Serum Prolactin Response Research Articles

Studies on Human Prolactin Radioimmunoassay Kit and Serum Prolactin Responses to TRH in Thyroid and Other Endocrine Disorders

Studies on Human Prolactin Radioimmunoassay Kit and Serum Prolactin Responses to TRH in Thyroid and Other Endocrine Disorders

The effect of stress on serum prolactin in the female rat.

SummaryChanges in serum prolactin in response to ether vapor, ether vapor plus serial bleeding, acute restraint and chronic restraint stresses were measured in cycling, castrate, pregnant, and lactating female Long-Evans rats. Serum prolactin was measured by radioimmunoassays in serial blood samples taken before and after administration of each stressor. Pretreatment prolactin levels were elevated in rats in the afternoon of proestrus and estrus, on Day 1 of pregnancy, and during lactation. Low initial prolactin concentrations were observed during diestrus, on the morning of estrus, and in castrate females. Low intensity stress, such as ether vapor alone, did not affect serum prolactin concentrations in any group tested. The effect of higher intensity stress was related to the pretreatment concentration of serum prolactin. If the initial prolactin levels were high, such as on the afternoon of proestrus and estrus, on Day 1 of pregnancy, and during lactation, high intensity stress was associated with a red...

The Effect of Aspirin and Indomethacin on the TRH Response in Man

A double-blind study of the effect of two inhibitors of prostaglandin synthesis on the TRH stimulation of serum TSH and prolactin was carried out in 35 normal males. The subjects were evaluated before and after the administration of indomethacin or aspirin for one week. Both indomethacin and aspirin lowered plasma prostaglandin E and F levels significantly. Indomethacin treatment had no effect on the serum TSH or prolactin response to 100 mug TRH or the serum T3 and T4 levels. In contrast, aspirin treatment significantly decreased the serum TSH response to TRH and significantly lowered mean total serum T3 (RIA) and T4 (D). There was no effect on the prolactin response to TRH. These findings suggest that aspirin blocks TRH responsiveness by a mechanism other than the inhibition of prostaglandin synthesis, probably by its previously demonstrated effect on increasing the fraction of unbound thyroid hormone.

Serum prolactin and growth hormone response to thyrotropin releasing hormone in prepubertal heifers.

Serum prolactin and growth hormone response to thyrotropin releasing hormone in prepubertal heifers.

Primary empty sella, galactorrhea, hyperprolactinemia and renal tubular acidosis

Discussed here is a 41 year old woman with galactorrhea associated with the empty sella syndrome and mild renal tubular acidosis. Basal serum prolactin (PRL) levels were normal, but a 24 hour serum PRL secretory profile demonstrated an increased mean PRL concentration. Serum PRL was appropriately suppressed by the administration of L-dopa; however, chlorpromazine stimulation resulted in a blunted serum PRL response. Pituitary luteinizing hormone, follicle stimulating hormone, ACTH and thyroid stimulating hormone levels were normal. Thus, galactorrhea associated with an enlarged sella does not establish the diagnosis of a pituitary tumor, and pneumoencephalography must be performed to exclude the empty sella syndrome.

Serum prolactin and LH responses to photoperiod in bull calves.

Two bull calves were subjected to changes in daily illumination over a 12-week interval, with ambient temperature maintained at 22 C. When photoperiod was shortened from 16 to 8 h, serum prolactin decreased from a maximum of 57 mg/ml to a minimum of 8 ng/ml. Conversely, with another 4 bulls, increasing the photoperiod from 8 to 16 h of light caused serum prolactin concentrations to increase from 25 to 100 ng/ml. The increase in serum prolactin in response to increasing photoperiod was delayed approximately 7 weeks, whereas the response to decreasing photoperiod was delayed only about 1 week. Changes in photoperiod had no effect on serum LH concentrations. We conclude that changes in photoperiod account, at least partially, for the seasonal changes in serum prolactin previously noted in cattle.

Response of Serum Prolactin to Exogenous Stimulation

Previous observations by other workers indicating suppression of serum prolactin (hPRL) by water loading could not be confirmed. Sequential testing using an acute water load in patients with various clinical diagnoses did not aid conclusively in differentiating functional hyperlactinemic states from pituitary adenoma. It was of interest that the acute ingestion of water resulted in a triphasic response in serum hPRL levels. The response to breast stimulation was more marked in patients with excessive breast hypertrophy and galactorrhea. This was in contrast to patients with hypo- or hyperthyroidism, anorexia nervosa, and our normal subjects. In response to breast stimulation, there was no difference among the normal group, women with functional hyperlactinemia, and patients with proven pituitary adenoma. When they were compared with other patient groups in this study, marked responsiveness was found in patients with amenorrhea and galactorrhea, amenorrhea with elevated hPRL levels without galactorrhea, breast hypertrophy, and adrenal overactivity in response to these two stimuli. The physiologic mechanisms resulting in the increase in serum hPRL levels seen in these patients remain unclear at the present time.

Thyrotrophin and prolactin responsiveness to thyrotrophin releasing hormone in Cushing's disease.

Serum thyrotrophin response to thyrotrophin releasing hormone was impaired in all of eight subjects with untreated Cushing's disease; while all of six similar subjects tested after adequate treatment by a pituitary implant of 198Au then showed a normal response. In all five of the untreated patients studied, the serum prolactin response to TRH was normal. Thus chronically excessive cortisol levels as seen in Cushing's disease inhibit pituitary TSH responsiveness to TRH without affecting the prolactin response to TRH. Evidently the release of TSH and of prolactin by TRH are governed by independent mechanisms.

Failure of insulin hypoglycemia to produce rise in serum prolactin

Serum prolactin and growth hormone responses to insulin-induced hypoglycemia were measured in 5 normal individuals. While growth hormone rose appropriately in all subjects studied, serum prolactin levels did not significantly change despite the production of symptomatic hypoglycemia during testing. Prolactin response to insulin hypoglycemia is not a useful diagnostic test for prolactin secretion and cannot be used as such for assessment of pituitary reserve.

Response of serum LH, FSH and prolactin to injection of synthetic LH-RH into rat anterior pituitary.

Changes in serum LH, FSH and prolactin were measured by radioimmunoassay following injection of synthetic LH-RH into the anterior pituitary and median eminence of rats. The time course of serum levels of LH and FSH after injection of synthetic LH-RH into the pituitary showed a peak at 15 min. The synthetic LH-RH had a more marked releasing effect on LH than on FSH. After injection of 20 ng into the pituitary, the serum LH rose to about 10.7 times the control level but the serum FSH only to about 1.8 times. A significant rise of serum LH over the control level was noted after injection of more than 0.2 ng of synthetic LH-RH, while that of serum FSH was after injection of more than 2 ng. An injection of 2 ng of synthetic LH-RH into the pituitary following 0.1 mug of estradiol benzoate resulted in a fall of serum LH and FSH levels, and a rise of serum prolactin level. An injection of 2 ng of synthetic LH-RH into the median eminence resulted in a tendency towards slight decrease in serum LH and FSH. No significant response of serum prolactin to synthetic LH-RH was noted.

Serum prolactin response to thyrotropin-releasing hormone in normal subjects and in patients with thyroid diseases (author's transl)

Synthetic thyrotropin-releasing hormone (TRH) has been shown to be a stimulator of prolactin release as well as of thyrotropin (TSH) release in normal man. This paper presents data concerning the effect of TRH on the PRL response in normal human subjects and in patients with thyroid diseases. Synthetic TRH (500 mug) was administered intravenously to 12 normal males, 12 normal females, 8 female patients with hyperthyroidism, and 8 female patients with primary hypothyroidism. Blood samples were taken for the determination of the serum prolactin(PRL) and thyrotropin (TSH concentrations. Serum PRL and TSH levels were determined by each specific and sensitive radioimmunoassay. The mean serum PRL level was 6.1 +/- 4.9 ng/ml (mean +/- SD) before TRH administration in normal females, and 4.9 +/- 5.0 ng/ml in normal males. The difference was not statistically significant. The serum PRL levels 15 min after TRH administration were significantly higher in females than in males (42.0 +/- 17.2 vs. 26.3 +/- 8.6 ng/ml, p smaller than 0.001). The mean serum PRL level before Trh administration in patients with hyperthyroidism was higher than in normal females (12.5 +/- 5.5 vs. 6.2 +/- 4.9 ng/ml, p smaller than 0.05), but the mean serum PRL level 30 min after TRH was lower in cases of hyperthyroidism than in normal females (14.3 +/- 5.0 vs. 44.1 +/- 13.7 ng/ml, p smaller than 0.05). The mean serum PRL level before TRH administration in primary hypothyroidism was significantly higher than in normal females (37.6 +/- 29.0 vs. 6.2 +/- 4.9 ng/ml, p smaller than 0.05) and serum PRL level after TRH was also higher in hypothyroidism than in normal females (132.8 +/- 83.4 vs. 42 +/- 17.2, p smaller than 0l05). There was a positive correlation between the maximum increase in serum PRL concentration above the base line (...PRL) and the increment in serum TSH (...TSH) after TRH administration in these subjects. In conclusion, the PRL response to TRH was greater in females than in males, abolished in hyperthyroidism and exaggerated in primary hypothyroidism. These results indicate that the thyroid hormone concentration influences the PRL response to TRH as well as TSH response.

Prolactin response to thyrotropin releasing hormone in normal subjects.

Synthetic thyrotropin releasing hormone (TRH) was administered intravenously to normal human subjects and the serum prolactin (PRL) response was measured. The effects of dose and of age and sex of the recipients on the PRL response were evaluated. The maximum increase in scrum PRL above the baseline level (max APRL) was used as the index of response. The max APRL increased linearly as a function of the log of the TRH dose between 6.25 and 100 μg of TRH, but did not increase further in response to 400 and 800 μg of TRH. Mean PRL responses did not vary with age in subjects of the same sex, but individual variability was greater in the older subjects of both sexes. PRL responses in each of 3 age groups of females, 20-39, 40-59 and 60-79 years old, were nearly double the responses observed in males of the same age groups (58.9 ± 4.7 ng/ml in all females vs 28.7 ± 2.4 ng/ml in all males, mean ± sem). In order to avoid diagnostic error in evaluating PRL response to TRH, criteria must be employed that are specif...