[Gonadotropin secretion following intravenous estradiol administration in normo- and hyperprolactinemic to sexually mature women].
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Biomedical subjects
Publications and source records attributed to W Hardt.
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Serum concentrations of the pregnancy-specific beta 1-glycoprotein (SP 1) and human placental lactogen (HPL) were measured by radioimmunoassay in 372 blood samples obtained from 40 women in the second half of a normal singleton pregnancy. The mean level of SP 1 steadily increased from 40 micrograms/ml in the 22nd week of pregnancy to 168 micrograms/ml in the 36th week of gestation and thereafter reached a plateau. The half-life of SP 1 during the first week after delivery was about 39 h. The clinical value of SP 1 in comparison to HPL estimations was assessed in a prospective study of a few high risk pregnancies. There were no significant differences between serum SP 1 and HPL levels in pregnancies complicated by preeclampsia with or without intrauterine growth retardation and in twin pregnancies. Serum HPL and SP 1 levels were equally effective in predicting placental insufficiency with fetal growth retardation.
The influence of lisuride, a new semisynthetic ergot derivative, was investigated in women during the puerperium. Treatment with 600 or 900 micrograms lisuride over 14 days (each test group n = 25) caused an immediate drop of elevated prolactin (PRL) levels in all patients in comparison to values seen in normal, nonpregnant women (less than 30 ng/ml). Such a sharp decline was not seen in two control groups of puerperal patients, nursing as well as nonnursing, placebo-treated women. The clinical efficacy in preventing or suppressing lactation was clear cut and comparable to the known PRL lowering effect of bromocryptine. Severe side effects were not observed during lisuride treatment with these dosages. The postsuckling PRL increase was abolished by a single oral dose of lisuride (100, 200, 300 micrograms), similar to that seen with bromocrytine (2.5 mg). The inhibition was dose dependent. Only doses of 200 and 300 micrograms showed, in comparison to a placebo group, a significant long-lasting (greater than 8 h) suppression of PRL secretion.
The regulation of the hypothalamic-hypophyseal-ovarian axis during puerperium is reviewed. The lactotrophic hormone prolactin is necessary for the growth of the milk producing system, initiation and maintenance of lactation. Inappropriate responsiveness of the hypothalamic-hypophyseal-ovarian system causes independent of the actual prolactin serum values postpartum amenorrhea during early puerperium. However, the duration of amenorrhea depends on the duration of breast-feeding. The prolactin peaks induced by suckling interfere with the reappearance of normal cyclic ovarian regulation.
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The effect of Ablacton, Estrovis 4000, 2 Brom-alpha-ergokryptin (Cb 154) and of Lisurid-hydrogenmaleate (LHM) on lactation and the serum concentration of prolactin postpartum was studied. 10 normal nursing postpartum patients served as control. LHM was tested in a double blind study compared to placebo. The serum prolactin (PRL) was determined daily for the first 10 postpartum days by radioimmunoassay. Inhibition of lactation was consistent with Cb 154 (89% of the cases). Within two to three days after the onset of treatment with Cb 154 the changes of pregnancy in the breasts had completely subsided. The sexual steroids resulted in inhibition of lactation in 60% of the postpartum patients but mastodynia continued. LHM showed no difference from group taking placebo. The serum prolactin levels postpartum remained as high as a nursing mother's or rose with the administration of steroids. The administration of Cb 154 resulted in a drop of the serum prolactin to non-pregnant levels with in 2 days. The serum prolactin levels under treatment with LHM were not different from the group slowly. In nursing mothers, the stimulus of suckling maintain the pituitary secretion of prolactin as showed by higher serum prolactin levels and a slower decreased to normals than in the non-nursing mothers.
The results of the treatment of 40 vesico-vaginal fistulas, 13 uretero-vesical fistulas, 2 ureto-uterine fistulas are 44 lower ureteral stenosis are reported. These developed following operative and radio-therapeutic treatment in gynaecology and obstetrics. The vesico-vaginal fistulas were operated through the vagine according to Fueth-Mayo. Even after failed primary operation a repeat vaginal operation was successful. In uretero-vesical fistulas a spontaneous healing cannot be expected later than 8 weeks after the primary operation and an operation for the fistula is then indicated. The results of 13 operations for uretero-vesical fistulas are described. In 12 cases a uretero-cystoneostomy was performed and in one case Boari plastic was done. Two ureto-uterine fistulas were treated by end to end anastomosis of the ureters which was successful. The treatment of post-operative stenosis of the ureter was primarily conservative and resulted in marked improvement on 18 of 24 cases. In 5 of 6 cases a ureto-cystonestomy or ureterolysis yielded good results.
In 9 hypogonadotrophic, normoprolactinemic women with primary or secondary amenorrhea, who were infertile, 16 treatment cycles with menopausal gonadotropin and chorionic gonadotropin (HMG-HCG) were carried out. Nine treatment cycles were monitored indirectly with the cervical factor and hormonal cytology. The concomitant serum estradiol and progesterone values were later determined by radioimmunoassays. The other 7 treatment cycles were monitored by daily serum estradiol determinations. There were 4 pregnancies. Successful induction of ovulation with subsequent pregnancies was only obtained in the treatment cycles monitored by serum estradiol determinations (pregnancy rate 60%). Classical signs of overstimulation with ascites and hydrothorax occurred twice in treatment cycles which were monitored by clinical means only. Neither the maturation index nor the cervical factor reflected a quantitative overstimulation of the ovaries. The daily radioimmunological determination of estradiol prevented overstimulation of the ovaries, and permitted optimal timing of the induction of ovulation with HCG. In our experience, the maturation index determined from vaginal cytology and the clinical determination of the cervical factor are inappropriate parameters to monitor individually a successful induction of ovulation with HMG-HCG.
A case of a premature infant with traumatic loss of the left arm and shoulder is reported. The trauma was caused by an ineffective interruption of pregnancy.
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