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Results for “hyperprolactinemia”

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PubMed1998

Hyperprolactinemia, a tool in treatment control of tetrahydrobiopterin deficiency: endocrine studies in an affected girl.

Severe tetrahydrobiopterin (BH4) deficiency is a naturally occurring model of cerebral catecholamine and serotonin shortage. Examination of the stimulated release and physiologic secretion pattern of several hormones in affected individuals permits certain conclusions concerning the involvement of these neurotransmitters in hormone regulation. Treatment, moreover, permits the ranking of the quality of the therapeutic regimens in use according to the degree of hormonal alteration. The 24-h secretion pattern of prolactin, GH, cortisol, and melatonin and the stimulated release of prolactin, GH, TSH, and gonadotropins were studied in an affected girl. Severe hyperprolactinemia with disruption of the pulsatile and circadian secretion pattern was the prevailing feature. The GH physiologic secretion pattern was not affected, but its stimulation was impaired. Melatonin displayed a normal circadian secretion pattern; the rhythm, however, was advanced by several hours. Conventional treatment of BH4 deficiency, i.e. BH4, 5-hydroxytryptophan, and L-DOPA/carbidopa (the last named given in three doses per day), suppresses prolactin levels merely for a few hours. L-DOPA/carbidopa given at shorter intervals or, even better, as a slow release preparation, is more effective in suppressing prolactin levels. Our data indicate immense hyperprolactinemia but few other hormonal disturbances in severe BH4 deficiency. Prolactin secretion may serve as an extremely sensitive marker for the hypothalamic dopamine content under different therapeutic regimens. Treatment with an L-DOPA/carbidopa slow release preparation produces virtually normal prolactin levels.

Adolescent↗

PubMed1988

Mass and in situ activity of tyrosine hydroxylase in the median eminence: effect of hyperprolactinemia.

The role of PRL in the control of catecholaminergic hypothalamic neurons of female rats was investigated. The in situ activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-3,4-dihydroxyphenylalanine (DOPA) in the median eminence (ME) after the administration of a DOPA decarboxylase inhibitor. The mass of TH was measured by an immunoblot assay using rat TH as the standard. Hyperprolactinemia was induced by pituitaries implanted beneath a renal capsule. Hyperprolactinemia resulted in a significant increase in the in situ activity of TH without an increase in TH mass. The release of dopamine from hypothalamic neurons was assessed by measuring the concentration of dopamine in hypophysial portal plasma. The mean concentration of dopamine in portal plasma of rats bearing pituitary implants was 3 times that in controls. When circulating PRL was neutralized by administration of antiserum against rat PRL, the activity of TH was reduced significantly compared to that in animals treated with preimmune serum. In animals bearing pituitary implants, phosphorylation of TH in the ME was not different from that in control animals. We conclude that the biosynthetic and secretory activities of dopaminergic neurons of the hypothalamus are potentiated by PRL, but the potentiation is not due to an increase in the mass of TH or to the capacity of the neurites of the ME to phosphorylate TH.

Animals↗

PubMed1998

Identification of mammosomatotrophs in the turkey hen pituitary: increased abundance during hyperprolactinemia.

We have previously reported that the hyperprolactinemia in incubating turkey hens is associated with recruitment of lactotrophs in the pituitary gland. In this study we have used double immunofluorescence and in situ hybridization histochemistry to 1) identify mammosomatotrophs in the anterior pituitary gland of egg-laying turkey hens and incubating hens, and 2) verify PRL gene expression within mammosomatotrophs by colocalizing PRL messenger RNA in GH-immunoreactive (ir) cells. The pituitaries of laying and incubating turkey hens were collected, and the midsagittal sections were dual labeled for either PRL and GH or PRL messenger RNA and GH. The plasma PRL concentrations were higher in incubating hens (231 +/- 10.6 ng/ml) than in laying hens (43 +/- 7.4 ng/ml; P < 0.01). In the midsagittal pituitary sections, mammosomatotrophs were predominantly found scattered in the caudal lobe of the anterior pituitary gland, in the ventral half of the cephalic lobe, and at the junction of cephalic and caudal lobes. In incubating hens, the proportion of mammosomatotrophs was 7.4 +/- 1.52% (mean +/- SEM) of the total number of GH-ir and/or PRL-ir cells counted, which was significantly higher (P < 0.05) than that found in laying hens (0.6 +/- 0.23%). Furthermore, PRL gene expression was observed in many GH-ir cells in the incubating hen pituitary gland. These data suggest that 1) mammosomatotrophs are present in the turkey pituitary gland, and 2) there is an increased abundance of mammosomatotrophs in the incubating turkey hen that may contribute to hyperprolactinemia.

Animals↗

PubMed2000

Exposure of newborn male and female rats to environmental estrogens: delayed and sustained hyperprolactinemia and alterations in estrogen receptor expression.

Environmental estrogens (xenoestrogens) are synthetic compounds that are abundant in the environment and mimic natural estrogens. The estrogenicity of two such compounds, bisphenol A (BPA) and octylphenol (OP), during development of the neuroendocrine system was investigated. The objective was to compare the effects of neonatal exposure to BPA, OP, and diethylstilbestrol (DES), a potent synthetic estrogen, on prepubertal serum PRL levels and estrogen receptor (ER) expression in the anterior pituitary and medial basal hypothalamus. Receptor expression in the uterus and prostate, two peripheral estrogen-responsive tissues, was also examined. Newborn male and female Fischer 344 rats were s.c. injected on days 1-5 after birth with corn oil (control), BPA and OP (100 or 500 microg/day), or DES (5 microg/day). Rats were bled on days 15, 20, and 25 and on the day of death (day 30), and serum PRL was analyzed by RIA. Relative expressions of ERalpha and ERbeta were determined by RT-PCR. BPA and OP induced delayed, but progressive, increases in serum PRL levels, up to 3-fold above control levels, in both males and females. The low dose of either compound was equally or more effective as the high dose in eliciting and sustaining elevated serum PRL levels, namely hyperprolactinemia. In contrast, the DES treatment resulted in a transient rise in serum PRL levels. BPA, OP, and, to a lesser extent, DES increased the expression of both ERalpha and ERbeta in the anterior pituitary of males, but not females, whereas the hypothalamic ERs were less responsive to these compounds. DES treatment caused down-regulation of ERalpha expression in the uterus and up-regulation of ERbeta in the prostate, whereas BPA or OP was without effect. In conclusion, exposure of newborn rats of either sex to environmental estrogens results in delayed and sustained hyperprolactinemia and differential alterations in ER expression in the hypothalamus and pituitary. DES appears to target the lower reproductive tract more effectively than the neuroendocrine system.

Animals↗

PubMed1989

The natural history of untreated hyperprolactinemia: a prospective analysis.

This report describes the results of a long term prospective study of 30 women with hyperprolactinemia who were not treated and who underwent yearly clinical, hormonal, and radiographic evaluation for an average of 5.2 yr (range 3-7 yr). At entry into the study 18 women had amenorrhea, 8 had oligomenorrhea, and 4 had regular menstrual periods. The initial mean serum PRL levels did not differ in women grouped according to menstrual function. Nine women (35%) had improvement in clinical symptoms. Serum PRL decreased, and menstrual periods normalized more often in those who initially had oligomenorrhea or regular menstrual periods. In most amenorrheic women serum PRL levels did not decline, and menstrual symptoms did not improve. Six of 30 women had an increase in serum PRL, 14 had no change, and 10 had a decrease, in 6 of whom serum PRL was normal at the last observation. Twenty-seven women had serial radiographic studies. Four (15%) of the 13 women with initially abnormal radiographic findings had normal studies later, 2 had tumor progression, and 7 no change. Four of 14 women who had normal radiographic studies initially developed radiographic evidence of a pituitary tumor, although the radiographic changes were minimal, and no patient developed a macroadenoma or pituitary hypofunction. Increases or decreases in serum PRL did not accurately predict changes in tumor size. Prior estrogen use and previous pregnancies did not increase the likelihood of tumor appearance or enhance tumor growth. The clinical presentation of the patient was an important factor in predicting which patients had a decline in serum PRL and resolution of symptoms. We conclude that patients with hyperprolactinemia are unlikely to have progression of their disease and may, in fact, have clinical and radiographic improvement.

Adult↗

PubMed1991

Naloxone increases the frequency of pulsatile luteinizing hormone secretion in women with hyperprolactinemia.

The ability to change the frequency and amplitude of pulsatile GnRH secretion may be an important mechanism in maintaining regular ovulatory cycles. Hyperprolactinemia is associated with anovulation and slow frequency LH (GnRH) secretion in women. To assess whether the slow frequency of LH (GnRH) secretion is due to increased opioid activity, we examined the effect of naloxone infusions in eight amenorrheic hyperprolactinemic women (mean +/- SE, serum PRL, 160 +/- 59 micrograms/L). After a baseline period, either saline or naloxone was infused for 8 h on separate days, and LH was measured in blood obtained at 15-min intervals. Additional samples were obtained for plasma FSH, PRL, estradiol, and progesterone. Responses to exogenous GnRH were assessed at the end of the infusions. LH pulse frequency increased in all subjects from a mean of 4.0 +/- 0.5 pulses/10 h (mean +/- SE) during saline infusion to 8.0 +/- 1.0 pulses/10 h during naloxone infusion (P less than 0.01). LH pulse amplitude did not change, and mean plasma LH increased from 7.4 +/- 0.8 IU/L (+/- SE) to 11.2 +/- 1.5 IU/L during naloxone (P less than 0.01). A small but significant increase was seen in mean plasma FSH. Plasma PRL, estradiol, and progesterone were unchanged by naloxone infusion. These data suggest that elevated serum PRL reduces the frequency of LH (GnRH) secretion by increasing hypothalamic opioid activity and suggest that the anovulation in hyperprolactinemia is consequent upon persistent slow frequency LH (GnRH) secretion.

Adult↗

PubMed1993

Acromegaly with hyperprolactinemia developed after bilateral adrenalectomy in a patient with Cushing's syndrome due to adrenocortical nodular hyperplasia.

A 27-yr-old woman was referred for evaluation of acromegaly and hyperprolactinemia. She had undergone left adrenalectomy at 12 and right adrenalectomy at 17 for Cushing's syndrome due to adrenocortical nodular hyperplasia. At this time a pituitary tumor was found by brain computerized tomography, but plasma levels of growth hormone (GH), prolactin (PRL) and adrenocorticotropin (ACTH) were normal. When she was 23, symptoms and signs of acromegaly and subsequently galactorrhea-amenorrhea had developed. Plasma GH and PRL were increased and she was followed up by the administration of bromocriptine (2.5 mg-12.5 mg/day, p.o.). However the plasma GH level had been increasing gradually. On admission, plasma GH and PRL were high (19.5 micrograms/L, 61.0 micrograms/L, respectively) and increased in response to thyrotropin releasing hormone (TRH, 500 micrograms i.v.). An intrasella mass, which had been detected when she was 17, had become enlarged and was removed by Hardy's operation. Microscopically, the resected tumor was an eosinophilic adenoma. Immunohistochemical studies showed GH, PRL and ACTH positive cells localized in the tumor. Immunoultrastructural analysis of the tumor confirmed that GH, PRL and ACTH were present in secretory granules and Golgi apparatus in the tumor cells. The patient was a rare case of acromegaly with hyperprolactinemia developed after bilateral adrenalectomy of Cushing's syndrome due to adrenocortical nodular hyperplasia, all of which manifestations may be caused by a GH, PRL and ACTH secreting pituitary adenoma.

Acromegaly↗

PubMed1989

Isolated ACTH deficiency associated with transient thyrotoxicosis and hyperprolactinemia.

A 43-year-old woman with isolated ACTH deficiency in association with transient thyrotoxicosis is reported. The initial evaluation revealed that plasma ACTH and cortisol did not respond to corticotropin-releasing hormone (CRH) in the presence of hyperthyroxinemia and hyperprolactinemia. During the replacement therapy with dexamethasone, she developed transient hypothyroxinemia with persistent hyperprolactinemia. Although thyroid open biopsy did not show any evidence of autoimmune thyroiditis or subacute thyroiditis, the data appear to provide other evidence of a possible relationship between acute adrenal insufficiency and transient thyroid dysfunction.

Adrenocorticotropic Hormone↗

PubMed1988

CQP 201-403, a new dopamine agonist in the treatment of hyperprolactinemia.

Current drugs used for hyperprolactinemia may have severe side effects. Effects and side effects of a new propylergoline derivate (CQP 201-403 SANDOZ) have been evaluated. Twenty-four otherwise healthy women (21-44 years) with hyperprolactinemia (35-318 micrograms/l) without extrasellar extension of pituitary adenomas took part in a randomized, double-blind study. Fasting prolactin levels measured on day 7 was significantly decreased when compared with day 1 (P less than 0.05) in all CQP groups, to 78% with 0.005 mg daily, to 40% with 0.015 mg daily, and to 27% with 0.025 mg CQP per day for one week. The levels in the control group did not change (96%). The area under the curve of the prolactin day curve (1-8 h after drug administration) decreased significantly (P less than 0.05) at all doses when day 7 was compared with day 1, to 77% with 0.005 mg, to 51% with 0.015 mg, and to 37% with 0.025 mg CQP. No change was seen in the control group (96%). Four patients (one on 0.005 mg, one on 0.015 mg, and two on 0.025 mg) experienced orthostatic hypotension while standing blood pressure was to be measured on the first day of treatment, and they had to lie down. CQP 201-403 lowers prolactin levels in hyperprolactinemic women at all doses employed. The effect was seen after the first dose of treatment, and lasted for at least 24 h. The adverse reactions are few and tolerable, and might be less than with current bromocriptine therapy.

Adult↗

PubMed1994

Enhanced cell proliferation by hyperprolactinemia in both exocrine and endocrine pancreas in mice.

Effects of hyperprolactinemia induced by ectopic anterior pituitary grafting on the pancreas were studied in male SHN mice. After pituitary grafting, the weight of pancreas rapidly increased. A similar increase in pancreatic weight was observed during lactation, a condition associated with elevated prolactin levels. Results of DNA and protein assays revealed that the increase in pancreatic weight in both pituitary-grafted and lactating mice was mainly due to the increase in the cell number, because the total DNA content per pancreas was greater in these mice than the controls. An increase in fluid volume or hypertrophy of cells also contributes to the weight increase; in contrast, the DNA and protein contents per unit tissue weight decrease. The rate of DNA synthesis determined by 5-bromo-2'-deoxyuridine labeling was higher both in acinar cells and islet B cells in pituitary-grafted mice than in the controls. Thus, hyperprolactinemia stimulates cell proliferation in exocrine pancreas as well as endocrine islets. The effect of prolactin seems to be indirect on acinar cells, because only B cells showed prolactin immunoreactivity in the mouse pancreas. In addition, insulin might not be a mediator of the prolactin effect on acinar cells, because the serum insulin level in pituitary-grafted mice failed to show any change.

Animals↗

PubMedDate not supplied

[Effects of metoclopramide-induced hyperprolactinemia on the murine corneal].

PURPOSE: To evaluate the morphological changes in murine cornea upon metoclopramide-induced hyperprolactinemia during the proestrous phase or pregnancy. METHODS: Forty adult mice were divided into two groups: (control) CTR1 and (treated with metoclopramide (MET1). After fifty days, half of the mice were sacrificed. The remaining animals were mated, and then labeled as pregnant controls (CTR2). Part of these animals were treated with metoclopramide and constituted the metoclopramide-treated pregnant (MET2) group. The groups CTR2 and MET2 were sacrificed on the 6th day of pregnancy. The hormonal levels were assessed by chemioluminescence and radioimmunoassay methods and the cornea was removed for the histomorphometric study. RESULTS: The epithelial, stromal, endothelial and total thickness in the experimental group was: MET1 and MET2 were higher than one in the control group: CTR1 and CTR2. There was a significant reduction of the hormonal level in the animals that received metoclopramide as compared to controls (CTR1: estradiol = 156.6 +/- 42.2 pg/ml; progesterone = 39.4 +/- 5.1 ng/ml; prolactin = 130.4 +/- 26.2 ng/ml; MET1: estradiol = 108.0 +/- 33.1 pg/ml; progesterone = 28.0 +/- 6.4 ng/ml; prolactin = 551.5 +/- 23.3 ng/ml; CTR2: estradiol = 354.0 +/- 56.0 pg/ml; progesterone = 251.0 +/- 56.0 ng/ml; prolactin = 423.2 +/- 28.1 ng/ml; MET2: estradiol = 293.0 +/- 43.0 pg/ml; progesterone = 184.0 +/- 33.0 ng/ml; prolactin = 823.1 +/- 51.1 ng/ml). CONCLUSION: The metoclopramide-induced hyperprolactinemia may increase corneal layers, mainly in pregnant mice. Possibly, this effect is related to reduction in estrogen and progesterone production.

Animals↗

PubMed1998

Hyperprolactinemia associated to calcification of the pituitary stalk. Case report.

In this work, the authors report the case of a female patient with 24 years of age with hyperprolactinemia, who presented a pituitary stalk calcification as seen by CT scan. Once other possible etiologies were excluded, we concluded that the calcification was probably related to hyperprolactinemia caused by interruption of the input of dopamine to the pituitary gland.

Adult↗

PubMed2003

Hyperprolactinemia: pathophysiology and management.

Hyperprolactinemia is commonly found in both female and male patients with abnormal sexual and/or reproductive function or with galactorrhea. If serum prolactin levels are above 200 microg/L, a prolactin-secreting pituitary adenoma (prolactinoma) is the underlying cause, but if levels are lower, differential diagnoses include the intake of various drugs, compression of the pituitary stalk by other pathology, hypothyroidism, renal failure, cirrhosis, chest wall lesions, or idiopathic hyperprolactinemia. When a pituitary tumor is present, patients often have pressure symptoms in addition to endocrine dysfunction, such as headaches, visual field defects, or cranial nerve deficits. The large majority of patients with prolactinomas, both micro- and macroprolactinomas, can be successfully treated with dopaminergic drugs as first-line treatment, with normalization of prolactin secretion and gonadal function, and with significant tumor shrinkage in a high percentage of cases. Surgical resection of the prolactinoma is the option for patients who may refuse or do not respond to long-term pharmacological therapy. Radiotherapy and/or estrogens are also reasonable choices if surgery fails. In patients with asymptomatic microprolactinoma no treatment needs to be given and a regular follow-up with serial prolactin measurements and pituitary imaging should be organized. Currently, the most commonly used dopamine agonists are bromocriptine, pergolide, quinagolide and cabergoline. When comparing the plasma half-life, efficacy and tolerability of these drugs, cabergoline seems to have the most favorable profile, followed by quinagolide. Ifprolactin levels are well controlled with dopamine agonist therapy, gradual tapering of the dose to the lowest effective amount is recommended, and in a number of cases medication can be stopped after several years. Evidence to date suggests that cabergoline and quinagolide appear to have a good safety profile for women who wish to conceive, but hard evidence proving that dopamine agonists do not provoke congenital malformations when taken during early pregnancy is currently only available for bromocriptine. Once pregnant, dopamine agonist therapy should be immediately stopped, unless growth of a macroprolactinoma is likely or pressure symptoms occur. At our institution patients with symptomatic prolactinomas, both micro- and macroadenomas, are treated with cabergoline as the first-line aproach. In the small group of patients who do not respond to this treatment, or who refuse long-term therapy, surgery is offered. Radiotherapy is given if both pharmacologic therapy and surgery fail.

Bromocriptine↗

PubMedDate not supplied

Evaluation of semen parameters in man with hyperprolactinemia induced by metoclopramide.

Hyperprolactinemia in man decreases libido and potency, but the few reports concerning its influence on spermatogenesis are contradictory. The aim of this study was to evaluate the effect of induced hyperprolactimemia on semen parameters. A total of 15 potentially fertile male volunteers, aged 28.2 +/- 4.3 years, were given 10 mg metoclopramide three times daily for 12 weeks. Serum and seminal plasma prolactin levels and semen parameters were determined before and 4, 8, and 12 weeks following initiation of metoclopramide administration. A fivefold increase of serum prolactin levels was observed, semen volume and abnormal sperm forms decreased, while spermatozoa velocity increased. On the contrary, no influence was noted on the number of spermatozoa per milliliter, the total number of spermatozoa, the percentage of motile spermatozoa, or the index of motility. Hyperprolactinemia seems to improve spermatozoal velocity and morphology, although direct effect of metoclopramide on these parameters cannot be excluded.

Adult↗

PubMedDate not supplied

Hyperprolactinemia in men with asthenozoospermia, oligozoospermia, or azoospermia.

The role of serum prolactin (PRL) in male infertility is still unclear. To assess the clinical significance of PRL determination during infertility studies, serum hormones and semen samples from 167 men attending the Andrology Clinic were analyzed, and PRL seric values were correlated with volume, sperm count, motility, viability, and morphology. The range of PRL levels (ng/mL) was 7.3 +/- 2.1 in the control group (n = 46), 13.9 +/- 6.6 in asthenozoospermic (n = 51), 12.6 +/- 7.8 in oligozoospermic (n = 42), and 10.9 +/- 4.8 in azoospermic patients (n = 28). Significantly higher (p < .0001) levels of PRL were found in the men with asthenozoospermia, oligozoospermia, and azoospermia. In the 121 infertile patients with abnormal semen analysis, serum PRL levels were below 14.0 ng/mL (normal mean + 3 SD) in 81 (66.9%) and above this level in 40 (33.1%) cases. Serum FSH and LH concentrations in azoospermic men were significantly higher (p < .0001) when compared with those of the control group, which indicates some disturbance of the spermatogenic process, and estradiol was significantly higher (p < .02) in oligozoospermic patients. No significant differences were found in serum testosterone. Twenty-one patients with idiopathic oligoasthenozoospermia and hyperprolactinemia were treated with 2.5 mg of bromocriptine daily for 6 months, resulting in a nonmeasurable effect on their sperm analysis. In conclusion, two-thirds of patients with oligozoospermia, asthenozoospermia, and azoospermia have normal PRL levels. Infertility in men due to moderate hyperprolactinemia could be associated with these sperm disturbances, but bromocriptine was of no therapeutic utility.

Adult↗

PubMed1996

A study of the clinical differences between women and men with hyperprolactinemia.

A group of 64 women and 14 men with hyperprolactinemia were followed up in an endocrine service center for a mean of 43 months. The various parameters in each sex were compared. The mean age at first visit was 49 years in the men and 36 years in the women (p < 0.001). The peak prolactin index levels were 13.7 in the men and 5.5 in the women (p < 0.002). Macroprolactinomas were significantly more prevalent in the men (p < 0.002). The women complained significantly more about headache (p < 0.02), malaise (p < 0.02), restlessness (p < 0.03) and fatigue (p < 0.04). These symptoms had no correlation with the prolactin level. Thus, in the men the clinical manifestations of hyperprolactinemia came to attention at an older age and had a connection with a higher prevalence of macroprolactinoma. The possible mechanisms are discussed. Vague complaints, reported more often by the women, do not seem to correlate with the prolactin level.

Adult↗

PubMed1996

Effect of estrogen on hyperprolactinemia-induced glucose intolerance in SHN mice.

The effects of prolactin (PRL) on circulating levels of glucose and insulin, and of estradiol on hyperprolactinemia-induced glucose intolerance of tissues were studied in pituitary-grafted SHN mice (PG mice) and sham-operated controls. Pituitary grafting (PG) decreased blood glucose levels in male mice at 1 and 3 months after the operation but did not alter those in females. PG had little effect on serum insulin levels in males, but increased those in females. In female mice at 2 months after PG, blood glucose levels were significantly higher at 1, 2, and 4 hr after glucose load when compared with those in controls. In contrast, there was no significant difference in blood glucose levels after glucose load between male PG and control mice. The rate at which blood glucose levels decreased was slower in female PG mice than in controls during the 30 min after insulin injection, whereas there was no difference in the rate after insulin injection between male PG and control mice. In ovariectomized (Ovx) mice, no significant difference was found in the blood glucose levels after a glucose load between PG and control groups at 2 months after PG. In Ovx mice treated daily with estrogen, however, a PG-dependent high level of blood glucose was observed after glucose load. These results suggest that hyperprolactinemia decreases glucose tolerance via an increase in insulin resistance in female SHN mice and that estrogen is essential to the expression of the PRL effect.

Animals↗

PubMed1989

Elevated serum lipids in hypogonadal men with and without hyperprolactinemia.

STUDY OBJECTIVE: To determine whether men with hypogonadism are at risk for hyperlipidemia. DESIGN: Case-control study. SETTING: Neuroendocrine clinical center of a referral-based university medical center. PATIENTS: Consecutive sample of 18 men with testosterone deficiency who had prolactin-secreting pituitary adenomas, 15 men with acquired secondary hypogonadism and normal prolactin levels, and 33 normal male controls. MEASUREMENTS AND MAIN RESULTS: We found a significant elevation in fasting cholesterol (6.23 +/- 0.28 mmol/L [mean +/- SE] compared with 5.17 +/- 0.13 mmol/L [241 +/- 11 mg/dL compared with 200 +/- 5 mg/dL], P less than 0.01), low density lipoprotein (LDL) cholesterol (4.11 +/- 0.23 mmol/L compared with 3.34 +/- 0.13 mmol/L [159 +/- 9 mg/dL compared with 129 +/- 5 mg/dL], P less than 0.05), and triglycerides (1.85 +/- 0.26 mmol/L compared with 1.11 +/- 0.07 mmol/L [164 +/- 23 mg/dL compared with 98 +/- 6 mg/dL], P less than 0.001) in men with hyperprolactinemia compared with controls. In the normoprolactinemic hypogonadal men, cholesterol (6.28 +/- 0.34 mmol/L [243 +/- 13 mg/dL], P less than 0.01), LDL cholesterol (4.34 +/- 0.34 mmol/L [168 +/- 13 mg/dL], P less than 0.01), and triglycerides (1.61 +/- 0.18 mmol/L [143 +/- 16 mg/dL], P less than 0.05) were also significantly higher than in the controls, and were the same as in the hyperprolactinemic men. High density lipoprotein (HDL) cholesterol did not differ among the three groups. CONCLUSIONS: Hypogonadism in men, with or without hyperprolactinemia, may be associated with elevation of fasting serum cholesterol, LDL cholesterol, and triglycerides compared with normal men. These data suggest that serum lipid levels should be evaluated in hypogonadal men. The presence of lipid abnormalities may affect the decision to treat testosterone deficiency in these patients.

Adolescent↗