Uterine peristalsis during the follicular phase of the menstrual cycle: effects of oestrogen, antioestrogen and oxytocin.
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Uterine peristalsis, directing sustained and rapid sperm transport from the external cervical os or the cervical crypts to the isthmic part of the tube ipsilateral to the dominant follicle, changes in direction and frequency during the menstrual cycle, with lowest activity during menstruation and highest activity at mid cycle. It was therefore suggested that uterine peristalsis is under the control of the dominant follicle with the additional involvement of oxytocin. To test this hypothesis, vaginal sonography of uterine peristalsis was performed in the early, mid and late proliferative phases, respectively, of cycles of women treated with oestradiol valerate and with human menopausal gonadotrophin following pituitary downregulation, with clomiphene citrate and with intravenous oxytocin, respectively. Administration of oestradiol valerate resulted in oestradiol serum concentrations comparable with the normal cycle with a simulation of the normal frequency of peristaltic contractions. Elevated oestradiol concentrations and bolus injections of oxytocin resulted in a significant increase in the frequency of peristaltic contractions in the early and mid follicular phases, respectively. Chlomiphene tended, though insignificantly so, to suppress the frequency of peristaltic waves in the presence of elevated oestradiol concentrations. In the late follicular phase of the cycle extremely elevated oestradiol concentrations as well as the injection of oxytocin resulted only in an insignificant further increase of peristaltic frequency. In the normal cycles, as well as during extremely elevated oestradiol concentrations and following oxytocin administration, the peristaltic contractions were always confined to the subendometrial layer of the muscular wall. The results and the review of literature indicate that uterine peristalsis during the follicular phase of the menstrual cycle is controlled by oestradiol released from the dominant follicle with the probable involvement of oxytocin, which is presumably stimulated together with its receptor within the endometrial-subendometrial unit and therefore acting in an autocrine/paracrine fashion. Since unphysiological stimulation with oestradiol and oxytocin did not significantly increase the frequency of uterine peristalsis in the late follicular phase of the cycle it is assumed that normal preovulatory frequency of uterine peristalsis is at a level which cannot be significantly surpassed due to phenomena of refractoriness of the system. (+info)
Paracrine changes in the peritoneal environment of women with endometriosis.
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During the past decade, macrophage-derived substances such as prostanoids, cytokines, growth factors and angiogenic factors have been detected in the peritoneal fluid of women with endometriosis. In particular, growth-promoting and angiogenic factors are considered to be substantially involved in the pathogenesis of endometriosis. In this study, vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF-beta) and intercellular adhesion molecule 1 (ICAM-1), substances recently detected in the peritoneal fluid of women with endometriosis, were assessed with regard to their concentrations in different stages of endometriosis and changes of the peritoneal paracrine activity after medical treatment with a gonadotrophin releasing hormone agonist (GnRHa). Peritoneal fluid was obtained from patients with endometriosis during laparoscopy before and after a 4-month treatment with a GnRHa. VEGF, TGF-beta and ICAM-1 could be detected in all women presenting with various stages of active endometriosis. After GnRHa therapy, all patients showed significant decreases in mean concentrations of VEGF (194+/-77 pg/ml), TGF-beta (902+/-273 pg/ml) and ICAM-1 (157+/-52 ng/ml). Patients with stage III and IV endometriosis (according to the rAFS score) had much higher concentrations of VEGF and TGF-beta before treatment compared with those patients with mild endometriosis (rAFS stages I and II). The most striking decrease in concentration was for TGF-beta, from 902 pg/ml before to 273 pg/ml after therapy. These results indicate an important role for paracrine activity in the establishment and maintenance of endometriosis. Indeed, treatment with a GnRHa may reduce paracrine activity in the peritoneal cavity via hypo-oestrogenism and provide proof of successful therapy. (+info)
Regression of endometrial hyperplasia after treatment with the gonadotrophin-releasing hormone analogue triptorelin: a prospective study.
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Endometrial hyperplasia is thought to be caused by the prolonged, unopposed oestrogenic stimulation of the endometrium. The regression of hyperplastic back to normal endometrium is the main purpose of any conservative treatment in order to prevent development of adenocarcinoma. The aim of this study was to evaluate the regression of hyperplastic to normal endometrium in patients with various forms of endometrial hyperplasia after treatment with the gonadotrophin-releasing hormone analogue (GnRHa) triptorelin for 6 months. Fifty-six patients with endometrial hyperplasia were enrolled in this trial; 39 patients (group I) presented simple hyperplasia, 14 (group II) complex hyperplasia and three (group III) atypical complex hyperplasia. All patients were treated with triptorelin for 6 months. Bleeding control during treatment was excellent. A post-treatment curettage for estimation of endometrial histology was performed on 54 out of 56 patients 100.1 +/- 44.7 days after the last triptorelin dose, following the restoration of pituitary function. Regression of hyperplastic to normal endometrium was observed in 32 (86.5%) out of 37 patients in group I and in 12 (85.7%) out of 14 in group II. Persistence of simple hyperplasia was found in five (14.5%) out of 37 patients in group I. Persistence of complex hyperplasia was found in 1 (7.1%) out of 14 patients and progression to atypical complex hyperplasia in another one (7.1%) woman in group II. In some of these cases, the presence of risk factors such as obesity, diabetes mellitus and ovulatory disturbances may contribute to the disease persistence despite therapy. On the other hand, in group III, none of the three patients had normal post-treatment endometrial histology. It seems, therefore, that in cases of endometrial hyperplasia without atypia, the administration of the GnRHa triptorelin is associated with high regression rates to normal endometrium. Conversely, the presence of atypia seems to be a poor prognostic factor. Treatment tolerance and bleeding control during therapy is excellent. (+info)
Treatment of uterine fibroid with triptorelin before hysterectomy.
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OBJECTIVE: To study the effects of pretreatment with triptorelin on uterine fibroid before abdominal hysterectomy. METHODS: Fifteen premenopausal Chinese women with symptomatic uterine fibroids requiring hysterectomy were recruited in the study. All patients received monthly intramuscular injections of 3.75 mg triptorelin for three months prior to abdominal hysterectomy. RESULTS: There was significant reduction in the serum levels of oestradiol (68.6%), progesterone (95.6%) and luteinizing hormone (73.9%) and in uterine (45.0%) and fibroid (68.0%) volumes. The serum level of follicle-stimulating hormone and haemoglobin concentration were not significantly different. CONCLUSIONS: Shrinkage of uterine fibroids can be achieved in women who are rendered hypoestrogenic with monthly injections of triptorelin for three months. This treatment modality may be of value prior to hysterectomy or myomectomy especially when the fibroid is large. (+info)
Effects of anabolic-androgenic steroid use or gonadal testosterone suppression on serum leptin concentration in men.
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OBJECTIVE: Serum leptin concentration shows a sexual dimorphism that is not accounted for by gender differences in adiposity. A strong inverse association exists between serum leptin and testosterone concentrations in men, pointing to a likely influence of gonadal sex steroids on serum leptin concentration. The aim of this study was to investigate whether manipulation of sex steroid hormones in men would alter serum leptin concentration independently of changes in fat mass. DESIGN AND METHODS: The effects of sex steroid suppression on serum leptin concentration were investigated in nine healthy men in whom testosterone had been reversibly suppressed for 5 weeks after treatment with intramuscular triptorelin. The effects of sex steroid supplementation were investigated in nine male bodybuilders who self-administered anabolic--androgenic steroids (AAS) for a mean period of 6.5 weeks. A control group received no hormonal treatment. RESULTS: Testosterone concentration was significantly reduced by triptorelin administration (7.32+/- 1.92ng/ml at baseline compared with 1.15+/-0.57ng/ml at 5 weeks, P=0.002). High-dose AAS use was confirmed by urine analysis. Body fat percentage was unaffected by the AAS or triptorelin intervention (P>0.19). Leptin concentration was significantly reduced after one cycle of AAS use (2.40+/-0. 98ng/ml off cycle compared with 1.63+/-0.37ng/ml on cycle, P=0.012), and was significantly increased by triptorelin administration (2. 96+/-1.50ng/ml at baseline compared with 6.63+/-4.67ng/ml at five weeks, P=0.004). No significant change occurred in the control group. CONCLUSION: Androgenic sex hormone supplementation decreases serum leptin concentration, whereas suppression increases serum leptin concentration, independently of changes in body fat mass in healthy men. The sexual dimorphism evident in serum leptin concentration is likely to be due to a suppressive effect of testosterone on serum leptin concentration in males. (+info)
Premenstrual attacks of acute intermittent porphyria: hormonal and metabolic aspects - a case report.
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We report the case of a 38-year-old woman with acute intermittent porphyria (AIP). Following the observation of an acute AIP attack in the patient's father, the diagnosis was established after genetic and biochemical examinations. At the age of 29, eight months after delivery of her first and only child, the patient was hospitalized due to a first proven attack of AIP. In the following years she suffered several premenstrual AIP attacks, with clinical symptoms ranging from abdominal pain to paralysis. One attack was accompanied by an increased urinary catecholamine output, strongly indicating adrenergic hyperactivity. The precipitation of acute episodes by secretion of gonadotrophins and a severe hyponatraemia due to a syndrome of inappropriate anti-diuretic hormone secretion indicated hypothalamic involvement in the pathogenesis of AIP. This patient has experienced an evolution of treatment regimens. At first, acute attacks were treated by i.v. hypertonic glucose. Afterwards propranolol was instituted as a maintenance therapy. Later on, i.v. injections of haem arginate were very successful in resolving acute AIP episodes. However, until therapy with an LHRH analogue was started, the patient continued to suffer premenstrual AIP attacks. These LHRH analogues cause hypothalamic inhibition of gonadotrophin secretion, with stabilization of endogenous ovarian steroid production at a low level, and therefore may be effective in preventing acute exacerbations of this disease. Since this patient went on a fixed regimen of an LHRH analogue combined with the lowest dose oestrogen patch her quality of life has improved substantially and she has not required hospitalization, now for over 3 years. (+info)
Analysis of the factors affecting auxological response to GnRH agonist treatment and final height outcome in girls with idiopathic central precocious puberty.
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The aim of this retrospective study was to analyze the factors which affected the auxological response to GnRH agonist treatment and the final height (FH) outcome in 71 girls with idiopathic and truly precocious (onset before 8 years) central puberty (CTPP) who had been treated with the same therapy protocol (Decapeptyl Depot, 60 microg/kg i.m. every 28 days) for at least 2 years (since 7.0+/-1. 3 (S.D.) years of age) and followed until puberty was completed and FH was reached. During the entire treatment period we observed: (a) a decrease of height standard deviation scores (SDS) (from 1.5+/-1.7 to 0.9+/-1.3 SDS, P<0.01); (b) a striking deceleration of bone age (BA), revealed by the subnormal DeltaBA:Deltachronological age (CA) ratio (0.2+/-0.1); (c) an increase of predicted adult height (from 155.6+/-7.0 to 160.7+/-6.7 cm, P<0.0005). Treatment interruption was followed by an important catch-down growth, with an FH (158.4+/-5.8 cm) lower (P<0.025) than that predicted at the end of therapy. However, FH fell within the population norm and the target range in respectively 87.3 and 90% of the patients. The tallest FH was recorded in the patients who started therapy at less than 6 years of age and in those who discontinued treatment at a BA of 12.0--12.5 years. At stepwise regression analysis, FH in the whole study population was positively affected by the following independent factors: (a) height at the end of therapy (F=45.45, P<0.0001); (b) pretreatment height (F=13.91, P<0.0005); (c) treatment duration (F=8. 51, P<0.005); (d) target height (TH) (F=7.70, P<0.01). We conclude that: (i) most girls with idiopathic CTPP treated by GnRH agonists may achieve an adult height within the population norm and/or their target range; (ii) the height gain from therapy onset until FH attainment, however, is generally rather limited (on average 2.9 cm) and only few patients are able to reach their target percentile; (iii) the most favorable height prognosis with respect to TH is generally observed in the subjects with the tallest height at the end of treatment and the lowest BA2:CA2 ratio, due to the important deterioration of height prognosis which frequently follows therapy interruption; (iv) FH is also significantly conditioned by both TH and treatment duration; (v) in order to strengthen the weak therapeutic effect of GnRH agonists in CTPP this treatment should be started as early as possible and discontinued at a BA of 12.0--12.5 years. (+info)
Luteal support with micronized progesterone following in-vitro fertilization using a down-regulation protocol with gonadotrophin-releasing hormone agonist: a comparative study between vaginal and oral administration.
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This study aimed to compare the efficacy of micronized progesterone administered as luteal support following ovulation induction for in-vitro fertilization (IVF)- embryo transfer in cycles using gonadotrophin-releasing hormone agonist, either orally (200 mgx4/day) or vaginally (100 mgx2/day) and to characterize the luteal phase hormonal profile during such treatments. A total of 64 high responder patients requiring intracytoplasmic sperm injection due to male factor infertility were prospectively randomized into two treatment groups. Patients treated orally or vaginally were comparable in age (31.9 +/- 6.1 versus 30.6 +/- 5.2; mean +/- SD), number of oocytes retrieved (17 +/- 8.2 versus 18 +/- 7.0), and number of embryos transferred (3.1 +/- 1.2 versus 2.7 +/- 0.9) per cycle. Following low dose vaginal treatment, a significantly higher implantation rate (30.7 versus 10.7%, P < 0.01), but similar clinical pregnancy rate (47.0 versus 33.3%) and ongoing pregnancy rate (41.1 versus 20.0%) was observed, compared with oral treatment. In conception cycles, luteal serum progesterone and oestrogen concentrations did not differ between the treatment groups. In non-conception cycles, late luteal progesterone concentrations were significantly lower following vaginal treatment. As low dose micronized progesterone administered vaginally is simple, easy and well tolerated, it could be recommended as the method of choice for luteal support, especially for high responder patients at risk for ovarian hyperstimulation syndrome. (+info)