Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Prolactin--analysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1987

Heterogeneous distribution of serum prolactin values in apparently healthy young women, and the effects of oral contraceptive medication.

Controversy over effects of oral contraceptives (OCs) on serum prolactin (PRL) levels from retrospective studies suggested performing a prospective study. Statistical analyses of PRL levels in 552 reproductive-age, nonmedicated women indicated a provisionally lognormal distribution of values less than 15 ng/ml, contaminated by a small number of abnormally high values less than or equal to 90 mg/ml. Truncated samples were used to estimate a "normal range" of PRL levels for three subsets of the study sample, classified according to number of weeks after pregnancy. Fifty-microgram estrogen-containing OCs doubled basal PRL levels at 5 to 8 weeks in those whose initial control values fell below 15 ng/ml, but the PRL elevation was no longer evident at 6 months of drug use. These OCs induced a small but significant lowering of PRL at 5 to 8 weeks in those with control levels of 15 ng/ml or higher. Thirty-five-microgram estrogen-containing OCs failed to alter PRL levels at 5 to 8 weeks in those with control values less than 15 ng/ml.

Age Factors↗
PubMed1979

Inherent ranges of seminal prolactin in pre- and postvasectomy subjects.

Seminal immunoreactive prolactin (i prolactin) was studied in 14 healthy subjects, ages 31 +/- 2 SEM, before and after undergoing elective vassectomy for birth control. Seminal plasma was separated within 2 hours of ejaculation, and prolactin was measured in duplicate by radioimmunoassay. The difference between the prevasectomy (mean +/- SEM 11.1 +/- 0.8 ng/ml) and postvasectomy seminal i prolactin (mean +/- 9.9 +/- 0.7 ng/ml) was statistically significant (mean +/- SEM 1.21 +/- 0.53 ng/ml, paired t-test, t = 2.36, P < 0.05). The mean prevasectomy seminal prolactin correlated with the corresponding mean postvasectomy value of the same subject (linear regression analyses, r = 0.77, P < 0.001). This study suggested that the accessory sex organs were the major source of seminal immunoreactive prolactin, and that a minor contribution might come from the in vivo presence of spermatozoa and/or testicular secretions. It also suggested that the magnitude of seminal immunoreactive prolactin was characteristic for each individual.

Adult↗
PubMed1975

Clinics in endocrinology and metabolism. Investigative procedures.

In patients with hypogonadism, the exact cause of the deficient androgenisation is not always clinically apparent. The data presented demonstrate that by means of hormone measurements, basally or after stimulation tests, the exact level of the lesion can usually be determined. This allows a decision with regard to appropriate therapy to be made on the basis of an accurate diagnosis. In many instances basal measurements of pituitary and gonadal hormones are all that is required to decide the level of the lesion. Care in interpreting basal levels is required, however, in view of methodological limitations and of known physiological variations with age, time of day and hour-to-hour fluctuations. If the basal hormone levels are borderline, or if the 'reserve function' of part or all of the hypothalamic-pituitary-gonadal axis needs to be assessed, than the appropriate stimulation test should be performed. The indication for these stimulation procedures and results obtained in different conditions are described and problems of interpretation discussed.

Adult↗
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↗