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At least 19 recordsLinked to original sources
PubMed1979

[Adrenocortical function in hyperprolactinemia. The study of glucocorticoids, mineralocorticoids and androgens in chronic and acute hyperprolactinemias (author's transl)].

Glucocorticoids, mineralocorticoids, and adrenal androgens were studied in 3 groups of patients: control subjects (group I), hyperprolactinemic subjects (group II) and miscellaneous patients including chromophobe adenomas and normalized hyperprolactinemic subjects treated with Bromocriptine (group III). All the patients were studied in the basal state and under various conditions: Metyrapone, ACTH, TRH for glucocorticoids, ACTH, TRH, saline perfusion for mineralocorticoids, ACTH and TRH for androgens. It is concluded that: the adrenal secretion of glucocorticoids, mineralocorticoids and androgens is not altered under basal conditions in chronic hyperprolactinemia nor during dynamic tests in chronic hyperprolactinemia (prolactin adenoma) nor in acute hyperprolactinemia (induced by TRH).

Acute Disease↗
PubMed1978

Alteration of feedback mechanism of estrogen on gonadotropin by sulpiride-induced hyperprolactinemia.

Four normally cycling women received an iv injection of 20 mg Premarin (conjugated estrogens equivalent to 20 mg estrone sulfate) on the seventh day of two consecutive cycles; the second experiment was performed under sulpiride-induced hyperprolactinemia (mean PRL level = 906 microU MRC standard 71/222 per ml; significantly 7.8 times greater than mean control level of 115 microU MRC standard 71/222 per ml, P less than 0.001). In comparison to the control experiment, sulpiride-induced hyperprolactinemia prevented the occurrence of any gonadotropin peak within the 84 h of estrogen administration; the negative feedback effect of estrogen on gonadotropin secretion was maintained and was even potentiated. These alterations of feedback mechanisms of estrogen were considered to be related to hyperprolactinemia itself rather than to sulpiride. Five other normally cycling women received iv injections of 100 microgram LRH on the 22nd day of a cycle under sulpiride-induced hyperprolactinemia since the onset of menstruation. Their mean LH response was somewhat greater (although not statistically significant) and their mean FSH response was considerably greater (P less than 0.001 at all times) than those of a control group of 10 women tested in their luteal phase. The results of these LRH tests under sulpiride-induced hyperprolactinemia give some support to the concept that hyperprolactinemia interferes at the hypothalamic or higher level with cyclic release of indogenous LRH.

Adolescent↗
PubMed1977

Hyperprolactinemia and hypogonadism in the human female.

Prolactin is a mammotropic hormone essential for the initiation of lactation. It also influences ovarian function; during hyperprolactinemia hypogonadism occurs. This is true for pathological forms of hyperprolactinemia but also for the early puerperium when there is physiological hyperprolactinemia. Amenorrhea is a better parameter of hyperprolactinemia than galactorrhea. The mechanisms by which prolactin disrupts ovarian function are not as yet fully understood; it probably alters hypothalamic neurotransmitter content through a direct feedback mechanism resulting in a decrease of Gn-RH. However, the direct effect of prolactin-producing pituitary tumors on the capacity of the gonadotrophs or a direct interference of prolactin at the gonadal level are also possibilities. Hyperprolactinemia can be treated very effectively with bromocriptine and this drug appears to have become the favorite form of treatment. In the case of obvious tumors hypophysectomy is indicated. When there are smaller tumors irradiation of the pituitary gland previous to bromocriptine treatment may prevent expansion of the gland during subsequent pregnancy.

Amenorrhea↗
PubMed2026

Macroprolactinemia as a diagnostic pitfall in hyperprolactinemia: a systematic review and quantitative synthesis.

CONTEXT: Macroprolactinemia is a well-recognized cause of hyperprolactinemia and an important diagnostic pitfall in endocrine practice. However, interpretation of published quantitative prolactin data remains sparse as studies vary in confirmation method, assay platform, polyethylene glycol (PEG) recovery cutoff, and reporting of prolactin measurement. EVIDENCE ACQUISITION: PubMed, Embase, Scopus, Web of Science, the Cochrane Library, and Google Scholar were systematically searched. Eligible studies reported macroprolactinemia-specific quantitative prolactin data in patients with confirmed macroprolactinemia defined by PEG precipitation, gel filtration chromatography (GFC), or both. Two reviewers independently performed study selection, data extraction, and quality assessment. Findings were summarized using study-level descriptive synthesis. The review was prospectively registered in PROSPERO and conducted in accordance with PRISMA 2020 guidelines. EVIDENCE SYNTHESIS: Forty-five studies encompassing 2853 macroprolactinemia cases from 21 413 screened patients with hyperprolactinemia across 22 countries were included. Among 33 studies eligible for primary quantitative analysis, the median study-level central total prolactin attributed to macroprolactinemia was 61.4 ng/mL ([IQR] 42.0-80.0; range 28.1-137.6), and the median study-level post-PEG monomeric prolactin was 11.7 ng/mL (IQR 8.3-13.2; range 4.0-17.0)). The median study-level maximum total prolactin was 264.5 ng/mL (IQR 97.0-425.5; range 81.8-663.0); extreme elevations were attributable to coexisting prolactinomas. CONCLUSION: In confirmed macroprolactinemia, total prolactin elevation is typically moderate, and post-PEG monomeric prolactin is usually within or near the normal range. The post-PEG monomeric prolactin value, rather than percent recovery alone, is the most informative parameter for distinguishing isolated macroprolactinemia from coexisting true hyperprolactinemia. These quantitative benchmarks may help clinicians to avoid unnecessary investigation or treatment.

Humans↗
PubMedDate not supplied

[Hyperprolactinemia and primary amenorrhea].

Six patients with primary amenorrhea and hyperprolactinemia are presented. The patients had normal secondary characteristics and normal body proportions. In four patients a tumour of the hypophysis was diagnosed radiologically, while in two patients the cause of hyperprolactinemia remained unknown. The gonadotropin concentration in the serum was normal. Reaction to Gn-RH was the same as that in women with the normal cycle in the follicular phase. In all the patients with function of the thyroid was normal. Primary amenorrhea was found in 14.6% of women with a disturbed cycle and hyperprolactinemia. In all the patients the administration of bromocryptin normalized prolactin concentrations, induced ovulation, and four patients became pregnant.

Amenorrhea↗
PubMed1978

[Drug therapy of hyperprolactinemia and acromegaly].

Hyperprolactinemia can be treated medically. Thus all patients with a normal sella turcica and those patients with only slight enlargement of the sella turcica can be treated medically with the dopaminagonist bromocriptine. This treatment is also indicated in paitents with postoperative persisting hyperprolactinemia. In contrast to hyperprolactinemia medical therapy of acromegaly is still in the experimental stage, through the dopaminagonist bromocriptine induces a decrease of growth hormone levels and improvement of the disease in many patients with acromegaly.

Acromegaly↗
PubMedDate not supplied

Failure of pyridoxine to effect neuroleptic-induced hyperprolactinemia in psychotic patients.

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.

Adult↗
PubMed1978

Effect of hyperprolactinemia on pituitary-adrenal function.

Three patients with hyperprolactinemia (2 with pituitary tumors and 1 with a hypothalamic disturbance) underwent evaluation of their hypothalamic-pituitary-adrenal axis using ACTH, metyrapone and in one case repetitive insulin tolerance tests. With the exception of a suggestion of a slight increase in adrenal responsiveness to pharmacological doses of ACTH in one of the patients, there was no alteration in the adrenal responsiveness of the 3 patients evaluated. We conclude that hyperprolactinemia probably does not systematically modify the responsiveness of the hypothalamic-pituitary-adrenal axis.

Adenoma, Chromophobe↗
PubMed1979

Lack of adrenal androgen stimulation by ACTH in extreme hyperprolactinemia.

Acute and prolonged alpha 1-24 corticotropin stimulation was performed on a treated chromophobe adenoma patient with partial ACTH deficiency and extreme hyperprolactinemia. Cortisol and aldosterone stimulated normally. However, the basal concentrations of androstenedione (A) and dehydroepiandrosterone (DHA) were low, and that of DHA-sulfate (DHAS) was undetectable. Furthermore, A and DHA did not stimulate normally, and DHAS did not stimulate at all. It has been claimed that adrenal androgen production is increased in hyperprolactinemia. However, the inability of prolactin (Prl) to maintain adrenal androgen (AA) secretion, with and without added ACTH, is demonstrated in this patient.

Adenoma, Chromophobe↗
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↗
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↗
PubMed1978

Value of luteinizing hormone-releasing hormone testing in bromocriptine treatment of amenorrhea and hyperprolactinemia in patients with pituitary tumors.

The results of bromocriptine treatment in 13 patients with radiologically evident pituitary tumors are described. A menorrhea was present in all patients, hyperprolactinemia in 12 of the 13 patients, and acromegaly in 3 patients. Five patients have previously been treated surgically and by radiotherapy because of suprasellar extension of the adenoma. Plasma prolactin levels after one single dose of 2.5 mg of bromocriptine were found to have no predictive value as to the dosage needed for treatment, whereas the plasma gonadotropin response after the administration of luteinizing hormone-releasing hormone appeared to be predictive with respect to the return of ovulation during bromocriptine therapy.

Adenoma↗
PubMed1978

Normal pregnancies after treatment of hyperprolactinemia with bromoergocryptine, despite suspected pituitary tumors.

Bromocryptine treatment was administered to 15 patients with amenorrhea and galactorrhea (AG) and to 1 patient with amenorrhea. All of them had increased plasma PRL levels. Of these 16 patients, 4 had a normal sella turcica (ST; group STO), 4 had a slight enlargement (group ST+), and 7 had a clear enlargement of ST (ST++) but no evidence of suprasellar extension. Ovulation was restored in 15 patients by bromocryptine treatment only. In one patient, ovulation resumed only after human pituitary gonadotropin treatment in combination with bromocryptine. There was no correlation between basal prolactinemia, PRL stimulability or suppressibility, the size of ST, or the efficiency of bromocryptine treatment. Every patient with normal LH response to either LRH or clomiphene or both resumed ovulation. Ovulation resumed in 3 patients among the 4 with abnormal LH response to either LRH or clomiphene or both. Among the 14 who desired pregnancy, 13 became pregnant. To date, 12 patients (ST++, 5; ST+, 3; STO, 4) have delivered normal babies. The courses of pregnancy were normal. During pregnancy, no change of ST was noted on lateral and frontal skull x-ray performed in every patient at trimonthly intervals. There was no change in the sellar index in 10 patients after pregnancy, as compared to the pretreatment status. In the presence of a pituitary adenoma or in patients with hyperprolactinemia and amenorrhea and galactorrhea, bromocryptine treatment may cure sterility without pituitary complication during pregnancy.

Adult↗
PubMed1979

Pituitary function testing in amenorrhea-galactorrhea-hyperprolactinemia.

Fifteen patients, age 16 to 55, presented with amenorrhea-galactorrhea-hyperprolactinemia. Pituitary function was evaluated by bolus injections of insulin, luteinizing hormone-releasing hormone (LHRH), and thyrotropin-releasing hormone (TRH) in 13 and by LHRH and TRH in 2. Responses to growth hormone (GH), thyroid-stimulating hormone (TSH), cortisol (F), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin were measured. GH, TSH, and F responses were normal in most cases. LH responses were decreased (P less than 0.025) in patients with abnormal sellar tomography, whereas FSH responses tended to decrease with elevated prolactin levels. Prolactin responses were absent in five of the seven cases which could be evaluated. The clinical value of such testing appears to be limited to an individualized basis, although some prognosis of ovulatory response to bromocriptine therapy may be obtained from the gonadotropin response.

Adolescent↗
PubMed1978

Hyperprolactinemia in multiple endocrine adenomatosis, type 1.

Three cases are described in which hyperprolactinemia occurred as a feature of multiple endocrine adenomatosis, type 1 (MEA-1); enlargement of the sella turcica varied from gross to absent, and serum prolactin (PRL) levels ranged from 21 to 1,000 ng/ml in these cases. Since PRL-secreting pituitary tumors may occur with variable presentation in MEA-1, periodic measurements of serum PRL levels should be carried out to detect this abnormality.

Adult↗
PubMed1979

Hyperprolactinemia and polycystic ovarian syndrome.

Prolactin and pituitary gonadotropin levels were studied in eight patients with polycystic ovarian syndrome. All women were of reproductive age and had had menstrual disorders since menarche. Three patients had hyperprolactinemia with or without galactorrhea and tomograms of the sella turcica revealed pituitary microadenomas. The remaining five patients with normal baseline prolactin levels had a prolactin stimulation test which used 25 mg of thorazine per os, and a prolactin suppression test using l-dopa 500 mg per os. Analysis of the results of these tests and a comparison with tests performed in five normal individuals used as controls showed significantly different responses in the two groups of women. The preliminary information obtained indicates that an abnormal prolactin secretion status may exist in the polycystic ovarian syndrome.

Adolescent↗