Endocrine effects of oestrogen withdrawal in long-term treated patients with prostatic adenocarcinoma

Eighteen patients with prostatic adenocarcinoma, treated with oestrogen for 45 months or more, were followed-up after withdrawal of oestrogen treatment. Serum concentrations of testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), oestradiol-17 beta, testosterone-oestradiol-binding globulin (TeBg) and prolactin were measured at different intervals between 3 and 42 months after cessation of treatment. Serum testosterone concentrations after cessation of oestrogen treatment were low (range 71.4 +/- 6.3 to 120.8 +/- 23.7 nmol/100ml), whereas the concentrations of LH (range 21.8 +/- 3.6 to 32.6 +/- 9.1 U/1) and FSH (range 31.2 +/- 5.5 to 54.7 +/- 9.5 U/1) were within or higher than the reference range. Prolactin (range 6.0 +/- 85.3 to 7.9 +/- 68.2 micrograms/1) was within the reference range. No significant changes in serum concentrations of testosterone, LH, FSH and prolactin occurred during the follow-up period. The serum concentrations of both oestradiol-17 beta and TeBg, found between 13 and 36 months after oestrogen cessation (range 43.8 +/- 4.6 to 46.2 +/- 5.9 and 64.0 +/- 2.5 to 86.0 +/- 10.0, respectively) were significantly lower than the concentrations found between 3 and 12 months (range 71.9 +/- 10.4 to 99.8 +/- 12.9 and 124.1 +/- 15.5 to 140.2 +/- 13.7, respectively). It is concluded that in patients with prostatic adenocarcinoma, long-term oestrogen treatment causes an irreversible impairment of Leydig cell function and consequently a reduced testosterone secretion after cessation of oestrogen treatment.     

Effect of adrenal steroids on testosterone and luteinizing hormone secretion in the ram

The effects of adrenal steroids on testosterone and LH secretion and changes in serum cortisol levels in response to treatments were studied in the ram. Acute administration of synthetic ACTH (10 micrograms/kg BW) elevated (P less than 0.01) serum cortisol and transiently suppressed (P less than 0.05) serum testosterone and LH. Acute dexamethasone treatment suppressed (P less than 0.01) serum cortisol, testosterone and LH. Administration of vehicle had no effect (P greater than 0.10) on serum hormone levels. These data support the contention that adrenal steroids inhibit testicular endocrine function indirectly by acting at the hypothalamic or pituitary level because both ACTH and dexamethasone treatments suppressed serum LH. To differentiate between hypothalamic and pituitary sites of action, the pituitary and testicular responses to an LHRH challenge (100 micrograms) were examined in rams chronically treated with dexamethasone (5 mg i.m., twice daily for 5 days). This treatment regimen suppressed (P less than 0.01) serum cortisol levels. Compared with controls, basal testosterone levels were suppressed (P less than 0.05) in dexamethasone-treated rams; however, no effect (P greater than 0.10) on the magnitude of the testosterone response to LHRH or on either basal or LHRH-stimulated LH secretion was observed. Thus, although a direct testicular effect cannot be eliminated, these data suggest that, in the ram, adrenal steroids inhibit testicular endocrine function by action at the level of the hypothalamus.     

Prolactinoma with a high adrenocorticotropic hormone level caused by meningitis--case report

A 69-year-old man was admitted semicomatose with high-grade fever and meningeal signs. Magnetic resonance imaging showed a supra- and intrasellar lesion. Hormone studies on admission showed increased serum prolactin, adrenocorticotropic hormone (ACTH), and cortisol titers. However, the serum ACTH and cortisol levels returned to normal after treatment of meningitis with an antimicrobial agent. The histological diagnosis was pituitary adenoma. Immunohistological staining showed positive reaction for prolactin but not for ACTH. This is a rare case of prolactinoma with a high serum ACTH level caused by meningitis.     

Some effects of treatment with ethinyl oestradiol with or without polyoestradiol phosphate in patients with prostatic carcinoma

Eleven patients with prostatic carcinoma were treated with ethinyl oestradiol (Etivex) 50 micrograms three times daily with and 10 patients without 80 mg polyoestradiol phosphate (Estradurin) monthly. Both forms of treatment produced a significant decrease in the serum testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) and a significant increase in the testosterone-oestradiol-binding globuline (TeBg). Serum prolactin was significantly higher at 1, 3 and 6 months after treatment, in all patients studied, but the concentrations found at 12 and 18 months did not differ from those before treatment. One out of 10 patients treated with ethinyl oestradiol had congestive heart failure. Five out of 11 patients treated with ethinyl oestradiol-polyoestradiol phosphate had cardiovascular or liver complications. Three of the 5 had thromboembolic complications. It is concluded that ethinyl oestradiol given in combination with polyoestradiol phosphate, was not superior in decreasing serum testosterone when compared to ethinyl oestradiol given alone. Furthermore, the oestrogens used, elevated prolactin only, during the first 6 months of treatment. There were fewer complications using ethinyl oestradiol alone than when using ethinyl oestradiol combined with polyoestradiol phosphate.     

Anterior and posterior pituitary function in brain-stem-dead donors. A possible role for hormonal replacement therapy

Blood samples were obtained, at the time of organ donation, from 31 consecutive brain-stem-dead (BSD) donors referred to one transplant coordinator during a 9-month period. Twenty-four cases (77%) had clinical diabetes insipidus (DI), which was poorly controlled with marked dehydration in a majority of cases (serum osmolality range 268-357; median 302 mOSM/kg). Serum triiodothyronine (T3) was subnormal in 25 (81%); all had normal or high serum reverse T3; and the serum free thyroxine (T4) index was subnormal in 9 (29%), and TSH was subnormal in 7 (23%). In no case were T4 and TSH both subnormal and results were typical of the sick euthyroid syndrome rather than TSH deficiency. Of 21 cases not receiving corticosteroids, 5 (24%) had a serum cortisol above 550 nmol/L (20 micrograms/dl), excluding ACTH deficiency, and only 1 had undetectable cortisol levels. Those with severe hypotension did not have significantly lower serum cortisol (mean 354 vs. 416; P greater than 0.5). Levels of prolactin, growth hormone, gonadotrophins, and gonadal steroids were variable, but only a minority were frankly deficient in these hormones. BSD donors frequently have DI, which is often managed poorly by nonspecialists and requires appropriate replacement therapy. In contrast most patients are not totally deficient in anterior pituitary hormones. Routine hormonal therapy with cortisol and T3 cannot, therefore, be justified on endocrinological grounds. Widespread introduction of such treatment should only follow controlled trials that clearly demonstrate clinically significant improvement in the transplanted organ function, without detriment to the donor.     

The effect of the chronic administration of a potent luteinizing hormone releasing hormone analog on the rat prostate

In order to assess the effect of the chronic administration of a potent luteinizing hormone releasing hormone analog, (D-SER(But)6) LHRH (1-9) nonapeptide-ethylamide (Buserelin, HOE 766) on the pituitary gonadal axis, and the prostate, adult male Wistar rats were administered either 0, 3, 10 or 50 micrograms./kg. body weight Buserelin subcutaneously daily. At 7, 21, 35 and 42 days of treatment, groups of animals were sacrificed and certain serum endocrine and grave metric parameters determined. In addition, at 1, 21 and 42 days of treatment the 1-hour response of serum LH and serum testosterone to a single injection of 10 micrograms./kg. body weight Buserelin was determined. All treatment doses had similar effects. Serum prolactin and the basal and "acute" response of serum LH to Buserelin (+ delta 5,000 per cent) were unaltered throughout treatment. Testes weight, testicular LH receptor content, and basal and "acute" concentrations of serum testosterone were markedly decreased by 42 days of treatment (48, 89, 88 and 88 per cent, respectively). Although seminal vesicle weight declined 50 per cent at 42 days of treatment, prostate weight was not altered from initial weight, but was significantly lower than age matched control at 42 days of treatment. Buserelin remains a potent stimulator of pituitary LH release even during chronic administration. It markedly reduces serum testosterone through a predominant testicular site of action. Buserelin treatment inhibits the growth of the normal prostate, but does not cause its regression.     

Heavy Resistance Training and Supplementation With the Alleged Testosterone Booster Nmda has No Effect on Body Composition,Muscle Performance,and Serum Hormones Associated With the Hypothalamo-Pituitary-Gonadal Axis in Resistance-Trained Males

The effects of 28 days of heavy resistance training while ingesting the alleged testosterone-boosting supplement, NMDA, were determined on body composition, muscle strength, serum cortisol, prolactin, and hormones associated with the hypothalamo-pituitary- gonadal (HPG) axis. Twenty resistance-trained males engaged in 28 days of resistance training 4 times/wk while orally ingesting daily either 1.78 g of placebo (PLAC) or NMDA. Data were analyzed with separate 2 x 2 ANOVA (p < 0.05). Criterion measures involved body composition, muscle strength, serum cortisol, prolactin, and gonadal hormone levels [free and total testosterone, luteininzing hormome (LH), gonadotrophin releasing hormone (GnRH), estradiol], and were assessed before (Day 0) and after (Day 29) resistance training and supplementation. No changes were noted for total body water and fat mass in response to resistance training (p > 0.05) or supplementation (p > 0.05). In regard to total body mass and fat-free mass, however, each was significantly increased in both groups in response to resistance training (p < 0.05), but were not affected by supplementation (p > 0.05). In both groups, lower-body muscle strength was significantly increased in response to resistance training (p < 0.05); however, supplementation had no effect (p > 0.05). All serum hormones (total and free testosterone, LH, GnRH, estradiol, cortisol, prolactin) were unaffected by resistance training (p > 0.05) or supplementation (p > 0.05). The gonadal hormones and cortisol and prolactin were unaffected by 28 days of NMDA supplementation and not associated with the observed increases in muscle strength and mass. At the dose provided, NMDA had no effect on HPG axis activity or ergogenic effects in skeletal muscle.

Key Points

• In response to 28 days of heavy resistance training and NMDA supplementation, similar increases in muscle mass and strength in both groups occurred; however, the increases were not different between supplement groups.
• The supplementation of NMDA had no preferential effect on augmenting testosterone or decreasing estrogen, cortisol, and prolactin.
• While resistance training was effective in increasing muscle mass and strength, it was not preferentially due to NMDA supplementation.
• At the dose provided, NMDA supplementation for 28 days combined with resistance training does not increases muscle mass and strength due to its ability to elevate endogenous testosterone levels and lower cortisol and prolactin when compared to placebo.

Key Words: D-Aspartic Acid, N-Methyl-D-Aspartic Acid, testosterone, resistance training     

Secretion of testicular steroids and gonadotrophins in hypothyroidism

Inconsistent alterations in gonadal steroidogenesis and pituitary functions have been reported in hypothyroid males. We have compared the lipid and endocrine profiles of the euthyroid and hypothyroid [thyroid-stimulating hormone (TSH) >100 mIU l(-1)] males. Hypothyroidism was found to be associated with an increase in the circulating level of total cholesterol and LDL-cholesterol (LDL-C) and a reduction in the levels of progesterone and testosterone, without any change in the serum levels of oestradiol and gonadotrophins. The failure of gonadotrophins to rise could be accounted by a normal level of serum oestradiol in the hypothyroid male. A mild hyperprolactinaemia was also noted in the hypothyroid patients. The reduction in serum testosterone level could be explained by (i) a reduced uptake of LDL-C by the Leydig cells and thereby a reduction in the synthesis of progesterone and consequentially testosterone, (ii) a further reduction in the rate of conversion of progesterone to testosterone, (iii) a higher rate of conversion of testosterone to oestradiol, (iv) a decrease in serum triiodothyronine and (v) hyperprolactinaemia. Rise in TSH needs to be investigated as a cause of the suppression of gonadal steroidogenesis.     

Routine hormone load tests are unnecessary in infertile men

A sample of 225 men examined at the Infertility Service Unit of this hospital had spermiograms, standardized in accordance with WHO guide lines, and a hormone stimulation test with injection of gonadotropin releasing hormone, thyrotropin releasing hormone, and ACTH. The serum concentrations of the following hormones were assessed: follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin, oestradiol (E), thyroid stimulating hormone, cortisol, 21-desoxycortisol, 17-hydroxypregnenolone, 17-hydroxyprogesterone, dehydroepiandrosterone, dehydroepiandrosteronesulphate, androstenedione, testosterone (T), and dihydrotestosterone. The results of the spermiograms were found to be related to the concentrations of the following hormones: FSH, LH, T, and E. Thyroid and adrenal function in men without signs of endocrinological diseases failed to influence spermatic parameters.     

Diet, absorption, and hormone studies in relation to body weight in obstructive airways disease.

Sixteen male patients with stable chronic obstructive airways disease were separated into two groups of eight according to arterial carbon dioxide tensions. Hypercapnia was associated with lower arterial oxygen tensions, higher red cell volume, and increased weight, while normocapnic subjects were decidedly thin. The considerable difference in body weight between the two groups could not be explained by variation in caloric intake, and malabsorption was excluded as a cause of weight loss in the underweight subjects. Serum tri-iodothyronine, thyroxine, cortisol, and oestradiol concentrations were similar and normal in each group, but both groups had significantly low testosterone values as compared with controls, values in the hypercapnic being appreciably lower than in the normocapnic group. The adrenal androgen dehydroepiandrosterone was significantly high in the normocapnic group and low in the hypercapnic group compared with controls. Serum pituitary luteinising and follicle stimulating hormones were normal, but three hypercapnic individuals had high serum prolactin values. Early morning urinary aldosterone values were significantly higher in the hypercapnic than in the normocapnic group. Such hormone comparisons have not previously been made in subjects with chronic obstructive airways disease grouped according to arterial blood gas values, and it is concluded that major alterations in adrenal and testicular function may occur, possibly due to pituitary suppression from hypoxia. Such hormonal changes might in part account for the contrasting alterations in body habitus found in this condition.     

Pituitary functions in the acute phase of traumatic brain injury: are they related to severity of the injury or mortality?

Primary objective: There are only limited data regarding pituitary functions in the acute phase of traumatic brain injury (TBI) and previous studies have been conducted in only small cohorts of subjects. Therefore we have investigated the pituitary functions in the early acute phase, within 24 hours of trauma, in 104 patients with TBI. Additionally, the relationships between basal pituitary hormones, severity of the trauma and mortality due to trauma were also investigated.

Methods and procedures: One hundred and four TBI patients were included in the study consecutively. All patients underwent basal hormonal evaluation within the first 24 hours of admission. Twenty of 104 patients died during the acute phase.

Main outcomes: Prolactin levels were negatively correlated with the Glasgow coma scale (GCS), cortisol levels were positively correlated with the GCS and cortisol levels were positively correlated with ACTH levels. Additionally there was a significant positive correlation between the total testosterone levels and the GCS in males. Logistic regression analysis revealed that mortality after TBI was unrelated to basal pituitary hormone levels. However age and GCS were significantly related to the mortality. The percentages of pituitary hormone deficiencies were as follows: 3.8% had TSH deficiency, 40.0% had gonadotrophin deficiency, 8.8% had ACTH deficiency and 20.0% had GH deficiency.

Conclusions: Present data clearly demonstrate that pituitary function is disturbed in TBI and the most frequently deficient pituitary hormones were gonadotrophins in the early acute phase of TBI. Basal hormone levels including cortisol, prolactin and total testosterone were related to the severity of the trauma. However there was no relation between basal hormones and mortality due to TBI. Age and GCS were significantly related to mortality.     

Serum hormone levels in men with end stage renal disease

Serum concentrations of testicular and adrenal androgens and androgen precursors, cortisol, unconjugated (E1) and total estrone (tE1; greater than or equal to 85% E1 sulfate), pituitary hormones, sex hormone binding globulin (SHBG) and albumin were measured in 14 male patients with non-diabetic end stage renal disease and in 28 age-matched healthy controls. The serum levels of the adrenal androgens 4-androstene 3,17-dione and dehydroepiandrosterone (DHA) were significantly lower and the levels of cortisol, LH, prolactin and tE1 significantly higher in the patients than in the controls. The ratios between E1 and tE1 and between DHA and DHA sulfate were strongly decreased in the patients. The findings are suggested to reflect different effects of the disease upon the metabolism of cortisol and of adrenal androgens and also the reduced or even absent urinary excretion, leading to a decreased metabolism of steroid conjugates.     

Effect of high-dose medroxyprogesterone acetate on plasma hormone levels and pain relief in patients with advanced prostatic cancer.

High-dose medroxyprogesterone acetate (MPA) was given orally to 7 patients with advanced prostatic cancer and severe pain due to bone metastases; 5 patients had stable and 2 had progressive disease. Pain relief was obtained in 6 patients. Two patients who reported complete relief of pain showed suppressed levels of gonadotrophins after MPA treatment. In the other patients, suppression of plasma gonadotrophin levels was observed before treatment. The plasma levels of prolactin, growth hormone and thyroid stimulating hormone were not affected by MPA. Only 1 patient showed suppression of plasma adrenocortical trophic hormone. The plasma levels of cortisol and dihydroepiandrosterone sulphate were suppressed in 6 patients, but there was no correlation between the suppression and the occurrence of pain relief. These findings suggest that the mechanism of pain relief by high-dose MPA may be very complicated.     

Change of serum adrenal androgens in prostatic cancer patients after bilateral orchidectomy or LHRH agonist treatment

Bilateral orchidectomy (ORX) or administration of luteinizing hormone releasing hormone agonist (LHRH) for prostatic cancer patients causes suppression of testicular androgens. However, the suppression of adrenal androgens by these treatments is controversial. We measured serum concentrations of testosterone (T), 4-androstene-3, 17-dione (A-dione), dehydroepiandrosterone (DHEA), LH, follicle-stimulating hormone (FSH), adrenocorticotropic hormone (ACTH) and cortisol before and after 3-12 months of the first hormonal treatment in 17 prostatic cancer patients who had received ORX (8 cases) or LHRH (9 cases). ORX and LHRH decreased serum T to the castration level significantly (ORX: p < 0.001, LHRH: p < 0.0001). ORX increased serum LH and FSH significantly (LH: p < 0.001, FSH: p < 0.001), whereas LHRH decreased LH and FSH significantly (LH: p < 0.05, FSH: p < 0.05). Neither treatment caused any significant change in ACTH or cortisol. ORX and LHRH decreased the serum A-dione significantly (ORX: p < 0.01, LHRH: p < 0.001). LHRH decreased the serum DHEA significantly (p < 0.01), whereas ORX did not decrease serum DHEA. These data suggest that "medical" and "surgical" castration, especially LHRH agonist, may decrease not only testicular androgens but also adrenal androgens.     

Testicular endocrine function after withdrawal of oestrogen treatment in patients with carcinoma of the prostate

The serum concentration of testosterone, luteinising hormone (LH), follicle stimulating hormone (FSH) and prolactin were determined at different intervals after withdrawal of oestrogen treatment in patients with prostatic carcinoma. Oestrogen therapy had been stopped in all patients because of the side effects of oestrogens. There was a negative correlation (r = -0.64) between serum testosterone concentrations and the duration of oestrogen treatment in patients investigated for more than 6 months after withdrawal of hormones. However, the decrease in testosterone concentration seems to be time-dependent. Thus patients who were treated for less than 3 years had normal testosterone concentrations approximately 6 months after withdrawal of the oestrogen therapy. This group of patients had a positive correlation (r = 0.49) between serum testosterone concentration and time elapsed after cessation of therapy. In contrast, patients treated for more than 3 years retained low testosterone concentrations even after 6 months. The other hormones did not vary between the groups. It is concluded that patients with carcinoma of the prostate treated with oestrogens for more than 3 years have an impaired Leydig cell function which might be irreversible.     

Gonadal function in patients with testicular germ cell tumors

The gonadal function of 18 patients with testicular germ cell tumors was evaluated. Seminal parameters after orchiectomy were examined in 15 patients. Six of them were available for follow-up observation after 2 or 3 courses of adjuvant chemotherapy. Serum gonadal hormones before and after orchiectomy were evaluated in 7 patients (testosterone and PRL were not examined in one patient). Five of 15 (33.3%), 8 of 15 (53.3%), 13 of 15 (86.7%), 7 of 13 (53.8%), and 9 of 12 (75.0%) had abnormal values in seminal volume, sperm concentration, motility, morphology, and vitality, respectively. The sperm concentration gradually improved after chemotherapy following orchiectomy in 5 of 6 (83.3%) patients. In all the patients examined, serum levels of follicular stimulating hormone (FSH), luteinizing hormone (LH), and prolactin (PRL) increased after orchiectomy. Serum levels of testosterone increased in 4 patients, but decreased in 2 after orchiectomy. These findings suggest that several factors, including preexisting intrinsic defect and disturbance of the hypothalamus-pituitary-gonadal axis, are involved in the deterioration of gonadal function in patients with testicular germ cell tumors.     

Hypoandrogenaemia is associated with subclinical hypothyroidism in men

Hypothyroidism has been shown to be associated with a reduction in serum testosterone level in males. This reduction in testosterone is reversible by thyroxine replacement therapy. However, to the best of our knowledge, it is not yet known, whether a similar reduction in serum testosterone level is observed in subclinically hypothyroid males [thyroid-stimulating hormone (TSH) < 10 mIU/L] in whom the benefits of thyroxine replacement therapy are still controversial. Our goal was to investigate the putative connections between subclinical hypothyroidism and the circulating levels of gonadotrophins and gonadal steroids in males (mean age +/- SEM, 34.67 +/- 1.52 years; ranging from 20 to 54 years). The serum samples from patients showing normal euthyroid and subclinical hypothyroid profiles (TSH < 10 mIU/L) were further analysed for the levels of luteinizing hormone, follicle-stimulating hormone, prolactin, testosterone, sex hormone-binding globulin, progesterone and oestradiol. Subclinical hypothyroidism was associated with a decrease in the levels of serum testosterone and its precursor progesterone. The data suggest that serum testosterone declines because of the non-availability of its precursor progesterone. The level of oestradiol was similar in both the groups, suggesting a greater conversion rate of testosterone to oestradiol in subclinically hypothyroid males, in order to maintain the oestradiol levels. Prolactin levels were slightly but significantly increased in subclinical hypothyroidism. To the best of our information this is a novel report, which shows a direct association between subclinical hypothyroidism and hypoandrogenaemia. Testosterone deficiency and its symptoms should be kept in view while managing subclinical hypothyroidism in male patients. Further studies are needed in order to reveal the physiological and molecular mechanisms leading to hypoandrogenaemia in subclinical hypothyroidism (TSH < 10 mIU/L).     

Anterior pituitary dysfunction in patients with chronic renal failure treated by hemodialysis or continuous ambulatory peritoneal dialysis

Cortisol, prolactin, and growth hormone responses to insulin-induced hypoglycemia were measured in 20 patients undergoing continuous ambulatory peritoneal dialysis or intermittent hemodialysis. The plasma cortisol responses were normal; however, the increments in serum prolactin and growth hormone concentrations were impaired in most patients. The growth hormone responses were lower (p less than 0.05) in those patients treated by continuous ambulatory peritoneal dialysis, but there were no other significant differences between the two patient groups. These results show that anterior pituitary dysfunction persists in some patients with chronic renal failure despite maintenance dialysis therapy.     

Changes in serum levels of LH, FSH, prolactin, testosterone, and cortisol associated with season and mating in male pygmy goats

Four male pygmy goats were used in a study designed to determine the effects of season on serum hormone (luteinizing hormone, follicle stimulating hormone, prolactin, testosterone, and cortisol) levels, testis size and libido, and the effects of mating on serum hormone profiles. Seasonal peaks were observed for prolactin in July, luteinizing hormone and follicle stimulating hormone in September, and testosterone in October. Luteinizing hormone peak frequency was greatest in September and was increased by mating activity in the months immediately preceding the breeding season. Scrotal circumference did not vary with season and libido showed no consistent seasonal pattern. Mating appeared to raise all hormone levels except during the months when these hormones were seasonally elevated. When episodic releases of luteinizing hormone occurred, they were associated with subsequent rises in serum testosterone levels. On some mating days, when episodic releases of luteinizing hormone were absent, changes in testosterone levels were highly correlated with changes in cortisol levels. It was concluded that both season and mating influence reproductive hormone levels in male pygmy goats.     

Prognostic value of serum hormone concentrations in prostatic cancer

Seventy-eight patients with cytologically and/or histologically confirmed prostatic cancer were randomly allocated to orchidectomy (ORX, n = 37) or combined intramuscular and oral estrogen treatment (ESTR, n = 41). Serum levels of testosterone (T), 17 alpha-hydroxyprogesterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, total estrone (tE1; sum of unconjugated and conjugated estrone, greater than or equal to 85% estrone sulfate), cortisol, luteinizing hormone, follicle-stimulating hormone, prolactin, growth hormone, sex hormone-binding globulin (SHBG), and albumin were determined prior to treatment and 12, 24, and 36 months after initiation of treatment. Fifty patients responded to treatment or had stable disease, and 28 did not respond (12 in the ORX and 16 in the ESTR group). There was no association between pretreatment hormone or protein levels and outcome of the treatment, neither in the total material nor within either of the two treatment subgroups. Significantly higher pretreatment levels of cortisol and prolactin and significantly lower levels of T, tE1, and albumin and a significantly lower T/SHBG-ratio (index on biologically active T) were found in patients with metastatic disease, compared with the patients without metastases. There was no association between testicular or adrenal androgens, SHBG, T/SHBG, and albumin values during treatment and the clinical outcome. The differences found between metastatic and nonmetastatic disease probably simply reflect the more stressful and catabolic condition and generally poorer health in patients with disseminated malignant disease. Furthermore, the study does not lend any support to the hypothesis that indicates an important role of adrenal "rest androgen" in prostatic cancer tumor growth.