Prolactin Hypersecretion Research Articles

Influence of thiouracil-induced hypothyroidism on adrenal and gonadal functions in adult female rats.

The effect of hypothyroidism on adrenals and gonads in adult female rats was investigated throughout the estrous cycle. Hypothyroidism was induced by administration of 4-Methyl-2-Thiouracil (Thiouracil) in the drinking water. The weight of ovaries and adrenals, and the plasma levels of corticosterone decreased in hypothyroid rats as compared with euthyroid rats throughout the estrous cycle. Hypothyroidism resulted in decreased concentrations of plasma LH on the day of diestrus and proestrus, whereas the plasma concentrations of prolactin and progesterone increased as compared with euthyroid rats. The weight of uteri and plasma concentrations of estradiol decreased during the day of diestrus and proestrus in hypothyroid rats as compared with euthyroid rats. To further clarify the dysfunction of hypothalamo-hypophysial-adrenal axis in hypothyroid rats, animals were stressed by immobilization for 3 hr. In hypothyroid rats, a marked increase in plasma levels of ACTH in response to immobilization stress was observed compared to euthyroid control, whereas increases in plasma concentrations of corticosterone were much smaller in hypothyroid than euthyroid rats. These results clearly indicate that hypothyroidism causes both gonadal and adrenal disturbances in adult female rats. The increased concentrations of plasma progesterone may be due to hypersecretion of prolactin during the day of proestrus and estrus, which in turn result in disruption of the estrous cycle.

ESTRADIOL IMPLANTS IN THE ARCUATE NUCLEUS INDUCE LACTOGENESIS IN VIRGIN RATS. ROLE OF PROGESTERONE

The aim of this study was to determine the effect of the centrally administered estradiol, and the effects of the consequent hypersecretion of prolactin (PRL) and progesterone, on lactogenesis as evaluated by mammary accumulation of casein and lactose. Bilateral cannulae containing 17β-estradiol or cholesterol were implanted in the arcuate nucleus of virgin rats on the day of estrus (Day 0). In the first experiment different groups of rats were killed on Days 6, 9, 15, 17, or 19. Trunk blood was collected and abdominal mammary glands were taken. In the second experiment, estradiol-implanted rats received the progesterone antagonist mifepristone or vehicle at 14.00 h on Day 8 or 16 post-implant, and were killed 28 or 48 h later. Serum PRL and progesterone and mammary casein were measured by RIA and lactose was determined by an enzymatic assay. Estradiol-implanted rats showed a significant increase in both milk components at all time points after implant compared to controls. On Day 9 after estradiol implant, mifepristone had no effect on mammary content of casein or lactose. By contrast, on Day 16, mifepristone markedly increased both casein and lactose contents without modifying serum PRL and progesterone concentrations. In conclusion, 17β-estradiol implants in the arcuate nucleus of virgin rats results in hyperprolactinaemia and stimulates mammary accumulation of casein and lactose in the absence of feto-placental units. Despite the prolonged luteal activation, the sustained high levels of circulating progesterone become inhibitory to lactogenesis after a relatively long period after implant.

Fertility impairment after mifepristone treatment to rats at proestrus: Actions on the hypothalamic-hypophyseal-ovarian axis

Accumulated evidence indicates that the antigestagen mifepristone affects the reproductive axis acting on hypothalamic, pituitary, ovarian, and uterine tissues. The purpose of this study was to further investigate which reproductive functions are impaired by the antagonist, critically compromising the reproductive process, leading to unsuccessful pregnancy. Circulating pituitary and ovarian hormones, sexual receptivity, ovulation, and implantation rates were studied in cycling rats receiving a single dose of mifepristone (1 or 10 mg/kg subcutaneously) at 12:00 proestrus, before luteinizing hormone (LH) stimulation of the ovulatory process. Mifepristone-treated rats had decreased preovulatory surges of LH and prolactin (PRL), and hypersecretion of LH, PRL, and progesterone at estrus. The sexual receptivity was dramatically affected by the antagonist as indicated by the profound decrease in the lordosis response evaluated on the night of proestrus. The number of ovulating animals and the number of oocytes recovered from the oviduct on the morning of estrus were not affected by mifepristone. The low number of rats that succeeded in mating with potent males became pregnant. However, they delivered an average of only two pups at parturition, indicating a failure in the implantation of the fertilized ova, as ovulation was not affected by the antagonist at the dose used. We conclude that a dramatic inhibition of the sexual receptivity and unsuccessful implantation, preceded by a reduction on LH and PRL secretion, are the major components leading to fertility impairment after a single dose of mifepristone administered before the preovulatory surge of LH.

GROWTH AND NEUROENDOCRINE DYSFUNCTION FOLLOWING THERAPY FOR CHILDHOOD CANCER

Poor linear growth and short adult stature are common complications following successful treatment of childhood cancer. Although several factors contribute to the impaired growth of these patients, growth potential is most reduced following radiotherapy to the head or spine. Younger age at treatment and female sex seem to be significant and independent risk factors for short adult height. Early diagnosis and timely therapy of the endocrine sequelae of cancer treatment (i.e., GH deficiency, hypothyroidism, and precocious puberty) ensure that these individuals will reach their optimum growth potential. For patients exposed to high-dose radiotherapy (> 35-40 Gy) to the region of the hypothalamus and pituitary gland, a variety of neuroendocrine abnormalities in addition to GH deficiency and early sexual development may occur, including deficiencies of LH/FSH, TSH, and ACTH as well as hypersecretion of prolactin. Because these problems may develop many years after irradiation, patients at risk for neuroendocrine disturbances require long-term endocrine follow-up.

Studies on the site of ethanol action in inducing prolactin release in male rats

Hypersecretion of prolactin (PRL) has been implicated as one of the factors that mediate ethanol-induced hypogonadism, but the site(s) is the central nervous system where ethanol acts to lead to the stimulation of PRL secretion is unknown. To clarify the site(s) of ethanol action, medial basal hypothalamic deafferentation (MBHD) or medial basal hypothalamic ablation (MBHA) were performed stereotaxically in male rats, and their PRL secretory capacity in response to acute ethanol administration was compared with that of intact or sham-operated controls. In intact control rats, plasma immunoreactive PRL concentration increased markedly ( P < .001 v saline injection) following ethanol 400 to 500 mg/100 g body weight (BW) intraperitoneally (IP). The PRL response was dose-related and reached a maximum plateau level at 15 minutes. Plasma PRL returned to a near-basal level by 60 minutes. The response was blocked completely ( P < .001) by pretreatment with dopamine (1 mg per rat), a specific inhibitor of adenohypophyseal PRL secretion. In sham-operated rats and in MBHD and MBHA rats, ethanol (500 mg/100 g BW IP) induced a significant ( P < .001 to .05) elevation of PRL relative to the respective saline treatment. The basal level was significantly ( P < .005) lower in the MBHD group (5.3 ± 0.9 ng/mL) and significantly ( P < .001) higher in the MBHA group (101.1 ± 15.7 ng/mL) than in the sham group (17.2 ± 5.9 ng/mL). These results suggest the following: (1) acute ethanol administration stimulates PRL secretion from the pituitary in a dose-related manner, (2) ethanol appears to have direct stimulatory effects on adenohypophyseal PRL secretion, and (3) extrahypothalamic brain areas exert a stimulatory influence and the hypothalamus an inhibitory influence on basal PRL secretion.

Absence of short-loop autoregulation of prolactin during late pregnancy in the rat

Animals bearing intrahypothalamic anterior pituitary (AP) grafts exhibit a central hyperprolactinemia, and thus, serve as a model for the study of short-loop feedback regulation of prolactin (PRL) secretion. We investigated the effects of intrahypothalamic AP grafts on PRL secretion during late pregnancy ( n = 7). A further group of five rats was injected with the dopamine agonist bromocriptine during late pregnancy and five control rats were treated with the bromocriptine-vehicle only. A nocturnal surge in plasma PRL concentrations was observed in the vehicle-injected control animals, peaking at 212 ± 11 ng/ml at 0300 h on the day of parturition. Despite the central hyper-prolactinemia due to the grafts, a similar PRL surge was observed in grafted animals, peaking at 205 ± 35 ng/ml at 0300 h on the day of parturition. Bromocriptine treatment completely blocked the nocturnal surge of PRL. These results suggest that short-loop feedback autoregulation of PRL secretion becomes less responsive or nonfunctional in the last 24 h of pregnancy in the rat. This apparent change in sensitivity of the autofeedback mechanism may be an important physiological mechanism to allow the hypersecretion of PRL during lactation.

Sustained Prolactin Release Associated with Precocious Ovarian Failure

Five women after precocious menopause and 1 patient with primary ovarian failure showed a simultaneous elevation of plasma gonadotropin and prolactin. The hypersecretion of plasma prolactin was still present 6 months after ovarian failure. After 12-18 months of observation while FSH and LH concentration remained elevated, prolactin concentrations normalized in 5 women and decreased in 1.

Effectivenesses of cabergoline in reducing follicle-stimulating hormone and prolactin hypersecretion from pituitary macroadenoma in an infertile woman

Dopaminergic drugs have been reported to be effective in the treatment of FSH-secreting adenomas. We describe the case of a young woman suffering from amenorrhea with radiologic signs of pituitary macroadenoma. The enlargement of both ovaries with hemorrhagic and serous cysts suggest that FSH was active biologically. The short-term (13 weeks) chronic treatment with 0.5 mg cabergoline one time per week, a dopaminergic drug with long-lasting effect, was effective in reducing FSH and PRL hypersecretion and restoring the function of the pituitary ovarian axis, as confirmed by the occurrence of pregnancy.

HIGH DOSE ESTROGENS IN GIRLS WITH TALL STATURE INDUCE A TRANSIENT PROLACTIN INCREASE

Estrogens are a potent stimulus of prolactin secretion as illustrated by the increase during female puberty. High estrogen levels may lead to lactotroph hyperplasia and even pituitary adenoma. Prolactinoma in a girl treated with estrogens has been described (J Ped 1988, 133:337-9). Methods: In 30 girls with constitutional tall stature prolactin levels were measured before, during and, in part of them, after Ethinyl Estradiol (EE) therapy, 200 microgram/day. At the start of treatment mean age was 12.7 yrs (range 10.3-15.9} and pubertal stage was B3-B4: all were premenarcheal. Reference data were obtained from 25 healthy girls with mean age 13.4 yrs (range 11.7-15.1), pubertal stage B3-B5 and pre- or perimenarcheal. Blood was drawn between 9.00 and 12.00 am. Results: In the control group mean prolactin was 0.19 U/l (range 0.09-0.37). In the EE group mean prolactin at the start of treatment was 0.19 U/l (range 0.05-0.51), not different from the control data. On EE (3-18 months) mean prolactin significantly increased (ANOVA P<0.001). Mean values at 3,6,9,12,15 and 18 months were 0.45. 0.41, 0.40. 0.33. 0.32 and 0.30 U/l respectively. The treatment values at each time were significantly higher compared to the control values as well (Wilcoxon P<0.001). After EE discontinuation prolactin values significantly decreased to 0.14 U/l (range 0.07-0.24), not different from pretreatment or control data. Conclusion: High dose estrogen treatment results in prolactin hypersecretion, which normalizes after estrogen withdrawal. Follow-up of these girls should be done to exclude long-term consequences as hyperprolactinoma and/or prolactinoma.

Properties of growth hormone and prolactin hypersecretion by the human infant on the day of birth.

The neonatal period is the only interval in postnatal life characterized by physiologically elevated plasma concentrations of GH and PRL, two hormones of common origin. To study the secretion of GH and PRL on the day of birth, we obtained at regular intervals (every 20 min for 6 h) blood from seven polycythemic newborns (gestational age 34-41 weeks; birthweight 1600-3960 g; postnatal age 6-23 h) during a therapeutic, standardized, isovolumetric, partial exchange transfusion. Serum GH concentrations were measured by RIA and PRL levels by immunoradiometric assay. Deconvolution analysis of the profiles revealed that all infants displayed a pulsatile pattern of amplified GH release (range 9-191 micrograms/L). Bursts of GH secretion occurred at a median interval of 73 min. The median serum GH half-life was 18 min. All infants had continuously elevated serum PRL concentrations (range 86-191 micrograms/L) and none appeared to release PRL episodically. There was no significant cross-correlation between the secretion of GH and PRL. Mean serum GH concentrations during the 6-h study were higher than in cord serum at birth, whereas PRL and insulin-like growth factor-1 levels were lower than at birth. In conclusion, the neonatal hypersomatotropism appears to be characterized by high-amplitude, high-frequency, pulsatile secretion of GH without a prolonged GH half-life, whereas hyperprolactinemia seems to result from GH-independent, continuous PRL release. The immediate postnatal rise of GH secretion in the human newborn may be related to decreased inhibition by circulating insulin-like growth factor-1.

Properties of growth hormone and prolactin hypersecretion by the human infant on the day of birth

Properties of growth hormone and prolactin hypersecretion by the human infant on the day of birth

Pituitary gigantism caused by growth hormone excess from infancy

A 2 1/4-year-old boy with pituitary gigantism had a large pituitary macroadenoma. Gross tumor removal has prevented further visual losses, but he has had persistent hypersecretion of growth hormone and prolactin. Treatment with somatostatin analog has decreased both hormone secretion and growth velocity.

A Case of Fibrous Dysplasia (McCune Albright Syndrome) Associated with Acromegaly

We report a case of a 47-year-old woman with McCune-Albright syndrome associated with unusual growth-hormone and prolactin hypersecretion. Acromegaly was suspected on clinical examination, and she was referred to us. She had no history of precocious puberty or pathological fracture. She was 154cm tall, weighing 62kg with so-called acromegalic facies. There were two lumps, one of which was on her right lateral forehead. The other on the right lower extremity seemed to be due to a bone deformity. Some brown pigmented macules with irregular borders were present on her lips and oral mucosa. Endocrine examination revealed elevated basal levels of plasma GH (54ng/ml) and PRL (36.2ng/ml), which paradoxically increased after injection of TRH. Plasma levels of these hormones did not change after LHRH test, and plasma GH level increased after GHRH test. A skull X-ray film showed a double floor of the sella turcia and hyperostotic formation of the right sphenoid bone. MRI and CT showed a tumor shadow in the right sella turcica. Bone roentogenography of the right fibula and tibia showed a large centrally expanding lesion with a ground-glass or cystic appearance and a thin cortex. The left fibula showed a similar lesion. We recognized similar findings in other bones which also showed abnormal accumulation in a radionuclide bone scan with 99mTc. On the basis of physical, endocrinological and roentogenographical examination, we diagnosed her as displaying McCune-Albright syndrome. We operated on her by transsphenoidal surgery and confirmed a functioning chromophobe adenoma which was removed during surgery. She has been free of GH and PRL hypersecretion since then. The pathology of the sphenoidal sinus affected with fibrous bone was in accordance with the findings of fibrous dysplasia. McCune-Albright syndrome (MCAS) is known as a syndrome characterized by polyostotic fibrous dysplasia and cutaneous pigmentation and multiple endocrinopathy. Its etiology is unknown. This syndrome with acromegaly is rare, and although 26 cases have been described in literature, pathological examinations have been undertaken in only three cases. This case was very rare and valuable because, by operating on her by the transsphenoidal route in spite of the sphenoidal sinus being affected with fibrous bone, we were able to confirm a chromophobe adenoma secreting both GH and PRL. We recognized that acromegaly with MCAS was endocrinologically, morphologically and immunohistologically the same as acromegaly without MCAS. Therefore, we concluded that acromegaly with MCAS is much the same as acromegaly without MCAS.

Pituitary‐gonadal hormones and adrenal androgens in non‐cirrhotic female alcoholics after cessation of alcohol intake

To investigate the sex-hormone profiles associated with chronic alcoholism in women we examined 16 non-cirrhotic alcohol abusers (aged 18-46 years). They were admitted for the treatment of alcoholism (duration of 2-16 yrs) to a social hospital for 6 weeks. Their mean daily alcohol consumption was 170 g. Blood samples for serum LH, FSH, prolactin (PRL), oestrone (E1), oestradiol (E2), progesterone (P), 17-alpha-hydroxyprogesterone (17-OHP), androstenedione (A) and dehydroepiandrosterone (DHEA) were drawn three times a week during the hospital stay. Similar blood samples were taken from 10 control women during one menstrual cycle. The cycles were anovulatory in two patients and in none of controls. Serum LH and FSH levels were similar in alcoholic and control women but serum concentrations of PRL were increased 2-4-fold in alcoholic women. In the patients serum, concentrations of E1 and E2 tended to be lower during the follicular and midcycle phases, as did those of P and 17-OHP during the luteal phase. Compared with the controls, serum levels of A were increased 2-3-fold in the patients. A parallel difference between the two groups was seen in serum DHEA concentrations. We conclude that until liver injury, even heavy alcohol drinking has only minor effects on the secretion of gonadotrophins and ovarian steroids. Hypersecretion of PRL and adrenal androgens may well be an initiating mechanism for sexual dysfunction of female alcoholics.

Childhood's enuresis in the history of women with hyperprolactinemic amenorrhea.

Hyperprolactinemia, or elevated levels of prolactin in blood, is a normal physiologic post-partum response in lactating women. Non-lactating women with hyperprolactinemia often present during the reproductive years since they may have amenorrhea, galactorrhea, or both. Hypersecretion of prolactin is most commonly due to pituitary adenomas. Women with hyperprolactinemic amenorrhea are often quite anxious, depressed and hostile. It has been hypothesized that these psychological symptoms might antecede the onset of hyperprolactinemia and that hyperprolactinemia may be associated with early developmental problems and may be psychogenic in origin. Twenty patients with hyperprolactinemic amenorrhea and twenty-one normoprolactinemic patients with amenorrhea had an interview covering psychiatric history in order to establish whether they had ever met DSM-III criteria for functional nocturnal enuresis at one time during their childhood. While seven out of twenty (35%) patients with hyperprolactinemic amenorrhea were found to have had functional enuresis during their childhood, only two out of twenty-one (9.5%) normoprolactinemic amenorrheic women reported having had functional enuresis. The difference between the two groups was statistically significant (chi-squared: 3.88; p less than 0.05). We postulate that early stress and developmental problems may present in children as psychological distress and functional enuresis and in women as psychological symptoms (e.g., anxiety and depression) and hyperprolactinemic amenorrhea.

Hypersecretion of Growth Hormone and Prolactin in McCune-Albright Syndrome*

Acromegaly and hyperprolactinemia have been reported in association with the McCune-Albright syndrome, but the pathophysiology of the GH and PRL hypersecretion that occurs in patients with this disorder has not been defined. We studied GH and PRL secretory dynamics in three patients with McCune-Albright syndrome and hypersecretion of these hormones. Each patient had excessive linear growth, glucose-non-suppressible plasma GH concentration, and GH responsiveness to TRH and GHRH. In response to exogenous GHRH, plasma GH concentrations rose approximately 2-fold in all three patients. Plasma GHRH levels were 20-40 ng/L (normal, less than 30). Study of the spontaneous GH secretory pattern in two patients indicated nocturnal augmentation of GH release. Bromocriptine therapy failed to reduce plasma GH in all patients; in one patient treatment with octreotide, a long-acting somatostatin analog, partially suppressed plasma GH and insulin-like growth factor I levels. These results suggest that hypersecretion of GH in the McCune-Albright syndrome is not due to ectopic GHRH production or autonomous somatotroph function. The results are similar to those described in classic acromegaly due to GH-secreting pituitary tumors. However, the lack of radiographic pituitary enlargement, the variable pituitary pathology reported in similar patients, and frequent concordance of GH and PRL excess suggest that the pathogenesis of this disorder may differ fundamentally from other forms of acromegaly or gigantism. The pathophysiology may reflect abnormal hypothalamic regulation and/or an embryological defect in pituitary cellular differentiation and function.

Neuroendocrine actions of nicotine and of exposure to cigarette smoke: Medical implications

Over many years a large number of studies have demonstrated that nicotine and exposure to cigarette smoke produce marked neuroendocrine changes in animals and in man. The initial effects of nicotine are characterized by a marked hypersecretion of ACTH, vasopressin, β-endorphin, prolactin and LH. Many of these very acute stimulatory effects of nicotine rapidly disappear, probably due to a desensitization of the central nicotinic cholinergic receptors involved. Instead, upon acute intermittent treatment with nicotine or exposure to cigarette smoke, an inhibition of prolactin, LH and TSH secretion occurs, which is associated with maintained hypersecretion of corticosterone. These effects are probably mediated via activation of central cholinergic receptors of the ganglionic type. Evidence indicates that the inhibitory effects of nicotine on LH and prolactin secretion are produced via an activation by these nicotinic receptors of the tubero-infundibular dopamine neurons, releasing dopamine as a prolactin inhibitory factor. Dopamine inhibits LHRH release via an axonic interaction involving D 1-like dopamine receptors in the median eminence. It therefore seems possible that the reduced fertility found in heavy smokers may be counteracted by D 1 receptor antagonists. The symptoms associated with glucocorticoid hypersecretion induced by nicotine is discussed considering not only the peripheral side effects but also permanent deficits in hippocampal glucocorticoid receptors and loss of hippocampal neurons. In view of the important influence of hormones on immune functions, it seems likely that smoking will cause disturbances in immune responsiveness. Finally, the nicotine-induced alterations of neuroendocrine function, especially in the pituitary-adrenal axis and in vasopressin release, may also lead to behavioural consequences in smokers, especially in the withdrawal phase.

Mixed growth hormone and prolactin-secreting human pituitary adenomas: a pathologic, immunocytochemical, ultrastructural, and immunoelectron microscopic study.

A study of 30 adenomas from patients with signs of growth hormone (GH) and prolactin (PRL) hypersecretion revealed the presence of mammosomatotroph cells (MSC) containing both hormones in all cases. Although the number of immunostained cells varied from case to case, in 14 of 25 tumors, all stained cells were MSC. Nine tumors had the ultrastructural appearance of densely granulated growth hormone adenomas, while 11 cases resembled sparsely granulated growth hormone adenomas with frequent fibrous bodies. Exocytosis was present in six of these 11 cases, a feature unusual for pure growth hormone adenomas. Nine tumors consisted of a mixture of cells with the morphology of GH and PRL cells. In the four cases examined, immunoelectron microscopy using double immunolabeling with protein A-gold particles revealed the presence of secretory granules containing both hormones in some tumor cells recognized as mammosomatotroph cells.

Dilated cardiomyopathy with neutropenia, short stature, and abnormal carnitine metabolism

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Secretory dynamics of bioactive and immunoreactive prolactin in polycystic ovary syndrome

To further investigate prolactin (PRL) secretion in polycystic ovary syndrome (PCO), the authors evaluated immunoreactive (immuno) and bioactive (bio) PRL levels in the basal state and in response to provocative testing with intravenous dopamine (DA), metoclopramide (MCP), and gonadotropin-releasing hormone (GnRH), before and after disulfiram. Basal measurements of immuno-PRL, bio-PRL, and the ratio of bio/immuno-PRL were similar in PCO and controls. The immuno-PRL decrement after DA was greater than that of bio-PRL in both groups (P less than 0.05). After MCP, immuno-PRL increased more than bio-PRL in PCO (P less than 0.01), and this immuno-PRL increment was greater than that of controls (P less than 0.05). Bio-PRL and immuno-PRL increased after GnRH in PCO, but not controls, and these responses were inhibited by disulfiram. These data confirm PRL hypersecretion in some women with PCO, which is better expressed by immunoreactivity than bioactivity. Given the assay systems and patients studied, bioactivity