Premenstrual syndrome no progesterone; premenstrual dysphoric disorder no serotonin deficiency.
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Biomedical subjects
Publications and source records attributed to H A van Leusden.
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Fifty postmenopausal women requiring hormone replacement therapy for the treatment of climacteric symptoms were recruited in six centers. All patients received a new combined norethisterone acetate (NETA)/oestradiol (E2)-TTS, (Estragest TTS, Ciba-Geigy Ltd), delivering 0.25 mg NETA and 50 micrograms E2 per day, continuously for 12 calendar months. Bleeding occurred in 38 (76%) of the 50 patients at any time during the 1 year treatment. The percentage of patients without bleeding increased gradually each month, from 24% in the second month to a relatively stable level of approximately 80% in month 7 and thereafter. Twenty-seven patients (54%) did not complete the whole trial period; 15 of which discontinued the treatment within the first few months due to irregular bleeding. In patients who remained in the trial, a clear decrease in the frequency and intensity of the bleeding was observed with time. Bleeding was mostly light or consisted of spotting only. None of the post-trial biopsies showed proliferation or hyperplasia of the endometrium. The treatment resulted in a substantial decrease of climacteric symptoms (Kupperman index) within 4 months and was well tolerated. It was concluded that the continuous NETA/E2-TTS treatment is an effective and safe alternative for the treatment of climacteric symptoms in selected patients.
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A nadir of LH precedes the onset of the flush and a flush is never seen without an LH pulse. However, after surgical and medical (GnRH agonist) hypophysectomy flushing occurs while LH is absent, thus LH itself is not the cause of the flush. GnRH agonist treatment induces low LH, whereas flushes remain, even when oestrogens are supplemented, suggesting that GnRH itself is the mediator. As flushes are preceded by a spike of LH-RH, GnRH involvement is most likely. Pulsatile administration of GnRH does not induce flushes, whereas continuous administration does. Thus it is the interference with the pulsatile pattern of GnRH that causes flushes. Even high doses of oestradiol during GnRH agonist treatment do not abolish flushes, whereas the alpha 2-adrenergic agonists such as clonidine and alpha-methyldopa abolish flushes during treatment with GnRH agonists. Thus, dysregulation of the GnRH releasing clock center in the nucleus arcuatus in the mediobasal hypothalamus is associated with altered central alpha-receptor activity which results in lowering of the set point of the central thermostat and the circulatory changes. The balance of evidence indicates that interference with the pulsatile pattern of GnRH causes the flush.
An increasing number of publications document regression of fibroids under treatment with gonadotropin releasing hormone (GnRH) agonists. However, recurrence after stopping treatment regularly counterbalances its benefit. We now report on 28 patients with intramural myomas, treated with triptorelin for 4-6 months and followed for 42-56 months. During or shortly after treatment, six patients entered menopause. In this group, a volume reduction of 71% was achieved and no surgery was needed thereafter. In 22 premenopausal women, a 64% decrease of uterine volumes was obtained at the end of treatment; the long-term reductive effect was 31%. When compared with initial values, a significant decrease was observed at the end of treatment (p = 0.0001) and of follow-up (p < 0.0005). In 13 (of 22) premenopausal patients, surgery was needed after triptorelin treatment for permanent control of fibroids. The remaining nine patients were free of symptoms after 42-56 months, having uteri in situ. These two groups differ significantly in pretreatment uterine volume (p < 0.001) and in reduction rate after therapy (p < 0.01), both parameters being higher in patients who finally needed surgery. In conclusion, triptorelin treatment is definitely beneficial in perimenopausal women and in nearly half of premenopausal women, in whom hysterectomy can be prevented. In the other half, surgery is necessary, despite significant volume reduction. These results need to be corroborated on larger groups of patients. More research is needed to explain different responses to treatment in premenopausal patients.
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Ten women with intramural leiomyomas were treated with the microencapsulated GnRH analogue Decapeptyl for 24 weeks. Four (4) mg Decapeptyl was injected, starting on day 21 of the menstrual cycle, and injections were repeated every 4 weeks for a total of 24 weeks. All patients showed a marked reduction in uterine size: before treatment it measured 284 +/- 57 cm3, after 8 weeks 122 +/- 33 cm3, and after 24 weeks 89 +/- 14 cm3. LH and estradiol decreased significantly; FSH decreased but not significantly; prolactin remained almost unaltered. Serum calcium, phosphate, alkaline phosphatase and osteocalcin increased, but, since calcium excretion (and hydroxyproline excretion) remained unaltered, these changes were considered to reflect increased bone turnover rather than bone loss. From these data it is concluded that Decapeptyl is very effective in reducing uterine fibroids, that treatment can be shorter than 6 months and that measurable bone loss did not occur.
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HCG and beta-HCG were determined in umbilical arterial and venous blood immediately after spontaneous term delivery. HCG and beta-HCG are present in higher concentrations in arterial than in venous umbilical cord blood. The data are consistent with the hypothesis that HCG and beta-HCG are produced in the fetal compartment of the human fetoplacental unit, with a larger contribution of the female fetus as compared with the male.
Lactating Texel ewes are hyperprolactinemic. Hyperprolactinemia persists for at least the first 50 h after weaning, when the udder is swollen and tender. Oral administration of bromocriptine lowers hyperprolactinemia dramatically within 4 h, correlated with 'shrinking' of the udder. During lowering of hyperprolactinemia there is no immediate increase in LH.
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