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PubMed1981

Endocrine profile of patients with post-tubal-ligation syndrome.

The endocrine profile of the midluteal phase was assessed in 29 patients with the post-tubal-ligation syndrome, consisting of pain, bleeding and premenstrual tension. Compared to normal controls, the patients had a high serum estradiol and a low serum progesterone level. This abnormal luteal function may be responsible for the symptoms observed and may also explain the failure to conceive following successful reversal of tubal ligation. It is recommended that patients seeking sterilization reversal be screened for abnormal luteal function preoperatively. Selection of sterilization procedures that minimize alteration in luteal function should be given high priority.

Adult↗
PubMed1981

The relation between oral contraceptive use and subsequent development of hyperprolactinemia.

Serum prolactin levels were determined in 123 patients who presented with menstrual irregularities and/or infertility of more than 1 year's duration. Sixty-three patients had hyperprolactinemia with serum prolactin levels of 26 to 843 ng/ml (normal 5 to 22 ng/ml); 44.4% of this group of patients received oral contraceptive for a period of 2 months to 7 years. Sixty patients were normoprolactinemic, with serum prolactin levels of 3 to 22 ng/ml; 33.4% of this group received oral contraceptives for a period of 6 months to 7 years. The age of presentation, onset of symptoms, age at which they started on oral contraceptives, and duration of use were tabulated. The data were analyzed using chi 2 test corrected for continuity. There was no significant difference in age at the time of evaluation between oral contraceptive users and nonusers with hyperprolactinemia. The relative odds developing hyperprolactinemia were 2.64 times greater among women who has used oral contraceptives for more than 1 year and 6.25 times greater if this use started before the age of 25.

Adolescent↗
PubMed1975

[The pulsatile LH fluctuation (spiking) dependent on the circulating prolactin. Studies during physiological (puerperium), functional pathological and TRH induced hyperprolactinemia].

The magnitude and frequency of episodic LH-fluctuations have been observed to change during the different phases of the menstrual cycle. A hypothalamic control center appears to be responsible for these variations. Disturbances of the hypothalamus often make themselves known through a lack of LH-episodes. Ahypothalamic derangement in women with functional amenorrhoea can result in a disregulation of gonadotropins as well as prolactin, thereby leading to hyperprolactinemia. One finds an inverse relationship between high prolactin secretion and cessation of or decreased pulsatile LH-secretion (spiking). LH-spiking was tested in physiological post partum, functional pathological and TRH-induced hyperprolactinemias. No LH-episodes were observed post partum after the end of HCG clearance although prolactin had returned to normal levels at 12 days p.p. The mode of LH-secretion in a group of functionally amenorrhoic patients was changed by a TRH-induced prolactin increase: the previously observed LH-spikes in these women could no longer be seen. Normal cycling women, however, were not affected. In patients with hyperprolactinemic anovulatory syndromes, prolactin suppressed LH-fluctuations reappeared after administration of 2-Bromo-alpha-ergocryptin. The inhibitory influence of hyperprolactinemia on the function of the gonadostat will be discussed. High plasma prolactin levels influence the cyclic and tonic hypothalamic function. Furthermore, prolactin appears to have a peripheral inhibitory influence on ovarian gonadotropin stimulation. Post partum anovulation and amenorrhoea can be caused by an antigonadotropic and antigonadic effect of prolactin.

Amenorrhea↗
PubMed1975

[TRH stimulation as an attempt at demonstration of the induction and involution of prolactin-secreting pituitary cells in pregnancy and puerperium and in pathological hyperprolactinemia].

The present paper discusses the relationship between functional hypertrophia or hyperplasia of the prolactin secreting cells in the pituitary and actual pituitary prolactin reserves in pregnant and post partum women. 35 randomly selected post partum patients from the 3rd to 12th day p.p. and 14 women in their 11th to 14th weeks of pregnancy volunteered to undergo a standard TRH-test. The control group consisted of 60 normoprolactinemic patients. Eleven pathologically hyperprolactinemic patients were compared to the normoprolactinemic and physiologically hyperprolactinemic groups. In all cases, plasma prolactin showed a linear decrease from the 3rd to 12th days post partum. The TRH induced increase became correspondingly greater as the basal prolactin levels decreased, i.e. an inverse relationship between these two parameters was seen. The TRH-induced increase was also always greater than the increase caused by suckling. A connection between prolactin and parity was not found. The inverse relationship between basal prolactin levels and the actual reserves which could be released by TRH stimulation can be explained in that there are two regulatory systems for prolactin. The estrogens stimulate basal prolactin and inhibit prolactin reserves. The actual prolactin reserve is, on the one hand, directly dependent on the degree of endogenous neurohormonal stimulation and, on the other hand, indirectly dependent on the endogenous estrogens through a feedback mechanism. The TRH-stimulation test is not suitable for determining a functional hypertrophia or hyperplasia of lactotropic pituitary cells.

Estrogens↗
PubMed1976

Prolactin binding to mammary gland, 7,12-dimethylbenz(a)-anthracene-induced mammary tumors, and liver in rats.

Specific binding of radioactively labeled prolactin was determined in membrane preparations from mammary glands and livers of rats during pregnancy and lactation. Prolactin binding to mammary gland increased throughout late pregnancy and early lactation, reached a maximum on Day 11 of lactation, and then declined. Maximum prolactin binding to liver membrane preparations was observed during late pregnancy and declined throughout lactation. Estradiol benzoate (20 mug/day), administered on Days 5 to 10 of lactation, reduced prolactin binding to mammary gland by 55%, increased binding to liver 2-fold, and reduced litter weight gain by 25%. Prolactin binding to 7,12-dimethylbenz(a)anthracene-induced mammary tumors was 3 times higher than that observed in lactating mammary gland. Administration of prolactin enhanced tumor growth but decreased specific prolactin binding to tumors. Lergotrile mesylate inhibited and estradiol benzoate (2 mug/day) enhanced tumor growth, but neither treatment affected prolactin binding to tumor membrane preparations. In contrast, higher doses of estradiol benzoate (20 mug/day) inhibited tumor growth and reduced prolactin binding. Prolactin binding varied widely within all groups of mammary tumors and was not clearly related to growth response or to altered circulating estrogen and/or prolactin levels. Hormone dependence in this animal tumor model is complex and may not be predicted on the basis of prolactin-binding capacity alone.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Pituitary-ovarian relationships preceding the menopause. I. A cross-sectional study of serum follice-stimulating hormone, luteinizing hormone, prolactin, estradiol, and progesterone levels.

Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, estradiol, and progesterone concentrations were measured in 58 ovulating women in different age groups (20 to 29, 34 to 39, 40 to 44, and 45 to 50 years) at five- to seven-day intervals through a single menstrual cycle and in 18 postmenopausal women sampled weekly five to six times. The over-all hormone patterns were similar in four premenopausal groups. However, mean serum FSH levels increased with age and significantly higher concentrations were found in the 40 to 50 years group than in the 20 to 29 year group. Serum LH levels did not show a similar rise with age, although follicular LH levels in the oldest group were higher than in the 20 to 29 year group. Prolactin and estradiol concentrations did not change with age prior to the menopause, but luteal progesterone levels were lower in the three older premenopausal groups than in the 20 to 29 year group. Postmenopausal women showed elevated FSH and LH, decreased prolactin, and negligible estradiol and progesterone levels. There was an over-all significant linear correlation between prolactin and estradiol concentrations. It appears that the menopause is preceded by several years of rising gonadotropin, predominantly FSH, levels. During this period, ovarian estrogen production appears to be maintained and ovulation continues, but luteal progesterone levels decline. It is likely that these premenopausal alterations in pituitary-ovarian relationships reflect depletion of ovarian follicles.

Adult↗