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At least 55 records · Page 3Linked to original sources
PubMed1989

Endocrine responses to growth hormone-releasing hormone, thyrotropin-releasing hormone and corticotropin-releasing hormone in depression.

To explore and to compare hypothalamic-pituitary-somatotropic (HPS), hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-adrenocortical (HPA) axis function in depression, 30 subjects (15 patients with a major depressive episode and individually matched controls) received 50 micrograms growth hormone-releasing hormone-44 amide at 9:00, 200 micrograms thyrotropin-releasing hormone (TRH) at 9:00 and 100 micrograms human corticotropin-releasing hormone (CRH) at 18:00 on consecutive days as an i.v. bolus dose. Compared with controls, depressed patients showed blunted growth hormone (GH) responses to GHRH, decreased TRH-induced thyrotropin (TSH) release and reduced corticotropin (ACTH) but normal cortisol secretion following CRH. ACTH secretion following CRH and TRH-induced TSH release were positively correlated across depressed patients and controls but no significant correlations between GH responses to GHRH and TRH-induced TSH release or ACTH and cortisol secretion following CRH administration were demonstrated. Our findings suggest that altered HPT and HPA axis function associated with depression are triggered by factors that are at least partly different from those that cause HPS system dysfunction. We conclude that the pathophysiological process resulting in aberrant neuroendocrine secretory dynamics associated with depression may primarily occur at a suprapituitary site, and that HPS, HPT and HPA axis dysfunction may be precipitated by complex central and peripheral regulatory mechanisms involving largely independent factors.

Adrenocorticotropic Hormone↗
PubMed2000

The roles of prolactin, growth hormone, insulin-like growth factor-I, and thyroid hormones in lymphocyte development and function: insights from genetic models of hormone and hormone receptor deficiency.

An extensive literature suggesting that PRL, GH, IGF-I, and thyroid hormones play an important role in immunity has evolved. Because the use of one or more of these hormones as immunostimulants in humans is being considered, it is of critical importance to resolve their precise role in immunity. This review addresses new experimental evidence from analysis of lymphocyte development and function in mice with genetic defects in expression of these hormones or their receptors that calls into question the presumed role played by some of these hormones and reveals unexpected effects of others. These recent findings from the mutant mouse models are integrated and placed in context of the wider literature on endocrine-immune system interactions. The hypothesis that will be developed is that, with the exception of a role for thyroid hormones in B cell development, PRL, GH, and IGF-I are not obligate immunoregulators. Instead, they apparently act as anabolic and stress-modulating hormones in most cells, including those of the immune system.

Animals↗
PubMed1993

Agonist-induced release of gonadotropin-releasing hormone, luteinizing hormone, and follicle-stimulating hormone and their associations with basal secretion of luteinizing hormone and follicle-stimulating hormone throughout lactation in sows.

Our working hypothesis was that the normal increase in basal secretion of LH and FSH during lactation in sows is paralleled by an increase in readily releasable pools of GnRH, LH, and FSH. Sows fitted with indwelling catheters and nursing 9-11 piglets were sampled on Days 1, 7, 14, and 21 (primiparous sows; n = 10; experiment 1) or Days 7 and 21 (multiparous sows; n = 10; experiment 2) of lactation. On each day, blood was collected at 10-min intervals for 2 h before one member of a pair of sows was infused (i.v.) with saline (n = 5) and the other with the neuroexcitatory amino acid N-methyl-DL-aspartic acid (NMA; 10 mg/kg b.w.) to measure readily releasable GnRH as estimated by LH release. Two hours later, each sow that had received saline was given GnRH (100 micrograms, i.v.) for estimation of releasable pools of pituitary LH and FSH. Responses to NMA and GnRH were estimated by area under the curve (ng.ml-1.min) of serum LH profiles for 1 h (NMA group) or 2 h (GnRH group) after treatment. Basal LH secretion in primiparous sows decreased from Day 1 to Day 7 and then returned to Day 1 values by Day 21. Similarly, in multiparous sows, basal LH was lower on Day 7 than on Day 21. Basal FSH secretion increased linearly as lactation progressed in primiparous and multiparous sows.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Stimulation of growth hormone release by luteinizing hormone-releasing hormone and melanocyte-stimulating hormone-release inhibiting hormone in the hypophysectomized rat bearing an ectopic pituitary.

Intrajugular administration of LHRH (0-6 and 1-2 mug) in hypophysectomized rats which received renal grafts of anterior pituitary induced a small but significant rise in plasma GH 5 and 10 min post-treatment. LHRH, at the same dose levels, was ineffective in weight-matched intact controls. MIF, at the dose of 1-2 mug, induced a slight GH rise 5 min after treatment in hypophysectomized trasnplanted rats, while it was ineffective in intact controls. Unlike the two hypothalamic peptides, alpha-MSH (0-6 and 1-2 mug) was ineffective as a GH-releaser in both transplanted and intact rats.

Animals↗
PubMed2000

Pituitary proopiomelanocortin-derived peptides and hypothalamus-pituitary-interrenal axis activity in gilthead sea bream (Sparus aurata) during prolonged crowding stress: differential regulation of adrenocorticotropin hormone and alpha-melanocyte-stimulating hormone release by corticotropin-releasing hormone and thyrotropin-releasing hormone.

Plasma levels of cortisol, growth hormone (GH), adrenocorticotropin hormone (ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), N-acetyl-beta-endorphin, in vitro ACTH-stimulated cortisol secretion, and in vitro corticotropin-releasing hormone (CRH)- and thyrotropin-releasing hormone (TRH)-stimulated ACTH and alpha-MSH secretion were investigated in gilthead sea bream exposed to high stocking density (30 kg m(-3)) for 23 days. Within 3 days after the onset of crowding, plasma levels of cortisol, ACTH, alpha-MSH, and N-acetyl-beta-endorphin were above control values. After 7 days, plasma parameters had returned to control levels, but at 23 days, cortisol, alpha-MSH, and N-acetyl-beta-endorphin levels were again elevated over controls, indicating a long-term activation of the melanotrope cells. In contrast, crowding stress elicited a prolonged reduction in plasma GH levels concomitant with the increased hypothalamus-pituitary-interrenal axis (HPI) activation. Crowding stress enhanced cortisol secretory activity of the unstimulated interrenal cells. However, interrenal tissue from crowded fish in vitro displayed an attenuated response to ACTH stimulation compared with tissue from control fish, indicating a desensitization of these cells to ACTH during crowding. The involvement of pituitary proopiomelanocortin-derived peptides in the HPI axis of sea bream is indicated by the observed modulation of the CRH and TRH responsiveness of the corticotropes and melanotropes in crowded fish. At day 1, when there were crowding-induced plasma increases in ACTH and alpha-MSH, there was an attenuated CRH-stimulated but not TRH-stimulated, ACTH release. However, at that time, CRH- and TRH-induced responses of alpha-MSH secretion, and the unstimulated secretory activity of the MSH cells, were enhanced in crowded sea bream. These data provide evidence for stimulatory roles of multiple hypothalamic (CRH and TRH) and pituitary (ACTH and alpha-MSH) peptides in the activation of the hypothalamus-pituitary-interrenal axis under crowding conditions in sea bream.

Adrenocorticotropic Hormone↗
PubMed1997

Growth hormone-releasing hormone and growth hormone-releasing peptide as therapeutic agents to enhance growth hormone secretion in disease and aging.

Growth hormone (GH) secretion is pulsatile and is tightly regulated. In this chapter the effects of aging, nutrition, the feedback effects of IGF-I, and the role of body composition in the decline of GH secretion will be discussed. In GH-deficient adults there is an increase in the amount of intra-abdominal (visceral) fat. Similarly, with increasing age, there is an increase in visceral fat and there is a tight correlation between 24-hour GH release and visceral fat in the elderly. This may have serious metabolic consequences, including insulin resistance and increased cardiovascular risk. There are at least four potential mechanisms for the age-related decline in GH secretion: 1) decreased release of growth hormone releasing-hormone (GHRH); 2) increased release of somatostatin; 3) enhanced sensitivity to IGF-I feedback; and 4) decreased somatotroph mass. The latter two potential mechanisms are discussed. There is little evidence that there is any change in sensitivity to IGF-I feedback with aging and the somatotroph cell mass appears to be preserved in older subjects. The GH axis may be stimulated by either GHRH or by growth hormone-releasing peptide (GHRP) and related compounds. Chronic therapy with GHRH in GH-deficient children restores GH secretion and accelerates linear growth. Mutations of the GHRH receptor lead to GH deficiency and short stature. This indicates the essential role of GHRH in regulation of GH secretion. Growth hormone releasing peptide was discovered in 1981. Recently, the GHRP/GH secretagogue receptor has been cloned and orally active GHRP mimetics have been developed. One such compound, MK-677, stimulates pulsatile GH secretion and its effects persist for 24 hours. Oral administration of MK-677 for a month in the elderly demonstrates that this route stimulates a physiologic pattern of GH secretion. The amplitude of the GH pulses was increased but the number of GH pulses was unchanged. Thus, in older individuals, the amount of GH secreted in 24 hours is restored toward that seen in young adults. This compound also enhances GH secretion in GH-deficient adults who had been GH-deficient during childhood. The development of stable, orally active molecules to stimulate the GHRP/GH secretagogue receptor is a practical reality. These GH secretagogues may have a therapeutic role in short stature and adult GH deficiency. In addition, the use of GH secretagogues in normal aging merits investigation, as growth hormone may regulate body composition in older adults.

Adult↗
PubMed1981

On the correlation of luteinizing hormone-releasing hormone, luteinizing hormone, follicle-stimulating hormone, and prolactin levels in plasma of women with normal menstrual cycles.

During seven follicular, five periovulatory, and seven luteal days of the menstrual cycle, concentrations of luteinizing hormone-releasing hormone (LHRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), total estrogen (TE), and progesterone (P) were measured every 20 minutes over a 3 or a 5 hour period in samples of venous plasma obtained from women with normal menstrual cycles. Episodic peaks of LHRH, LH, and PRL and less pronounced elevations of FSH were observed. Correlation analysis of the study demonstrated the following: (1) During early follicular and late luteal days, a synchrony was observed between LHRH and LH pulses and trends. There was a positive correlation between LHRH and LH levels only during the early follicular days (p less than 0.05), demonstrating a probable LHRH control of LH release. (2) When TE and TE/P concentrations increased during the late follicular and early luteal days, respectively, no correlation was present between LHRH and LH levels and trends. (3) Neither a synchrony nor a correlation was detectable between LHRH and FSH pulses or levels during any of the cycle days. (4) A statistical correlation existed between LH and PRL concentrations during various days of the cycle, more specifically during the periovulatory period, suggesting a common release mechanism for these two pituitary hormones.

Adult↗
PubMed1976

The effect of repeated injections of synthetic luteinizing hormone-releasing hormone on the response of plasma luteinizing hormone and follicle-stimulating hormone in young hypogonadotropic-hypogonadal patients.

Sixteen patients, ages 14 to 18, eleven with isolated gonadotropin deficiency and five with sporadic multiple pituitary hormone deficiency, were subjected to a course of five daily intramuscular injections of synthetic luteinizing hormone releasing hormone (LH-RH), 100 mug/day. Before and after the course of intramuscular injections, a rapid LH-RH test (by a one-bolus intravenous injection of 50 mug/sq m) was performed and the responses of plasma LH and follicle-stimulating hormone were measured by a radioimmunoassay method. The patients could be divided into three groups according to the response of the plasma LH to the second LH-RH test: group A, five patients with a significantly higher response of plasma LH to the second LH-RH test: group B, nine patients with a less significantly higher response of the plasma LH to the second LH-RH test; and group C, two patients with very low or no response to either stimulation used in this study. The patients in the three groups may represent different etiologic entities, namely that of a separate hypothalamic lesion, a "mixed" pituitary and hypothalamic lesion, and a "pure" pituitary lesion, respectively. It is concluded that the proposed procedure provides a useful tool for discriminating etiologic groups in patients with abnormal gonadotropic secretion. Recognition of tertiary hypogonadism (primary, pure, hypothalamic gonadotropin-releasing hormone deficiency) is of practical importance in selecting those patients who can benefit from long standing LH-RH therapy.

Adolescent↗
PubMed1981

Long-term effect of D-Trp6-luteinizing hormone-releasing hormone on testicular size and luteinizing hormone, follicle-stimulating hormone, and testosterone levels in hypothalamic hypogonadotropic males.

Six men, ages 18 to 34 years, with hypothalamic hypogonadotropism were treated with D-Trp6-luteinizing hormone-releasing hormone (10 micrograms intramuscularly on alternate days) for a period of 6 months. They underwent an intravenous luteinizing hormone-releasing hormone (LH-RH) test (50 micrograms/sq m) before and after 1, 3, and 6 months of treatment. During the first 3 months of therapy, the mean (+/- standard deviation) testicular volume increased from 3.5 +/- 1.0 ml to 6.0 +/- 2.0 ml, but decreased to 5.0 +/- 1.0 ml after 6 months. A significant increase in the plasma LH response to LH-RH over pretreatment levels was noted after 1 month (10.2 +/- 4.2 mIU/ml versus 1.6 +/- 1.0 mIU/ml, P less than 0.001) and 3 months (3.0 +/- 1.6 mIU/ml, P less than 0.01) with a subsequent decline to pretreatment levels after 6 months of treatment. The follicle-stimulating hormone response to LH-RH was not significant. It is concluded that D-Trp6-LH-RH induced an initial stimulation in these patients but, probably because of the excessively high dose used, a paradoxical inhibitory response was obtained after 3 months of therapy.

Adolescent↗
PubMed1976

Luteinizing hormone and follicle stimulating hormone and the response to luteinizing hormone releasing hormone in relation to sex and age.

Serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) before and after intravenous injection of luteinizing hormone releasing hormone (LHRH) were studied in 71 male and female subjects of various ages. Mean basal FSH and LH levels were not significantly different in the male groups, except that FSH was significantly higher in the very old subjects. Postmenopausal female subjects had much higher concentrations of both hormones than had premenopausal women. LH was higher in female subjects shortly after the menopause than in very old female subjects. The serum concentrations of both FSH and LH 30 min. after intravenous injection of 200 mug LHRH were not different from the 60 min. values. There was no significant difference in the response of LH in the male groups. The peak FSH concentration was higher in the very old male subjects. Postmenopausal women had a much higher peak concentration of both FSH and LH than had younger subjects. The increment of LH, but not of FSH, was larger in female subjects shortly after the menopause than in very old female subjects. In both sexes there was a significant correlation between the basal FSH/LH ratio and age. In younger male subjects there was a close positive correlation between basal LH and serum testosterone, in older male subjects this correlation was negative and significant.

Adult↗
PubMed1977

Luteinizing hormone responses to luteinizing hormone releasing hormone, and growth hormone and cortisol responses to insulin induced hypoglycaemia in functional secondary amenorrhoea.

Luteinizing hormone (LH) responses to luteinizing hormone releasing hormone (LHRH), and growth hormone (GH) and cortisol responses to insulin induced hypoglycaemia were studied in 56 women classified into 4 distinct groups of functional secondary amenorrhoea. The groups were: I, self-induced weight reduction (20 patients); II, post pill amenorrhoea (14 patients); III, anorexia nervosa (10 patients); and IV, idiopathic secondary amenorrhoea (12 patients). Only patients with no overlapping anamnestic factors were included. Group I patients had the most heavily impaired LHRH-LH responses, and the GH response to hypoglycaemia was smaller than in other groups. Cortisol responses were normal. Group II patients showed blunted LH responses and normal GH and cortisol responses. Group III patients showed normal or exaggerated LH responses in the recovery phase of anorexia nervosa, while those two patients who were in the static phase of the illness had impaired responses. GH responses varied greatly. Group IV patients had normal basal levels of LH and normal LH, GH and cortisol responses. The restoration of LH response is not solely correlated to body mass, since patients recovering from anorexia nervosa showed greater LHRH-LH responses with nutritional rehabilitation at 76% of ideal body weight than patients with self-induced weight reduction at 87% of ideal body weight. In idiopathic amenorrhoea the hypothalamic pituitary axis seems to be practically intact. The function of hypothalamic-pituitary axis may be impaired selectively in functional amenorrhoea. Corticotrophin releasing hormone function remains intact, and GH-response may be impaired or normal independently of the LH-response to LHRH. In self-induced weight reduction both functions were impaired. These tests are easily carried out with out-patients, and they give more information about the functional state of hypothalamic-pituitary axis than basal analyses of hypothalamic-pituitary axis than basal analyses of gonadotrophins and oestrogens. However, a single pathologic reading in the LH response is not specific enough to indicate to which group of amenorrhoea the patients belong, but these tests together elucidate the severity of lesion in hypothalamic pituitary axis.

Adolescent↗
PubMed1993

Effects of pyridostigmine, corticotropin-releasing hormone and growth hormone-releasing hormone on the pituitary-adrenal axis and on growth hormone secretion in dementia.

Alterations of neuroendocrinological indices determined by the impaired regulating effects of cholinergic neurotransmission have been described in primary dementia. In this study we have evaluated the effects of acetylcholinesterase inhibition by pyridostigmine on growth hormone (GH), adrenocorticotropic hormone (ACTH) and cortisol secretion and on their responses to GH-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) in 7 patients with primary degenerative dementia and in 8 sex- and age-matched controls. Demented subjects showed higher cortisol basal levels and lower ACTH levels than controls. Pyridostigmine increased the GH response to GHRH in both groups, the effect being significantly enhanced in patients. An increase of ACTH and cortisol levels was found in both groups after pyridostigmine and CRH administration. Pyridostigmine pretreatment significantly increased the ACTH response to CRH in controls but not in patients. The obtained data may indicate that a muscarinic receptor upregulation and an impairment of somatostatinergic function are operative in the regulation of GH secretion in dementia. An underlying hyperactivity of the hypothalamic-pituitary-adrenal axis impairs the responses of ACTH and cortisol to CRH in this disorder.

Adrenocorticotropic Hormone↗
PubMed1988

Sex differences in the responses of hypothalamic luteinizing hormone-releasing hormone and catecholamine systems to ovarian hormones and naloxone: implications for sexual differentiation of luteinizing hormone secretion in rats.

Normal male rats, or female rats exposed neonatally to androgens or estrogens, do not respond in adulthood to ovarian hormone treatments that stimulate preovulatory-like surges of luteinizing hormone (LH) or mating behavior in normal females. As an attempt to understand the neurochemical basis for this insensitivity, the present studies tested whether sex differences also exist with respect to several important neural events that are antecedent to and essential for the appearance of an LH surge induced by ovarian hormone treatment. Administration of estradiol via Silastic capsules to adult, gonadectomized rats resulted in a suppression of LH release that was equivalent in males and females, but only the estrogen-primed females responded to injections of progesterone with an LH surge. Similarly, in estrogen-primed females but not males, progesterone induced a presurge sequential accumulation and decline of LH-releasing hormone (LH-RH) concentrations in the median eminence and increased the turnover rates of norepinephrine (NE) and epinephrine (E) in the medial basal hypothalamus during the time of LH-RH accumulation. Ovarian hormones may activate NE and E release in females by removing a tonic inhibition over catecholamine release exerted by endogenous opioids. In order to test whether direct antagonism of opiate mechanisms would produce equivalent neuroendocrine or neurochemical responses in males and females, additional studies tested the effects of the opiate receptor blocker naloxone on LH release and on activity of catecholamines in the medial basal hypothalamus. In contrast to females, estrogen-primed male rats did not display either an increase in serum LH or an enhancement of the alpha-methyltyrosine-induced decline of NE or E after treatment with naloxone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of protein deficiency on luteinizing hormone releasing hormone (LHRH), gonadotropin releasing hormone associated peptide (GAP) and luteinizing hormone (LH) immunocytochemistry in the hypothalamus and pituitary gland of prepubertal ewes.

Growing female lambs were fed diets containing 14.2% (standard) or 8.1% (protein restricted) of proteins to determine their effects on puberty and luteinizing hormone releasing hormone (LHRH), gonadotropin hormone associated peptide (GAP), luteinizing hormone (LH) hormonal system. At the end of the experiment (30-34 weeks of age), hypothalamic LHRH, GAP and pituitary LH were analysed by immunocytochemical methods using specific antibodies. Plasma LH were determined by radioimmunoassay at 21 weeks of age. It was found that lowering of the dietary proteins content decreased the concentration of basal plasma LH significantly in lambs of 21 weeks of age. None of the sheep of this group reached sexual maturity at the same time as the animals of the standard group. However, immunoreactive (ir) LHRH neuronal system of protein restricted lambs was normally developed: Numerous irLHRH perikarya, dense network of axons and abundant material stored in the nerve terminals were well visualized in the typical sites of the preoptico-septal area, hypothalamus and the median eminence (ME). Gonadotropin associated peptide (GAP) of the LHRH precursor was present in the same populations of neurons that contained LHRH in the sheep brain. The proportion of pituitary LH-cells was three fold higher in pituitaries of the nutritionally restricted group. They displayed hypertrophy and very strong immunoreaction. These results show that protein deficiency in diets of growing female sheep delays their puberty but does not impair the synthesis and processing of LHRH in the brain neurons and synthesis of LH in pituitary cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Gonadotropin-releasing hormone neurons in the preoptic-hypothalamic region of the rat contain lamprey gonadotropin-releasing hormone III, mammalian luteinizing hormone-releasing hormone, or both peptides.

This study utilized a newly developed antiserum, specific for lamprey gonadotropin-releasing hormone III (l-GnRH-III), to determine the following: in which regions of the rat hypothalamus the neuronal perikarya producing l-GnRH-III are localized; and whether this peptide, known to selectively induce follicle-stimulating hormone release, is coexpressed in neurons containing mammalian luteinizing hormone-releasing hormone (m-LHRH). Double-label immunocytochemistry was performed by using an l-GnRH-III polyclonal antiserum and an LHRH monoclonal antiserum. Immunopositive neurons for l-GnRH-III, m-LHRH, or neurons coexpressing both peptides were detected within the organum vasculosum lamina terminalis (OVLT) region of the preoptic area (POA). Caudal to the OVLT, l-GnRH-III-positive neurons were also observed dorso-medially, above the third ventricle in the medial POA. The m-LHRH neurons were not observed in this area. The lateral POA region contained neurons positive for both peptides along with single-labeled neurons for each peptide. Importantly, neurons that expressed l-GnRH-III, m-LHRH, or both peptides were also detected in the ventral regions of the rostral hypothalamus, dorsolateral to the borders of the supraoptic nuclei. In both of these latter areas, neurons containing l-GnRH-III were slightly dorsal to neurons containing only m-LHRH. The l-GnRH-III perikarya and fibers were eliminated by absorption of the primary antiserum with l-GnRH-III, but not by l-GnRH-I, chicken-GnRH-II, or m-LHRH. These results indicate that, unlike other isoforms of GnRH found in the mammalian brain, l-GnRH-III neurons not only are observed in regions that control follicle-stimulating hormone release but also are colocalized with m-LHRH neurons in areas primarily controlling LH release. These findings suggest an interrelationship between these two peptides in the control of gonadotropin secretion.

Animals↗
PubMed2004

Chemohormonal therapy as primary treatment for metastatic prostate cancer: a randomized study of estramustine phosphate plus luteinizing hormone-releasing hormone agonist versus flutamide plus luteinizing hormone-releasing hormone agonist.

BACKGROUND: The present study was undertaken mainly to investigate whether chemohormonal therapy with estramustine phosphate plus luteinizing hormone-releasing hormone (LHRH) agonist has a more beneficial effect than the hormonal therapy with flutamide plus LHRH agonist for newly diagnosed patients with metastatic prostate cancer. METHODS: A total of 57 patients with metastatic prostate cancer aged 59-80 years (median 74 years) were entered in the study and were randomized to the treatment of estramustine phosphate (560 mg/day) plus LHRH agonist (estramustine group) or flutamide (375 mg/day) plus LHRH agonist (flutamide group) with stratification for the degree of performance status, histological differentiation and bone metastasis. RESULTS: Both of the treatment regimens were well tolerated with similar incidences of adverse drug reactions. The overall response rates (complete response plus partial response) at 12 weeks after treatment in the estramustine and flutamide groups were 76 and 55%, respectively. The median time to objective progression for the estramustine group (25.4 months) was longer than that of the flutamide group (14.6 months). The serum levels of follicle stimulating hormone and testosterone were significantly lower in the estramustine group. CONCLUSIONS: Chemohormonal therapy with estramustine phosphate plus LHRH agonist showed longer clinical progression-free survival than the hormonal therapy with flutamide plus LHRH agonist (P = 0.03), although there was no significant difference in the overall survival. A larger-scaled trial with more statistical power is required to clarify that the former regimen is more beneficial than the latter for newly diagnosed patients with advanced prostate cancer.

Aged↗