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PubMed1995

Successful conservative treatment of catamenial pneumothorax with GnRH agonist.

A thirty four year old woman with recurrent catamenial pneumothorax is described. Pleural endometriosis was suspected and cytologic examination of fluid drained from the right pleural cavity showed glandular cell clusters of probable endometrial origin. The patient received a long-acting GnRH agonist (Triptorelin-Arvekap-Ipsen) 3.75 mg/month I.M. for nine months and remains asymptomatic with regular periods 12 months after discontinuing the treatment.

Adult↗
PubMed1997

Intermittent Etidronate partially prevents bone loss in hirsute hyperandrogenic women treated with GnRH agonist.

Treatment with gonadotropin-releasing hormone (GnRH) agonist leads to enhanced bone turnover and accelerated bone loss in premenopausal women with endometriosis, uterine leiomyomatomas and hirsutism. Sodium etidronate is a powerful inhibitor of bone resorption which had been proven efficacious in the prevention and treatment of postmenopausal osteoporosis. The objective of this study was to evaluate the skeletal effects of 6 months of therapy with the depot preparation of the GnRH agonist triptorelin (decapeptil 3.75 mg intramuscularly every 4 weeks) in 24 hirsute patients, aged 24-33 years, with hyperandrogenic chronic anovulation. Ten patients also received cyclical etidronate in an oral dose of 400 mg/day for 2 weeks, followed by an 11-week period of 500 mg/day elemental oral calcium (one cycle). The remaining 14 patients received 500 mg/day of elemental calcium continuously. After 6 months all treatments were discontinued for at least a further 6 months. Bone mineral density (BMD) at lumbar spine and hip (dual-energy X-ray absorptiometry, Sophos LXRA, France) and biochemical markers (serum alkaline phosphatase, osteocalcin, urinary N-telopeptide and hydroxyproline/creatinine ratio) were evaluated at baseline, 6 months and 12 months. In the group given GnRH agonist alone BMD fell significantly at all measured skeletal sites during the first 6 months. In the patients treated with etidronate a significant decrease in BMD was observed at lumbar spine but not in the femoral neck and trochanter, and the changes at lumbar spine and trochanter were significantly smaller than those in the control group. At 6 months bone turnover was also increased in patients treated with GnRH and calcium. Cyclical etidronate prevented the increase in biochemical markers of bone formation and resorption, with the exception of calcium/creatinine excretion, which was significantly increased in both groups. Six months after treatment withdrawal BMD did not recover in either group. Biochemical markers (N-telopeptide, serum alkaline phosphatase) remained increased in those patients previously treated with calcium alone while they remained close to baseline values in the patients treated with cyclical etidronate. Our study indicates that: (1) GnRH agonist therapy causes remarkable bone loss in young individuals with androgen excess who are expected to have increased bone mass; (2) this bone loss can be partially prevented by intermittent cyclical etidronate therapy.

Adult↗
PubMed1990

Compared effects of GnRH analogs and 4-hydroxytamoxifen on growth and steroid receptors in antiestrogen sensitive and resistant MCF-7 breast cancer cell sublines.

Antiestrogens, such as tamoxifen, have a direct antitumor action and are widely used in cancer therapy. The direct antitumor action of GnRH analogs has been documented in both in vitro and clinical studies. GnRH analog direct action could therefore provide an alternative approach in postmenopausal patients developing antiestrogen resistance, a frequent cause of relapse during hormonal treatment of breast cancer. This study was carried out to compare the effects of two GnRH analogs (the agonist Decapeptyl and the antagonist BIM 21009C) and the antiestrogen 4-hydroxy-tamoxifen (OH-TAM) on proliferation in antiestrogen-responsive or antiestrogen-resistant human breast cancer cell lines (MCF-7, MCF-7 LY2). Ineffective when used without estrogen stimulation, both of the GnRH analogs and OH-TAM inhibit the 17 beta-estradiol-stimulated growth of the estrogen-responsive cell line MCF-7. Compared with parental MCF-7 cell line responsiveness, the antiestrogen-resistant variant MCF-7 LY2 appears to be resistant to GnRH analogs. These findings indicate similarities between the two types of compounds with regard to their antiestrogenic effects on growth observed in vitro. However, since unlike OH-TAM, Decapeptyl displays no effect on steroid receptor levels of sensitive MCF-7 cells, the intracellular inhibitory mechanisms of these drugs are probably in part different. This study suggests that the direct effect of the studied GnRH analogs would not be a potent tool for treating antiestrogen-resistant breast tumors.

Antineoplastic Agents↗
PubMed1992

Inhibition of growth of MCF-7 MIII human breast carcinoma in nude mice by treatment with agonists or antagonists of LH-RH.

Human breast carcinoma (MCF-7 MIII), which exhibits an estrogen-independent but estrogen-responsive phenotype, was xenografted in 8-9-week-old intact female athymic nude mice without estrogen supplementation. In this model, we investigated inhibitory effects of the modern luteinizing hormone-releasing hormone (LH-RH) antagonist SB-75 and the agonist D-Trp6-LH-RH. The analogs were administered in the form of sustained delivery systems (microcapsules and microgranules). In the first experiment, treatment lasted 10 weeks. After 9 weeks of treatment, a significant inhibition of tumor volume was first found only in the group treated with SB-75, but the final tumor volume was significantly suppressed both by D-Trp6-LH-RH and SB-75. In the second experiment, treatment was started 70 days after tumor transplantation and was continued for 6 weeks. Chronic treatment with SB-75 or D-Trp6-LH-RH appeared to completely arrest tumor growth as measured by tumor volume, percentage change in tumor volume, and tumor weight. Serum estradiol was suppressed to undetectable levels and LH levels were also diminished. Histologically, the regressive changes in the treated tumors were due to the enhancement of apoptosis (programmed cell death) of tumor cells. Membrane receptor assays showed that LH-RH binding sites were down-regulated in tumor cells after treatment with SB-75 or D-Trp6-LH-RH. The results indicate that the antagonist SB-75, released from sustained delivery systems, can inhibit the growth of MCF-7 MIII tumors as effectively as the agonist D-Trp6-LH-RH, but more rapidly. In view of its immediate blockade of the pituitary-gonadal axis and the absence of side effects, the LH-RH antagonist SB-75 might be considered as a possible new hormonal agent for the treatment of breast cancer.

Adenocarcinoma↗
PubMed1993

Reduction of bone density: an effect of gonadotropin releasing hormone analogue treatment in central precocious puberty.

Gonadal steroids drive the significant bone mineral increase that occurs at puberty. Oestrogen deprivation in women results in bone loss. We investigated bone mineralization by single photon absorptiometry in girls with central precocious puberty (n = 13, age 3.8-8.5 years) before and during 1 year of treatment with gonadotropin releasing hormone analogue (GnRH-a = long-acting D-Trp6-GnRH, 60 micrograms i.m. every 28 days). Before GnRH-a therapy, bone mineral density (BMD) was significantly higher in patients than in ten control girls matched for chronological age (patients 0.575 +/- 0.097 g/cm2, controls 0.433 +/- 0.049 g/cm2, P < 0.001). Patient BMD was not significantly different from that of ten control girls matched according to patient bone, age (0.550 +/- 0.046 g/cm2, P = NS). During GnRH-a treatment, pituitary-gonadal axis was suppressed and patient BMD significantly decreased (6 months: -6.0%, P < 0.002 vs baseline; 12 months: -8.0%, P < 0.001 vs baseline). We conclude that in girls with precocious puberty the activation of gonadal steroid secretion induces an increase in bone mineralization and that oestrogen deprivation by GnRH-a treatment caused a significant decrease in BMD.

Absorptiometry, Photon↗
PubMed1993

Failure to improve height prediction in short-stature pubertal adolescents by inhibiting puberty with luteinizing hormone-releasing hormone analogue.

A group of 17 endocrinologically normal short stature adolescent (9 females aged 11.8 +/- 1.5 years and 8 males aged 13.2 +/- 1.1 years) referred at a pubertal stage II-III according to Tanner with a height prediction below -2.5 SD according to Bayley and Pinneau, were treated with long-acting D-Trp6-luteinizing hormone-releasing hormone (3.75 mg i.m. monthly for 24 months) and observed for a period of 13.4 +/- 5.8 months. Pubertal progression was suppressed during the 2 years of analogue therapy, then resumed shortly after the end of treatment. Annual growth rate remained in the prepubertal range during the treatment period and did not increase with the resumption of sexual development. A reduced rate of bone maturation was observed during the 2 years of analogue treatment without clear-cut improvement of the height to bone age relationship at the end of the treatment nor after the post-treatment observation period. Thus, after approximately 3 years of study, no significant improvement of predicted adult stature was obtained. There were no side-effects, but psychological problems mainly related to the failure to increase height. Though methods for predicting adult height are not accurate, these data suggest that use of luteinizing hormone-releasing hormone analogue in endocrinologically normal short subjects entering puberty at normal age with a poor height prognosis does not offer enough possible advantages on growth to offset the possible psychological drawbacks, and cannot be considered as routine treatment in this situation.

Adolescent↗
PubMed1992

Predictive factors for the effect of gonadotrophin releasing hormone analogue therapy on the height of girls with idiopathic central precocious puberty.

The factors influencing the final height of central precocious puberty patients treated with gonadotrophin releasing hormone (GnRH) analogues remain a critical issue. This study compares the predicted final height before and after GnRH analogue therapy to identify predictive factors for final height. Fourteen girls with idiopathic central precocious puberty were treated with a GnRH analogue. All had an active non-regressive form before therapy, full and permanent suppression of oestrogenic activity during therapy (duration greater than 2 years, 3.1 +/- 0.3 years, mean +/- SEM), and the pubertal pituitary-ovarian axis had normalized in all of them 1 year after the cessation of therapy. The mean predicted final height increased from 152 +/- 1.8 cm before therapy to 162.2 +/- 1.2 cm (P less than 0.01) at the last evaluation performed 4.5 +/- 0.3 years after the onset of therapy. The mean gain in predicted final height between the onset of therapy and the last evaluation was 10.2 +/- 1.1 cm. It was correlated with the following data recorded at the onset of therapy: bone age advance over chronological age (r = 0.66, P less than 0.02), predicted final height at the onset of therapy (r = -0.76, P less than 0.001), and the difference between the target height and the predicted height at onset of therapy (r = 0.76, P less than 0.001). We conclude that GnRH analogue therapy is more likely to improve final height prognosis in girls who initially present with a markedly advanced bone age and a great difference between their target and predicted heights. Both these parameters reflect the severity of the disease at diagnosis.

Body Height↗
PubMed1992

Evaluation of binding of cytotoxic analogs of luteinizing hormone-releasing hormone to human breast cancer and mouse MXT mammary tumor.

The binding characteristics of several cytotoxic analogs of luteinizing hormone-releasing hormone (LH-RH) developed in our laboratory were examined in membranes from human breast cancer and estrogen independent MXT mammary cancer. Specific binding of [125I]D-Trp6-LH-RH and the cytotoxic LH-RH analog [125I]T-98 ([D-Lys6]LH-RH coupled to glutaryl-2-(hydroxymethyl)anthraquinone) (HMAQG) was demonstrated in membrane preparations from human breast and MXT mammary tumor cells. Ligand binding of T-98 was specific, saturable, and dependent on temperature, time, and plasma membrane concentration. Analysis of the binding data showed that in human breast cancer, interaction of [125I]T-98 was consistent with the presence of two classes of LH-RH receptors, one class showing high affinity and low capacity, and the other class showing low affinity and high capacity binding. In membranes from MXT mammary cancer, T-98 bound to one class of saturable, specific, noncooperative binding sites with high affinity and low capacity. The rates of association and dissociation for [125I]T-98 were calculated to be 4.757 x 10(8) M-1 min-1 and 0.016 min-1 (t1/2 = 38.7) in membranes from MXT mammary cancer. In human breast cancer, association rate constants (K1a and K1b) were 2.3 x 10(6) M-1 min-1 for binding to high affinity and 1.8 x 10(4) M-1 min-1 for binding to low affinity binding sites. Dissociation rate constants were K-1a = 0.0801 min-1 (t1/2a = 63.4 min) and K-1b = 0.0467 min-1 (t1/2b = 23.5 min), respectively. [125I]T-98 was not displaced by either unlabeled somatostatin or epidermal growth factor, but was displaced completely by unlabeled T-98 or [D-Trp6]LH-RH. The analysis of displacement curves of [D-Trp6]LH-RH by cytotoxic agonists and antagonists of LH-RH synthesized in our laboratory showed that T-121, AJ-11, T-120, T-133, and T-98 were the most potent in displacing [125I]D-Trp6-LH-RH from breast and MXT cancer membranes. Binding kinetics and analyses of displacement curves of [125I]D-Trp6-LH-RH and [125I]T-98 in membranes of human breast cancer and estrogen independent MXT mouse mammary cancer suggest that binding of the cytotoxic analog T-98 to the LH-RH receptor proceeds reversibly like that of its congeners without cytotoxic radicals. Our findings may provide a stimulus for further studies with LH-RH analogs carrying cytotoxic radicals.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of somatostatin, or a combination.

Female BDF1 mice inoculated with MXT (3.2) estrogen independent mouse mammary carcinoma were treated for three weeks with microcapsules of the luteinizing hormone-releasing hormone (LH-RH) agonist [D-Trp6]LH-RH, the antagonist SB-75, the somatostatin analog RC-160, or combinations. The lack of estrogen dependence of the tumor was proved by bilateral surgical ovariectomy, which had no effect. In two experiments, treatment with 25 micrograms/day doses of each analog alone resulted in a significant inhibition of tumor growth as shown by a 40-53% inhibition of tumor volumes, 38-43% decrease in tumor weights, and histological signs of tumor regression. However, the combination of SB-75 or [D-Trp6]LH-RH with somatostatin analog RC-160 caused greater reduction of tumor volume (68 and 61%) or tumor weights (59 and 56%), than single analogs, and histologically the occurrence of apoptosis and decrease in AgNOR numbers was more pronounced in the groups receiving combination therapy. Specific binding sites for [D-Trp6]LH-RH, EGF, and IGF-I were demonstrated in the tumor membranes. The binding capacity of LH-RH receptors was decreased by treatment with the analogs, the greatest down-regulation being caused by combination therapy. A significant decrease in EGF binding capacity was observed after treatment with the LH-RH analogs, alone or especially in combination with somatostatin analog RC-160. The combination of these analogs also caused a reduction in IGF-I receptors. The finding that LH-RH agonists and antagonists and somatostatin analogs inhibit the growth of estrogen independent mammary tumors, and that combinations are more effective than single analogs, might be of practical importance in human breast cancer therapy.

Amino Acid Sequence↗
PubMed1996

The impact of D-Trp6 LH-RH on plasma lipid levels.

BACKGROUND: There is increasing evidence regarding the correlation between the risk of death from cardiovascular disease and low levels of HDL-cholesterol or high plasma concentrations of LDL-cholesterol, total cholesterol, and triglycerides. Gonadotropin releasing hormone (GhRH) analogues are widely used in assisted reproduction programs. Therefore, it seems important to evaluate possible changes in serum lipoprotein levels following treatment with these compounds. PURPOSE: Our purpose was to assess possible lipoprotein changes following administration of the long-acting GnRH analogue, D-Trp6 luteinizing hormone-releasing hormone (LH-RH). DESIGN: Serum levels of cholesterol, HDL-cholesterol, LDL-cholesterol, and triglicerydes were determined before and after 6 weeks of treatment. RESULTS: No significant changes in either cholesterol or HDL-cholesterol, LDL-cholesterol, or triglicerydes following treatment with D-Trp6 LH-RH were demonstrated in the group of 25 patients investigated. CONCLUSIONS: Short-term use of D-Trp6 LH-RH is not associated with any significant change in plasma lipid levels. Further studies are still required with patients undergoing repeated treatment cycles, especially those who exhibit elevated pretreatment plasma lipid levels, to confirm the long-term safety of GnRH analogues with respect to lipid metabolism.

Arteriosclerosis↗
PubMed1995

Bone loss during gonadotropin releasing hormone agonist treatment and use of nasal calcitonin.

Gonadotropin releasing hormone (GnRH) agonists have shown to be effective in the treatment of several sex-hormone-dependent conditions. However, their use could be limited by the bone loss they induce. To evaluate the use of nasal salmon calcitonin (sCT) in preventing this bone loss, 40 patients with endometriosis were treated for 6 months with triptoreline (3.75 mg monthly) and calcium (1 g daily), and randomized in three groups-placebo, sCT 100 IU daily and sCT 200 IU daily-in a prospective double-masked study. Dual-energy X-ray absorptiometry and biochemical parameters were used to evaluate the benefit of the treatment. At baseline, there were no statistically significant differences between the groups. After 6 months, estradiol and biochemical markers of bone metabolism were at postmenopausal levels, with no difference between the groups. There was no difference in bone loss in the three groups, at all sites. Mean lumbar bone loss was 4.01 +/- 2.59% (mean +/- SD) in this population. In this study dosages of 100 IU and 200 IU daily of nasal sCT were insufficient to prevent bone loss during GnRH agonist treatment.

Absorptiometry, Photon↗
PubMed1980

Hormonal and behavioral response of male chimpanzees to a long-acting analogue of gonadotropin-releasing hormone.

A long-acting preparation of gonadotropin-releasing hormone (GnRH) was administered to three adult male chimpanzees living in a socially integrated group. Hormonal changes and behavioral responses were monitored for 8 days. Blood serum levels of luteinizing hormone peaked at about 8 hr and returned to baseline at 48 hr. Total serum testosterone reached the highest levels of 140% above baseline at 24 hr and returned to baseline after 48 hr. Out of a wide variety of behaviors observed in detail, only one cluster of three related behaviors showed even a suggestion of response: The two measures of activity, lone travel (p < 0.05) and distance traveled (p < 0.1), decreased on the day of hormone administration followed by an increase on the 2 subsequent days, and idle time (p < 0.1) revealed the reciprocal pattern. In view of various reports of behavioral effects of GnRH in other species, it is particularly noteworthly that parameters of sexual and agonistic behavior of male chimpanzees definitely did not change.

Agonistic Behavior↗
PubMed1990

Treatment of children with central precocious puberty by a slow-release gonadotropin-releasing hormone agonist.

A total of 82 patients (74 girls, 8 boys) are presently participating in an international multicentre trial for treatment of central precocious puberty (CPP) with a slow release gonadotropin-releasing hormone (GnRH) agonist depot preparation: Decapeptyl-Depot (DD). Of these patients, 53 (3 boys) were previously untreated (group 1) and 29 (5 boys) have been treated before with either a short-acting GnRH analogue or cyproterone acetate (group 2). Fifty-one patients (44 girls, 7 boys) were treated with DD for 12 months or more. Basal plasma luteinizing hormone (LH) levels decreased in both groups after 1 year of therapy. The LH response to intravenous GnRH was reduced in both groups. Basal plasma follicle stimulating hormone (FSH) levels decreased in both groups. Stimulated FSH levels were reduced in both groups after 1 year of DD treatment. Plasma oestradiol levels in the girls decreased to prepubertal levels in both groups. In all patients the clinical signs of precocious gonadarche such as breast development and menstruations (girls) and an increased testis volume (boys), did not further progress and sometimes regressed in several patients. Growth velocity decreased in the girls of group 1 from 9.0 +/- 0.72 cm/year (mean +/- SEM) in the last half-year before treatment to 6.3 +/- 0.50 in the first half-year of treatment (P less than 0.01) and to 4.5 +/- 0.23 cm/year in the second half-year (P less than 0.01). After 12 months a stabilization of growth velocity was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Height↗
PubMed1995

Comparison between nafarelin acetate and D-Trp6-LHRH for temporary pituitary suppression in in vitro fertilization (IVF) patients: a prospective crossover study.

PURPOSE: Nafarelin acetate is a new gonadotropin releasing (GnRH) agonist analogue with unique potency, intranasal administration, and convenient storage. Hence, nafarelin was considered as an alternative for temporary pituitary suppression in patients undergoing ovulation induction in IVF. A crossover treatment in a prospective study was performed including 40 women with bilateral obstructed tubes and normal ovarian function, treated in 80 ovulation induction cycles using the long protocol. Twenty patients used nafarelin acetate 600 micrograms/daily in their first cycle and received D-Trp6-LHRH, 0.5 mg/daily, in their following cycle. The other 20 women used decapeptyl in their cycle and received nafarelin in the second. RESULTS: Estradiol suppression was achieved by both D-Trp6-LHRH and nafarelin at equal time intervals. The average total number of ampoules (P = 0.0005) and the length of administration of hMG required for ovarian stimulation (P = 0.0002) and the time interval between GnRHa initiation to oocyte retrieval (P = 0.04) was significantly lower in nafarelin cycles. The number and the distribution between large and small follicles as well as the average number of oocytes retrieved did not differ between the two GnRH analogues. CONCLUSION: Our results demonstrate that nafarelin acetate is comparable to D-Trp6-LHRH for temporary pituitary suppression used for controlled ovarian stimulation in IVF patients. However, using nafarelin ovarian stimulation was achieved with few ampoules of hMG, administered for a shorter period of time, thus with a lesser cost.

Adult↗
PubMed1996

Chronic GnRH agonist administration down-regulates platelet serotonin transporter in women undergoing assisted reproductive treatment.

The effect of pretreatment with the gonadotropin releasing hormone (GnRH) agonist D-Trp6-LHRH (Decapeptyl) on platelet serotonin transporter in women undergoing assisted reproductive treatment (ART) was investigated and compared with women treated with human menopausal gonadotropin (Pergonal). The study group (n = 10) was exposed for 12 days to 3.2 mg Decapeptyl C.R. while a comparison group (n = 9) was exposed to 11 days of human meno-pausal gonadotropin (Pergonal). All patients were assessed with the Hamilton depression and anxiety scales before and after treatment, and platelet and plasma samples were collected at the same time points. Plasma levels of estradiol, progesterone. FSH and LH were determined by radioimmunoassay (RIA). Platelet serotonin transporter was labeled using high affinity [3H]imipramine binding. The GnRH analogue induced ovarian suppression as reflected by low plasma estradiol levels, while Pergonal administration induced ovarian stimulation. An elevation in the Hamilton depression and anxiety scale scores was observed in the Decapeptyl treated group; this mood alteration was associated with a significant decrease (19%, P < 0.05) in the density (Bmax) of platelet [3H]imipramine binding sites. No significant change was observed in the Bmax of the Pergonal treated group. These results indicate that ovarian suppression (menopausal-like state) in young women is associated with depressed and anxious mood and decreased serotonin transporter density.

Adult↗
PubMed1989

[Combined GnRH analogs/hMG/hCG treatment].

Ovarian stimulation with human menopausal gonadotropins after Gn-RH-analogue induced pituitary desensitization has been shown to optimize the follicular maturation. This is mostly due to the avoidance of irregular endogenous LG-reactions which occur during hMG-therapy in about one third of the treatment cycles. In several studies using Buserelin or Decapeptyl as Gn-RH-analogue 282 patients were treated for in vitro fertilization, gamete intrafallopian transfer or as part of an "in vivo" therapy. Pregnancy rates were significantly improved in all groups: HMG/hCG therapy resulted in a pregnancy rate of 17% per patient whereas by the combined therapy in 25% of the patients a pregnancy was achieved.

Buserelin↗