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Biomedical subjects

J Soria

Publications and source records attributed to J Soria.

At least 199 records · Page 11Linked to original sources
PubMed1977

Gonadotropic responsiveness to clomiphene, LRH, estradiol, and bromocriptine in galactorrheic women.

Twenty hyperprolactinemic patients with galactorrhea were studied to determine their gonadotropic responses to various stimuli. Five women lacked response to gonadotropin following the administration of clomiphene citrate. Ten patients who had luteinizing hormone releasing hormone (LRH) tests before and during bromocriptine administration exhibited varied FSH and LH responses that apparently were unaffected by bromocriptine therapy. A loss of the normal positive feedback of estrogens at the level of the hypothalamus was demonstrated in most patients before and during bromocriptine therapy. Long-term treatment with bromocriptine in 11 women resulted in a decrease of serum prolactin, cessation of lactation in all, and pregnancy in 8. These results suggest that the failure of normal secretion of gonadotropins in hyperprolactinemic women may result from 1) inadequate release of endogenous LRH, and 2) loss of the positive feedback of estrogens, as a result of the same hypothalamic disturbance that provokes the hyperprolactinemia. In turn, the elevated prolactin levels may exert a short-loop negative feedback at the hypothalamic level, inhibiting cyclic gonadotropin release.

Bromocriptine↗
PubMed1977

[Gonadotropin reserve in anorexia nervosa].

Four patients with anorexia nervosa were studied. All patients in the acute stage of the illness had low serum luteinizing hormone (LH) levels which were unresponsive to clomiphene. The four women showed almost no LH response on a single iv injection of 100 mug LH-RH; however, the FSH response was similar to that of normal eumenorrheic women. When the patients had regained weight the LH levels were normal, and they responded normally to LH-RH. These results seem to suggest that impaired hypothalamic function is the cause of gonadotropin deficiency in most patients with anorexia nervosa.

Anorexia Nervosa↗
PubMed1977

Relationship of maternal, fetal, and amniotic fluid prolactin levels.

Serum prolactin (PRL) was measured by radioimmunoassay in 80 women in serum and amniotic fluid during various stages of normal pregnancy and at delivery. In addition, prolactin levels were measured in cord sera at 60 newborns. PRL levels in maternal serum progressively increased during pregnancy, and they were lower than the corresponding levels in amniotic fluid. A relative decline in the amniotic fluid prolactin between the 39th and the 40th week of gestation was observed. The mean concentration of PRL in umbilical blood was significant lower than that in maternal blood at delivery. The lack of correlation between the PRL in amniotic fluid and the levels found in maternal and newborns serum suggests an independient source of PRL in each of the three compartments.

Amniotic Fluid↗
PubMed1977

Anterior pituitary function during early neonatal period.

Anterior pituitary responsiveness to parturition was studied in 28 normal newborn infants. Cord blood sera samples were obtained for measurement of TSH, HGH, PRL, and FSH at birth and at intervals during four hours. The neonate infant's pituitary response to parturition consists of both PRL and TSH increments, which is probably mediated by an increase in TRH release.

Fetal Blood↗
PubMed1976

Long-term administration of thyrotropin-releasing hormone and its effect on gonadotropin secretion in eumenorrheic women.

Thyrotropin-releasing hormone (TRH) was administered orally in doses of 60 mg/day to six women for two consecutive menstrual cycles. Daily serum samples were obtained for radioimmunoassay of luteinizing hormone, follicle-stimulating hormone, prolactin (PRL), and 17beta-estradiol secretory response. TRH was ineffective in interfering with normal gonadotropin and estradiol secretion, and failed to inhibit ovulation. The length of the luteal phase was not affected by TRH in the two cycles of treatment as demonstrated by basal body temperature, pregnanediol excretion, and endometrial biopsy. Long-term TRH administration induced an elevation of PRL serum levels that were not persistent and showed wide spikes. From these studies it is concluded that oral TRH at a dosage of 60 mg/day is unable to modify gonadotropin secretion and ovarian responsiveness in normally menstruating women.

Adult↗
PubMed1976

Therapeutic use of gonadoliberin (follicle-stimulating hormone/luteinizing hormone-releasing hormone) in women.

Certain conclusions may be drawn from the present review: 1. Synthetic FSH/LH-RH may induce ovulation; therefore, a therapeutic effect has been established in some cases of anovulatory infertility, but it is still difficult to assess the correct dose of FSH/LH-RH because of individual variations in response. 2. Gonadoliberin may also be used to induce ovulation after follicular maturation has been evoked by other agents. FSH/LH-RH can be utilized for supplementing the LH surge after clomiphene therapy in cases of clomiphene failure. When associated with HMG, the synthetic decapeptide may be helpful in avoiding the ovarian hyperstimulation syndrome. 3. The "triggering" of ovulation by a continuous infusion of FSH/LH-RH might be a convenient means of controlling the timing of ovulation. 4. It is expected that FSH/LH-RH blocking analogs may be used to inhibit both LH and FSH release induced by endogenous gonadoliberin in women seeking contraception.

Anovulation↗
PubMed1976

Further observations on postpartum ovarian refractoriness: effect of gonadal stimulation in women receiving bromocryptine.

It has been reported previously that the administration of human menopausal gonadotrophins (HMG) to lactating and non-lactating women from day 5 to day 9 postpartum elicited no significant elevation of urinary oestrogens or serum oestradiol within 15 days after delivery. In order to study further the role of prolactin on this ovarian refractoriness, five women receiving 7-5 mg of bromocryptine (CB-154) daily were given HMG at a dose of 300 iu per day, from day 5 to day 10 post-delivery. In all women serum oestradiol and urinary oestrogens showed no significant elevation within the 2 weeks after delivery. Serum prolactin was elevated in all cases and fell to normal nonpregnant levels immediately after CB-154 was administered. The suggestion that prolactin may possess antigonadotrophic activity at the ovarian level is not supported by the data presented here. The deficient ovarian response to gonadotrophin stimulation could be due to either the intraovarian effect of the high amounts of circulating steroids produced during gestation or to some unknown mechanism.

Bromocriptine↗
PubMed1976

The effect of oral administration of thyrotropin-releasing hormone on lactation.

Sixteen puerperal women between the ages of 17-30 years, were studied in a double blind trial during the four weeks postpartum. Eight women received orally 20 mg of synthetic TRH three times a day, 30 minutes before the corresponding breast feeding; the remaining group received a placebo in the same fashion. The women receiving TRH exhibited higher basal concentrations of serum PRL as well as a higher increment in response to suckling; however, the PRL concentrations before and after breast feeding in this group were similar to those of the control group by the fourth week postpartum. TRH treatment showed no effect on the yield or content of milk during the four-week period. In a conjoint study, PRL concentrations did not rise after TRH administration in women with defective lactation, suggesting that some impairment of the PRL release mechanism was present. TRH caused no clinical hyperthyroidism in the mothers nor in the children. Serial determinations of serum T3 and TBG revealed values within the normal limits. It was also observed that TRH administration had no effect on FSH and LH secretion, and gonadotropin secretion was not inhibited despite of the increments on PRL concentrations. In both groups, suckling had no effect on serum levels of pituitary gonadotropins determined before and after breast feeding. We have concluded that in full lactating mothers: a) the oral administration of TRH produced a marked increment in PRL concentration but no significant augmentation of milk production was observed; b) in some cases of hypogalactia, TRH did not improve the milk production; and c) the PRL-enhanced secretion showed no effect on gonadotropin secretion.

Administration, Oral↗
PubMed1976

Effect of prolactin suppression on gonadotrophic secretion in the puerperium.

Serum levels of prolactin (PRL), FSH, LH and oestradiol-17 beta were determined by radioimmunoassay in 57 lactating women and in 20 women in whom lactation was inhibited by ergocryptine (CS-154). Women who breast fed their infants exhibited high PRL levels which abruptly declined within 48 h post-partum, and remained low for the duration of the study. Serum FSH was undetectable during the first week post-partum in lactating as well as in CB-154 treated women. Thereafter, lactating women showed increasing FSH levels which reached a maximum by the third week post-partum. These FSH values were higher in lactating women than in the CBS-154 treated group. In contrast, LH levels were higher in those women receiving CB-154. Serum oestradiol-17 beta remained in low levels throughout the study, and no difference was observed between the two groups of subjects. From these results it seems that: 1) inhibition of PRL secretion leads to a faster recovery of gonadotrophin secretion toward the "menstrual type", and 2) PRL suppression produces no effect on the ovarian oestrogen production.

Adolescent↗
PubMed1976

Serum FSH and synthetic LHRG response in pregnant women at term and in the newborn.

Serum immunoreactive FSH was undetectable in a) pregnant women past 38 weeks of gestation, b) newborn infants, and c) anencephalic infants. The intravenous administration of 100 mug of synthetic LHRH elicited no FSH release in each instance. These results seem to indicate that the absence of FSH in serum in pregnant women in the last trimester, as well as in the newborn, is due to the suppressive effect on the anterior pituitary of the increased amount of circulating sex steroids.

Anencephaly↗