Biomedical subjects

J Schoemaker

Publications and source records attributed to J Schoemaker.

At least 127 records · Page 7Linked to original sources

PubMed1989

The significance of preoperative hysterosalpingography and laparoscopy for predicting the pregnancy outcome in patients with a bilateral hydrosalpinx.

We analyzed the importance of 3 factors derived from the HSG (nature of the mucosal pattern, diameter of the hydrosalpinx, expandability of the ampulla) and of four factors from the findings at laparoscopy (extent of adhesions, nature of adhesions, thickness of tubal wall and diameter of the hydrosalpinx) for predicting the pregnancy outcome in 98 patients with bilateral hydrosalpinx. Each factor was categorized into 3 scores and each patient was scored for both the right and the left tube, resulting in 6 score-combinations. An association between the pregnancy prospects based on the score-combinations and the actual pregnancy outcome seemed to be present for all factors evaluated, except for the extent of adhesions and the diameter of the hydrosalpinx (laparoscopy). The results further indicate that a favourable score on the nature of mucosal pattern in one or both tubes concurs with good pregnancy prospects. In contrast, the presence of an unfavourable score for most of the other factors in at least one tube is associated with a poor fertility prognosis, regardless of the condition of the other tube.

Evaluation Studies as Topic↗

PubMed1989

Premature ovarian failure. I: The association with autoimmunity.

Twenty-four patients were investigated for non-organ-specific and organ-specific autoantibodies (Aab) in order to establish a relationship between premature ovarian failure (POF) and autosensitization. Regarding the non-organ-specific Aab, prevalences of clearly raised ANA (42%), nDNA Ab (25%), rheumatoid factors (41%) and smooth muscle Aab (53%) were found in the POF patients. Less outspoken higher prevalences of organ-specific Aab in these patients were also found: parietal cell Aab (23%), islet of Langerhans Aab (20%). Fifteen percent of the patients showed Aab to the adrenal gland, and a single patient had Aab towards the steroid-producing cells (Stpc) of the ovary. Although no single immune parameter could be clearly identified to correlate with POF, autoimmune (AI) phenomena were detected in the majority of the patients (92%). Since AI disease could be present for a considerable time without any clinical symptoms, a further immunological screening and follow up of POF patients may enable us to better understand and manage these patients.

Adolescent↗

PubMed1989

Premature ovarian failure. II: Considerations of cellular immunity defects.

Twenty-three patients with premature ovarian failure (POF), were investigated on the basis of cell-mediated immunity. An increase in T-cells and especially T-helper cells was found in the group of POF patients, while T-suppressor cells and B-cells did not exceed the counts compared to healthy controls matched for age and sex. The macrophage migration inhibition factor (MIF) assay showed a decreased activity towards Haemophiles influenza. Candida albicans and Varidase antigens in the POF group. Levels of immunoglobulins (IgG, IgA, IgE and IgM) did not exceed the normal levels. The relationship between the hormonal status of POF patients and their immunological profile is discussed.

Adolescent↗

PubMed1989

Effects of LHRH antagonist administration to immature male rats on sexual development.

Gonadotropin secretion in immature male rats was inhibited by administration of a potent LHRH antagonist (LHRH-A): from 6 to 15 days of age (early onset/short-term treatment), from 6 to 48 days of age (early onset/long-term treatment) or from 22 to 31 days of age (late onset/short-term treatment). Balano-preputial separation was retarded by 9 or 13 days (short-term treatments) or by about 40 days (long-term treatment). Adult testicular weight was lowered and plasma FSH was increased after early, but not after late onset of LHRH-A treatment. Plasma LH and testosterone levels were not affected by any of the LHRH-A treatments. Fertility was diminished after early onset LHRH-A administration only. Adult precopulatory and copulatory behavior were severely affected after early onset of LHRH-A treatment. Intensity of precopulatory anogenital inspection was increased. The copulatory pattern was incomplete with absence of ejaculatory behavior during sexual behavior tests. Sexual behavior was not affected after late onset of LHRH-A treatment. Thus, administration of LHRH-A to immature male rats delays balano-preputial separation irrespective of the age of onset of LHRH-A treatment. In contrast, effects on adult FSH levels, testicular weight, fertility and sexual behavior depend on age and duration of LHRH-A administration.

Animals↗

PubMed1989

Ovulation induction with pulsatile luteinizing hormone-releasing hormone in women with clomiphene citrate-resistant polycystic ovary-like disease: endocrine results.

The pituitary and gonadal response to pulsatile luteinizing hormone-releasing hormone (LH-RH) administration during the first and consecutive second treatment unit (TU) was studied in nine women with clomiphene citrate-resistant polycystic ovary-like disease (PCOD). The control group consisted of eight eumenorrheic women. Luteinizing hormone levels, LH amplitudes, and total urinary excretion/24 hours did not differ between ovulatory and anovulatory TUs, but were significantly higher compared with the control group. Follicle-stimulating hormone (FSH) in PCOD did not differ from normal cycles. Androgen values in the anovulatory TUs were significantly higher compared with the ovulatory TUs (P = 0.001). We conclude that LH-RH therapy may result in ovulation; however, it does not redress the intrinsic abnormality in PCOD and FSH, and androgen levels do not seem to be critical in ovulation induction.

Adult↗

PubMed1989

Pregnancy rate is significantly higher in in vitro fertilization procedure with spermatozoa isolated from nonliquefying semen in which liquefaction is induced by alpha-amylase.

In 115 patients (group I) in which normal liquefaction of semen occurred, the fertilization rate of the yielded oocytes was 71.2% after standard in vitro fertilization procedure, and the viable pregnancy rate per patient per cycle was 13.0%. In a comparable group of 26 patients (group II), in which semen liquefaction did not occur spontaneously, alpha-amylase was added in order to liquefy the semen. In this group, the fertilization rate was 86.7% of the yielded oocytes, and the viable pregnancy rate per patient per cycle was 26.9% (P less than 0.05). It is concluded that alpha-amylase can be of use to liquefy nonliquefying semen, and that the resultant spermatozoa have a positive effect on pregnancy results.

Adult↗

PubMed1989

Luteinizing hormone and follicle stimulating hormone secretion patterns in boys throughout puberty measured using highly sensitive immunoradiometric assays.

Pulsatile gonadotrophin secretion patterns were studied in 32 normal boys (chronological age, CA 7.2-14.6 years) at different stages of pubertal development (5 in stage G1, 11 in G2, 5 in G3, 4 in G4, 7 in G5). Plasma LH and FSH concentrations were measured at 10 min intervals from 1200 to 1800 h and from 2400 to 0600 h using an immunoradiometric assay with a lower limit of detection of 0.15 IU/l for both LH and FSH. Plasma testosterone (T) was measured hourly. In the young prepubertal boys plasma LH was not detectable during day or night. In contrast, plasma FSH ranged from 0.7 to 1.4 IU/l. Plasma T was not detectable either (less than 0.25 nmol/l). In the older prepubertal boys a discrete pulsatile LH pattern (2 per 6 h) became discernible only during the night (range 0.1-0.4 IU/l). Plasma FSH also revealed a pulsatile pattern only during the night (2 per 6 h), while plasma T still remained undetectable. In the early pubertal boys (G2) a median daytime LH value of 0.37 IU/l was determined with 1 pulse per 6 h and at night definite LH pulses (4 per 6 h) were found in all boys (range 0.4-4.7 IU/l). Plasma FSH increased considerably to a median level of 2.50 IU/l during the day; most boys had a pulsatile FSH pattern (one per 6 h). Plasma T became detectable during the day (median 0.54 nmol/l) and night (median 1.16 nmol/l). With the progression of puberty the mean plasma level of LH and FSH, the LH/FSH pulse number and the LH/FSH pulse amplitude increased; plasma T rose as well, more obviously during the night. In G5, however, the LH pulse number decreased, while the LH level and pulse amplitude still increased, presumably as a result of the increased negative feedback action of sex steroids. Simultaneous LH/FSH pulses developed during the night at onset of puberty but during the day only towards the end of pubertal development. The use of these novel highly sensitive IRMA methods demonstrated nocturnal LH and both diurnal and nocturnal FSH pulsatility to be present in older prepubertal boys. The early detectable FSH level plus the existence of solitary FSH pulses throughout puberty as well as in adult men support the hypothesis of the existence of a GnRH-independent FSH secretion in men. Our results are in accordance with the following hypotheses: (1) puberty is brought about by GnRH secretion increasing with time, both in frequency and amplitude, and first appearing during the night.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1989

Administration of a GnRH-antagonist to immature rats affects subsequent female and male pubertal development differently.

Gonadotropin secretion was inhibited in immature male and female rats by sc administration of the GnRH-antagonist ORG30276 (GnRH-A) on days 6, 9, 12 and 15. In GnRH-A-treated females this resulted in suppression of the temporarily increased plasma LH and FSH levels, which normally occur in prepubertal female rats. Ovarian weight was decreased. Although vaginal opening in GnRH-A-treated rats occurred earlier, the age of 1st estrus and the number of ova shed at first ovulation were not affected. Fertility at 4 months of age was normal. After initial suppression of gonadotropin levels, the FSH levels in GnRH-A-treated males, however, sharply increased to about twice the control levels. Plasma FSH remained elevated at least until 4 months of age. The LH levels at adult age were not affected by antagonist treatment and neither were testosterone levels. Testicular weight was decreased by GnRH-A from about 50% on day 15 to about 30% at 4 months of age. Pubertal development as measured by balano-preputial separation was delayed by about 7-10 days. At 4 months of age fertility was decreased. Thus, suppression of early gonadotropin secretion by GnRH-A treatment had dramatic effects on subsequent pubertal development in the male, but not in the female rat.

Age Factors↗

PubMed1989

Acute desensitization of pituitary FSH response to LHRH in ovariectomized rats: further evidence that in the presence of ovarian proteins the LHRH-dependent, LH-like component of FSH release becomes apparent.

Pulsatile release of LHRH and short-term pituitary desensitization to LHRH in the rat are believed to be necessary for the maintenance of LH pulsatility. In contrast, FSH release is partly induced by LHRH release and is partly LHRH-independent. This LHRH-independent release of FSH is subject to inhibitory feedback control by ovarian proteins (probably inhibin), and may obscure an LHRH-induced short-term loss of pituitary FSH responsiveness to LHRH. The object of this study was to establish whether short-term pituitary desensitization to single doses of LHRH results not only in a loss of LH response, but also of FSH response. Ovariectomized rats were used to eliminate the influence of steroid feedback. A group of ovariectomized rats was pretreated with steroid-free bovine follicular fluid (bFF) to suppress LHRH-independent FSH release, and phenobarbital to suppress LHRH-dependent FSH release respectively, 7 and 1 h before administration of LHRH. Another group received phenobarbital only. The animals were injected sequentially with either low or high doses of LHRH (1.25 or 10 ng/100 g body weight at times 0 and at 80, 120 or 180 min, and 6.25 or 50 ng/100 g at 60 min). Blood was taken for FSH measurements before and 5 and 10 min after each injection. Rats pretreated with bFF and phenobarbital showed an acute FSH response related to the dose of injected LHRH. No dose-response curve was seen in animals which had only been pretreated with phenobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

The frequency of pulsatile luteinizing hormone-releasing hormone treatment and luteinizing hormone and follicle-stimulating hormone secretion in women with amenorrhea of suprapituitary origin.

The influence of luteinizing hormone-releasing hormone (LH-RH) pulse frequency on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) was studied in hypogonadotropic hypogonadal women. They received three regimens of 5 days of pulsatile LH-RH (5 micrograms/pulse) given at 30-, 90-, or 180-minute intervals, with at least 6 weeks between treatments. On day 1, LH and FSH increased in proportion to the LH-RH pulse frequency. After 5 days of treatment with the 30- and 90-minute intervals, LH was still elevated, but FSH had returned to pretreatment levels together with a decline of the FSH response. The LH response only declined during treatment with the 30-minute pulse interval. During each treatment, estradiol (E2) increased. Explanations for dissociation between LH and FSH secretion during treatment with higher LH-RH pulse frequencies could be: (1) desensitization of FSH rather than LH secretion on LH-RH; (2) a differential effect of E2 on LH and FSH; (3) nonsteroidal ovarian factors selectively regulating LH and/or FSH release.

Adult↗

PubMed1988

Luteinizing hormone secretion patterns in boys at the onset of puberty measured using a highly sensitive immunoradiometric assay.

Pulsatile LH secretion was studied in 3 prepubertal and 11 early pubertal boys by measuring plasma LH concentrations at 10-min intervals from 1200-1800 h and from 2400-0600 h using an immunoradiometric assay with a lower limit of detection of 0.10 IU/L. Plasma testosterone (T) was measured hourly. In the prepubertal boys plasma LH was not detectable during the daytime but at night 20- to 300-min periods of detectable, but low (less than 0.5 IU/L) plasma LH values occurred. A discrete episodic LH pattern was discernible, and the median number of pulses was 2 during the 6-h nocturnal sampling periods. Plasma T was not detectable (less than 1.0 nmol/L). In the pubertal boys most daytime plasma LH values were greater than 0.3 IU/L, with periods of values of 0.1-0.3 IU/L and short periods of undetectable levels as well. At night definite pulses, up to 4.7 IU/L, were found in all boys. The median number of pulses was 4 during the 6-h nocturnal sampling period. Plasma T was detectable at night in 5 of these 11 boys. The results strongly suggest that at the onset of puberty prepubertal boys (G1) have no LH secretion during the day but intermittent gonadotrophic activity during the night. In early puberty LH secretion increases in amplitude as well as frequency to a clear pulsatile pattern during the night, sometimes with pulses during the day as well.

Adolescent↗

PubMed1988

The influence of pulsatile GnRH administration to the ovariectomized rat on the pituitary response to GnRH and the occurrence of spontaneous LH pulses.

Otherwise untreated adult ovariectomized rats were given pulses of GnRH (5 ng/100 g body weight iv) once every 60 or 120 min for 24 or 96 h. On the first and last day of the experiment plasma LH was estimated during the administration of GnRH pulses. Endogenous LH pulses between exogenously generated LH pulses were observed in nearly all animals on both the first and the last day, without any change in nadir and amplitude values. Shortly after an injection of GnRH, the spontaneous LH pulses were fewer than expected. The number of these pulses, however, increased again with time after the injections. The response to exogenous GnRH was reduced on the last day of the experiment. However, not all GnRH injections led to LH pulses. Most injections which did not result in an LH pulse appeared to be given within 15 min after a preceding endogenous LH pulse. The results obtained are in agreement with the hypothesis of an acute short-lasting desensitization of the pituitary gland caused by exogenous as well as endogenous pulses of GnRH.

Animals↗

PubMed1988

Pulsatile GnRH treatment of the ovariectomized rat and release of LH and FSH.

The effect of pulsatile GnRH administration on the levels of LH and FSH was investigated in rats that had been ovariectomized 2 weeks earlier. Also the asynchronous occurrence of endogenous and GnRH-induced LH and FSH pulses was analysed. A small pulse dose of GnRH (1.25 ng/100 g) was given iv at a frequency of once every 60 min or once every 120 min during 24 h. A larger dose of 5 ng/100 g was given once every 60 or 120 min during either 24 h or 96 h. Blood was sampled arterially every 5 min around the two first and last GnRH injections and LH and FSH were measured. Only the treatment with the larger GnRH pulse dose resulted in a change of LH and FSH plasma levels. LH levels declined under all circumstances, whereas FSH was found to be increased temporarily after 24 h of treatment. The pituitary LH response to pulses of GnRH (5 ng/100 g) decreased irrespective of the frequency or duration with which GnRH was administered. There was a marked asynchronicity between LH and FSH pulses and almost every injection of GnRH (5 ng/100 g) resulted in clear LH pulses but not in FSH pulses.

Animals↗

PubMed1988

Pituitary response during pulsatile luteinizing hormone-releasing hormone ovulation--induction in patients with clomiphene citrate-resistant polycystic ovary-like disease.

The pituitary response to pulsatile luteinizing hormone-releasing hormone (LRH) was studied in 6 women with clomiphene-resistant polycystic ovary-like disease (PCOD). PCOD was defined as oligomenorrhea, elevated luteinizing hormone (LH), normal follicle-stimulating hormone (FSH), and, in general, elevated androgens. LRH was administered in a pulsatile way, chronically, with a pulse dose of 20 micrograms and a pulse interval of 60, 90 and 120 minutes. Blood was drawn every 10 minutes for 6 hours, at the start of therapy (pulse study 1) and 9-15 days after the start of therapy (pulse study 2). Five patients ovulated within 10 days of therapy, which meant that pulse study 2 was performed during the luteal phase. One patient remained anovulatory. The follicular and luteal response during LRH therapy was comparable to that of normal cycles, although the pituitary response was enhanced in PCOD at the start of therapy, which might be related to the state in which the ovary finds itself with respect to follicular development. Desensitization for LH to LRH occurred only incidentally during pulse study 1. Desensitization for FSH to LRH already developed during pulse study 1 and continued to existed during therapy. The 60, 90 and 120 minute LRH pulse interval regimes resulted in LH nadir intervals with wide ranges, although the medians were 60, 90 and 120 minutes respectively.

Adult↗

PubMed1988

Pulsatile LH-RH treatment induces a relatively low response of LH and FSH, while discontinuation enhances the response in women with amenorrhea of suprapituitary origin.

Five women with amenorrhea of suprapituitary origin were given intravenous injections of 10 micrograms LH-RH every 90 minutes for 4 days by means of a portable infusion pump. Immediately before and after this, the LH and FSH responses to a test dose of 100 micrograms LH-RH were measured. Four days after discontinuation of the treatment, so that LH and FSH could be measured, blood was sampled every 10 minutes for a period of 6 hours, during which 20 micrograms LH-RH was injected intravenously every hour. Finally, a test dose of 100 micrograms LH-RH was given. The whole procedure was repeated at least 6 weeks later, but this time hourly injections of 100 micrograms LH-RH were given 4 days after discontinuation of the pulsatile LH-RH treatment. Four days after the pulsatile LH-RH treatment was stopped, increased LH and FSH responses to LH-RH were observed. These could be reduced by 6 injections, given hourly, of either 20 or 100 micrograms LH-RH. Although the totally released amount of both LH and FSH did not differ between the two treatment regimens irrespective of the LH-RH dose used, the response of both gonadotropins to the LH-RH test dose after the hourly 100 micrograms LH-RH injections was significantly lower. This indicated that desensitization can be attributed, at least in part, to a lower responsiveness of LH and FSH to LH-RH when pulsatile LH-RH is given. Low responses during treatment with pulsatile LH-RH could not be related to higher concentrations of plasma estradiol. We conclude that women with amenorrhea of suprapituitary origin who are treated with pulsatile LH-RH have a low state of responsiveness to LH-RH, which can be caused by the presence of the LH-RH and might be attributed in part to desensitization by LH-RH. Removal of the LH-RH results in an enhancement of the responsiveness, as the pituitary gland might have recovered from this desensitization.

Adult↗

PubMed1987

The chance of spontaneous conception for the infertile couple referred to an academic clinic for reproductive endocrinology and fertility in The Netherlands.

892 infertile couples were studied retrospectively over a 4 year and 7 month period for their chance of spontaneous conception after first attendance at the clinic. The Kaplan-Meier method was used for all calculations. Most of the spontaneous conceptions took place within two years. As the age of the female patient increased, beginning at age 30, the cumulative spontaneous conception rate decreased. The same was true for the duration of infertility beginning at 4.5 years. The influence of the latter was more important. The cumulative conception rate was not influenced by whether the infertility was primary or secondary. Patients referred by a general physician had a better chance of achieving spontaneous conception than patients referred by a gynaecologist. It is concluded that time plays a significant role in the achievement of pregnancies in our clinic, but should no longer be relied upon two years after entering the clinic.

Adolescent↗

PubMed1987

Short-term pituitary desensitization to luteinizing hormone-releasing hormone (LH-RH) after pulsatile LH-RH administration in women with amenorrhea of suprapituitary origin.

The existence of a short-term pituitary desensitization in luteinizing hormone (LH) release to single doses of luteinizing hormone-releasing hormone (LH-RH) in the ovariectomized rat was recently disclosed. The purpose of the present study was to investigate whether this refractoriness is also present in humans. Blood from six women with amenorrhea of suprapituitary origin was sampled every 10 minutes for 300 minutes for determination of LH and follicle-stimulating hormone (FSH). A pulse of 20 micrograms LH-RH was given intravenously 90 and 210 minutes after the first blood sample, and 2 micrograms LH-RH was given 30, 150, 240, and 270 minutes after t0. The mean maximal increments of LH and FSH were compared. The LH response to a 2-micrograms LH-RH bolus given 30 (t240) or 60 (t150) minutes after a 20-micrograms LH-RH pulse was significantly decreased, compared with the initial response to this dose at t30. For both LH and FSH, the response to 2 micrograms LH-RH given 30 minutes after the 20-micrograms pulse (t240) was almost absent, compared with 60 (t150) minutes after the 20-micrograms dose. We conclude that a short-term pituitary refractoriness to LH-RH is present after administration of single pulses of LH-RH in women with amenorrhea of suprapituitary origin and pulses of LH-RH in the physiologic range (2 micrograms) given to these women do not always generate LH and FSH increments that are identifiable as significant hormone pulses.

Adult↗

PubMed1987

Induction of first cycles in primary hypothalamic amenorrhea with pulsatile luteinizing hormone-releasing hormone: a mirror of female pubertal development.

During pubertal development in girls, the attainment of regular ovulatory menstrual cycles usually is preceded by cycles that are either anovulatory or show a defective luteal phase. It is not known whether these defective cycles are caused by inadequate luteinizing hormone-releasing hormone (LH-RH) secretion or by an inadequate response of the pituitary-ovarian axis to LH-RH stimulation. To shed new light on this matter, the authors analyzed endocrine data from 12 menstrual cycles induced by pulsatile LH-RH therapy in five women with primary amenorrhea of hypothalamic origin. Anovulatory cycles occurred with and without an increase in estrogen excretion and with and without a luteinizing hormone surge. In addition, ovulatory cycles with and without deficient corpus luteum function were observed. Most of these types of anovulatory and ovulatory menstrual cycles also have been described during normal puberty. Therefore, these observations suggest that, during normal pubertal development, maturation of the pituitary gonadotropes and of the ovary occurs, as well as the increased secretion of LH-RH from the hypothalamus, which the overall process depends upon.

Adolescent↗