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Results for “hyperprolactinemia”

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PubMed1984

Effect of hyperprolactinemia and age on the hypogonadism of uremic men on hemodialysis.

Primary hypogonadism has been commonly reported among uremic men on hemodialysis, characterized by low testosterone levels, increased luteinizing hormone and sometimes follicle-stimulating hormone levels. Little is known about the influence of hyperprolactinemia and age on this hypogonadism. In 149 hemodialysis patients and in 60 healthy subjects the serum levels of testosterone (T), gonadotropins (LH and FSH) and prolactin (PRL) were assessed through radioimmunoassay. Mean +/- SD hormone levels were: T 274 +/- 125 ng/100 ml, lower than controls; LH 44.7 +/- 46.1 mlU/ml and FSH 17.6 +/- 18.4 mIU/ml, both higher than controls. PRL 31.3 +/- 49.4 ng/ml, higher than controls. A positive correlation between LH and FSH, a negative correlation between PRL and both T and LH was found. Moreover T and FSH were correlated with age only in the normoprolactinemic patients. These data suggest: a common damaging mechanism by uremia on both interstitial and tubular structures of the testis; a central antigonadal influence of hyperprolactinemia even if a direct action on the testis cannot be excluded; a worsening action of age on the gonadal function of these patients.

Adult↗

PubMed1978

Transsphenoidal microsurgery for pituitary tumors associated with hyperprolactinemia.

The results of transsphenoidal microsurgery in treating 37 patients (30 women and seven men) with pituitary tumors associated with hyperprolactinemia are presented. Immediate (10-day) postoperative fasting prolactin levels were normal (less than 25 ng/ml) in 19 of 26 patients whose preoperative prolactin level was less than 200 ng/ml, and in only three of 11 patients in whom preoperative prolactin was greater than 200 ng/ml. Twelve of 13 patients with normal preoperative pituitary-target organ function maintained normal axes postoperatively. Thirteen other patients had preoperative deficiencies in one or more pituitary-target organ axes. Postoperatively, in these latter 13 patients, a pituitary-target organ axis that was deficient preoperatively returned to normal in six cases; there was no change in five, and there was impairment in another axis in four instances. Although gross total tumor removal was believed to be complete in 35 of 37 patients, serial postoperative prolactin determinations in four of these 35 patients indicate tumor regrowth. The authors conclude that transsphenoidal microsurgery is currently the operative procedure of choice for the majority of pituitary tumors associated with hyperprolactinemia.

Adenoma, Acidophil↗

PubMed1981

Hyperprolactinemia and hyperadrenocorticism accompanied by normal blood pressure in Sprague-Dawley rats.

Pituitary glands removed from adult female normotensive Sprague-Dawley (S-D) rats were implanted beneath the renal capsule of 100-day male S-D rats. Female neonatal S-D rats were given a single sc injection of 1.25 mg of testosterone proprionate (TP) suspended in sesame oil. Systolic blood pressure and blood samples were taken at various time intervals postimplantation and TP treatment prio to autopsy. Both the TP treatment and pituitary implants caused hyperprolactinemia, increased adrenal weight concomitant with thymus gland involution, hypersecretion of corticosterone, but no increase in systolic blood pressure. It is suggested that the failure of these hyperprolactinemic S-D rats to develop hypertension was due to the absence of a genetically mediated hypertensinogenic factor present in this normotensive strain which is activated by chronic hyperprolactinemia.

Adrenal Glands↗

PubMed1977

[Dynamics of hormonal modifications induced by bromocryptin during hyperprolactinemia].

In a group of 16 females and 2 males with hypogonadism and hyperprolactinemia, bromocriptine was found to suppress prolactin (PRL) high levels within one day without further significant lowering during a 3 weeks longitudinal survey. The usually effective dosage was 5 mg per day. On the contrary, sex hormones did not vary initially and increased secondarily only in those patients resuming gonadal activity. The changes were either cyclical or heterogenous when the first cycle was anovulatory. This latter situation could sometimes but not always be attributed to persistent hyperprolactinemia. Menstruation resumed in 11 patients. Persistance of hypogonadism in the remainder could be explained by incomplete PRL reduction in one case and probability of previous hypothalamo-pituitary damage in six. The latter hypothesis was based in part on impaired gonadotropins responses to LH RH which were not modified by the treatment.

Adolescent↗

PubMed1985

[The coincidence of gonadal dysgenesis and hyperprolactinemia].

It was reported about 6 female patients aged from 3 to 31 years (average age 18 years) with gonadal dysgenesis and hyperprolactinemia. Beside one all these females were not treated with synthetic sexual steroids. In 5 of the 6 patients both hyperprolactinemic and hypergonadotropic serum levels were observed. In one case the gonadotropic serum levels were normal. In 4 patients a stimulation test with GRH-TRH or Arg-GRH-TRH, respectively, was performed. In patients with gonadal dysgenesis a change on the area of the hypothalamic-hypophyseal axis is supposed to cause the hyperprolactinemia.

Adolescent↗

PubMed1985

[Functional hyperprolactinemia].

Treatment remains the same whether there is true idiopathic hyperprolactinemia or microadenomas too small to be detectable by methods of investigation. Bromocriptine has an antitumoral effect and treatment can often be stopped after the disappearance of a microadenoma or even of a larger adenoma. "Cure" of idiopathic hyperprolactinemia is rarer.

Adenoma↗

PubMed1978

[Primary dysmenorrhoea and hyperprolactinemia (author's transl)].

Between 5 and 10% of all young girls and women suffer of severe primary dysmenorrhoea which interfers monthly with their activities. In this type of primary dysmenorrhoea we found hyperprolactinemia in 13 of 15 women who were examined. All 15 patients had a pituitary tumour ruled out and were treated with Bromo-ergocryptine (parlodel). Eight patients became free of symptoms and five were well improved. The possible correlation of hyperprolactinemia to premenstrual tension and severe primary dysmenorrhoea is discussed.

Adolescent↗

PubMed1984

Galactorrhea-amenorrhea and hyperprolactinemia associated with pituitary tumors of growth-hormone- and adrenocorticotropic-hormone-secreting cells. A report of two cases.

In women with galactorrhea, amenorrhea/oligomenorrhea, hyperprolactinemia and radiographic evidence of a pituitary tumor, the presumed etiology is usually a primary prolactin-secreting tumor. We treated two patients whose presenting symptoms (galactorrhea and oligomenorrhea) and initial investigation (which showed radiographic enlargement of the sella and hyperprolactinemia) suggested a prolactin-secreting pituitary tumor. However, after further endocrinologic investigation, transsphenoidal exploration and ultrastructural-immunohistologic evaluation of the excised pituitary tumors, the tumors were found to be composed of cells characteristic of growth-hormone and adrenocorticotropic-hormone production. These data are consistent with the hypothesis that any factor or factors increasing intrasellar pressure, including pituitary tumors originating in cells other than galactotrophs, can elevate serum prolactin and present clinically as galactorrhea-amenorrhea. They suggest further that a diligent search be done for elevations of other pituitary trophic hormones when a pituitary tumor is suspected in order not to overlook other kinds of serious endocrinopathy.

Adenoma↗

PubMed1983

[Hyperprolactinemia in chronic renal insufficiency: an interesting model of hypothalamo-hypophyseal dysfunction].

It is note that hyperprolactinemia is frequently associated to chronic renal failure (CRF). The etiopathogenesis of this endocrine disorder is not clearly understood, trying to evaluate the possible hypothalamic-pituitary cause we have evaluated the Prl levels under some pharmacological tests: TRH (200 mcg i.v.),Domperidone (DOM)(10 mg i.v.),Nomifensine (NOM)(200 mg p.o.)and Bromocriptine (BRC)(2.5 mg p.o.) in 3 groups of patients: CRF(8 cases), dysfunctional (8 cases) and tumoral (9 cases) hyperPrl. Prl plasma levels have been evaluated by RIA (kits,Biodata,Roma). In patients affected by CRF either direct (BRC) than indirect (NOM) agonist acting dopaminergic drugs failed to induce a reduction in Prl plasma levels, like to tumoral patients for NOM, and in contrast to the significant decrease after BRC (-70%) in tumoral and (-74%) in dysfunctional and NOM (-50%) observed in dysfunctional patients. CRF and dysfunctional patients showed significant response to TRH and DOM, being prolactinoma bearing patients unresponsive to these tests. These results show an hyporesponsivity of pituitary Prl secreting cells to dopaminergic control suggesting the existence of central etiopathological factor in inducing hyperprolactinemia in CRF patients.

Adult↗

PubMed1984

Hyperprolactinemia in polycystic ovary syndrome.

With the use of multiple blood sampling, the prevalence of hyperprolactinemia in 150 consecutive patients with polycystic ovary syndrome (PCO) was found to be 17%. To further compare these two groups of PCO patients, the pituitary responses to gonadotropin-releasing hormone and thyrotropin-releasing hormone and the adrenal responses to dexamethasone suppression and adrenocorticotropic hormone stimulation were evaluated in 40 normoprolactinemic and 10 hyperprolactinemic PCO patients. Adrenal and pituitary perturbation tests were normal in both groups of PCO patients. Besides the higher levels of prolactin, the hyperprolactinemic patients also had higher blood levels of thyrotropin and testosterone, a higher luteinizing hormone/follicle-stimulating hormone ratio, lower levels of follicle-stimulating hormone, and lower follicle-stimulating hormone responses to gonadotropin-releasing hormone. Our data are consistent with the hypothesis that in some cases, the pathogenesis of PCO may be due to a central deficiency in dopaminergic activity at the basal hypothalamus. The hyperprolactinemia observed in a significant number of PCO patients may reflect a greater deficiency of hypothalamic dopamine, as manifested by the basal elevations of both prolactin and thyrotropin levels.

Adrenal Cortex Hormones↗

PubMed1984

Hyperprolactinemia and male infertility.

Four patients suffering from oligospermia and infertility were found to have slightly to moderately elevated serum prolactin levels consistently. Their testicular biopsy specimens showed varying degrees of impairment of spermatogenesis ranging from hypospermatogenesis to complete absence of germ cells. The usual known causes of hyperprolactinemia, such as pituitary or suprasellar tumors, hypothyroidism, intake of certain medications that deplete the dopamine levels of the hypothalamus or block the action of dopamine on the pituitary, were absent. These patients are described in view of recent clinical and experimental reports implicating hyperprolactinemia as a cause of male infertility.

Adult↗

PubMed1978

Sellar enlargement with hyperprolactinemia and a Rathke's pouch cyst.

A woman with secondary amenorrhea was found to have hyperprolactinemia without clinical galactorrhea. Radiological findings of an enlarged sella turcica with displacement of the pituitary stalk were considered consistent with a prolactin macroadenoma. Treatment with bromocriptine corrected the amenorrhea and hyperprolactinemia, and the patient inadvertently became pregnant. However, no complications to the mother or fetus occurred during pregnancy or postpartum. On transsphenoidal surgery three months postpartum, the unexpected presence of a large Rathke's pouch cyst with a microadenomatous or nodular hyperplasia type of prolactin-secreting tumor was observed to account for the preoperative clinical and radiological findings.

Adult↗

PubMed1983

Hyperprolactinemia and pregnancy. Clinical series.

We report 15 cases of pregnancy in 11 patients with hyperprolactinemia. These patients initially went to our Gynecologic Endocrinology Center for various menstrual troubles. They were all treated with bromocriptine, except one whose hyperprolactinemia was diagnosed when she had already started a gonadotropin therapy, since HPRL assays performed elsewhere had given normal results. In 6 patients we diagnosed prolactin-secreting pituitary adenoma. Only two patients underwent adenomectomy. All patients gave up bromocryptine as soon as their pregnancy was detected. Two patients had two subsequent pregnancies, another one had three. All pregnancies were single. The only twin pregnancy followed a gonadotropin therapy. One of the 15 pregnancies ended with abortion at the 12th week; another one (twin) with spontaneous delivery at the 37th week; 13 with term-delivery. They all had physiologic courses, except for one case of threatened abortion and one case of diabetes insipidus at the 9th month. None of the 15 newborns (7 SGA and 8 AGA) showed malformations. No sign or symptom of tumour growth was detected in the patients affected by pituitary adenoma.

Adenoma↗

PubMed1980

Galactorrhea and hyperprolactinemia during treatment of polycystic ovary syndrome.

The serum concentration of prolactin and the presence of galactorrhea were evaluated systematically in a prospective study of the effect of medroxyprogesterone acetate (MPA) in polycystic ovary syndrome (PCO). In 21 patients, the diagnosis of PCO was made by laparoscopy. Three women presented with galactorrhea and increased prolactin levels, 2 had galactorrhea with normal prolactin levels, and 3 had an isolated elevation in the serum concentration of prolactin. Treatment with MPA induced galactorrhea in 10 additional patients. Elevated levels of prolactin were detected in 18 of the patients during treatment. There was no correlation between the score for galactorrhea and the level of prolactin. Tomograms of the sella turcica were abnormal in 3 of 8 patients with hyperprolactinemia. The authors conclude that galactorrhea and/or hyperprolactinemia are important side effects of MPA in patients with PCO.

Adolescent↗

PubMed1983

Coexistent primary empty sella syndrome and hyperprolactinemia. Report of 11 cases.

The series involved 11 women with concurrent hyperprolactinemia and primary empty sella syndrome. Eight had amenorrhea and six had galactorrhea. All 11 patients had intact hypothalamic-pituitary function, except for having elevated prolactin levels that ranged from 33 to 498 ng/mL. One patient had primary hypothyroidism. Radiologic investigations included sellar polytomography in eight cases, computed tomography of the head in eight cases, bilateral carotid angiography in six cases, and pneumoencephalography in three cases. Of eight patients undergoing transsphenoidal exploratory surgery, one had a pituitary microadenoma and an empty sella while seven had only an empty sella with a flattened pituitary gland. Conventional histologic methods (seven cases) and immunocytologic studies (three cases) of the pituitary gland showed no abnormalities. The cause of this syndrome is unknown. It should be recognized that hyperprolactinemia, with or without galactorrhea-amenorrhea, may occur in association with an empty sella in the absence of an associated pituitary tumor.

Adult↗

PubMed1982

hyperprolactinemia of portal hypertension in rats.

Plasma prolactin levels are often raised in patients with liver cirrhosis and portal hypertension. To obtain more insight into the underlying mechanisms we examined the synthesis and release of prolactin in male rats with partially ligated portal veins. Portal hypertension led to an increase in pituitary prolactin, plasma prolactin, and plasma 17 beta-estradiol, and a decrease in hypophyseal stalk dopamine levels. Castration decreased plasma prolactin levels and prevented the induction of hyperprolactinemia by portal hypertension. Administration of dihydrotestosterone to castrated animals did not affect prolactin levels in the pituitary gland or in the plasma. Plasma tryptophan and tyrosine concentrations did not change in portal hypertension. A low protein diet caused a decrease in plasma tryptophan and an increase in plasma tyrosine levels without affecting prolactin levels in either controls or portal hypertensive rats. The hyperprolactinemia of portal hypertension is probably caused by elevated estrogen levels which interfere with hypothalamic dopamine release. Changes in plasma amino acid levels are of little importance in the regulation of prolactin release in portal hypertensive rats.U

Animals↗

PubMed1981

Estrogen and the puberty-advancing effect of hyperprolactinemia in female rats.

Female Wistar rats were twice daily injected with 10 IU prolactin from 21 days of age to vaginal opening (VO). Precocious VO and ovulation followed by an ovarian cycle of normal length were recorded following this treatment. Hyperprolactinemia induced by the implantation of one pituitary under the kidney capsule of 23-day-old females resulted in advancement of VO but, probably due to the antiovulatory and luteotropic effects of the permanently elevated prolactin levels, the first ovulation occurred only at the normal time of puberty onset, and the first ovarian cycle was significantly lengthened. An increase uterine but not of ovarian weight was induced by both treatments indicating enhanced estrogen secretion. Daily injections of 0.05 or 0.1 microgram estradiol benzoate per 100 g b.w. administered during different periods between day 21 and VO, however, were ineffective in accelerating sexual maturation. The findings suggest that the puberty-advancing effect of hyperprolactinemia does not primarily depend upon the stimulation of ovarian estrogen secretion.

Animals↗

PubMed1981

[Hyperprolactinemia and catalepsy induced by haloperidol].

The effect of endogenous hyperprolactinemia induced by pituitary transplantation under the kidney capsule on haloperidol induced catalepsy was evaluated in male Wistar rats treated with two doses of the drug (500 gamma/kg; 2 mg/kg i.p.). Rats of 220 +/- 30 g received intraperitoneal injection of haloperidol. Every five minutes following drug administration the rats were assessed for catalepsy by placing the forepaw on a horizontal bar, and observed for two minutes. Data obtained show that hyperprolactinemia potentiates the cataleptic score in rats treated with dose of 500 gamma/kg i.p., while no significant difference was observed between hyperprolactinemic rats and control rats, at the dose of 2 mg/kg i.p. of haloperidol.

Animals↗