation of long-term estrogen therapy in patients with prostatic carcinoma is without value, since testosterone levels do not change despite cessation of estrogen treatment or after orchidectomy.

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“…As some up-to-date studies have shown, the prostatic gland seems to constitute not only the testosterone-related tissues but also to have prolactin receptors which play an important role in the pathogen esis of prostatic cancer. The synthesis of androgens depends not only on the gonadotropic hormones (lutein izing hormone and follicle-stimulating hormone), but also on prolactin which, moreover, speeds up the accu mulation of testosterone by prostatic cells [1,2,16,20], The harmful properties of prolactin as well as its high blood serum levels found in prostatic cancer patients treated with estrogens in 1978 led Jeromin to introduce in Poland a new drug into the treatment of carcinoma of the prostate, namely an antagonist of prolactin, bromo criptine (Parlodel, Sandoz) [3,8,14,17,18].…”

mentioning

confidence: 99%

Clinical Follow-Up of Prostatic Cancer Patients under Intermittent Treatment with Fosfestrol and Bromocriptine

Jeromin¹

1988

Urol Int

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A clinical follow-up is presented of 152 patients with newly diagnosed prostatic cancer, confirmed histopathologically and intermittently treated with Fosfestrol and bromocriptine in the last few years. The optimal dosage of Fosfestrol and bromocriptine was established on the basis of serum testosterone and prolactin levels. The reduction of Fosfestrol dosage combined with bromocriptine and the intermittent administration of estrogens resulted in a prolongation of the period of sensitivity to female hormones, in a better tolerance for the drugs, and in a reduced number of side effects.

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Carcinoma of prostate: response of plasma luteinizing hormone and testosterone to oestrogen therapy.

Cited by 73 publications

References 9 publications

Effects of Castration, Testosterone, Estradiol, and Prolactin on Specific Prolactin-Binding Activity in Ventral Prostate of Male Rats

Effects of Castration, Testosterone, Estradiol, and Prolactin on Specific Prolactin-Binding Activity in Ventral Prostate of Male Rats

Effect of Orchidectomy Performed after Cessation of Estrogen Therapy on Serum Testosterone Concentrations in Patients with Prostatic Carcinoma

Clinical Follow-Up of Prostatic Cancer Patients under Intermittent Treatment with Fosfestrol and Bromocriptine

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