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PubMed1999

A multicenter phase II study with triptorelin (sustained-release LHRH agonist) in advanced or recurrent endometrial carcinoma: a French anticancer federation study.

The objective of this phase II multicenter study was to assess the efficacy and tolerance of triptorelin (a sustained-release LHRH agonist) in advanced or recurrent endometrial cancer. A total of 101 monthly intramuscular injections were administered to 24 eligible patients (median number/patient = 3; range 1-12). Mainly due to progression, only 16 patients received 3 or more injections. Among the 23 evaluable patients, 1 complete and 1 partial response (response rate of 8.7%) and 5 disease stabilizations were observed, often of long duration, but never in an irradiated area or after progestogens treatment failure. Median survival for eligible patients was 7.2 months (range: 1-36 months). Only grade 1 toxicities possibly related to the treatment were observed in 4 patients. In conclusion, triptorelin was safe, well tolerated, and easily manageable, and the very low toxicity did not impair the quality of life in these patients with a very poor prognosis. Although the response rate was disappointing, several patients showed early evidence of efficacy which may be of long duration. Response rates range between 0 and 45% in different published studies. Additional studies with stricter inclusion criteria and a larger sample size are necessary to better evaluate the role of LHRH agonists in endometrial adenocarcinomas.

Adult↗
PubMed2000

Luteinizing hormone-releasing hormone agonist triptorelin and antagonist cetrorelix inhibit EGF-induced c-fos expression in human gynecological cancers.

OBJECTIVES: Spontaneous and epidermal growth-factor-induced proliferation of human gynecological cancer cell lines is dose- and time-dependently reduced by treatment with the luteinizing hormone-releasing hormone (LHRH) agonist triptorelin and antagonist Cetrorelix. This antiproliferative activity is probably directly mediated through the LHRH receptors expressed by the tumor cells interacting with growth-factor-dependent mitogenic signal transduction. We have examined whether epidermal growth-factor (EGF)-induced expression of the early response gene c-fos is reduced by LHRH analogs. METHODS: Human endometrial (Ishikawa, Hec-1A), ovarian (EFO-21, EFO-27, SK-OV-3), and breast cancer cell lines (MCF-7) were rendered quiescent by incubation (72 h) in the absence of fetal calf serum and phenol red. This was followed by a 15-min incubation in the absence or presence of the LHRH agonist triptorelin (100 nM) or the antagonist Cetrorelix (100 nM) before the cells were stimulated for 10 min with EGF (100 nM). C-fos mRNA expression was determined by semi-quantitative RT-PCR using a synthetic DNA fragment as internal standard. C-Fos protein synthesis was determined by SDS-PAGE and semi-quantitative Western blotting. RESULTS: In cells derived from endometrial and ovarian cancer, maximal c-fos mRNA expression (seven- to ninefold over basal level) was obtained 30 min after EGF stimulation. In the breast cancer cell line MCF-7 this effect was obtained 60 min after EGF treatment. In all of the lines expressing LHRH receptor, EGF-induced c-fos mRNA expression as well as c-Fos protein synthesis was dose-dependently reduced by treatment with LHRH agonists and antagonists. At 100 nM concentrations of the LHRH analogs, c-fos expression was reduced to baseline levels. No effect of LHRH analogs on EGF-induced c-fos expression was observed in the ovarian cancer cell line SK-OV-3, which does not express the LHRH receptor. CONCLUSIONS: These results suggest that the binding of LHRH agonists and antagonists to their receptors inhibits the mitogenic signal transduction pathway of the EGF receptor in endometrial, ovarian, and breast cancer cell lines. The coupling of both signal transduction systems mediates the antiproliferative effect of LHRH analogs.

Antineoplastic Agents, Hormonal↗
PubMed1994

Attempted protection of spermatogenesis from irradiation in patients with seminoma by D-Tryptophan-6 luteinizing hormone releasing hormone.

Possible protective effects of D-Tryptophan-6 luteinizing hormone releasing hormone (D-Trp-6-LH-RH) against irradiation-induced testicular damage were investigated for the first time in patients with seminoma. After unilateral orchiectomy 12 men were allocated to receive the long-acting gonadotropin releasing hormone (GnRH) agonist D-Trp-6-LH-RH prior to and for the duration of radiotherapy. Eight patients with the same disease served as a control group. In contrast to several trials to protect spermatogenesis from chemotherapy by GnRH agonists, we first suppressed the pituitary-testicular axis before starting the treatment. As a new schedule this adjuvant GnRH agonist treatment was combined with cyproterone acetate for the first 20 days to diminish the amount and the duration of the initial stimulation of gonadotropins and testosterone. Irradiation started after suppression of the pituitary-gonadal axis. In all patients luteinizing hormone and testosterone were completely suppressed throughout the treatment compared to the controls, whereas the initial suppression of follicle-stimulating hormone was not completely maintained until radiotherapy was completed. At the follow-up at 18 months after completion of therapy, all patients reached their initial concentration of gonadotropins, testosterone, and motile spermatozoa independently of D-Trp-6-LH-RH treatment. With the dose and schedule investigated, the GnRH agonist showed no protective effects against testicular damage caused by radiotherapy.

Adult↗
PubMed1987

Gonadotropin production and release in female goldfish (Carassius auratus) after administration of pimozide and an LHRH analogue as studied by electron microscopy and radioimmunoassay.

The effect of pimozide and an LHRH-analogue (LHRH-A) on gonadotropic cells of the goldfish pituitary gland were described qualitatively and quantitatively. A scale of four categories was devised to reflect various ultrastructural appearances of the cells. Experimental animals were divided into a control group, a group injected with LHRH-A alone, pimozide alone, and groups receiving these two substances in combination. Fish injected with the single substance were killed 12 h after injection while the groups receiving the combined treatments were killed at 4, 12 and 48 h. Serum levels of gonadotropin measured by radioimmunoassay were used to indicate whether an increase in hormone release had occurred. An immunocytochemical technique, the protein A-gold procedure, assured that the cells studied were gonadotropes. The control group showed variation in the profiles of gonadotropic cells. The single treatment groups showed some increase in secretory inclusions. At 4 h after injection the combined treatment caused a significant increase in hormone granules; at 12 and 48 h there was a gradual decrease in content of secretory products, and an increase in vacuolization. The results indicate that the combined pimozide and LHRH-A treatment stimulated gonadotropin production as well as release.

Animals↗
PubMed1991

LHRH analogues do not protect the germinal epithelium during chemotherapy. An experimental animal investigation.

The protective effect of Decapeptyl, a D-Trp6-LHRH analogue, on the germinal epithelium of rats during chemotherapy was examined in an experimental animal study. Four groups were formed consisting of 15 (groups A and B) and 20 (groups C and D) Sprague-Dawley rats, respectively. The animals were treated as follows: group A (control group) was given 0.9% NaCl i.m.; group B (LHRH group) D-Trp6-LHRH analogue (Decapeptyl); group C (LHRH + chemotherapy group) Decapeptyl + cyclophosphamide; group D (chemotherapy group) cyclophosphamide. The gonads were removed before therapy was initiated and on days 13, 52, and 182 after treatment and examined histologically. In addition, follicle-stimulating hormone (FSH) levels in the serum, a sensitive indicator of tubular damage, were determined. The most damaging effects of chemotherapy on histology and hormone levels were observed in the animals in group C, which were additionally treated with LHRH analogues. Therefore, it is not possible to protect the germinal epithelium of the rat with LHRH analogues during chemotherapy.

Animals↗
PubMed1993

Total and regional bone mineral content in women treated with GnRH agonists.

Changes in bone mineral content induced by GnRH agonists were investigated by measuring total body bone mineral content (TBBM) and regional bone mineral content (BMC) (arms, legs, trunk, pelvis) and densities with dual energy X-ray absorptiometry in 25 premenopausal women before and after a 6-month treatment with gonadotropin-releasing hormone (GnRH) agonists. Biological markers of bone remodeling, estrogens, luteinizing hormone, and follicle-stimulating hormone were also measured. Weight and body mass index increased significantly after treatment (P < 0.05), and TBBM, corrected for weight (TBBM/W), decreased (P < 0.001). The changes in BMC that we observed ranged from +2.5% to -6.9%. The greatest decrease in regional BMC occurred in the trunk (4.4%, P < 0.001), with TBBM decreasing by 2.1% (P < 0.001). No significant changes were observed in the limbs. Tartrate-resistant acid phosphatase (TRAP) increased significantly after treatment (P < 0.001) and a significant negative correlation between TRAP and TBBM (P < 0.001) and between TRAP and estradiol (P < 0.001) were observed before treatment. The lack of changes observed in the BMC of the limbs indicate that GnRH agonists cause a preferential loss of BMC in trunk osseous structures, a situation similar to that of the first years of menopause.

Absorptiometry, Photon↗
PubMed1992

The effect of a synthetic GnRH analogue on catamenial epilepsy: a study in ten patients.

Ten female patients suffering from catamenial epilepsy were treated with a synthetic analogue of the gonadotrophin releasing hormone (GnRH) in addition to antiepileptic drugs. Three of the patients became seizure free, in four patients seizure frequency decreased and in one patient seizures were of shorter duration. In only two of the patients was there no therapeutic effect. Adverse effects, including hot flushes, headache and increase in weight, were noticed in eight patients. These results support the hypothesis that treatment with a synthetic GnRH analogue might be helpful in patients with intractable catamenial epilepsies.

Adult↗
PubMed1991

Combined gonadotropin releasing hormone agonist/human menopausal gonadotropin therapy (GnRH-a/hMG) in normal, high, and poor responders to hMG.

Patients who failed to conceive after gonadotropin stimulation in in vitro fertilization treatment were classified into normal, high, or poor responders. They were routinely offered another cycle with a combination of a gonadotropin releasing hormone agonist and gonadotropin therapy (in order to evaluate whether this combined therapy could improve their response). The gonadotropin-induced cycle was compared with the combined therapy cycle. With the combination treatment, in the normal responders the phase of ovarian stimulation was significantly (P less than 0.001) prolonged, and the number of follicles and oocytes collected (5.7 +/- 0.7 vs 3.1 +/- 0.4) was increased, without any change in serum estradiol level compared to the control cycle. In high responders the number of oocytes was not modified by the combined treatment compared with the control cycle. However, serum estradiol level was significantly (P less than 0.005) decreased. The combined therapy did not modify any parameter of response in poor responders. We conclude that the response to combined agonist/gonadotropin therapy is dependent on the patient's own basal response. No improvement in response was expected in poor responders.

Delayed-Action Preparations↗
PubMed1991

The use of long-acting gonadotropin-releasing hormone agonist (GnRH-a; decapeptyl) and gonadotropins versus short-acting GnRH-a (buserelin) and gonadotropins before and during ovarian stimulation for in vitro fertilization (IVF).

The efficiency of two ovarian stimulation protocols using different gonadotropin-releasing hormone agonists (GnRH-a) for in vitro fertilization (IVF) was examined and compared with human menopausal gonadotropin (hMG)-only stimulation. Fifty-four patients who had 57 aspiration cycles were treated with protocol 1, which consisted of long-acting GnRH-a D-Trp6 (Decapeptyl Depot) and hMG. Protocol 2 entailed intranasal administration of short-acting GnRH-a (Buserelin) and human menopausal gonadotropin (hMG) in 66 women who underwent 70 aspiration cycles. Fifty-five patients who had 59 ovum pickups (OPU) treated with hMG only served as a control. No differences were observed in cycle parameters and hormonal concentrations among the three groups. The total clinical pregnancy rates per OPU for patients receiving protocols 1 and 2 were 12.3 and 27.1%, respectively (P less than 0.05). The pregnancy loss was significantly lower in protocol 2 than in protocol 1 (26.3 versus 71.4%; P less than 0.05). Our data show superiority of short-acting GnRH-a over the long-acting agents in achievement of pregnancy and its outcome, though neither was significantly different from the hMG-only protocol.

Adult↗
PubMed1992

Treatment of experimental DMBA induced mammary carcinoma with Cetrorelix (SB-75): a potent antagonist of luteinizing hormone-releasing hormone.

Cetrorelix, (Ac-D-Nal(2)1, D-Phe(4Cl)2, D-Pal(3)3, D-Cit6, D-Ala10)-LHRH (SB-75) is a new highly potent antagonist of LH-RH. In the model of DMBA-induced mammary carcinoma, this antagonist was very effective in reducing tumor mass. A rapid decrease in tumor weights to levels below 0.1 g total tumor mass was achieved with 300 micrograms/kg given sc. daily for 14 days. The weights of uteri and ovaries were reduced to about 40-50% of control values. In all treated rats the estrus cycle was interrupted and the animals remained in a state of anestrus. Microscopically, the effects of Cetrorelix on the tumors were characterized by a loss of mitotic activity, marked regression with apoptosis, an increase of stroma and differentiation towards a normal mammary architecture. On the basis of a dose-response curve, a dose of 100 micrograms/kg/d of Cetrorelix was determined as sufficient for a full antitumor response. Large DMBA-tumors with total tumor mass of about 6 g could also be treated very effectively with a dose of 100 micrograms/kg/d. To achieve a complete tumor regression, the treatment had to last 34 days. After the cessation of treatment with 100 micrograms/kg/d and regrowth of the tumors the animals were treated with the agonist Decapeptyl (Trp6-LHRH) using a dose of 50 micrograms/rat/d for 14 days. Again, the tumors responded well and regressed within 10 days. The treatment with an overlapping dose schedule of Cetrorelix and Decapeptyl showed a continuous antitumor response. A transient stimulation of tumor growth by the LH-RH agonist was not observed under these experimental conditions. In ovariectomized rats bearing DMBA-tumors, treatment with Cetrorelix and estradiol, produced no tumor growth inhibition as compared to estradiol control group, indicating that there is no estrogen nullifying effect of this antagonist on tumor cells in this model. On the basis of these results, Cetrorelix is a highly effective antitumor agent in this breast cancer model, which might also be useful under clinical conditions.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Luteinizing response to human chorionic gonadotropin does not predict outcome in gonadotropin releasing hormone agonist-suppressed/human menopausal gonadotropin-stimulated in vitro fertilization (IVF) cycles.

OBJECTIVE: The purpose of this study was to determine if early luteinizing potential in gonadotropin releasing hormone agonist (GnRH-a)-suppressed/human menopausal gonadotropin (hMG)-stimulated IVF cycles is predictive of cycle outcome. DESIGN, PATIENTS: The study was a prospective evaluation of 41 women beginning a GnRH-a-suppressed/hMG-stimulated IVF cycle. SETTING: The in vitro fertilization program of a tertiary care institution was the study setting. MAIN OUTCOME MEASURES: The main outcome measures were (1) estradiol (E2) and progesterone (P) levels on the day of human chorionic gonadotropin (hCG) administration and the following day and (2) the ovarian response to ovulation induction and clinical outcome. RESULTS: Ten of the 41 women achieved a clinical pregnancy (24.4%). There was no significant difference in progesterone (P) levels on the day of or the day following hCG administration between the pregnant and the nonpregnant groups. Both groups exhibited a significant rise in P level in response to hCG. There was no significant difference in E2 levels on the day of hCG between the two groups. The serum E2 did not rise significantly in response to hCG in either group. Patients who became pregnant had significantly more oocytes retrieved, fertilized, cleaved, and transferred. CONCLUSIONS: Clinical response and outcome in GnRH-a-suppressed/hMG-stimulated IVF cycles are not predicted by early luteinizing potential as indicated by the response of E2 or P to hCG.

Adult↗
PubMed1992

Leuprolide acetate elevates prolactin during ovarian stimulation with gonadotropins.

OBJECTIVE: The purpose of this study was to determine whether gonadotropin-releasing hormone agonist further increases the prolactin rise accompanying ovarian stimulation. DESIGN: Serum prolactin concentrations were compared between cycles with and cycles without the use of leuprolide acetate (LA) matched for estradiol levels. Relationships of prolactin levels to cycle outcomes were examined. SETTING: The study took place at a private fertility center. PATIENTS: Patients were women receiving stimulation for oocyte retrieval using human menopausal gonadotropins. INTERVENTIONS: No interventions were used. MAIN OUTCOME MEASURES: Serum prolactin level, fertilization rate, embryo quality, and pregnancy were the main outcome measures. RESULTS: Higher serum prolactin was associated with both higher estradiol levels and use of LA but did not have any effects on fertilization rate, embryo quality, or occurrence of pregnancy. CONCLUSION: LA stimulates prolactin release during ovarian stimulation but without apparent consequence.

Chorionic Gonadotropin↗
PubMed1992

Hormonal stimulation for in vitro fertilization: a comparison of fertilization rates and cytogenetic findings in unfertilized oocytes.

OBJECTIVE: The purpose of this study was to compare fertilization and aneuploidy rates after two stimulation protocols in an IVF program. DESIGN: This was a retrospective study. SETTING: The study took place in the IVF laboratory of an Infertility Department. METHODS: In 349 treatment cycles, clomiphene citrate (CC) and human menopausal gonadotropin (hMG) were used in one group (N = 233) and hMG after treatment with a gonadotropin-releasing hormone agonist (GnRHa) in two other groups (long protocol): goserelin (N = 73) and buserelin (N = 43). Cytogenetic analysis was performed on all unfertilized oocytes in both groups. RESULTS: Fertilization rates were significantly higher in the GnRHa/hMG group than in the CC/hMG group, but cleavage rates and embryo quality were not different. Of 736 oocytes prepared for cytogenetic analysis, 256 were karyotyped: 172 were found to be euploid and 84 aneuploid. More oocytes were aneuploid in the GnRHa/hMG group than in the CC/hMG group and this difference was statistically different after analysis of the data using a specially designed mathematical model. CONCLUSION: If no selection against chromosomally abnormal oocytes takes place at the time of fertilization, more abnormal oocytes are harvested with GnRHa/hMG protocols than with CC/hMG. If, on the other hand, there is a selection against oocytes with some chromosomal imbalance, there is no intrinsic effect of GnRH agonists on the chromosomal complement of the oocyte, and the real aneuploidy frequency in all oocytes, fertilized and unfertilized, is the same in the GnRHa/hMG and in the CC/hMG group.

Aneuploidy↗
PubMed1993

The impact of D-Trp6 luteinizing hormone-releasing hormone (LH-RH) on carbohydrate metabolism.

BACKGROUND: The population exposed to repeated cycles of gonadotropin-releasing hormone analogue treatment before in vitro fertilization is growing rapidly. Sex steroids have been shown to induce changes in carbohydrate metabolism. In view of the effect of gonadotropin-releasing hormone analogues on sex steroid levels, it seems of interest to investigate carbohydrate metabolism following treatment with these compounds. PURPOSE: Our purpose was to assess possible changes in glucose tolerance following administration of the long-acting gonadotropin-releasing hormone and analogue, D-Trp6 LH-RH. DESIGN: A 3-hr oral glucose tolerance test with 100 g glucose was performed on all patients, before and after 6 weeks of treatment. RESULTS: No significant changes in either glucose tolerance or insulin levels following treatment with D-Trp6 LH-RH were demonstrated in the group of 25 women investigated. CONCLUSION: With respect to carbohydrate metabolism, D-Trp6 LH-RH may safely be administered to healthy women. Further studies are still required to assess the safety of this GnRH analogue when treating potentially diabetic and diabetic patients.

Adult↗
PubMed1993

Effect of treatment with LHRH analogs containing cytotoxic radicals on the binding characteristics of receptors for luteinizing-hormone-releasing hormone in MXT mouse mammary carcinoma.

Binding capacities and apparent dissociation constants of receptors for luteinizing-hormone-releasing hormone (LHRH) were investigated in estrogen-independent MXT mammary cancers of untreated mice and after in vivo treatment with agonistic or antagonistic analogs of LHRH containing cytotoxic radicals: AJ-04 (agonist [D-Lys6]LHRH linked to methotrexate), T-98-([D-Lys6]LHRH coupled to glutaryl-2-(hydroxmethyl)anthraquinone (G-HMAQ)) and T-121/B (LHRH antagonist T-147 containing two residues of G-HMAQ), which induced tumor growth inhibition. The effects were compared to LHRH agonist [D-Trp6]LHRH and carriers [D-Lys6]LHRH, LHRH antagonist T-147, as well as to methotrexate, G-HMAQ and surgical bilateral overiectomy. Analysis of the binding data revealed that in control tumors the interaction of 125I-[D-TRP6]LHRH was consistent with the presence of one class of saturable, specific, noncooperative, high-affinity and low-capacity binding sites. Chronic treatment of mice bearing MXT tumors with LHRH analogs AJ-04 and T-121/B carrying cytotoxic radicals, but not with T-98 produced significant down-regulation of membrane receptors for LHRH. The largest decrease in dissociation binding constant and Bmax of receptors for LHRH was also found in animals treated with T-121/B. Specific, high affinity binding of 125I-labelled epidermal growth factor (EGF) was detected in the membranes from control and treated MXT tumors. Treatment with cytotoxic LHRH analogs, AJ-04, T-98 and especially with T-121/B, reduced maximal binding capacity of EGF receptors. Our results indicate that LHRH analogs carrying cytotoxic radicals retain their hormonal activity and inhibit tumor growth while inducing down-regulation of LHRH receptors. In addition, probably both components of the cytotoxic LHRH analog, peptide carriers and cytotoxic radicals, reduce the binding capacity of EGF receptors, which might be useful in the treatment of breast cancer.

Amino Acid Sequence↗