Disease relevance of Hyperprolactinemia

• In addition to vasopressin deficiency, two patients had mild hyperprolactinemia and nine had impaired secretory responses of growth hormone to insulin-induced hypoglycemia [1].
• Mice with a disrupted D2 dopamine receptor gene had chronic hyperprolactinemia and developed anterior lobe lactotroph hyperplasia without evidence of adenomatous transformation [2].
• Metabolic clearance rates (MCR) and production rates (PR) of prolactin (PRL) have been determined by the constant infusion to equilibrium technique in 11 normal subjects, 6 patients with hyperthyroidism, 4 patients with hypothyroidism, and 9 patients with hyperprolactinemia [3].
• The hyperprolactinemia of portal hypertension is probably caused by elevated estrogen levels which interfere with hypothalamic dopamine release [4].
• Masked hyperprolactinemia in a case of aldosterone-producing adrenal adenoma [5].

Psychiatry related information on Hyperprolactinemia

• Six women with primary hyperprolactinemia (mean prolactin level, 50 ng/ml) were matched with six normal women on eight factors influencing life style [6].
• OBJECTIVE: Little is known about the relationship between recent life events and onset of hyperprolactinemia, despite the well-known effect of acute psychological stress on prolactin levels in healthy subjects [7].
• Use of the dopamine agonists bromocriptine and cabergoline in the management of risperidone-induced hyperprolactinemia in patients with psychotic disorders [8].
• The need for routine prolactin (PRL) measurement in the initial evaluation of erectile dysfunction (ED) has been questioned because of the low rate of hyperprolactinemia (HP) in these men and the costs involved [9].
• METHODS: We describe a 19-year-old woman with paranoid schizophrenia who was taking thioridazine (a phenothiazine), in whom hyperprolactinemia, galactorrhea, oligomenorrhea, and a reversible anatomic pituitary abnormality developed [10].

High impact information on Hyperprolactinemia

• Among 41 patients (22 women and 19 men) with hyperprolactinemia who took pergolide for three months or more, prolactin levels fell to normal in 37 and remained slightly elevated in 2 [11].
• In hyperprolactinemia, cortical bone mass is decreased and the magnitude of the decrease correlates with the severity of the estrogen deficiency [12].
• However, Prlr(-/-) mice exhibited more profound hyperprolactinemia and larger tumors than did age-matched Drd2(-/-) mice, and there were additive effects in compound homozygous mutant male mice [13].
• Pituitary lactotroph hyperplasia and chronic hyperprolactinemia in dopamine D2 receptor-deficient mice [2].
• Castration decreased plasma prolactin levels and prevented the induction of hyperprolactinemia by portal hypertension [4].

Chemical compound and disease context of Hyperprolactinemia

• These data show that chronic hyperprolactinemia and testosterone deficiency in men have deleterious and previously unrecognized extragonadal effects that may be alleviated after normalization of hormone concentrations [14].
• A mean basal prolactin level above 150 ng/ml or an increase of more than 100 ng/ml after TRH administration in a patient with hyperprolactinemia unresponsive to chlorpromazine stimulation strongly suggests a prolactin-secreting tumor [15].
• Patients who remained hypogonadal despite the reversal of hyperprolactinemia had no change in radial (0.76 +/- 0.03 to 0.76 +/- 0.04 g/cm2) or vertebral bone density (105 +/- 10 to 103 +/- 9 mg of potassium phosphate, dibasic/cm3) [16].
• We found transient hyperprolactinemia following complex partial seizures but little change in serum gonadotropins, thyroid-stimulating hormone, growth hormone, or cortisol [17].
• Perphenazine, 1 mg i.m. daily, a dose known to cause hyperprolactinemia, also impaired the efficacy of A-43818 [18].

Biological context of Hyperprolactinemia

• Primary empty sella, hyperprolactinemia, and isolated ACTH deficiency after postpartum hemorrhage [19].
• The scores of 14 women with hyperprolactinemia on the Symptom Rating Test and the Symptom Questionnaire were compared with those of nonpsychotic women attending a psychiatric clinic, women attending a family practice clinic, and female nonpatient employees [20].
• It is evident that hyperprolactinemia or sulpiride treatment do not change the circulating concentrations of sex steroids and hPL between 6--11 of normal gestation [21].
• Supporting this position, chronic elevations of PRL (hyperprolactinemia) produce pronounced reductions in animal sexual activity, and significant reduction of libido and gonadal function in both men and women [22].
• Preoperative hormone data revealed hyperprolactinemia (97 ng/ml), low plasma cortisol levels without circadian rhythm, undetectable plasma ACTH, and normal plasma FSH and LH levels, with an impaired response to LRH [23].

Anatomical context of Hyperprolactinemia

• Normal skull film, tomogram views of the sella turcica, and computerized axial tomography scan suggested that long-term estrogen administration caused sustained hyperprolactinemia with levels that ranged between 21 and 83 ng/mL throughout the ensuing year [24].
• Patients on chronic hemodialysis have abnormal hypothalamo-hypophyseal thyroid and gonadal functions, including blunted TSH response to TRH, hyperprolactinemia, elevated basal levels of LH with exaggerated response to GnRH, and depressed FSH secretory response to GnRH [25].
• Since DHAS is virtually an exclusive product of the adrenal cortex, and since high PRL levels appear to inhibit ovarian steroid production, the findings suggest that hyperprolactinemia selectively stimulates adrenocortical androgen production [26].
• Idiopathic hyperprolactinemia (IH) can be defined as the presence of elevated serum PRL levels in a patient in the absence of demonstrable pituitary or central nervous system disease and of any other recognized cause of increased PRL secretion [27].
• Metoclopramide-induced hyperprolactinemia impairs ovarian follicle maturation and corpus luteum function in women [28].

Gene context of Hyperprolactinemia

• Previous investigations have demonstrated that GnRH agonists also suppress GHRH-stimulated GH release in normal men and women and PRL levels in subjects with hyperprolactinemia [29].
• This suggests that hyperprolactinemia inhibits GnRH-R responses to GnRH in females by a direct action on the pituitary gonadotroph [30].
• Suckling-induced hyperprolactinemia did not participate in the increase in ARH NPY activity, whereas it played a major stimulatory role in suckling-induced activation of NPY neurons in the DMH and an inhibitory role in suckling-induced suppression of TIDA activity [31].
• Specifically, hyperprolactinemia gives rise to prostate hyperplasia, and prostate size is reduced in PRL-deficient mice [32].
• Since hyperprolactinemia associates in these patients with depressed EPO production, it may be regarded as a compensatory mechanism for the reduced availability of the hemopoietic factor [33].

Analytical, diagnostic and therapeutic context of Hyperprolactinemia

• Eight women with amenorrhea, galactorrhea, and hyperprolactinemia, of whom six had macroadenomas and two had microadenomas, were treated with conventional (cobalt-60) external radiotherapy, and their progress was monitored for eight to 15 years [34].
• Normalization of androgen and sex hormone-binding globulin levels after treatment of hyperprolactinemia [35].
• Oral glucose tolerance tests were performed on nine normal women during late pregnancy who had physiological hyperprolactinemia comparable to that in the AGS group [36].
• Ovariectomy attenuated hyperprolactinemia and after 18 months, D2R(-/-) mice had average pituitary weights of 4 mg, compared with 60 mg in the intact group [37].
• Compared with risperidone, olanzapine causes greater increases in weight gain and body mass index but less hyperprolactinemia [38].

References