PubMed Health⌕ Search

Biomedical subjects

B Couzinet

Publications and source records attributed to B Couzinet.

At least 19 recordsLinked to original sources
PubMed1992

The incidence of late-onset congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency among hirsute women.

OBJECTIVE: The present study was designed to determine the incidence of 3 beta-hydroxysteroid dehydrogenase deficiency (3 beta-HSD) in adult women with hyperandrogenism. DESIGN AND PATIENTS: In 78 hirsute patients and 30 normal women in the same age range, an ACTH stimulation test was performed on day 5 of the cycle by administration of a single bolus of 0.25 mg ACTH-(1-24) at 0800 h. MEASUREMENTS: The following steroids were measured before, 30 and 60 minutes after ACTH injection: delta 5-pregnenolone (delta 5-P), 17-hydroxy-delta 5-pregnenolone (17-OH delta 5-P), dehydroepiandrosterone (DHEA), delta 5-androstenediol, progesterone (P), 17-hydroxyprogesterone (17-OHP), androstenedione (A), testosterone (T) and cortisol. RESULTS: Maximum ACTH-stimulated values of delta 5-steroids were in excess of the 90% confidence limits of the control group in 19 hirsute women. Ten patients had an isolated increase in delta 5-P, 17-OH delta 5-P, DHEA or delta 5-androstenediol. Nine patients had an increase in two delta 5 steroids and none had increased values of three or four delta 5 steroids. The ratios of 17-OH delta 5-P to 17-OHP, DHEA to A, delta 5-P to P and delta 5-androstenediol to T were increased in 5, 1, 1 and 1 patients respectively. No patient had elevated values of more than one ratio. CONCLUSIONS: Using stringent diagnostic criteria, partial 3 beta-HSD deficiency was excluded in all 78 patients and therefore appears to be a rare disorder.

3-Hydroxysteroid Dehydrogenases↗
PubMed1992

Progesterone stimulates luteinizing hormone secretion by acting directly on the pituitary.

To determine if progesterone (P) does affect gonadotropin secretion by acting directly on the pituitary, six women with hypothalamic gonadotropin deficiency were studied. They were treated with 17 beta-estradiol (E2; 2 mg/day, orally) to induce P receptors and maintain constant plasma E2 levels during two 15-day periods separated by 1 month. GnRH was administered iv at a dose of 10 microgram/pulse every 90 min during the last 5 days of E2 treatment. Either P (400 mg/day) or a placebo was administered intravaginally in a cross-over randomized design during the 5 days of pulsatile GnRH therapy. A baseline study of pulsatile LH secretion was performed, with sampling performed every 10 min for 8 h. The sampling was then repeated on day 15 of each study period at the end of pulsatile GnRH administration. Plasma levels of E2 and P were measured every day during the 5 days of either GnRH and P or GnRH and placebo treatment. In the six patients, the observed apulsatile pattern of LH during the baseline study confirmed the diagnosis of complete gonadotropin deficiency. Plasma E2 levels were not significantly different at the time of each pulse analysis (288 +/- 61 vs. 252 +/- 77 pmol/L). The plasma P level achieved with the vaginal pessaries was 22 +/- 5 nmol/L. P treatment resulted in all cases in a significant increase in the mean plasma LH level (5.2 +/- 0.9 vs. 3.6 +/- 0.7 IU/L after GnRH plus placebo; P less than 0.001). Furthermore, LH pulse amplitude was significantly increased by P compared to placebo (3.1 +/- 0.3 vs. 1.4 +/- 0.1 IU/L, respectively; P less than 0.01). Mean plasma FSH levels were significantly increased by GnRH regardless of whether P or placebo was present. In conclusion, these data indicate that a short exposure to physiological levels of P in the range of early luteal phase levels has a stimulatory effect on LH secretion by acting directly at the pituitary level.

Activity Cycles↗
PubMed1992

Differing responses of plasma bioactive and immunoreactive follicle-stimulating hormone and luteinizing hormone to gonadotropin-releasing hormone antagonist and agonist treatments in postmenopausal women.

Plasma bioactive (B) and immunoreactive (I) FSH and LH were measured every 10 min for 8 h in the same postmenopausal women in a three-phase study: 1) during normal pulsatile gonadotropin secretion (basal study; n = 8), 2) 8 h after a single injection of a GnRH antagonist (5 mg Nal-Glu, sc; n = 5), and 3) 21 days after a GnRH agonist injection (D-Trp6, 3.75 mg depot preparation, im; n = 7). I-FSH and I-LH were measured by monoclonal antibody immunoradiometric assays. B-FSH and B-LH were measured in selected samples with the immature rat granulosa cell and mouse interstitial cell assays, respectively. Significant pulsatility of B- and I-FSH and LH was demonstrated in the basal samples, but only the B/I ratio of LH was slightly elevated within the secretion peaks. After GnRH antagonist treatment, I-FSH decreased from a mean pretreatment level of 55.7 +/- 7.8 IU/L by 26% (P less than 0.001), and B-FSH from 313.8 +/- 61.9 IU/L by 44% (P less than 0.01). The B/I ratio decreased from 6.4 +/- 1.7 to 4.5 +/- 1.0 (P less than 0.05). After agonist treatment, the I- and B-FSH levels decreased by 92% and 83% (P less than 0.0001), respectively, but the B/I ratio increased to 17.3 +/- 4.7 (P less than 0.05). The concentrations of I- and B-LH decreased by 75% and 80%, respectively (P less than 0.001), after antagonist treatment. After agonist treatment, I-LH decreased by 92%, and B-LH by 93% (P less than 0.0001). No changes in the B/I ratios of LH were found after either treatment. In conclusion, no changes were found in the quality of circulating LH during the treatments, whereas the antagonist treatment decreased and the agonist treatment increased the B/I ratio of FSH. These findings provide further evidence that the qualitative responses of FSH and LH to treatment with the same GnRH analog are different, and that the suppressive mechanisms of GnRH antagonist and agonist action on gonadotropin secretion are different.

Adult↗
PubMed1991

Steroid control of gonadotropin secretion.

Current knowledge about the mechanism and site of action of estradiol (E2) and progesterone (P) during the menstrual cycle and the physiological role of androgens is reviewed. In normal women, the positive feedback effect of E2 at the pituitary level is the principal event of the follicular phase inducing the LH surge. P, by its negative feedback at the hypothalamic level and by its positive feedback at the pituitary level regulates GnRH and LH secretion during the luteal phase. Androgens do not directly play a role in gonadotropin regulation.

Androgens↗
PubMed1991

Effects of gonadotrophin releasing hormone antagonist and agonist on the pulsatile release of gonadotrophins and alpha-subunit in postmenopausal women.

OBJECTIVE: The present study was designed to further assess the mechanism of action of GnRH and GnRH analogues. DESIGN AND PATIENTS: Both the Nal-Glu GnRH antagonist and the D-Trp6 GnRH agonist were administered sequentially to nine normal, post-menopausal women. MEASUREMENTS: A baseline study of pulsatile LH, FSH and free alpha-subunit secretion was performed, with sampling every 10 min for 8 h, and then repeated 8 h after a single subcutaneous injection of Nal-Glu GnRH antagonist (5 mg). Sampling was repeated 21 days after the intramuscular injection of a depot preparation of D-Trp6 GnRH (3.75 mg) in the same women. RESULTS: The baseline sampling period showed synchronous pulses of LH and free alpha-subunit. The antagonist Nal-Glu decreased plasma LH (71%) and free alpha-subunit (43%). However, with the single dose of 5 mg, pulsatile LH and free alpha-subunit release were not completely suppressed and remained temporally correlated. The GnRH agonist had a potent inhibitory action on plasma immunoreactive LH (IRMA) (93%). In contrast, it increased the mean plasma levels of free alpha-subunit from 1.66 +/- 0.01 to 5.06 +/- 0.02 micrograms/l (205%). The pulsatile secretory patterns of both LH and free alpha-subunit were abolished by the agonist. Immunoreactive FSH levels were decreased by the antagonist (24%) and suppressed by the agonist (93%). CONCLUSIONS: The pulsatile study confirms the different mechanism of action of GnRH analogues. Following antagonist administration, low amplitude free alpha-subunit pulses persist and are synchronous with residual LH pulses. In contrast, LH and free alpha-subunit are not maintained under agonist treatment. These data provide evidence for the differential regulation of LH and free alpha-subunit by GnRH.

Female↗
PubMed1990

Late luteal administration of the antiprogesterone RU486 in normal women: effects on the menstrual cycle events and fertility control in a long-term study.

Twelve regularly cycling women, with contraindications to other methods of contraception, received RU486 (Roussel UCLAF, Romainville, France), once a month as a method of fertility control. The study was designed for 18 consecutive cycles. Each patient recorded basal body temperature, detected urinary luteinizing hormone peak, and collected saliva samples during each luteal phase for progesterone (P) determinations. A single dose of RU486, 600 mg, was given on the day before the expected date of the menses and 8 days later in case of continuing pregnancy after the first dose. Blood samples were collected for estradiol, P, and beta-human chorionic gonadotropin analyses on these two occasions. The compliance was poor and the results of only 137 cycles were obtained. The menstrual cyclicity was not significantly modified during this long-term study. Of the 137 cycles, 22 pregnancies occurred (16%), and 4 (18.2%) were not interrupted by the second dose of RU486. Thus, because of the high failure rate, use of RU486 at the time of the natural P withdrawal cannot be advocated as a "once-a-month" contragestive agent.

Adult↗
PubMed1989

[Free alpha-subunit glycoprotein hormones: physiological and pathological data].

The glycoprotein hormone alpha-subunit is secreted as a free molecule as well as a molecule combined to a glycoprotein hormone beta-subunit. In human subjects, plasma levels of the free alpha-subunit were measured by means of a specific radioimmunoassay. Plasma concentrations were high during the neonatal period, then decreased to a nadir at the age of 6 years. A significant pubertal increase occurred in both sexes, more pronounced in girls. In female subjects mean levels (+/- SEM) were 0.21 +/- 0.05 before puberty and 0.51 +/- 0.03 ng 1 degrees IRP-hCG alpha/ml in follicular phase. During menstrual cycle, a typical preovulatory surge was seen simultaneous with the LH surge. During aging, plasma levels increased slowly in males, abruptly in menopausal females. The pituitary reserve as assessed by LH-RH stimulation test (100 micrograms i.v./m2) exhibited a significant pubertal maturation in boys and girls. Chronic administration of LH-RH agonist induced a marked increase of alpha-subunit levels, whereas LH levels were deeply suppressed. LH-RH injections in children treated for precocious puberty with a LH-RH agonist induced a significant release of alpha-subunit despite an almost complete abolition of LH release. In conclusion, from a quantitative point of view, the glyco-protein hormone alpha-subunit is a major secretory product of the pituitary. It seems that there is a specific regulation of its secretion, resembling but not identical to LH secretion regulation. Whether or not it plays a biological role remains uncertain.

Child↗
PubMed1989

Effects of a pure antiandrogen on gonadotropin secretion in normal women and in polycystic ovarian disease.

To assess the role of androgens in gonadotropin regulation in women, we studied the effects of a pure nonsteroidal antiandrogen, Anandron (Cassenne, Paris, France). Nine normally cycling women (group 1) with acne and/or seborrhoea and nine patients with polycystic ovarian disease (PCOD) (group 2) received Anandron (100 mg twice a day) and a placebo. Both treatments were administered orally, in a cross-over randomized design, for two consecutive cycles (group 1) or months (group 2) separated by one cycle or 1 month. Luteinizing hormone (LH) pulse frequency and amplitude (cluster analysis), basal and gonadotropin-releasing hormone (GnRH)-stimulated plasma LH/follicle-stimulating hormone (FSH) levels were determined on day 5 of each treatment or placebo cycle. On days 5, 10, 20, and 24 of each cycle or month, plasma estradiol (E2), estrone (E1), testosterone (T), dihydrotestosterone (DHT), androstenedione (A), dehydroepiandrosterone sulfate (DHAS), sex hormone-binding globulin (SHBG) levels, and urinary androstanediol glucuronide (3 alpha-diol G) were measured. Plasma progesterone (P) levels were determined on days 20 and 24 of each cycle (group 1) and on days 5, 10, 20, and 24 (group 2). In both groups, seborrhea and acne decreased markedly within the first month and practically disappeared after 2 months of Anandron treatment. No adverse side effects were reported. None of the normal patients had any disturbance of menstrual cycles as assessed by basal body temperature shift, ultrasonography, and plasma P levels. In PCOD patients, cycles remained anovulatory.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effects of vasoactive intestinal polypeptide, TRH, and dopamine on prolactin secretion in estrogen-primed postmenopausal women.

Prolactin secretion is influenced by at least three important hypothalamic neurotransmitters: TRH, vasoactive intestinal polypeptide and dopamine. The purpose of this study was to determine whether, in estradiol-primed postmenopausal women, the PRL response to TRH, vasoactive intestinal polypeptide, and dopamine differed. Ten postmenopausal women were studied during treatment with estradiol benzoate at a dose of 0.625 mg per day during 15 days. TRH (200 micrograms iv), saline infusion, vasoactive intestinal polypeptide (75 micrograms infused iv during 15 min), coadministration of vasoactive intestinal polypeptide and TRH, and dopamine (4 micrograms.kg-1.min-1 iv for 3 h) were administered for 5 consecutive days before and during the last 5 days of estradiol benzoate treatment. Before estradiol benzoate administration, the PRL, response to TRH was significantly greater than that of vasoactive intestinal polypeptide. Estradiol benzoate treatment increased significantly the PRL release induced by TRH (p less than 0.01), but did not modify the response to vasoactive intestinal polypeptide. At the end of estradiol benzoate treatment, the maximal increase in PRL after the combined (vasoactive intestinal polypeptide + TRH) test was greater than that obtained with TRH alone and occurred earlier (p less than 0.04). Dopamine suppressed PRL secretion to a similar extent after estradiol benzoate treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Dopamine↗
PubMed1988

Stimulation of ovarian follicular maturation with pure follicle-stimulating hormone in women with gonadotropin deficiency.

According to the 2-cell theory, ovarian steroidogenesis requires the coordinate action of both FSH and LH. To evaluate the relative importance of these hormones in follicular maturation, a randomized cross-over study was performed in 10 women with complete gonadotropin deficiency (absence of pulsatile LH secretion and no LH response to LHRH). Five women were treated with highly purified FSH (LH bioactivity, 0.09%) and 3 months later with human menopausal gonadotropin (hMG; LH bioactivity, 65%), each given for 10 days at a daily dose of 225 IU FSH, im. The sequence was reversed in the other 5 women. hCG (5000 IU) was administered im 24 h after the last injection of FSH or hMG. Plasma estradiol (E2), estrone (E1), androstenedione (A), testosterone, LH, and FSH concentrations and urinary LH and FSH were measured daily by RIA. Ultrasonography was performed during each treatment and 2 days after each hCG injection. After FSH treatment, mean plasma and urinary FSH levels increased, mean plasma LH did not change, and urinary LH increased slightly but not significantly from 91 +/- 32 (SE) to 164 +/- 55 mIU/24 h (10(-3) IU/24 h). After hMG treatment, mean plasma and urinary LH and FSH levels increased accordingly. The mean basal plasma E2 [11 +/- 1 pg/mL (40 +/- 4 pmol/L)] and E1 [14 +/- 4 pg/mL (52 +/- 15 pmol/L)] levels increased after FSH treatment to 207 +/- 69 pg/mL (760 +/- 253 pmol/L) and 82 +/- 21 pg/mL (303 +/- 78 pmol/L), respectively (P less than 0.01), but plasma A did not change. In response to hMG, the mean plasma E2, E1, A, and testosterone levels increased more than during FSH treatment. Ultrasonography revealed multiple preovulatory follicles (greater than or equal to 16 mm) in 2 women after hMG and 1 woman after FSH treatment; therefore, hCG was not administered. In 3 women given FSH, hCG did not induce ovulation. hCG induced ovulation in 8 women given hMG and in 6 women given FSH, based on ultrasonography and plasma progesterone levels. Thus, in the presence of profound gonadotropin deficiency pharmacological doses of FSH, with minute LH contamination, are capable of stimulating ovarian follicular maturation, underlining the key role of FSH in folliculogenesis.

Adolescent↗
PubMed1987

[Contragestion].

Explore the source record for details and available documents.

Contraceptives, Postcoital↗
PubMed1987

Comparative effects of cyproterone acetate or a long-acting LHRH agonist in polycystic ovarian disease.

A randomized cross-over study was done to compare the therapeutic efficacy of cyproterone acetate (CPA, 50 mg/day orally) and a depot preparation of the LHRH superagonist (D-Trp6 LHRH 3 mg i.m. once a month) in 10 patients with polycystic ovarian disease (PCO). The two treatment periods were separated by 6 months. Both treatments resulted in marked clinical improvement. In response to CPA treatment, basal plasma gonadotropin, estradiol, estrone, testosterone and androstenedione levels significantly decreased. In response to D-Trp6 LHRH, both basal and stimulated gonadotropin levels were completely suppressed after 3 weeks of treatment. After initial elevation on day 2, plasma ovarian steroid levels fell into the castrate range, without any change in dehydroepiandrosterone sulfate levels. Urinary 3 alpha-androstanediol excretion decreased significantly. In patients with PCO, LHRH-A induced more complete gonadotropin inhibition than did CPA. However, following cessation of either therapy, the disease rapidly recurred.

Adult↗
PubMed1986

Termination of early pregnancy by the progesterone antagonist RU 486 (Mifepristone).

We studied the effects of the progesterone antagonist RU 486 in 100 women with early, unwanted pregnancy (within 10 days of the expected onset of the missed menstrual period). Thirty-four women received oral doses of 400 mg (in four days), 26 received 600 mg (in four days), and 40 received 800 mg (in two days). Uterine bleeding occurred in all patients within four days of the first dose and continued for 5 to 17 days. In 85 of the women, a dramatic decrease in the plasma chorionic gonadotropin level was observed on day 6, and an empty uterus was confirmed by ultrasonography on day 13. Hence, these women were considered to have had a complete abortion. Fifteen subjects had persistently elevated plasma chorionic gonadotropin levels on day 6 and were considered not to have responded to RU 486. They all had uterine evacuation, which was facilitated by a softening of the cervix. The percentage of women with complete abortion was similar in all dosage groups. Furthermore, plasma levels of immunoreactive RU 486 were similar in subjects with and without complete abortion. The only important side effect observed in the responders was prolonged uterine bleeding in 18 percent, but neither blood transfusion nor curettage was required. We conclude that RU 486 is an effective and safe method for termination of very early pregnancy but that it should be used only under close medical supervision.

Abortifacient Agents↗
PubMed1986

Pulsatile luteinizing hormone releasing hormone treatment for induction of ovulation. Radioimmunoassay of plasma LHRH and comparative study of subcutaneous versus intravenous routes of administration.

To investigate the efficacy of the different routes of luteinizing hormone releasing hormone (LHRH) administration upon pituitary responsiveness, we compared plasma LHRH concentrations and pituitary LH responses in four patients with hypothalamic amenorrhea treated with pulsatile LHRH. A portable computerized infusion pump delivered sc or iv LHRH pulses of 5, 10 or 20 micrograms every 90 min. Comparison of the two modes of LHRH delivery was performed using radioimmunoassay of exogenous LHRH and studying its pharmacokinetics for a 3 pulses period. With 10 micrograms of LHRH given iv, plasma LHRH levels increased between 700 and 1000 pg/ml within 3 min and returned to basal levels in 30 min. When given sc (10 micrograms), plasma LHRH levels peaked between 80 and 100 pg/ml in 15 min and returned to basal levels 60 min later. In one patient treated with 5 micrograms per pulse iv or sc, plasma LHRH increased to 380 and 60 pg/ml respectively. In all patients, computerized analysis of LH pulses was performed during sc and iv LHRH administration. LH pulsatile release displayed a similar rhythm period with both routes. However, for the same dose of LHRH (10 micrograms), the adjusted mean of LH plasma levels was lower with the sc route. In conclusions, the pharmacokinetics of LHRH administered sc or iv displayed a similar pattern but, with equivalent doses, higher plasma LHRH levels are attained with the iv route. Concomitantly, the mean LH levels were also greater after iv administration. Ovulation can be successfully induced by both pulsatile iv and sc LHRH therapy. However, with the sc route, a higher dose of LHRH should be used to prevent a delay of ovulation or a luteal deficiency.

Adult↗
PubMed1986

Interactions of oestradiol benzoate and promegestone upon basal and TRH-induced prolactin secretion in postmenopausal women.

The interactions of ovarian steroids with PRL secretion in women are still controversial. Ten healthy postmenopausal women, on no medication, received during the first period of 2 months later in a cross-over design study, i.m. injections of 0.625 mg of oestradiol benzoate (EB) alone for 10 d or in combination with 750 micrograms/d of a pure progestin promegestone for 10 d. A TRH (200 micrograms i.v.) stimulation test was performed before the start and at the completion of each treatment period. Basal plasma gonadotrophins, PRL and oestradiol were measured every day by radioimmunoassay. The EB-induced rise in oestradiol levels was similar during the two periods. In response to EB treatment serum PRL levels increased from 6.1 +/- 0.9 ng/ml to 22.9 +/- 3.4 ng/ml. With the addition of promegestone, the increase in PRL, from 6.7 +/- 1.3 ng/ml to 13.8 +/- 2.5 ng/ml, was significantly diminished (P less than 0.001). The PRL release induced by TRH was significantly greater with EB treatment than was the response with the combined treatment (P less than 0.05, Wilcoxon test to compare the areas under the curves). These data suggest that in postmenopausal women oestrogens act as stimulators of PRL release and promegestone is able to partially counteract the stimulatory effect of oestradiol benzoate upon basal and TRH-stimulated PRL secretion.

Drug Interactions↗