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Biomedical subjects

S J Nillius

Publications and source records attributed to S J Nillius.

At least 55 records · Page 3Linked to original sources
PubMed1981

Endometrial patterns in women on chronic luteinizing hormone-releasing hormone agonist treatment for contraception.

Endometrial biopsy specimens were obtained from 12 healthy women under chronic intranasal luteinizing hormone-releasing hormone (LH-RH) agonist treatment for evaluation of the risk of endometrial hyperplasia during long-term inhibition of ovulation. A single daily dose of 400 or 600 microgram of the superactive LH-RH agonist D-Ser(TBU)6-EA10-LH-RH was given for 13 to 55 weeks. Treatment was monitored by clinical examination, basal body temperature (BBT) recordings, and frequently taken venous blood specimens for determination of estradiol and progesterone. Ovulation was inhibited during all but 2 of the 102 treatment cycles. No pregnancy occurred. Six of the women had slight menstrual-like bleeding, and six hac amenorrhea during the treatment period. No dysfunctional uterine bleeding occurred. The dominating histologic picture of the 17 endometrial biopsies, obtained after 78 to 380 days of treatment, was inactive or weak proliferative glands with slightly atrophic stroma. There were no signs of hyperplasia. After discontinuation of treatment ovulatory menstrual cycle rapidly returned.

Administration, Intranasal↗
PubMed1981

46,XY male pseudohermaphroditism due to early foetal testicular dysgenesis.

A 17 year old patient with female phenotype and 46,XY karyotype presented because of primary amenorrhoea. Enlarged clitoris and pubic hair were observed and no breast development. Gonadotrophin values were greatly raised into the castrate range, while testosterone was at the upper limit of the normal range for females. No uterus, Fallopian tubes or remnants of Mullerian and Wolffian products were found at laparotomy. Bilateral inguinal masses were removed and proved to be testicular tissue. This case report shows that gonads can be present in patients with the clinical and endocrinological characteristics of the syndrome of 'true agonadism'.

Adolescent↗
PubMed1981

Effects of bromocriptine-induced pregnancy on prolactin-secreting pituitary tumours.

Twenty-eight women with hyperprolactinaemia and amenorrhoea received bromocriptine treatment which resulted in 31 term pregnancies. Bromocriptine treatment was stopped as soon as pregnancy was established. Nineteen of the women had radiological signs of a pituitary tumour. The pregnancies were clinically uneventful in all cases except one who developed headache. Post-partum sellar X-ray showed pregnancy-induced enlargement of the pituitary fossa in 4 of the 28 women. Regression of the radiological changes occurred in 3 of the 4 women within 2 years after the delivery. The women with abnormal sellar X-rays had no difference in the mean prolactin levels before treatment and after pregnancy and lactation while all the women with normal sellae had lower prolactin levels after pregnancy than before. Three women resumed regular spontaneous menstruations after pregnancy and lactation but only one conceived again. Thus, serious pituitary tumour complications are rare in hyperprolactinaemic women with bromocriptine-induced pregnancies. The pregnancy does not worsen the condition. Resolution of hyperprolactinaemia after bromocriptine-induced pregnancy is an unfrequent finding.

Adult↗
PubMed1981

Ultrasonic measurement of ovarian follicles, ovarian and uterine size during induction of ovulation with human gonadotrophins.

Twelve anovulatory women were examined by compound B-mode and real-time ultrasound scanning during incubation of follicular maturation and ovulation by human gonadotrophins. The treatment was monitored by daily serum oestrogen determinations. Ovarian follicles became visible on the ultrasound scans after 4 days of treatment, on average. The mean follicular diameter at that time was 8 mm. Multiple follicles developed in all but one of the 12 patients. At induction of ovulation the diameter of the dominant follicle varied between 15 and 22 mm. The serum oestrogen level was related to the number of follicles, the diameter of the greatest follicle and the ovarian size. There was a marked increase in the ovarian size during the treatment. The size of the uterus also increased. Ultrasound may be a valuable complement to daily oestrogen determinations for monitoring human gonadotrophin therapy.

Adult↗
PubMed1980

Luteolysis induced by a luteinizing hormone-releasing hormone agonist is prevented by human chorionic gonadotropin.

The superactive stimulatory luteinizing hormone-releasing hormone (LRH) analogue D-Ser(TBU)6-EA10-LRh was administered intranasally to five healthy women in a daily dose of 600 microgram during two successive days of the mid-luteal phase. Both the basal serum progesterone levels and the length of the luteal phase were reduced, i.e. luteolysis occurred. Three women who were given additional treatment with human chorionic gonadotropin (HCG) in a daily intramuscular dose of 1500 IU for 10 days, had increased basal progesterone levels and a prolongation of the luteal phase. Thus, HCG prevented the luteolytic effect caused by the LRH agonist.

Adult↗
PubMed1980

Effects of a luteinizing hormone-releasing hormone agonist on luteal function in women.

The potent stimulatory luteinizing hormone-releasing hormone (LRH) analogue D-Ser(TBU)6-EA10-LRH was administered once daily during the luteal phase of the human menstrual cycle. The treatment was instituted in the early or mid-luteal phase of the cycle. Early luteal phase institution of intranasal treatment with 600 micrograms of the LRH agonist once daily reduced the basal progesterone levels during the luteal phase in 4 women but did not cause premature onset of menstruation. Mid-luteal phase institution of subcutaneous treatment with 10 micrograms of the LRH agonist once daily did not affect the progesterone levels or reduce the length of the luteal phase in 5 women. Thus, daily postovulatory administration of the LRH agonist D-Ser(TBU)6-EA10-LRH did not cause luteolysis in normally cycling women.

Adult↗
PubMed1980

Chronic effects of the stimulatory luteinizing hormone-releasing hormone analogue D-Ser (TBU) 6-EA 10-LRH on the gonadotrophin and gonadal steroid secretion in women with amenorrhoea.

The agonistic analogue of luteinizing hormone-releasing hormone (LRH) D-Ser-(TBU) 6-EA10-LRH was given subcutaneously or intranasally to 21 women with longstanding secondary amenorrhoea in an attempt to induce follicular maturation and ovulation. Seven women were given daily subcutaneous injections of 10 /micrograms of the LRH analogue for 21 days. The pituitary and ovarian responses were monitored by follicle-stimulating hormone (FSH), luteinizing hormone (LH), oestradiol (E2) and progesterone (P) in serum. A significant increase of the E2 levels in blood was seen during the first three days of treatment but the E2 elevations were not sustained. No signs of follicular maturation were detected during the treatment. Intranasal treatment with the LRH agonist was instituted in 14 women. Repeated daily low intranasal spray doses (1 - 10 /micrograms) were given. The treatment was continued for 2 - 4 weeks. Intranasal doses of 5 /micrograms and below were ineffective in increasing gonadotrophin and gonadal steroid secretion. An initial gonadotrophin release was observed after intranasal doses of 10 /micrograms and there was a slight increase of the E2 concentrations in serum during the first 2 - 3 days. The pituitary responsiveness to the agonist then decreased markedly during the treatment. None of the 14 women showed signs of follicular maturation during or after the treatment. The pituitary desensitization caused by this potent agonistic LRH analogue seems to limit its therapeutic use for treatment of anovulatory infertility.

Adolescent↗
PubMed1980

Chronic treatment with the gonadotropin-releasing hormone agonist D-Ser(TBU)6-EA10-LRH for contraception in women and men.

The stimulatory analogue of luteinizing hormone-releasing hormone (LRH) D-Ser(TBU)6-EA10-LRH was administered subcutaneously (sc) or intranasally to 10 women with amenorrhea and to 44 healthy female and male volunteers. The LRH agonist evoked a pronounced initial release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) but the gonadotropin response decreased during the course of the chronic treatment. Ovulation could not be induced in seven amenorrheic women who were given prolonged treatment with the analogue. In normally ovulating women, ovulation was inhibited during chronic treatment with a daily sc dose of 5 microgram or a daily intranasal dose of 400 microgram. In four healthy men treated with 5 microgram of the LRH agonist daily over 17 weeks basal FSH, LH, and testosterone levels decreased but spermatogenesis and potency were unaffected. The negative effects on testosterone secretion may limit the use of the LRH agonist for male contraception. Chronic intranasal administration of the stimulatory LRH analogue paradoxically inhibited ovulation and proved to be a safe and effective new approach to contraception in women.

Administration, Intranasal↗
PubMed1979

Intranasal gonadotropin-releasing hormone agonist as a contraceptive agent.

The stimulatory luteinising hormone-releasing hormone (LRH) analogue D-Ser(TBU)6-EA10-LRH was administered intranasally once daily to twenty-seven regularly menstruating women to determine its efficacy as a contraceptive agent. Ovulation was inhibited during all but 2 of the 89 treatment months. The failures were due to initial technical problems with the nasal spray. Twenty-one of the twenty-seven women had slight menstrual-like anovulatory bleeds during the 3--6 month trial. The remaining six women were amenorrhoeic. Ovulatory menstrual cycles rapidly returned after discontinuation of treatment. There were no serious side-effects.

Administration, Intranasal↗
PubMed1979

Bromocriptine treatment of seven women with primary amenorrhoea and prolactin-secreting pituitary tumours.

Seven women with primary amenorrhoea and hyperprolactinaemia were treated with bromocriptine. All the women had started to develop secondary sex characteristics at normal age but pubertal development stopped and menarche did not occur. Radiological signs of a pituitary tumour were found in all the women. Before the pituitary tumour was diagnosed, four women had been given longterm cyclical oestrogen replacement therapy. Three women had received primary tumour therapy with surgery and/or irradiation but had persistent hyperprolactinaemia. The basal luteinizing hormone (LH) levels were low in four of the women while all the women had normal basal levels of follicle-stimulating hormone (FSH) and normal or exaggerated gonadotrophin responses to luteinizing hormone-releasing hormone (LHRH). None of the women had evidence of endogenous oestrogen production before treatment. Bromocriptine treatment normalized the raised serum prolactin levels (46-2900 microgram/l) in all but one woman, in whom the prolactin level decreased from 160 to 38 microgram/l. Regular ovulatory menstrual cycles appeared in four women, one of whom had previously been treated by transsphenoidal adenomectomy followed by external irradiation. Two other women with persistent hyperprolactinaemia after previous surgical and/or irradiation treatment of large pituitary tumours did not menstruate after more than one year of treatment with bromocriptine. One infertile patient with a microadenoma conceived at the first ovulation on therapy and developed symptoms and signs of tumour growth during pregnancy.

Adenoma, Chromophobe↗
PubMed1979

Reduced gonadotropin secretion in postmenopausal women during treatment with a stimulatory LRH analogue.

The potent and long-acting LRH agonist D-Ser(TBU)6-EA10-LRH was administered in a daily subcutaneous dose of 5 microgram to 5 postmenopausal women for a period of 10 days. The LRH analogue produced a significant decrease in both the basal FSH and LH levels and the gonadotropin responses to the agonist. The estrogen levels in serum remained unchanged during the study period. The results suggest that D-Ser(TBU)6-EA10-LRH has a direct inhibitory effect at the pituitary level.

Aged↗
PubMed1979

Inhibitory effects on gonadotrophin secretion and gonadal function in men during chronic treatment with a potent stimulatory luteinizing hormone-releasing hormone analogue.

Long-term treatment with the potent and long-acting stimulatory luteinizing hormone-releasing hormone (LRH) analogue D-Ser(TBU)6-EA10-LRH was given to 4 healthy men to study its effects on pituitary gonadotropin secretion and gonadal function. Five micrograms of the LRH agonist was self-administered sc once daily over 17 weeks. Weekly basal blood samples were obtained for determination of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolacting (PRL) and testosterone. The gonadotrophin responses to the LRH analogue were also determined during the treatment period. LRH tests were performed after treatment. Seminal fluid specimens were collected during and after treatment. A reduction of the basal serum gonadotrophin and testosterone levels were observed during the treatment period. The FSH and LH responses to the analogue were also diminished. After discontinuation of treatment the gonadotrophin and testosterone concentrations returned to pre-treatment levels within a week. The PRL levels and the seminal fluid specimens did not show any significant changes during the study period. The results suggest that chronic treatment with D-Ser(TBU)6-EA10-LRH has an inhibitory effect on the pituitary gonadotrophin secretion in healthy men. It seems likely that the reduced testosterone level is secondary to the diminished gonadotrophin secretion.

Adult↗
PubMed1979

Pituitary responsiveness to luteinizing hormone-releasing hormone during treatment with subdermal D-norgestrel implants in women.

It has previously been reported that subdermal implants containing d-norgestrel inhibit ovulation through blockage of the positive feedback action of estrogen on luteinizing hormone (LH) release. In this study 100 micrograms of LH-releasing hormone (LRH) were injected intravenously to test the pituitary reserve capacity for gonadotrophin secretion in three women with three 40 mg d-norgestrel rods implanted subdermally for more than one year. The gonadotrophin release to LRH varied and seemed related to the ovarian steroid concentrations at the time of the LRH infusion in a manner similar to that seen during the normal menstrual cycle. It is concluded that low plasma levels of d-norgestreol do not inhibit the pituitary responsiveness to LRH. The results indicate that the blocking action of the gestagen on the positive feedback of estradiol on LH release occurs at the hypothalamus or higher CNS centers.

Adult↗