Biomedical subjects

J Sandow

Publications and source records attributed to J Sandow.

At least 19 recordsLinked to original sources

PubMed2004

Analysis of the anorectic efficacy of HMR1426 in rodents and its effects on gastric emptying in rats.

OBJECTIVES: Pharmacodynamics of HMR1426 in rodents. SUBJECTS: Male and female rats and male mice. MEASUREMENTS: 24 h feed consumption was measured. From the time curves IC(50) values of HMR1426 were calculated. Microanalysis of feeding behavior was determined. Macronutrient preference was measured, by offering rats three different diets. Gastric emptying was measured after liquid gastric loads or solid meals. In rats with gastric cannulas, milk consumption was measured with closed or open cannulas. Diabetes-related parameters and thyroid hormones were measured. RESULTS: HMR1426 inhibited feed consumption dose-dependently in rodents. Microstructural analysis of feeding after HMR1426 differed from central acting anorectics. HMR1426 inhibited consumption of fat- and carbohydrate-enriched diets. Gastric emptying was dose- and time-dependently delayed. Gastric emptying correlated with the time course of the anorectic effect. In sham-fed rats, HMR1426 had no anorectic effect with open cannulas. Anorectic effect occurred with closed cannulas. We proved that HMR1426 is not a CCK(A) agonist. CONCLUSION: The correlation between anorectic properties of HMR1426 and gastric emptying suggests that gastric emptying may cause the anorectic properties of HMR1426. The differences in microstructural feeding behavior between HMR1426 and centrally active anorectics makes it unlikely that HMR1426 acts via the CNS. Evidence for a peripheral mode of action is derived from sham-fed rats with open gastric fistula. When the milk fed was drained, HMR1426 was ineffective. HMR1426 is not a CCK(A) agonist. The molecular action of HMR1426 causing gastric emptying and its anorectic properties are under investigation.

Animals↗

PubMed2001

Sex steroids used in hormonal treatment increase vascular procoagulant activity by inducing thrombin receptor (PAR-1) expression: role of the glucocorticoid receptor.

BACKGROUND: The use of sex steroids in oral contraception or hormonal replacement therapy is associated with an increased risk of cardiovascular thromboembolic complications. Although both the estrogen and the progestin components have been involved, the underlying mechanisms responsible are unclear. METHODS AND RESULTS: This study examined whether sex steroids promote hemostasis indirectly by increasing the procoagulant activity of blood vessels. Treatment of vascular smooth muscle cells with several progestins (progesterone, 3-keto-desogestrel, gestodene, and medroxyprogesterone acetate) upregulated proteolytically activatable thrombin receptor (PAR-1) expression, resulting in a potentiated thrombin-induced tissue factor expression and surface procoagulant activity. In contrast, neither the progestins levonorgestrel, norethisterone, and norgestimate nor the synthetic estrogen 17alpha-ethinylestradiol had such effects. The effect of the stimulatory progestins, which induce glucocorticoid-like effects in several cell systems, was mimicked by dexamethasone and inhibited by the progesterone and glucocorticoid receptor antagonist RU-38486. In addition, long-term administration of progesterone, 3-keto-desogestrel, or medroxyprogesterone acetate to ovariectomized rats increased PAR-1 protein level in the arterial wall, resulting in an increased responsiveness of isolated aortic rings to thrombin. CONCLUSIONS: These data demonstrate that several progestins markedly potentiate the vascular procoagulant effects of thrombin by increasing the availability of membrane thrombin receptors in the smooth muscle, an effect that is most likely due to their glucocorticoid-like activity.

Animals↗

PubMed2000

Validation of excised bovine nasal mucosa as in vitro model to study drug transport and metabolic pathways in nasal epithelium.

The present work aims at the validation of excised bovine nasal mucosa as an in vitro model to address transport and metabolism pathways relative to the nasal mucosal uptake of therapeutic peptides. Preservation of the viability of the excised tissue in the course of in vitro studies of up to 3 h was demonstrated by (i) positive viability staining, (ii) constant transepithelial electrical resistance (42 +/- 12 Omega cm(2)), (iii) constant rates of metabolic turnover, and (iv) linear permeation profiles of therapeutic peptides and (3)H-mannitol. Using 1-leucine-4-methoxy-2-naphthylamide as a model substrate, we observed no difference between bovine and human nasal aminopeptidase activity. By a series of therapeutic peptides, no direct correlation was found between their effective permeability coefficients (from 0. 1 x 10(-5) to 5 x 10(-5) cm s(-1)) and their respective molecular masses (from 417 to 3,432 Da), indicating that other factors dominate nasal permeability. For instance, the permeabilities of metabolically labile peptides were concentration dependent and saturable, as demonstrated for two short thymopoietin fragments, Arg-Lys-Asp (TP3) and Arg-Lys-Asp-Val (TP4). By permeation studies using gonadorelin and two gonadorelin derivatives, buserelin and Hoe 013, without and in the presence of the chemical enhancer bacitracin, we also verified the ability of the model to assess chemical enhancer effects and their reversibility. In conclusion, our work demonstrates the potential of the investigated in vitro model, excised bovine nasal mucosa, to explore mechanistic aspects of nasal transport and metabolism of therapeutic peptides.

Absorption↗

PubMed1997

Impact of congenital or experimental hypogonadotrophism on the radiation sensitivity of the mouse ovary.

As the numbers of young people making a full recovery from haematological malignancy continue to rise, reproductive science must investigate ways of ameliorating the sterilizing effects of high-dose chemotherapy and total body irradiation. Because there is conflicting evidence as to whether lower serum gonadotrophin concentrations have any protective effect on the gonads, a study was designed to test whether either congenital or experimentally induced hypogonadism reduces the radiosensitivity of the mouse ovary. Test subjects were either homozygous for the hpg locus or animals of normal phenotype treated with a gonadotrophin-releasing hormone antagonist. At 14 days after receiving a single dose of 0.1, 0.2 or 0.3 Gy X-rays or a sham procedure, primordial follicles in the ovaries of the two experimental groups and controls were counted in serial histological sections. The doses at which half of the follicles were lost (LD50) were estimated as 0.11 +/- 0.02, 0.19 +/- 0.02 and 0.17 +/- 0.02 Gy respectively. There was no significant difference between the controls and the antagonist-treated animals, but the congenitally hypogonadal group was unexpectedly more sensitive to radiation. Either way, these results do not support the hypothesis that the ovary is protected from radiation injury by lower gonadotrophin concentrations.

Animals↗

PubMed1996

S- and C-glycopeptide derivatives of an LH-RH agonist.

The S- and C-glycosylated nonapeptides 1 and 2 were synthesized as analogs of the non-glycosylated LH-RH agonist buserelin (pGlu-His-Trp-Ser-Tyr-D-Ser(tBu)-Leu-Arg-Pro-NHEt) by segment condensation in solution. 1 and 2 differ from this peptide in the amino acid in position 6. In the first case (1), D-serine (tBu) is substituted by D-cysteine carrying a rhamnosyl residue, in the second case (2) D-alanine carrying a galactosyl moiety bound as C-glycoside is incorporated. The bioactivity of both glycopeptides as fertility drugs was determined from the dose dependent LH release in male rats. Additionally, in female rats the ovulation rate was assessed. As a result the analog 1 exhibits a similar biological activity as buserelin while analog 2 shows about 25% of this potency. Compared to buserelin the solubility of the analogs 1 and 2 in aqueous buffer is improved by more than two orders of magnitude due to the carbohydrate moieties.

Alanine↗

PubMed1995

Pathways of degradation of buserelin by rat kidney membrane.

The pathways of in vitro degradation of the gonadotropin-releasing hormone (GnRH) analog buserelin [pGlu-His-Trp-Ser-Tyr-D-Ser(tBu)-Leu-Arg- ProNHEt, B1-9] by the rat kidney membrane fraction was investigated using high-performance liquid chromatography for the separation of the peptide products and electrospray mass spectrometry for their identification. The N-terminal peptides B1-4, B1-3, B1-2, C-terminal peptides B3-9, B4-9, B5-9, B6-9, middle sequence B3-4 and the amino acids Trp, Ser and Tyr were found to be formed. However, due to extreme differences in the stability of the peptides toward the battery of membrane enzymes (B1-2, B6-9 >> B1-3, B5-9 >> B1-9 >> B1-4 > B4-9 > B3-9, B3-4), the final products of buserelin degradation were B1-2, B1-3, B5-9, and B6-9 and the amino acids Ser and, corresponding to the formation of B1-2 and B6-9, Trp and Tyr, respectively. The sequences B3-9, B4-9 and B3-4 were clearly detectable only when the inhibitors of aminopeptidases amastatin and bestatin were included in the incubations.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1993

Effects of the luteinizing-hormone-releasing hormone (LHRH) antagonist ramorelix (hoe013) and the LHRH agonist buserelin on dimethylbenz[]anthracene-induced mammary carcinoma: studies with slow-release formulations.

Luteinizing-hormone-releasing hormone (LHRH) agonists and antagonists are antigonadotropic agents for reversible ovarian/testicular suppression in gynaecology and in oncology. Pituitary inhibition and suppression of the gonadal steroids can be maintained with continuous release rates from biodegradable implants or microparticles. The effects of curative and preventive treatment with slow-release formulations of the LHRH agonist buserelin (implants and microparticles) and the LHRH antagonist ramorelix (hoe013) (microparticles) on dimethylbenz[a]anthracene(DMBA)-induced mammary tumours in rats and the pharmacokinetics of these formulations are described. In addition, direct effects of the LHRH antagonist ramorelix on tumour growth were studied. The release rates of the implants (polylactide-glycolide 75:25) and the microparticles (polylactide-glycolide 50:50) were calculated from urinary excretion of the peptides. The curative treatment started at the time of full tumour development (76 days after DMBA induction). A single buserelin implant injection (3.3 mg peptide) resulted in a dramatic tumour regression within 14 days, which was comparable to ovariectomy. It prevented tumour progression for 120 days. Previous studies in rats have shown that ramorelix microparticles (3.6 mg peptide) have a shorter duration of action (about 14 days) in suppression of gonadal function when compared to buserelin microparticles (3.6 mg peptide), where the suppression lasted for about 35 days. As expected, a single injection of ramorelix microparticles (3.6 mg peptide) inhibited tumour progression for only 14 days. This short action is due to a different release profile of the ramorelix microparticles and the different specific activities of peptides incorporated. In the preventive experiments animals were treated 17 days after DMBA induction before tumour development. Treatment with buserelin implants (3.3 mg peptide) every 56 days or with buserelin microparticles (3.6 mg peptide) every 28 days and the treatment with ramorelix microparticles (1.8 mg peptide) every 7 days prevented the development of tumours. Six weeks after the last injection of ramorelix microparticles a strong tumour progression was seen. There was a clear correlation between peptide release and tumour inhibition. The implants and the microparticles were well tolerated, no tissue reaction or side-effects of ramorelix were seen. Treatment of ovariectomized oestradiol-substituted DMBA-treated rats resulted in a marginal (not significant) inhibition in tumour development. LHRH antagonists in slow-release formulations (microparticles or implants) represent a new approach in treatment of hormone-dependent tumours because of the immediate onset of gonadal function and the increased drug efficacy due to the controlled release from biodegradable microparticles.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1992

Long-acting gonadotrophin releasing hormone agonist implant causes variable duration of suppression of ovarian steroid and inhibin secretion.

OBJECTIVE: The duration of action of a gonadotrophin releasing hormone (GnRH) agonist implant designed to be effective for 3 months was investigated in women by monitoring drug release and ovarian hormone secretion. Serum inhibin secretion was measured to determine whether the secondary rise in serum FSH concentrations observed during long-term GnRH agonist treatment was attributable to changes in inhibin secretion. DESIGN AND PATIENTS: The implants of slowly biodegradable polylactide/glycolide (molar ratio 75:25) containing 3.3 mg buserelin, D-Ser (But)6-GnRH (1-9)-nonapeptide-ethylamide, in a rod 1 cm long and 0.13 cm diameter were injected s.c. in patients with endometriosis (3.3 mg buserelin in four patients, 6.6 mg buserelin in six patients). MEASUREMENTS: Urinary secretion of oestrone, pregnanediol, LH and buserelin were determined in daily samples collected for 2 cycles before treatment, during treatment, and for 2 recovery cycles. Oestradiol, progesterone, inhibin, LH and FSH were measured in serum collected once per week. RESULTS: In all patients ovarian hormone secretion was suppressed successfully but considerable variability occurred in the length of time taken for ovarian function to recommence, time to return to ovulation being 100-194 days (median 118 days) (3.3 mg group) and 79-290 (median 178 days) (6.6 mg group). After implant injection, there was a rapid rise in the urinary buserelin excretion followed by an early fast phase of buserelin release, half life (t1/2) = 9 days for 3.3 mg implant and 11 days for 6.6 mg implant. This was followed by a second phase representing a plateau of release, t1/2 = 50 days (3.3 mg implant) and 90 days (6.6 mg implant). During this second phase, an excretion rate of greater than 0.2 nmol buserelin/mol Cr was associated with oestrone excretion at or below early follicular phase values. Once buserelin excretion fell below 0.1 nmol/mol Cr, ovarian function returned in all patients. The period for which buserelin secretion was maintained between 0.1 and 0.2 nmol/mol Cr corresponded to the time taken to recovery of ovulatory cycles in 8/10 of the women. In 9/10 patients serum immunoreactive inhibin concentrations declined at 2 weeks, along with the suppression of oestradiol, and remained suppressed throughout the period of anovulation. Recovery of FSH secretion began after 4-5 weeks. CONCLUSIONS: While this implant should have important clinical application where chronic treatment is indicated, further work is needed on design of long-term implants so that such preparations can be used when precise return to ovarian activity is required. A fall in inhibin secretion may contribute to the secondary rise in FSH by withdrawal of negative feedback but these events are not closely correlated.

Adult↗

PubMed1992

Pharmacokinetics of the gonadotropin-releasing hormone agonist buserelin after injection of a slow-release preparation in normal men.

The pharmacokinetics of the gonadotropin-releasing hormone (GnRH) agonist buserelin (D-Ser(BUt)6-GnRH-(1-9) nonapeptide-ethylamide, Hoe 766, CAS 57982-77-1) after injection of a slow-release preparation was investigated in 16 healthy young male volunteers. Eight volunteers received a buserelin implant of 3.3 mg and 8 volunteers one of 6.6 mg by subcutaneous injection. In order to prevent androgen deficiency symptoms caused by the GnRH agonist all volunteers were injected with an initial loading dose of 400 mg of the androgen 19-nortestosterone hexyloxyphenylpropionate one week prior to the buserelin administration, followed by injections of 200 mg once every three weeks up to week 23. Maximal buserelin serum levels were measured two days after injection of the implant. Following a slow decrease in serum concentrations up to week 8, serum buserelin had disappeared by week 14 in the 3.3 mg group and by week 17 in the 6.6 mg group. The areas-under-the-serum-concentration-versus-time-curves (AUCs) for the 3.3 and 6.6 mg implants were 691 +/- 60 ng x h/ml and 1050 +/- 102 ng x h/ml, respectively (p less than 0.01). The mean residence times (MRTs) of buserelin after administration of 3.3 mg and 6.6 mg buserelin implant were 4.7 +/- 0.4 and 4.1 +/- 0.3 weeks, respectively (p greater than 0.05). Urinary excretion of buserelin showed a similar pharmacokinetic profile. However, urinary buserelin was still detectable at very low concentrations by the end of the study, i.e. 29 weeks after implant injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

The relation between pharmacokinetics and endocrine effects of buserelin implants in patients with mastalgia.

Six patients with mastalgia were treated with polylactide/glycolide 50:50 implants containing 6.6 mg buserelin once every 4 weeks, to study the relationship between buserelin pharmacokinetics and suppression of pituitary-ovarian function. On the first treatment day there was an initial rise in plasma and urinary buserelin levels followed by a rapid fall during the next 2 days. After a plateau phase (60-80 micrograms/g creatinine) urinary buserelin/creatinine ratios decreased slowly to a mean value of 25 micrograms/g creatinine 4 weeks after implantation. Plasma oestradiol concentrations dropped to castrate values within 2 weeks of treatment reaching a mean concentration of 17 pmol/l compared to 27 pmol/l (P less than 0.01) determined in 680 postmenopausal control women. After the last implant injection urinary buserelin/creatinine ratios remained relatively high (greater than 5 micrograms/g creatinine) during more than 8 weeks followed by an exponential decrease (half-life of buserelin release: 15 days) to undetectable buserelin levels at 16-22 weeks after the last implantation. A rise of suppressed plasma oestradiol concentrations to above castrate levels was found 15-20 weeks after the last buserelin implantation, at a time when urinary buserelin excretion had decreased below 0.2 micrograms/g creatinine. It is concluded that after initial suppression of pituitary-ovarian function only very low concentrations of buserelin are needed to maintain suppression of ovarian activity by using slow release preparations.

Adult↗

PubMed1990

Pharmacokinetics and endocrine effects of slow release formulations of LHRH analogues.

The LHRH agonists are antigonadotropic agents for reversible ovarian suppression in gynaecology and in oncology. In oncology, pituitary inhibition is maintained with high release rates preferably by implant or microcapsule injection. The pharmacokinetics of buserelin after injection, infusion, and during implant treatment (controlled release) are described. The release rate is monitored by urinary buserelin excretion (fractional excretion of 30% of the daily dose). During therapy, LHRH agonists in serum are measured by specific radioimmunoassays, with or without extraction. A more convenient non-invasive procedure is to measure the amount of buserelin in 24-h urine samples (during injections or nasal spray), or the urinary buserelin/creatinine ratio in morning urine samples (during infusions or implants). After high dose injection, buserelin has a half-life of 80 min, therapeutic plasma concentrations are maintained for 8-12 h. In long-term maintenance with buserelin implants (polylactide-glycolide, 75:25), serum concentrations and urinary excretion showed an extended plateau phase indicating a suitable dose interval of 2-3 months. In endometriosis and leiomyoma, the minimum release rate (urinary buserelin) required for maintenance of steroid suppression was established (buserelin excretion of about 0.5 microgram/g creatinine). Buserelin implants in prostate carcinoma are effective for 2 or 3 months, after a single dose of 6.6 or 10 mg buserelin, respectively. A consistent suppression of serum testosterone secretion was confirmed for more than 2 yr. Buserelin microparticles are effective in rhesus monkeys to completely suppress follicular maturation and oestrogen secretion during 4-6 weeks after a single dose of 3.6 mg buserelin. Recent results on the controlled release of an LHRH antagonist (Hoe 013) from biodegradable microparticles in rats with DMBA-induced mammary tumours indicate that tumour suppression by LHRH antagonists is well tolerated and highly effective. The local tolerance at the injection site of antagonist microparticles is excellent as in the case of LHRH agonists like buserelin.

Animals↗

PubMed1990

Long-term suppression of ovarian function by a luteinizing-hormone releasing hormone agonist implant in patients with endometriosis.

Ten endometriosis patients received luteinizing hormone releasing hormone (LH-RH) agonist (buserelin) implant injections (6.6 mg subcutaneously) at days 0, 42, 84 and 126. Serum LH and follicle-stimulating hormone (FSH) were lowered by day 14. Luteinizing hormone remained at basal concentrations while FSH returned to values in the low-normal range of the menstrual cycle by day 35. At the end of the luteal phase during which treatment commenced, estrone and pregnanediol declined and remained at postmenopausal or early follicular phase values until days 305 to 460. Time to first ovulation ranged from 321 to 481 days after starting treatment. After the initial menstruation, only three instances of bleeding occurred during treatment. Pelvic pain was relieved or markedly reduced by day 42 and remained absent throughout the period of ovarian suppression. These results indicate the potential of a long-acting LH-RH agonist implant to form the basis for the treatment of symptomatic endometriosis.

Administration, Intranasal↗

PubMed1990

Three-monthly GnRH agonist (buserelin) for prostatic cancer.

A new slow release formulation of buserelin given as a 3-monthly depot injection has been evaluated in 4 patients with advanced prostatic cancer previously maintained on shorter acting depots. Treatment was maintained for a mean period of 21 months. Steady state urinary buserelin concentrations were reached by the beginning of the third treatment week and maintained until the end of the third treatment month. Serum testosterone remained suppressed in the castrate range for the duration of the study. Seven previously untreated patients were entered into treatment. Serum testosterone was suppressed into the castrate range between the seventh and fourteenth days after implantation. This preparation offers an advantage for the patient and clinician over existing methods of GnRH analogue administration and will now enter further clinical trial.

Buserelin↗

PubMed1990

Pituitary-testicular function is suppressed by an LHRH antagonist but not by an LHRH agonist in the marmoset monkey.

The use of pituitary desensitization by an LHRH agonist (buserelin) to examine pituitary-testicular function was investigated in a New World primate. Six adult male marmoset monkeys were injected s.c. with an LHRH agonist implant (1.5 mg in a rod 0.5 cm long). Pharmacokinetics, determined by radioimmunoassay of urinary buserelin, revealed a rapid initial release of the agonist followed by a steady decline during a 200-day period. The LHRH agonist treatment resulted in a rapid initial rise in plasma LH followed by a return to mean values similar to those seen in the control samples by 7 days after implantation. Using the present protocol, no evidence of subsequent pituitary desensitization or suppression of testicular function was observed, plasma concentrations of LH and testosterone remaining within the normal range during the 200-day study period. In contrast, pituitary-testicular function was suppressed in the male marmoset after blockade of pituitary LHRH receptors by an LHRH antagonist. Five adults were treated with a single s.c. injection of the antagonist [Ac-D-Nal(2)1,D-pCl-Phe2,D-Trp3,D-Ser(Rha)6,AzGlyNH2(10)]-LHRH at a dose of 300 micrograms/kg. The LHRH antagonist induced a marked suppression of plasma LH and testosterone by 6-8 h, the low levels being maintained for 24-48 h. These results show that, whereas treatment with an LHRH antagonist can inhibit pituitary-testicular function in the male marmoset, it may be that desensitization cannot be induced by the LHRH agonist used.

Animals↗

PubMed1989

Pharmacokinetics and endocrine effects of the LHR analogue buserelin after subcutaneous implantation of a slow release preparation in prostatic cancer patients.

The pharmacokinetics and endocrine effects of the LHRH analogue buserelin [D-Ser(TBU)6-LHRH], released from biodegradable implants, were studied in 14 patients with stage C and D prostate cancer. Six patients received a subcutaneous implant of 3.3 mg buserelin monthly, and 8 patients received a subcutaneous implant of 6.6 mg buserelin every two months. Serum levels of buserelin decreased rapidly immediately after implantation. After 1-2 weeks a more gradual decline occurred, while in the two-monthly treated group a third phase of the elimination curve started after 5 weeks. Mean serum buserelin levels just before the next implantation in the two groups were not different. Urinary excretion of buserelin followed the same pattern. Serum LH levels in both groups became non-detectable 2 weeks after the first implant. This decrease of LH levels was accompanied by a suppression of serum testosterone to concentrations below 1 nmol/l (castration level). Side effects were not different from those observed with the intranasal application of buserelin. It is concluded that the subcutaneous application of buserelin is an easily administered form of treatment which has more profound and more reliable endocrine effects when compared with the intranasal administration of the drug. The greatest advantage of the new preparation is that the intervals between applications may be prolonged to at least 2 months.

Aged↗

PubMed1989

A pharmacological evaluation of a new 3-month depot preparation of buserelin for prostatic cancer.

A new slow-release formulation of buserelin given as a 3-month depot injection was evaluated in four patients with advanced prostatic cancer. Treatment was maintained for a mean period of 15 months. Steady-state urinary buserelin concentrations were reached by the beginning of the 3rd week of treatment and maintained until the end of the 3rd month. Serum testosterone remained suppressed in the castrate range for the duration of the study. This preparation offers an advantage for the patient and clinician over existing methods of gonadotrophin-releasing hormone (GnRH) analogue administration and will enter further clinical trial.

Buserelin↗

PubMed1989

Treatment of uterine fibroids with implants of gonadotropin-releasing hormone agonist: assessment by hysterography.

The effect of a potent, subcutaneously injected gonadotropin-releasing hormone (GnRH analog) (Buserelin, Hoechst, Frankfurt/Main West Germany) on the size of uterine leiomyomas and the uterine cavity area was studied in a group of 20 women. In all patients except 1, the uterine cavity area calculated by hysterosalpingography was decreased, with an average decrease of 35% (from 12.0 +/- 5.4 cm2 to 7.8 +/- 3.3 cm2) by 8 weeks of therapy. Significant decrease was observed in the group of women with initial uterine cavity area greater than 10 cm2. In patients with very large submucous fibroids, myomectomy by hysteroscopy and neodymium:YAG laser was easily performed. Rapid relief of symptoms such as menometrorrhagia permits the restoration of a normal hemoglobin concentration. In conclusion, use of GnRH analog represents an adjunct for preoperative reduction of tumor size and may permit surgical treatment by hysteroscopy.

Adult↗

PubMed1989

Administration of nasal Buserelin as compared with subcutaneous Buserelin implant for endometriosis.

One hundred infertile patients with laparoscopically confirmed ovarian endometriosis were treated with either intranasal (IN) Buserelin (Hoechst, AG, Frankfurt am Main, West Germany) (300 micrograms three times a day) or subcutaneous (SC) Buserelin implant (6.6 mg Buserelin). Serum estradiol was suppressed in the menopausal range in both groups, but the inhibition of the pituitary ovarian axis appeared more profound and consistent in the SC group than in the IN group. Laparoscopic findings proved that the SC Buserelin emerged superior to the IN Buserelin. Indeed, the score of endometriotic lesions and the ovarian cyst diameter were more reduced in the SC group than in the IN group. Moreover, the histologic study showed a lower incidence of active endometriosis and a lower mitotic index of ovarian endometrial epithelium in the SC group than in the IN group. In conclusion, the release of a gonadotropin-releasing hormone agonist by a biodegradable implant achieved better efficacy in reducing endometriotic lesions than the IN mode of administration.

Administration, Intranasal↗