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PubMed2004

Gonadotropin releasing hormone antagonists and cryopreservation outcome: a review.

REVIEW: The outcome of freeze-thaw cycles with pronuclear stage oocytes or embryos, derived from collecting cycles stimulated with gonadotropin-releasing hormone (GnRH)-antagonists' protocols, was reviewed. CONCLUSION: The viability of cryopreserved pronuclear stage oocytes and embryos, the quality of transferred embryos and the pregnancy rates of the freeze-thaw cycles seem to be satisfactory regardless of the type and dose of GnRH-antagonist.

Cryopreservation↗
PubMed2003

Quantitative calcaneal ultrasound parameters and bone mineral density at final height in girls treated with depot gonadotrophin-releasing hormone agonist for central precocious puberty or idiopathic short stature.

UNLABELLED: To evaluate the effect of gonadotrophin-releasing hormone (GnRH) agonist treatment on bone quality at final height, we studied girls with central precocious puberty (CPP) and with idiopathic short stature (ISS). A total of 25 Caucasian girls were included: group A (n=14) with idiopathic CPP (mean age at start 7.4 years) and group B (n=11) with ISS (mean age at start 11.7 years). Treatment duration was 3.8 and 1.7 years respectively. The quantitative ultrasound parameters (QUS) broadband ultrasound attenuation (BUA) and speed of sound (SOS) were measured at the calcaneus (UBIS 3000 device). Lumbar spine bone mineral density (BMD; L2-L4) was measured by dual energy X-ray absorptiometry (DXA) (Hologic QDR1000). Measurements were performed at final height and expressed as Z-scores corrected for bone age. Mean Z-scores of QUS parameters, areal BMD and volumetric BMD (BMDvol) were above -1 in both groups (group A: BUA Z-score -0.21, SOS Z-score -0.29, BMD Z-score 0.02, BMDvol Z-score 0.05, group B: BUA Z-score -0.93, SOS Z-score -0.40, BMD Z-score -0.86, BMDvol Z-score -0.68), although mean Z-scores of BUA and areal BMD in group B were significantly different from zero (P=0.03 and P=0.02 respectively). Mean Z-score BMDvol was not significantly different from zero (P=0.05), we found no significant difference between the groups for BMDvol (P=0.13). CONCLUSION: Although quantitative ultrasound parameters parameters and bone mineral density were normal in girls with central precocious puberty at final height after gonadotrophin-releasing hormone agonist treatment, mean Z-score for broadband ultrasound attenuation and areal bone mineral density were significantly different from zero and mean Z-score for volumetric bone mineral density was (just) not significantly different from zero in idiopathic short stature girls with normal puberty treated with gonadotrophin-releasing hormone agonists. Therefore we cannot say that this treatment is safe in these girls with regard to bone health.

Absorptiometry, Photon↗
PubMed1998

Effect of central precocious puberty and gonadotropin-releasing hormone analogue treatment on peak bone mass and final height in females.

UNLABELLED: To evaluate the effect of central precocious puberty (CPP) and its treatment with gonadotropin-releasing hormone (GnRH) analogues on final height and peak bone mass (PBM), we measured lumbar bone mineral density (BMD) in 23 girls at final height. Patients were distributed in two groups. Group 1: 14 patients with progressive CPP were treated with GnRH analogues; seven patients received buserelin (1600 microg/daily), subsequently switched to depot triptorelin (60 microg/kg/26-28 days); seven patients were treated with depot triptorelin (60 microg/kg/26-28 days); mean age of treatment was 6.2 years (range 2.7-7.8 years); the treatment was discontinued at the mean age of 10.1 years (range 8.7-11.3 years); final height was reached at the mean age 13.4 years (range 12.0-14.9 years). Group 2: 9 patients (mean age 6.5 years, range 4.8-7.7 years) with a slowly progressing variant of CPP were followed without treatment; final height was reached at the mean age 13.6 years (range 12.5-14.8 years). Lumbar BMD (L2-L4 by dual energy X-ray absorptiometry) was measured in all patients at final height. In group 1, final height (158.9+/-5.4 cm) was significantly greater than the pre-treatment predicted height (153.5+/-7.2 cm, P < 0.001), but significantly lower than mid-parental height (163.2+/-6.2 cm, P < 0.005). Subdividing the girls of group 1 according to the bone age at discontinuation of therapy (i.e. < or =11.5 years, n=5, or > or =12.0 years, n=9), the former patients had a final height significantly higher than the latter (163.7+/-3.9 cm vs 156.5+/-4.6 cm, P < 0.02). In group 2, final height (161.8+/-4.6 cm) was similar to the pre-treatment predicted height (163.1+/-6.2 cm, P=NS) and was not significantly different from mid-parental height (161.0+/-5.9 cm). BMD values (group 1: 1.11+/-0.14 g/cm2, group 2: 1.22+/-0.08 g/cm2) were not significantly different from those of a control group (1.18+/-0.10 g/cm; n=20, age 16.3-20.5 years) and the patients' mothers (group 1: 1.16+/-0.07 g/cm2, n=11, age 32.9-45.1 years; group 2: 1.20+/-0.08 g/cm2, n=7, age 33.5-46.5 years). In group 1, the girls who stopped therapy at a bone age < or =11.5 years had significantly higher BMD (1.22+/-0.10 g/cm2) compared to those who discontinued therapy at a bone age > or =12.0 years (1.04+/-0.12 g/ cm2, P < 0.05). CONCLUSION: In girls with progressive CPP, long-term treatment with GnRH analogues improves final height. A subset of patients with CPP does not require treatment because good statural outcome (slowly progressing variant). In CPP, the abnormal onset of puberty and the long-term GnRH analogue treatment do not impair the achievement of PBM. In GnRH treated patients, the discontinuation of therapy at an appropriate bone age for pubertal onset may improve both final height and PBM.

Adolescent↗
PubMed2000

Final height, gonadal function and bone mineral density of adolescent males with central precocious puberty after therapy with gonadotropin-releasing hormone analogues.

UNLABELLED: Few data are available on the outcome of boys with central precocious puberty (CPP) treated with gonadotropin-releasing hormone (GnRH) analogues. We report on final height, endocrine and exocrine testicular function, and bone mineral density (BMD) in nine males (age 16.7 +/- 1.5 years) treated with GnRH analogues from the age 6.0 +/- 1.8 years for a mean period of 5.6 +/- 2.4 years. The following parameters were evaluated: final height, serum gonadotropin and gonadal steroid levels, spermarche, semen analysis, area and volumetric BMD. Final height (-0.4 +/- 1.1 SDS) was significantly higher than pre-treatment predicted adult height (-2.0 +/- 1.2 SDS) and not significantly different than midparental height (-0.1 +/- 0.8 SDS). Pubertal response of gonadotropins to GnRH test occurred within 1.5 years (mean 0.7 +/- 0.4 years) and spermarche (n = 7) from 0.7 to 3 years (1.8 +/- 0.9 years) after the discontinuation of GnRH analogue therapy. No alteration in semen analysis was found (n = 6, sperm count, 10(6)/ml: 52.0 +/- 18.7; normal motility (%): 49.5 +/- 18.7; atypical morphology (%): 44.5 +/- 11.4). Area and volumetric BMD were not reduced (0.2 +/- 1.0 SDS and -0.1 +/- 0.9 SDS, respectively). CONCLUSION: Long-term treatment with gonadotropin-releasing hormone analogues improves final height in boys with central precocious puberty. Post-therapy data demonstrating normal endocrine and exocrine testicular function support the safety of gonadotropin-releasing hormone analogues on reproductive function. Long-term pharmacological suppression of testicular function in childhood does not impair bone mineral density in late adolescence.

Adolescent↗
PubMed2005

Single and repeated GnRH agonist stimulation tests compared with basal markers of ovarian reserve in the prediction of outcome in IVF.

PURPOSE: To study the value of a single or repeated GnRH agonist stimulation test (GAST) in predicting outcome in IVF compared to basal ovarian reserve tests. METHODS: A total of 57 women was included. In a cycle prior to the IVF treatment, on day 3, an antral follicle count (AFC) was performed and blood taken for basal FSH, inhibin B and E2 measurements, followed by a subcutaneous injection of 100 microg triptorelin for the purpose of the GAST. Twenty-four hours later blood sampling was repeated. All the tests were repeated in a subsequent cycle. From the GAST E2 and inhibin B response were used as test parameters. The outcome measures were poor ovarian response and ongoing pregnancy. Group comparisons were done using the Mann-Whitney or chi-square test. Univariate and multivariate logistic regression was applied to assess which test revealed the highest predictive accuracy as expressed in the area under receiver-operating characteristic curve (ROC(AUC)). Clinical value was compared by calculating classical test characteristics for the best logistic models. RESULTS: All the basal and GAST variables were significantly different in the poor responders (n = 19) compared to normal responders (n = 38). In the univariate analysis on cycle 1 tests the AFC was the best predictor for poor ovarian response, while in cycle 2 the E2 response in the GAST performed best (ROC(AUC) of 0.91 for both). Multivariate analysis of the basal variables led to the selection of AFC and inhibin B in cycle 1, yielding a ROC(AUC) of 0.96. Mean E2 response was selected in a multivariate analysis of the repeated GAST variables (ROC(AUC) 0.91). At a specificity level of -0.90, several logistic models including GAST variables appeared to have a sensitivity (-0.80), positive predictive value (-0.82) and false positive rate (-0.18), comparable to a logistic model containing AFC and inhibin B. None of the test variables showed a significant relation with ongoing pregnancy. CONCLUSIONS: The GAST has a rather good ability to predict poor response in IVF. However, comparing the predictive accuracy and clinical value of the GAST with a day 3 AFC and inhibin B, it appeared that neither a single nor a repeated GAST performed better. In addition, the predictive ability towards ongoing pregnancy is poor. Therefore, the use of the GAST as a predictor of outcome in IVF should not be advocated.

Adult↗
PubMed2005

Differences in serum LH and FSH levels using depot or daily GnRH agonists in controlled ovarian stimulation: influence on ovarian response and outcome of ART.

PURPOSE: To study effects of endogenous LH levels on ovarian response and outcome in ART cycles a controlled study was performed with two patient groups differing in the intensity of pituitary downregulation. METHODS: Group I (n = 27) received 3.75 mg of the GnRH agonist triptorelin acetate depot, group II (n = 54) was given 0.1 mg triptorelin acetate daily, followed by ovarian stimulation with recombinant FSH. RESULTS: After downregulation serum LH and FSH levels were significantly lower in group I. Patients of group I needed significantly higher FSH doses to achieve comparable levels of serum estradiol and preovulatory follicles. The number of retrieved oocytes and transferable embryos was lower in group I. CONCLUSION: Patients with profound endogenous LH suppression by depot GnRH agonists show higher FSH stimulation dose requirements and lower oocyte number and fertilization rate, indicating a need for minimal LH activity in folliculogenesis and oocyte development.

Adult↗
PubMed2006

Efficacy of subcutaneous administration of gonadotropin-releasing hormone agonist on idiopathic central precocious puberty.

In order to assess the feasibility of subcutaneous administration of Triptorelin with 6-week intervals for the suppression of pituitary-gonadal axis and changes of clinical signs in girls with idiopathic central precocious puberty (ICPP), 46 girls with ICPP were treated with GnRHa. Triptorelin (Decapeptyl, 3.75 mg) was administered subcutaneously (SC) at 6-weeks intervals or intramuscularly (IM) at 4-weeks intervals randomly for more than 12 months consecutively. During GnRHa therapy, clinical parameters and laboratory data, including height, weight, pubertal stage, bone age, uterine volume and ovarian size, serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol (E2), were monitored and analyzed. It was found that both treatment regimes led to regression of precocious puberty and reversal of secondary sexual characteristics. Breast developments regressed. Uterine volume was decreased after treatment, but there was no statistically significant difference. Mean ovarian volume did not change significantly during treatment. The height velocity was decreased significantly from 6.3+/-1.4 cm/year to 5.8+/-1.2 cm/year in group SC and 6.7+/-1.3 cm/year to 5.4+/-1.0 cm/year in group IM, respectively. The rate of bone maturation was reduced significantly during treatment. The ratio of deltaBA/deltaCA was 1.2+/-0.2 or 1.3+/-0.3 at the onset of therapy and decreased significantly after the treatment to 0.7+/-0.2 or 0.9+/-0.1, respectively. The predicted adult height was increased significantly and progressively during therapy. The levels of serum LH, FSH and E2 returned to the prepubertal condition. No significant side effects of therapy were noted. The most common side effect during SC treatment was that a non-irritating, 1 cm in diameter mass was palpated at the site of subcutaneous injection in the abdominal wall of patients, which disappeared after 6-12 weeks. Two girls had minimal withdrawal vaginal bleeding episodes after the first injection. It was concluded that both IM and SC triptorelin administrations were clinically effective. They induce profound suppression of hypothalamic-pituitary-gonadal axis while stabilizing height velocity, slowing bone maturation and increasing predicted adult height. These results suggest that subcutaneous injection of triptorelin in 6-weeks intervals at a dosage of 3.75 mg be a safe and acceptable regimen for ICPP

Bone Development↗
PubMed2006

Impact of neoadjuvant hormonal therapy on dose-volume histograms in patients with localized prostate cancer under radical radiation therapy.

INTRODUCTION: Prostate volume involves a defined toxicity predictor in the radiation therapy of localized prostate cancer. Neoadjuvant hormone therapy (nHT) can reduce prostate volume and, therefore, the planned volume. The objective of this study was to establish if the value of nHT reduces the planned volume and if this reduction correlates with a reduction of the dose received in the target organs. MATERIAL AND METHODS: 28 patients diagnosed of localized prostate cancer and referred to our departments for radiation therapy with radical intention, in the period ranging between April 2002 and October 2003, were included prospectively. The patients received nHT (triptorelin + flutamide) for 2 months and adjuvant HT until completing 2 years in the high-risk cases. A transrectal ultrasound study was performed in all patients, simulation CT and planning before the start of HT and after 2 months of treatment. The radiation therapy was carried out with 6 or 18 MV LINAC photons, with a dose fractioning scheme of 5 x 180-200 cGy, a total dosage of 66-72 Gy to prostate, 56 Gy to seminal vesicles and, in the high-risk cases, 46 Gy to pelvic lymph nodes. RESULTS: The distribution according to risk group was: low risk 3.6%, intermediate risk 28.6% and high risk 67.9%. By transrectal ultrasound, prostate volume on diagnosis was 50.65 cc pre HT and 38.97 cc post HT (p < 0.001), which means a volume reduction of 24%. The comparative analysis of the dose-volume histograms of the first versus the second CT shows a reduction in the planned volume GTV1 (prostate) (81.33 cc vs 63.96 cc, p < 0.05), PTV1 (prostate and margin) (197.51 cc vs 168.38 cc, p < 0.001) and PTV2 (prostate, vesicles and margin) (340.5 cc vs 307.26 cc, p < 0.05), a reduction of the maximum dose in the seminal vesicles (70.2 versus 68.75 Gy, p < 0.05), a reduction of the mean dose in the seminal vesicles (65.07 Gy versus 63.07 Gy, p < 0.05), PTV2 (67.72 Gy versus 66.9 Gy, p < 0.01) and PTV3 (prostate, vesicles, pelvic lymph nodes and margin) (58.86 Gy versus 57.21 Gy, p < 0.01), a reduction of the D90 in the seminal vesicles (61.83 Gy versus 60.06 Gy, p < 0.05) and PTV2 (61.04 Gy versus 59.45 Gy, p < 0.05) and a reduction of V60 of the rectum (32.45% versus 28.22%, p < 0.05) and V60 of the bladder (41.78% versus 31.67%, p < 0.005). CONCLUSIONS: Neoadjuvant hormone therapy reduces significantly prostate volume and as a result the planned volume and consequently the rectal and bladder V60 can be significantly reduced.

Aged↗
PubMed1990

The effect of large uterine fibroids on urinary bladder function and symptoms.

Fourteen patients with large uterine fibroids and urinary symptoms were treated with monthly injections of [D-Trp6]-luteinizing hormone-releasing hormone microcapsules. The average uterine size before treatment was 728 ml; it dropped to 323 ml (a drop of 55%) after treatment. Urinary symptoms of diurnal frequency disappeared in 11 of 12 patients (p less than 0.005) after the reduction of uterine size. Urgency decreased in 11 of 13 (p less than 0.005) and nocturia in eight of 10 (p less than 0.02). No differences were found before and after treatment in the symptoms of urge incontinence and stress incontinence in the cystometric and urethral pressure profile measurements. Urinary symptoms of frequency, urgency, and nocturia may be caused by the direct pressure exerted on the bladder by the enlarged uterus. Symptoms of urge incontinence and stress incontinence deserve a more specific treatment as they are not related to uterine size.

Adult↗
PubMed1991

Fibrocystic disease of the breast in premenopausal women: histohormonal correlation and response to luteinizing hormone releasing hormone analog treatment.

Sixty-six patients with fibrocystic mastopathy were enrolled in the trial after being selected according to clinical, radioultrasonographic, and histologic criteria. No characteristic hormonal profile was noted in most patients (52%). Estrogen receptors or progesterone receptors, or both, were found in 57% of patients. Hormone receptor levels were correlated with atypical proliferative mastopathy (87.5%). Mastopathy was associated with a uterine fibroma or a fibromatous uterus in 73% of cases. All patients received intramuscular injections of a sustained delivery system (microcapsules) of luteinizing hormone releasing hormone agonist [D-Trp6]-LHRH, Ipsen-Biotech, Paris) for 3 to 6 months. In case of partial response at 3 months, an antiestrogen (tamoxifen, 40 mg/day, for estrogen receptor-predominant lesions) or a progestin (cyproterone acetate, 50 mg/day, for progesterone receptor-predominant lesions) was added to the luteinizing hormone releasing hormone agonist. A complete response was observed in more than half of the patients (n = 35, 53%) treated by [D-Trp6]-LHRH alone (n = 29) or associated with tamoxifen (n = 4) or cyproterone acetate (n = 2). A significant partial response was observed in 30 other patients (45%). Additionally, half of them received inhibitory drugs. The best responses were seen with cyst reformation (complete response, 100%) and fibrous block. Clinical responses to treatment with [D-Trp6]-LHRH alone were independent of hormone receptor status, but synergistic effects occurred with concomitant use of the corresponding inhibitory drugs. We conclude that chronic mastopathy, particularly when associated with uterine fibroma, can be successfully treated by luteinizing hormone releasing hormone analogs in premenopausal women.

Adult↗
PubMed1993

Impact of medical treatment of endometriosis on bone mass.

A review of studies examining the effect of medical therapy of endometriosis on bone mass and potential approaches to preventing bone loss was undertaken. Studies specifically examining bone density in women with endometriosis treated medically were used. Reports on effects of oral contraceptives and progestins on bone mass were derived from women using them for contraception. Oral contraceptives and medroxyprogesterone acetate apparently did not adversely affect bone mass. While initial studies with dual-photon absorptiometry were unable to detect appreciable bone loss with gonadotropin-releasing hormone agonist, subsequent studies have invariably found significant bone loss beginning as early as 3 months of treatment. Quantitated computerized tomography always shows significant trabecular bone loss of the vertebrae and hip with gonadotropin-releasing hormone agonist. Depot preparations appear to produce more marked loss than daily injections of intranasal spray. Recent studies indicate recovery of bone loss may take longer than 6 months or even 1 year after discontinuation of therapy with considerable individual variation. Danazol produced bone gain. Bone loss with gonadotropin-releasing hormone agonists could be prevented or attenuated with progestins, and this is worthy of further studies. Impact of medical therapy on bone mass should be a practical consideration in the selection of patients, in repeat medical therapy for recurrence of endometriosis, and in formulation of medical therapy so as to attenuate or overcome such silent adverse effects.

Bone Density↗
PubMed1984

Administration of human pancreatic growth hormone-releasing factor (GRF) analogs enhances responsiveness of cultured rat pituitary cells to GRF.

The aim of this study was to investigate whether anterior pituitary responsiveness to human pancreatic growth hormone-releasing factor containing 29 amino acids (GRF-29) can be modulated by GRF-29 itself. Male rats were injected (sc) daily for 3 days with 50 ug of GRF-29, or were treated twice daily for 14 days with 5 ug of [D-Ala-2]-GRF-29 (a potent GRF agonist). Control animals were injected with saline. After the last injection, pituitaries were removed, dispersed, cultured for 96 h and then challenged with either GRF-29 or [D-Trp-6]-LHRH (a LHRH agonist). Cultured cells from analog-treated rats were more responsive to GRF-29 stimulation than were cells obtained from controls. In contrast, neither treatment altered the response to [D-Trp-6]-LHRH. These studies indicate that periodic administration of GRF analogs can increase hypophyseal GRF responsiveness. Such control may be an important component in the physiological regulation of GH secretion and has important implications for potential therapeutic uses of GRF analogs.

Animals↗
PubMed1992

Cloning, sequencing, and expression of human gonadotropin releasing hormone (GnRH) receptor.

Gonadotropin releasing hormone is a hypothalamic decapeptide that stimulates the release of gonadotropic hormones from the anterior pituitary gland. Therapeutically, the human pituitary GnRH receptor is the target of agonists used in the suppression of prostate cancer. Here we report the isolation of a cDNA representing this receptor. It encodes a protein with a transmembrane topology similar with that of other G protein-coupled, 7-transmembrane receptors. Binding studies of the cloned receptor demonstrate high affinity and pharmacological properties similar with the native human pituitary GnRH receptor. Northern blot and reverse transcriptase/PCR analysis revealed that its mRNA is expressed in pituitary, ovary, testis, breast, and prostate but not in liver and spleen. Availability of a human GnRH receptor cDNA should permit the design of improved analogs for therapeutic applications.

Amino Acid Sequence↗
PubMed1983

Administration of agonistic and antagonistic analogues of LH-RH induce anovulation in Macaca fasicularis.

This study was designed to compare the effects of [N-Ac-D-Trp1,3, D-p-Cl-Phe2, D-Phe6, D-Ala10] (A-LH-RH), an inhibitory analogue, and D-Trp6-LH-RH, an agonist of LH-RH, administered to normally cycling cynomologous monkeys. Animals were divided into three groups (n = 5 each), each group receiving one of the following daily during the first 25 days of the menstrual cycle: 1) 20 micrograms of D-Trp6-LH-RH daily, 2) 1 mg of A-LH-RH, and 3) vehicle. Ovulation was established by serial laparoscopies and serum estradiol measurement. Controls presented normal cycles, as evidenced by ovulation day, luteal phase length and hormone levels. Ovulation was completely inhibited during drug administration in all animals of groups 1 and 2. Luteal phase length of all monkeys that ovulated was normal. The present data, therefore, not only show evidence for a consistent anovulatory effect of agonistic and antagonistic analogues of LH-RH in non-human primates, but also open a new approach for non-steroidal contraception.

Animals↗
PubMed1983

Thermal stability of a long-acting analogue of luteinizing hormone releasing hormone (D-trp6-pro9-NEt-LHRH).

The stability of solutions of a long-acting analogue of luteinizing hormone releasing hormone (D-trp6-pro9-NEt-LHRH [LHRHa] after heating to 60C for 5 days, after repeated freezing and thawing, and after refrigeration at 4C for 8 days has been examined. None of the treatments caused a detectable alteration in the HPLC profile, and none caused a significant change in biological activity in vivo. It is concluded that D-trp6-pro9-NEt-LHRH can withstand mild heating, repeated freezing and thawing, and short-term refrigeration without apparent change in HPLC profile or biological activity. It is also concluded that the results obtained with the HPLC method correlate well with the results from the in vivo bioassay.

Animals↗