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A male neonate with marked breast hypertrophy associated with transient hyperprolactinemia is reported. The breast hypertrophy resolved when the serum prolactin levels decreased to normal. Ultrasonographic finding of the breast hypertrophy are presented. It is not known if the hyperprolactinemia was etiologically related to the breast hypertrophy.
OBJECTIVE: The aim of this study was to investigate whether fluoxetine given to castrated and noncastrated rats caused hyperprolactinemia and its effects with respect to adenomyosis. DESIGN: Fluoxetine, a serotonin reuptake inhibitor, was given to Wistar Albino rats for 98 days to produce hyperprolactinemia. The drug was given to two groups consisting of castrated and noncastrated rats and compared to two groups of castrated and noncastrated controls. Prolactin levels were measured and the uteri of the rats were removed for histopathological analysis at the end of 98 days. SETTING: Marmara University School of Medicine, Department of Histology and Embryology, Zeynep Kamil Women and Children's Hospital. MAIN OUTCOME MEASURES: Serum prolactin levels, uterine histopathology. RESULTS: The prolactin levels of castrated and noncastrated groups treated with fluoxetine were statistically significantly higher when compared to their respective control groups. Histological studies revealed 11 cases of adenomyosis, all within the noncastrated group receiving fluoxetine. CONCLUSION: It was suggested that high serum prolactin levels cause degeneration of myometrial cells in the presence of ovarian steroids that results in a myometrial invasion by endometrial stroma. This invasion eventually progresses to adenomyosis.
OBJECTIVE: To study prospectively the serum prolactin (PRL) concentrations among male patients with systemic lupus erythematosus (SLE) and their possible relationship to disease activity and manifestations. METHODS: Serum PRL levels were measured by radioimmunoassay in 31 male patients with SLE and 31 age matched controls. Demographic, clinical, and laboratory features of the patients were obtained. Mean PRL levels from both groups were compared, and PRL from patients with SLE was correlated with variables of disease activity, including the SLE Disease Activity Index (SLEDAI), complement level, and anti-dsDNA titer. Thirteen patients were followed serially and changes in PRL levels in relation to fluctuation in disease activity were evaluated. RESULTS: Mean PRL levels were higher in male patients with SLE than healthy controls; however, the difference did not reach statistical significance (230 vs 194 mIU/l; p = 0.06). Hyperprolactinemia was found in 4 patients (13%) and was not associated with particular clinical manifestations or autoantibodies. Considering all patients as a whole, PRL levels did not correlate with variables of disease activity and there was no difference in PRL between patients with active versus inactive disease. A subanalysis of the 4 hyperprolactinemic patients revealed a higher SLEDAI score than those with normal PRL (8.8 vs 3.7; p = 0.20); however, the difference was not statistically significant. Among the hyperprolactinemic patients, PRL levels did not correlate with SLEDAI score or anti-dsDNA titer. Prospective studies of PRL levels in 13 patients did not indicate a role of PRL in the monitoring of disease activity or predicting relapses. CONCLUSION: Hyperprolactinemia occurred in a small proportion of male patients with SLE and its significance remained unclear. Serum PRL level did not correlate with disease activity and was not a reliable marker for disease monitoring.
The growth-promoting effect of prolactin on the ventral prostate lobe, the anterior prostate lobe (or coagulating gland), and seminal vesicles has been studied before, during and after puberty in rats up to 5 months of age. Pituitaries from female rats were grafted under the renal capsule of 23-26-day-old male rats. Within 1/2 month substantial (five- to ten-fold) hyperprolactinemia occurred followed by a gradual decline; levels were still high 4 months after grafting. A statistically significant increase in the weight of the seminal vesicles and the ventral and anterior prostate lobes was observed 1 month after implantation. This effect was only maintained for the seminal vesicles during the next 3 months. Hyperprolactinemia did not influence testosterone metabolism. In the ventral prostate lobe, 1 month after grafting, the nuclear androgen receptor content increased, whereas the cytosolic androgen receptor content decreased. These results suggest that the growth-promoting effect of prolactin, on the ventral prostate lobe of the rat, is brought about by an increased translocation of the androgen receptor.
The rat ventral prostate contains prolactin receptors, and during sexual maturation prolactin stimulates the growth of this gland. The aim of the present investigation was to evaluate whether prolactin is involved in the regulation of the number of its own receptor sites in the rat ventral prostate. To this end, the content of prolactin receptors was estimated in prostate membranes of control and chronically hyperprolactinemic rats both before and after in vitro desaturation with 4 M MgCl2. Hyperprolactinemia resulted in a 40% increase in the number of available prolactin receptors (P less than 0.05). In vitro desaturation of receptors resulted in loss of 84% of protein and 36 +/- 6% and 52 +/- 6% of prolactin receptors from ventral prostate membranes of control and hyperprolactinemic rats respectively (P less than 0.05). We have concluded that the rat ventral prostate membranes are not suited to in vitro desaturation of prolactin receptors with MgCl2. From the increase in the number of available prolactin receptors after hyperprolactinemia we have concluded that prolactin is involved in the regulation of the number of its own receptors in the rat ventral prostate.
Metastases to the pituitary gland from systemic cancers is a rare phenomenon and usually occurs in patients with disseminated disease. The neurohypophysis is the most commonly involved site, and diabetes insipidus is the most common presentation in these patients. Breast and lung cancer are the most common cancers metastasizing to the pituitary. Involvement of the pituitary by renal cell carcinoma (RCC) is exceedingly rare. Mild-to-moderate degree of hyperprolactinemia is a rare presentation of pituitary metastases. We report the case of a woman with metastatic RCC to the pituitary presenting an unusually high degree of hyperprolactinemia.
OBJECTIVE: A correct differential diagnosis of patients with mild hyperprolactinemia is essential to select the most appropriate treatment modality. CLINICAL PRESENTATION: A 50-yr-old woman presented to our Department for evaluation of an intra- and suprasellar mass causing progressive visual defect. Mild hyperprolactinemia causing menstrual irregularities was diagnosed in February 1989. In 1992, serum PRL levels ranged from 50 to 70 microg/l and magnetic resonance imaging (MRI) of the hypothalamic-pituitary region showed the presence of a 7 mm microadenoma. Bromocriptine therapy resulted in normalization of PRL levels and menstrual cycle, while a repeat MRI showed no change. Menses stopped in March 1998, when the patient was 46 yr old. Subsequently, the patient complained of worsening headaches and, starting from July 2001, visual disturbances. In March 2002, MRI showed a large pituitary tumor, measuring 40x37x28 mm. In May 2002, the patient was operated through the transsphenoidal approach with apparent total tumor removal. Histological examination confirmed a pituitary adenoma that stained negative for all pituitary hormones. Four months after surgery, the patient reported an improvement of visual function. MRI of the hypothalamic-pituitary region, performed 4, 13 and 25 months after surgery, showed a partially empty sella with no evidence of residual tumor. CONCLUSIONS: This case suggests that, to exclude the alternative diagnosis of nonfunctioning pituitary adenoma or another mass lesion of the hypothalamic-pituitary region, repeat neuroimaging studies during long-term follow-up may be advisable in patients with presumed microprolactinoma who did not show reduction of the tumor during dopaminergic therapy.
The effects of acute and repeated administration of pyridoxine on serum prolactin levels were studied in 18 chronic schizophrenics, 10 women and 8 men, in whom hyperprolactinemia had been induced by long-term treatment with phenothiazines, haloperidol, sulpiride or clopentixol. The patients were divided into 5 groups: group 1 received 300 mg of the vitamin per os in a single dose; group 2 received 300 mg of the vitamin per os for 7 days; group 3 received 300 mg of the vitamin iv as a single bolus; group 4 received 600 mg of the vitamin iv as a single bolus; group 5 received 1200 mg of the vitamin per os in a single dose. Prolactin levels were examined before and 15, 30, 60, 90, 120 and 150 min after the single administration of pyridoxine, either iv or per os, and on days 3,5, 7 of the chronic administration. There was no decrease in prolactin levels either after oral or iv administration of the drug, given in single or repeated doses. Therefore, this treatment is not useful for the suppression of hyperprolactinemia induced by neuroleptics.
To better understand the state of dopamine (DA) neurotransmission in the tuberoinfundibular DA system (TIDA), monoiodotyrosine (3-iodo-L-tyrosine, MIT), a potent inhibitor of DA synthesis, was acutely administered to 8 normal women, 7 postpartum women, 8 women with pathological hyperprolactinemia and 5 women after successful removal of a prolactinoma. The effects on plasma prolactin (PRL) and thyrotropin (TSH) were compared to those induced in the same subjects by the DA receptor antagonist domperidone (DOM). MIT (1 gpo) and DOM (10 mg iv) induced qualitatively similar hormonal responses, although the PRL- and TSH-releasing effects of DOM were always greater than those of MIT. In control subjects, MIT treatment induced a consistent rise in plasma PRL (peak increment 45.2 +/- 13 ng/ml at 120 min); in the same subjects DOM induced a prompter and higher PRL response, (peak increment 147.8 +/- 26 ng/ml at 30 min). MIT failed to alter plasma TSH levels, while DOM induced a significant rise in plasma TSH. In postpartum women MIT induced a prompter and higher PRL rise than that occurring in controls (peak increment 180.3 +/- 20 ng/ml at 90 min), though also in this instance DOM proved to be a more potent PRL releaser (peak increment 345.7 +/- 88 ng/ml at 30 min) than MIT. MIT was unable to stimulate TSH secretion, while DOM induced a significant rise in plasma TSH. In women with pathological hyperprolactinemia MIT failed to alter baseline PRL levels while DOM slightly increased them (peak increment 14.7 +/- 3 ng/ml at 30 min).(ABSTRACT TRUNCATED AT 250 WORDS)
Since dopamine (DA) has been implicated in the inhibitory control of both TSH and LH, we have compared TSH and LH levels following dopamine (DA) receptor blockade with domperidone in patients with hyperprolactinemia due to presumed prolactinomas. Eight euthyroid patients (aged 19-37 yr) with presumed prolactinomas each received domperidone (10 mg iv) at 11:00 and 23:00 h and tests were separated by at least one week. Basal TSH levels were significantly greater at 23:00 than at 11:00 h (2.7 +/- 0.5 vs 1.7 +/- 0.4 mU/l, mean +/- SE, p less than 0.01) whereas basal LH levels did not differ. All subjects showed clear rises in basal TSH levels following drug administration and these were significantly greater at 23:00 than at 11:00 h (p less than 0.02 at each time point). In contrast there was no alteration in LH levels following drug administration at either time of day. These data suggest that the mechanisms underlying the dopaminergic control of TSH and LH are different in these patients. Furthermore the data argue against an anterior pituitary or median eminence site of action of DA in the inhibition of LH release in hyperprolactinemia since domperidone does not penetrate the blood brain barrier to any appreciable extent.
This 55-year-old woman presented with primary adrenal insufficiency that led to multiple endocrine gland dysfunctions. Despite symptoms suggestive of hypothyroidism, she had mildly elevated serum thyroid hormone levels associated with elevated thyrotropin levels, hyperprolactinemia, and mild hypercalcemia. These abnormalities corrected with corticosteroid replacement but could be reproduced, in part, when the corticosteroids were temporarily withdrawn. The findings in this patient suggest that physiologic concentrations of glucocorticoids modulate prolactin secretion and the pituitary-thyroid axis. Adrenal insufficiency should be considered in the differential diagnosis of hyperprolactinemia and hyperthyrotropinemia with or without associated hyperthyroxinemia.
The effects of alpha- and beta-adrenergic blocking agents on the serum prolactin levels of six women with hyperprolactinemia and galactorrhea were investigated. There was no indication that pituitary adenomas were etiologic agents for the hyperprolactinemia. Serum prolactin could be lowered with oral L-dopa. When intravenous phentolamine (an alpha-adrenergic blocking agent) or intravenous propranolol (a beta-adrenergic blocking agent) were administered for 1 hour, there was no significant change in serum prolactin levels.
A primary "empty" sella may be associated with significant hypothalamic-pituitary dysfunction. This report characterizes the endocrinologic and radiographic findings in six patients with hyperprolactinemia (range 34.3 to 1,170 ng/ml) ultimately found to have an enlarged empty sella. Lateral skull x-ray films and thin-section tomograms were suggestive of pituitary tumors in all patients. Four patients underwent transphenoidal sellar exploration after pneumoencephalography (PEG) failed to demonstrate air within the sella. The inability of PEG to demonstrate an empty sella in two patients was explainable on the basis of an intact diaphragma sellae with previous transient intrasellar pathology responsible for the sellar enlargement. Dynamic hypothalamic-pituitary testing yielded no consistent pattern of response. These studies suggest that an empty sella: (1) may be associated with hyperprolactinemia, regardless of etiology, (2) is not diagnosable by dynamic hormonal testing, and (3) may be indistinguishable from a pituitary tumor by current radiographic techniques.
Several investigators have suggested that normal responsiveness to dopamine is exhibited by pituitary lactotrophs in patients with idiopathic hyperprolactinemia and prolactinomas. These studies, however, have employed dopamine infusion rates that produced supraphysiologic serum dopamine concentrations. In order to further examine this issue, we infused graded doses of dopamine to normal men and women as well as to patients with idiopathic hyperprolactinemia and prolactinomas. Dopamine infusion rates as low as 0.004 micrograms/kg/min, which were associated with physiologic serum dopamine levels, produced significant (p less than 0.01) suppression of prolactin in normal women and in normal males (p less than 0.05). In contrast, a 10-fold increase in the dopamine infusion rate, 0.04 micrograms/kg/min, was required in the hyperprolactinemic subjects to produce prolactin suppression similar to that found in the control subjects. Hence, prolactin secretion in both tumors and other hyperprolactinemic states is associated with a resistance to suppression by dopamine.
Ninety-four women and seven men were treated with low dose bromocriptine for (a) hyperprolactinemia or (b) normoprolactinemia but with galactorrhea and a pituitary adenoma. All the pituitary adenomas became smaller or remained the same. Prolactin levels decreased with treatment and inappropriate galactorrhea improved in the 53 patients except for 7 where there was no change. Of the 41 women with premenstrual mastalgia 78% improved with treatment. Of the 74 women with ovulatory problems, a biphasic pattern was restored in 65 patients. Thirty-two patients out of the 92 trying to conceive achieved a pregnancy with an abortion rate of 12.5% and non-lethal congenital abnormality of 9.8% (2.1% in Singapore population). Fertility was restored in 3 hyperprolactinemic oligospermic males and improved libido was professed by most of the treated men. Side effects were present but were on the whole tolerable. Pregnancy rate was better in those with high levels of prolactin (greater than 1000 miU/l) than in those with hyperprolactinemia of between 500 and 1000 miU/l although this was not statistically significant chi 2 = 0.69. In the lower hyperprolactinemic range there was noticeable number of patients with endometriosis and increased luteinizing hormone (LH) levels.
Serum prolactin (PRL) concentrations, as well as body, epididymal white adipose tissue (EWAT), and testes weights, decrease in Siberian hamsters (Phodopus sungorus sungorus) following short-photoperiod exposure. Previously, we have shown that lesions of the suprachiasmatic nucleus of the hypothalamus (SCNx) block regression of the testes and decreases in body weight and EWAT caused by short day-like, timed daily subcutaneous melatonin infusions in pinealectomized Siberian hamsters and elevate dramatically serum PRL concentrations. We also have shown that SCNx, as well as lesions of the paraventricular nucleus of the hypothalamus (PVNx) and an area immediately ventral to the PVN (subPVN), promote accelerated testicular recrudescence, increases in EWAT and body weights, and increases in serum PRL concentrations, in short-day (SD)-housed, photoregressed Siberian hamsters. The stimulation of the testes seen in these previous studies could have been due to the lesion-induced increases in serum PRL concentrations. Therefore, the purpose of the present experiment was to test whether experimentally induced hyperprolactinemia could stimulate testicular recrudescence. This was accomplished by giving photoregressed, SD-housed Siberian hamsters chronic subcutaneous infusions of ovine PRL (oPRL) to mimic either long-day- or lesion-induced serum concentrations of hamster prolactin (hPRL). No increase in testes, body, or EWAT weights were observed following 5 weeks of oPRL infusions in either group compared with their vehicle-infused counterparts. These data suggest that hyperprolactinemia was not solely responsible for the stimulation of testicular recrudescence in SCNx or PVNx photoregressed, or SCNx pinealectomized hamsters receiving timed melatonin infusions seen previously.
To evaluate the synergistic effect of estrogens and progesterone on prolactin secretion, rhesus and cynomolgus monkeys in the early follicular phase received estradiol benzoate (100 microgram/kg/day, sc) alone for 14 days, then in combination with progesterone (subcutaneous silastic capsule) for an additional 14 days. Blood was drawn daily by femoral venipuncture under ketamine hydrochloride anesthesia (15 mg/kg). Similarly, this protocol for exogenous steroid treatment was employed in a monkey having a chronically indwelling (femoral insertion into the vena cava) cannula maintained by a vest and mobile tether apparatus; however, no anesthesia was used to obtain serum specimens. In addition, this assembly was applied to six monkeys to determine the acute effects of ketamine hydrochloride on prolactin secretion. Concentrations of prolactin, estradiol-17 beta, and progesterone in serum were determined by conventional radioimmunoassays. Under estrogen therapy alone, mean circulating prolactin levels declined from approximately 15 to less than 5 ng/ml; in contrast, the addition of progesterone caused an abrupt serum prolactin elevation, approximately 8-12 fold. This estradiol-progesterone course led to sustained hyperprolactinemia in the chronically catheterized monkey, whereas ketamine administration raised serum prolactin only briefly, the elevation lasting less than three hours after injection. These findings establish that an estrogen-progesterone synergy, separate from the transient effects of ketamine, induced hyperprolactinemia in cycling monkeys having prevailing levels of estrogen and progesterone near those characteristic of late gestation, when sustained prolactin elevations are observed normally.
An intrasellar chordoma in a patient with diplopia and hyperprolactinemia is presented. A brief review of the literature on intrasellar chordomas and the potential etiology for the hyperprolactinemia in this patient are discussed.