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Hormone-releasing Hormone (hormone-releasing + hormone)
Kinds of Hormone-releasing Hormone Terms modified by Hormone-releasing Hormone Selected AbstractsEffect of oxytocin on nitric oxide activity controlling gonadotropin secretion in humansEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2003P. Chiodera Abstract Background Previously described inhibitory effects of the nitric oxide synthase (NOS) inhibitor L-NAME on luteinizing hormone-releasing hormone (LH-RH)-induced LH and follicle stimulating hormone (FSH) secretion in humans suggested modulation by nitric oxide (NO) of the gonadotropin-releasing action of LH-RH. Design In order to establish whether oxytocin (OT) participates in this regulatory mechanism, 10 normal men were treated with LH-RH (100 µg as an i.v. bolus) given alone or in the presence of L-NAME (40 µg kg,1 injected plus 50 µg kg,1 infused i.v. for 60 min), OT (2 IU injected plus 4 IU infused i.v. for 60 min) or a combination of both drugs. Results The administration of OT was unable to change the gonadotropin responses to LH-RH. In contrast, L-NAME significantly reduced both FSH and LH increments induced by LH-RH. When L-NAME was given in the presence of OT, the LH and FSH responses to LH-RH were similar to those observed after the administration of LH-RH alone. Conclusion These data suggest antagonistic actions of OT and L-NAME in the control of NOS activity in regulation of gonadotropin secretion induced by LH-RH. [source] Netrin 1-mediated chemoattraction regulates the migratory pathway of LHRH neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2004Gerald A. Schwarting Abstract Luteinizing hormone-releasing hormone (LHRH) neurons migrate from the vomeronasal organ (VNO) to the forebrain in all mammals studied. In mice, the direction of LHRH neuron migration is dependent upon axons that originate in the VNO, but bypass the olfactory bulb and project caudally into the basal forebrain. Thus, factors that guide this unique subset of vomeronasal axons that comprise the caudal vomeronasal nerve (cVNN) are candidates for regulating the migration of LHRH neurons. We previously showed that deleted in colorectal cancer (DCC) is expressed by neurons that migrate out of the VNO during development [Schwarting et al. (2001) J. Neurosci., 21, 911,919]. We examined LHRH neuron migration in Dcc,/, mice and found that trajectories of the cVNN and positions of LHRH neurons are abnormal. Here we extend these studies to show that cVNN trajectories and LHRH cell migration in netrin 1 (Ntn1) mutant mice are also abnormal. Substantially reduced numbers of LHRH neurons are found in the basal forebrain and many LHRH neurons migrate into the cerebral cortex of Ntn1 knockout mice. In contrast, migration of LHRH cells is normal in Unc5h3rcm mutant mice. These results are consistent with the idea that the chemoattraction of DCC+ vomeronasal axons by a gradient of netrin 1 protein in the ventral forebrain guides the cVNN, which, in turn, determines the direction of LHRH neuron migration in the forebrain. Loss of function through a genetic deletion in either Dcc or Ntn1 results in the migration of many LHRH neurons to inappropriate destinations. [source] The effect of GHRH antagonists on human glioblastomas and their mechanism of action,INTERNATIONAL JOURNAL OF CANCER, Issue 10 2010Eva Pozsgai Abstract The effects of new growth hormone-releasing hormone (GHRH) antagonists JMR-132 and MIA-602 and their mechanism of action were investigated on 2 human glioblastoma cell lines, DBTRG-05 and U-87MG, in vitro and in vivo. GHRH receptors and their main splice variant, SV1 were found on both cell lines. After treatment with JMR-132 or MIA-602, the cell viability decreased significantly. A major decrease in the levels of phospho-Akt, phospho-GSK3, and phosho-ERK 1/2 was detected at 5 and 10 min following treatment with the GHRH antagonists, whereas elevated levels of phospho-p38 were observed at 24 hr. The expression of caspase-3 and poly(ADP-ribose) (PARP), as the downstream executioners of apoptosis were found to be significantly elevated after treatment. Following treatment of the glioblastoma cells with GHRH antagonists, nuclear translocation of apoptosis inducing factor (AIF) and Endonuclease G (Endo G) and the mitochondrial release of cytochrome c (cyt c) were detected, indicating that the cells were undergoing apoptosis. In cells treated with GHRH antagonists, the collapse of the mitochondrial membrane potential was shown with fluorescence microscopy and JC-1 membrane potential sensitive dye. There were no significant differences between results obtained in DBTRG-05 or U-87MG cell lines. After treatment with MIA-602 and JMR-132, the reduction rate in the growth of DBTRG-05 glioblastoma, xenografted into nude mice, was significant and tumor doubling time was also significantly extended when compared with controls. Our study demonstrates that GHRH antagonists induce apoptosis through key proapoptotic pathways and shows the efficacy of MIA-602 for experimental treatment of glioblastoma. [source] Clinical experience of hormone therapy to bone metastatic prostate cancerINTERNATIONAL JOURNAL OF UROLOGY, Issue 5 2006MASAMI WAKISAKA Background:, A novel hormone therapy was instituted against prostate cancer with bone metastases and its therapeutic efficacy was investigated. Methods:, A total of 35 patients who had been pathologically diagnosed with carcinoma of the prostate between January 1994 and December 2003 were entered into the present study. Patients aged over 80 years were excluded from the study. As for the treatment methodology, diethylstilbestrol diphosphate (DES-P) at 500 mg/day was intravenously injected for 20,40 days, followed by monotherapy with an analog of luteinizing hormone-releasing hormone (LHRH). In all subjects, surgical castration was not conducted. The survival rate was analysed according to the method of Kaplan,Meier. Results:, One of the 35 patients was excluded from the study as this patient did not meet the inclusion criteria. There were four patients who dropped out of the study. On histology, 17 patients had moderately differentiated adenocarcinomas and 17 patients had poorly differentiated adenocarcinomas. As for the extent of disease (EOD), the patients were classified as with a score of 1 in 10 patients, 2 in 13 patients, 3 in 7 patients and 4 in 4 patients. The 5-year progression-free survival rate and overall survival rate were 24.3% and 60.6%, respectively. Conclusion:, Our new hormone therapy in the management of prostate cancer metastatic to the bone has demonstrated markedly superior therapeutic results compared to those so far obtained. [source] Neoadjuvant flutamide monotherapy for locally confined prostate cancerINTERNATIONAL JOURNAL OF UROLOGY, Issue 4 2003KOJI YOSHIMURA Abstract Background: We compared the clinical effects and impact on quality of life (QOL) of patients who received a 3-month course of flutamide monotherapy before radical prostatectomy with those who received a 3-month course of luteinizing hormone-releasing hormone (LHRH) agonist monotherapy. Methods: Thirty-seven patients with non-metastatic prostate cancer were enrolled in this study (19, flutamide; 18, LHRH agonist). The rates of change of serum prostate-specific antigen (PSA) and testosterone levels, downsizing of prostate volume, the rate of organ confined disease, adverse effects and perioperative scores measured using the European Organization for Research and Treatment of Cancer Prostate Cancer Quality of Life Questionnaire (EORTC-P) and the Sapporo Medical University Sexual Function Questionnaire (SMUF) were analyzed. Results: At radical prostatectomy, pathological variables were not significantly different in the two groups. Serum testosterone level was significantly higher (mean 359.2 compared to 10.5, P < 0.001), complete response rate of PSA (13% compared to 57%, P = 0.028) and rate of downsizing of prostate volume (mean, ,17.7% compared to ,35.4%, P = 0.038) were significantly lower in the flutamide group than in the LHRH group. After neoadjuvant hormone therapy, the scores on the sexual problem domain of EORTC-P (P = 0.033) and sexual desire score of SMUF (P = 0.021) were significantly higher in the flutamide group than in the LHRH group. At a median follow-up of 34 months after prostatectomy, biochemical failure-free survival rate in the flutamide group did not differ from that in the LHRH group. Conclusion: This study suggests that flutamide monotherapy can be an acceptable modality as an option for neoadjuvant hormone therapy. [source] Divergent Regulation of Hypothalamic Neuropeptide Y and Agouti-Related Protein by Photoperiod in F344 rats With Differential Food Intake and GrowthJOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2009A. W. Ross Hypothalamic genes involved in food intake and growth regulation were studied in F344 rats in response to photoperiod. Two sub-strains were identified: F344/NHsd (F344/N) and F344/NCrHsd (F344/NCr); sensitive and relatively insensitive to photoperiod respectively. In F344/N rats, marked, but opposite, changes in the genes for neuropeptide Y (NPY) (+97.5%) and agouti-related protein (AgRP) (,39.3%) expression in the arcuate nucleus were observed in response to short (8 : 16 h light/dark cycle, SD) relative to long (16 : 8 h light/dark cycle, LD) day photoperiods. Changes were associated with both reduced food intake and growth. Expression of the genes for cocaine and amphetamine-regulated transcript (CART) and pro-opiomelanocortin (POMC) in the arcuate nucleus was unchanged by photoperiod. POMC in the ependymal layer around the third ventricle was markedly inhibited by SD. Parallel decreases in the genes for growth hormone-releasing hormone (GHRH) and somatostatin (Somatostatin) mRNA in the arcuate nucleus and Somatostatin in the periventricular nucleus were observed in SD. Serum levels of insulin-like growth factor (IGF)-1 and insulin were lower in F344/N rats in SD, whereas neither leptin nor corticosterone levels were affected. By contrast, F344/NCr rats that show only minor food intake and growth rate changes showed minimal responses in these genes and hormones. Thus, NPY/AgRP neurones may be pivotal to the photoperiodic regulation of food intake and growth. Potentially, the SD increase in NPY expression may inhibit growth by decreasing GHRH and Somatostatin expression, whereas the decrease in AgRP expression probably leads to reduced food intake. The present study reveals an atypical and divergent regulation of NPY and AgRP, which may relate to their separate roles with respect to growth and food intake, respectively. [source] Rapid Action of Oestrogen in Luteinising Hormone-Releasing Hormone Neurones: The Role of GPR30JOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009E. Terasawa Previously, we have shown that 17,-oestradiol (E2) induces an increase in firing activity and modifies the pattern of intracellular calcium ([Ca2+]i) oscillations with a latency < 1 min in primate luteinising hormone-releasing hormone (LHRH) neurones. A recent study also indicates that E2, the nuclear membrane impermeable oestrogen, oestrogen-dendrimer conjugate, and the plasma membrane impermeable oestrogen, E2 -BSA conjugate, all similarly stimulated LHRH release within 10 min of exposure in primate LHRH neurones, indicating that the rapid action of E2 is caused by membrane signalling. The results from a series of studies further suggest that the rapid action of E2 in primate LHRH neurones appears to be mediated by GPR30. Although the oestrogen receptor antagonist, ICI 182, 780, neither blocked the E2 -induced LHRH release nor the E2 -induced changes in [Ca2+]i oscillations, E2 application to cells treated with pertussis toxin failed to result in these changes in primate LHRH neurones. Moreover, knockdown of GPR30 in primate LHRH neurones by transfection with human small interference RNA for GPR30 completely abrogated the E2 -induced changes in [Ca2+]i oscillations, whereas transfection with control siRNA did not. Finally, the GPR30 agonist, G1, resulted in changes in [Ca2+]i oscillations similar to those observed with E2. In this review, we discuss the possible role of G-protein coupled receptors in the rapid action of oestrogen in neuronal cells. [source] Hypothalamic Control of Anterior Pituitary Function: A HistoryJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2008H. Charlton The concept of neurohumoral control of anterior pituitary function championed by Geoffrey Harris was based upon clinical and biological observation backed by rigorous experimental testing. The areas of the brain involved in the control of gonadotrophic hormone synthesis and release were identified by electrical stimulation, lesioning and fibre tract cutting. The medial preoptic area (MPOA) proved to be a major integrating centre, with axon terminals from this region terminating at the median eminence releasing factors into the portal vessels to give a direct route from brain to pituitary. It took over a decade before the gonadotrophic hormone-releasing hormone (GnRH) was isolated, sequenced and synthesised. With antibodies raised against this peptide, the MPOA was identified as a site rich in GnRH neurones and the hormone was detected at high levels in portal blood extracts. A natural knockout of the GnRH gene was discovered in a hypogonadal (hpg) mouse. Hormone injections, gene replacement methods and neural grafting in these mutants all confirmed the central role of GnRH in reproduction. The modern techniques of molecular biology have allowed us to extend our knowledge base. In the last few years the role of kisspeptin and its receptor (GPR54) in the control of the GnRH neurone has added a further level of hypothalamic involvement in the modulation of reproduction. [source] Noradrenergic Regulation of Hypothalamic Cells that Produce Growth Hormone-Releasing Hormone and Somatostatin and the Effect of Altered Adiposity in SheepJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2005J. Iqbal Abstract The growth hormone (GH) axis is sensitive to alteration in body weight and there is evidence that central noradrenergic systems regulate neurones that produce growth hormone-releasing hormone (GHRH) and somatostatin (SRIF). This study reports semiquantitative estimates of the noradrenergic input to neuroendocrine GHRH and SRIF neurones in the sheep of different body weights. We also studied the effects of altered body weight on expression of dopamine ,-hydroxylase (DBH), the enzyme that produces noradrenalin from dopamine. Ovariectomised ewes were made Lean (39.6 ± 2.6 kg; Mean ± SEM) by dietary restriction, whereas Normally Fed animals (61.2 ± 0.8 kg) were maintained on a regular diet. Brains were perfused for immunohistochemistry and in situ hybridisation. The Mean ± SEM number of GHRH-immunoreactive (-IR) cells was lower in Normally Fed (65 ± 7) than in Lean (115 ± 14) animals, whereas the number of SRIF-IR cells was similar in the two groups (Normally Fed, 196 ± 17; Lean 230 ± 21). Confocal microscopic analysis revealed that the percentage of GHRH-IR cells (Normally Fed 36 ± 1.5% versus Lean 32 ± 4.6%) and percentage of SRIF-IR cells (Normally Fed 30 ± 40.4% versus Lean 32 ± 2.3%) contacted by noradrenergic fibres did not change with body weight. FluoroGold retrograde tracer injections confirmed that noradrenergic projections to the arcuate nucleus are from ventrolateral medulla and noradrenergic projections to periventricular nucleus arise from the ventrolateral medulla, nucleus of solitary tract, locus coeruleus (LC) and the parabrachial nucleus (PBN). DBH expressing cells were identified using immunohistochemistry and in situ hybridisation and the level of expression (silver grains/cell) quantified by image analysis. The number of DBH cells was similar in Normally Fed and Lean animals, but the level of expression/cell was lower (P < 0.02) in the PBN and LC of Lean animals. These results provide an anatomical basis for the noradrenergic regulation of GHRH and SRIF cells and GH secretion. Altered activity or noradrenergic neurones in the PBN and LC that occur with reduced body weight may be relevant to the control of GH axis. [source] Expression of Three Gene Families Encoding Cell,Cell Communication Molecules in the Prepubertal Nonhuman Primate HypothalamusJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2005A. E. Mungenast Abstract Transsynaptic and glial,neuronal communication are important components of the mechanism underlying the pubertal activation of luteinizing hormone-releasing hormone (LHRH) secretion. The molecules required for the architectural organization of these cell,cell interactions have not been identified. We now show that the hypothalamus of the prepubertal female rhesus monkey expresses a multiplicity of genes encoding three families of adhesion/signalling proteins involved in the structural definition of both neurone-to-neurone and bi-directional neurone,glia communication. These include the neurexin/neuroligin (NRX/NRL) and protocadherin-, (PCDH,) families of synaptic specifiers/adhesion molecules, and key components of the contactin-dependent neuronal,glial adhesiveness complex, including contactin/F3 itself, the contactin-associated protein-1 (CASPR1), and the glial receptor protein tyrosine phosphatase ,. Prominently expressed among members of the NRX family is the neurexin isoform involved in the specification of glutamatergic synapses. Although NRXs, PCDH,s and CASPR1 transcripts are mostly detected in neurones, the topography of expression appears different. NRX1 mRNA-containing neurones are scattered throughout the hypothalamus, PCDH, mRNA transcripts appear more abundant in neurones of the arcuate nucleus and periventricular region, and neurones positive for CASPR1 mRNA exhibit a particularly striking distribution pattern that delineates the hypothalamus. Examination of LHRH neurones, using the LHRH-secreting cell line GT1-7, showed that these cells contain transcripts encoding NRXs and one of their ligands (NRL1), at least one PCDH, (CNR-8/PCDH,10), and the CASPR1/contactin complex. The results indicate that the prepubertal female monkey hypothalamus contains a plethora of adhesion/signalling molecules with different but complementary functions, and that an LHRH neuronal cell line expresses key components of this structural complex. The presence of such cell,cell communication machinery in the neuroendocrine brain suggests an integrated participation of their individual components in the central control of female sexual development. [source] Drug adsorption in human skin: A streaming potential studyJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 12 2003Johanna Raiman Abstract The objective of this study was to investigate the drug adsorption process in human skin using in vitro streaming potential measurements. Streaming potential is an electrokinetic phenomenon, which reflects both the charge density and the pore size of a membrane. Thus, the adsorption of charged solutes on the pore walls can be detected as a change of streaming potential, viz., as a change in the slope ,E/,P. In these streaming potential measurements, hydrophilic nadolol and luteinizing hormone-releasing hormone, and lipophilic propranolol and Nafarelin were used as model drugs. As could be expected, the hydrophilic drugs did not change the slope. The more lipophilic propranolol and Nafarelin, instead, changed the slope. Propranolol changed the slope gradually from negative to positive when the concentration was increased from 1 to 10 mM. With Nafarelin, a straight line with a slope of about 0 was obtained at pH 7.3 and an ascending curve at pH 4.2. These results indicate that the negative charges on the pore walls of human skin are blocked by adsorption of the lipophilic cations. The adsorption of lipophilic cations in the skin alters the permselectivity of the skin, which, in turn, may lead to the inhibition of electroosmotic flow across the skin during iontophoresis and to the shut down of transdermal drug permeation of higher molecular weight drugs. © 2003 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 92:2366,2372, 2003 [source] Granuloma caused by subcutaneous injection of leuprorelin acetate product: Case report and histopathological findingsTHE JOURNAL OF DERMATOLOGY, Issue 10 2006Takeshi OUCHI ABSTRACT Leuprorelin acetate is a luteinizing hormone-releasing hormone (LH-RH) analog, which is used for chemical castration. Chemical castration treatment has an especially important role for prostate cancer. To ensure ongoing chemical castration, a novel sustained-action injection system using spherical microcapsules has been developed. We report a patient who had granuloma caused by administration of the 11.25 mg leuprorelin acetate product. Histological examination revealed many giant cells with vacuoles. On the basis of reported cases, these vacuoles are characteristic for the granuloma caused by leuprorelin acetate product. The vacuoles in the granuloma are the same size as the microcapsules, and their shape is almost spherical. We assume that the vacuoles in the granuloma are actually the microcapsules. We expect that there will be investigations regarding the procatarctic cause of granuloma formation. [source] Abarelix and other gonadotrophin-releasing hormone antagonists in prostate cancerBJU INTERNATIONAL, Issue 11 2009Roger S. Kirby Hormonal therapy is the main recommended treatment for locally advanced and metastatic prostate cancer. Luteinizing hormone-releasing hormone (LHRH) agonists, such as buserelin, goserelin, leuprorelin and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels. However, this reduction is accompanied by a well described increase or ,surge' in LH and testosterone levels, necessitating the concomitant administration of an antiandrogen to combat the potential effects of transient acceleration in cancer activity. Two pure GnRH antagonists have been developed, abarelix and degarelix, that are devoid of any agonist effect on the GnRH receptor and consequently do not result in testosterone flare. Abarelix was the first GnRH antagonist to be developed and was approved by the USA Food and Drug Administration in 2004 for the initiation of hormonal castration in advanced or metastasizing hormone-dependent prostate carcinoma, when rapid androgen suppression is necessary. Clinical data on both abarelix and degarelix show that they can produce rapid and sustained decreases in testosterone to castrate levels without the need for co-administration of an antiandrogen, and with a very low complication rate in the short term. [source] Assessing the attitudes to prostate cancer treatment among European male patientsBJU INTERNATIONAL, Issue 2007Claude Schulman OBJECTIVES, To understand the attitudes of patients with prostate cancer toward the disease in general and to the use of hormone therapy as treatment; to assess unmet needs in the management of prostate cancer; and to gauge patient receptivity to a potential 6-month formulation of a luteinizing hormone-releasing hormone (LHRH) agonist. PATIENTS AND METHODS, Face-to-face interviews, lasting 50 min on average, were conducted during January and February 2007 with 200 European men who had been diagnosed with prostate cancer. RESULTS, Most patients were very satisfied with their physician, particularly with specialists, with 94% of men being satisfied with their expertise and 67% fully trusting the recommended treatment. Therapeutic efficacy was considered the most crucial aspect of treatment, although maintaining their lifestyle during treatment was also considered important (83% of patients). In all, 67% of patients believed that consideration should be given to lifestyle needs when selecting treatment; however, over half (55%) had never raised lifestyle issues with their physicians. Most patients would prefer fewer injections, with 68% (135/200) preferring 6-monthly injections over 3- or 1-monthly depots. Perceived advantages of 6-monthly injections include less discomfort/pain, more quality of life, fewer reminders of the disease and more ability to undertake activities without restriction. CONCLUSIONS, Patients with prostate cancer are generally very satisfied with their physicians and the information they receive, yet find it difficult to communicate their lifestyle needs. Most patients would prefer 6-monthly LHRH agonist therapy due to the many advantages associated with fewer injections, including its efficacy in reducing testosterone levels. Improving patients' willingness to raise lifestyle issues with their physicians, providing more effective patient-physician communication and less frequent injections might assist in achieving both optimal control of testosterone and optimal management of prostate cancer. [source] Efficacy of primary hormone therapy for localized or locally advanced prostate cancer: results of a 10-year follow-upBJU INTERNATIONAL, Issue 3 2006HIDEYUKI AKAZA OBJECTIVE To evaluate the efficacy of primary hormone therapy for localized or locally advanced prostate cancer, by analysing the 10-year survival rates for men with localized or locally advanced prostate cancer treated with primary hormone therapy or prostatectomy. PATIENTS AND METHODS Between February 1993 and March 1995, men with T1b, T1c or T2-3 N0M0 prostate cancer were enrolled. In all, 176 men who had a prostatectomy were assigned to Study 1 and were given adjuvant luteinizing hormone-releasing hormone (LHRH) agonist; 151 men who did not have a prostatectomy were assigned to Study 2 and had LHRH agonist monotherapy or combined androgen blockade. They were followed until death, loss to follow-up, or until the end of the observation period (31 March 2004). We analysed all cases in each study as a single population, and compared Study 1 with Study 2. RESULTS The mean patient ages were 67.2 years in Study 1 and 75.7 years in Study 2. During a median of 10.4 years of follow-up, 20 men in Study 1 and 17 in Study 2 died from prostate cancer, and 21 men in Study 1 and 50 in Study 2 died from other causes. In Study 1, the 10-year overall survival rate was 73% and the 10-year cause-specific survival rate was 86%, vs 41% and 78% in Study 2. Overall survival curves were similar to expected survival curves in both studies. There was no significant difference between studies in cause-specific survival. CONCLUSIONS The progression of prostate cancer was retarded by primary hormone therapy in men with localized or locally advanced prostate cancer. With primary hormone therapy or prostatectomy, the men had a life-expectancy similar to that of the normal population. [source] The significance of serum levels of insulin-like growth factor-1 in patients with prostate cancerBJU INTERNATIONAL, Issue 1 2000R. Kurek Objectives,To compare the serum levels of insulin-like growth factor-1 (IGF-1) in patients with prostate cancer and in control patients with no malignancy, and to evaluate any possible influence of testicular androgen withdrawal on the level of IGF-1 in patients with prostate cancer. Patients and methods,IGF-1 was measured in serum samples from 238 patients using both a chemiluminescence method and a radio-immunoassay. From a subgroup of 19 patients presenting with newly diagnosed carcinoma of the prostate, IGF-1 and testosterone values were measured before and during the course of testicular androgen with-drawal, achieved by the administration of luteinizing hormone-releasing hormone (LHRH) analogues combined with anti-androgens. Results,There were no significant differences in the mean serum levels of IGF-1 patients with and without prostate cancer (158.6 and 159.1 ng/mL, respect-ively). There were no significant differences in mean IGF-1 levels before and after antiandrogen therapy; the mean (median, sd, range) levels of testosterone (µg/L) and IGF-1 (ng/mL) before androgen withdrawal were 4.81 (4.84, 1.26, 3.11,6.93) and 157.1 (152.5, 26.7, 122.8,195.1). After androgen withdrawal the corresponding values were 0.303 (0.218, 0.24, 0.13,0.81) and 169.7 (31.7, 168.6, 124.9,227.6). A linear regression analysis (P = 0.76) and Spearman rank order correlation test (correlation coefficient ,0.0613, P = 0.64) showed no association between levels of testosterone and IGF-1. Freeze and thaw cycles applied to the samples had no effect on the IGF-1 values measured. Conclusions,There was no significant association between IGF-1 serum levels and prostate cancer. Short-term androgen withdrawal using LHRH anal-ogues combined with anti-androgens had no effect on the levels of IGF-1. [source] | ||||||||||