Hormone profile in hyperprolactinemic infertile men

Serum levels of FSH, LH, prolactin, testosterone, and estradiol in 46 infertile men with hyperprolactinemia were compared with the same in 50 infertile and 30 fertile men with normal serum prolactin levels. Serum FSH levels in hyperprolactinemic men were significantly higher than in the other groups, indicating disturbance of spermatogenic process among those men. Significantly raised serum LH levels were in infertile men with serum prolactin over 1000 U/liter. All men with hyperprolactinemia had significantly lower serum testosterone levels than other infertile and fertile men. Although serum testosterone was not under the lower limit of normal range and high LH levels demonstrated disturbance of Leydig cell function in hyperprolactinemic infertile men, serum estradiol levels were not different among investigated groups. Azoospermic men with raised serum prolactin had higher serum FSH and LH levels than oligospermic men with hyperprolactinemia. These data demonstrated disturbance in hypothalamopituitary-testicular axis in infertile men with hyperprolactinemia. Further studies of prolactin in males with reproductive failure could probably clear this problem.     

The specificity of serum prolactin as a diagnostic indicator of pituitary adenoma.

Serum prolactin levels were determined in 205 patients with a variety of intracranial diseases, including 70 cases with pituitary tumors. It is concluded that although the absence of elevated prolactin levels does not help to rule out pituitary pathology, the presence of hyperprolactinemia is highly specific for diseases of the pituitary and hypothalamus, and prolactin determination should be part of the regular work-up of pituitary tumor suspects. Excluding known causes of hyperprolactinemia, such as tranquilizing drug ingestion, the presence of neurological disease outside the hypothalamic-pituitary area was not associated with increased serum prolactin concentrations.     

Hyperprolactinemia and impotence

One hundred impotent men and 15 sexually active male volunteers served as the source for this study. Serum prolactin was estimated in all cases using radioimmunoassay technique. Cases with hyperprolactinemia were treated with bromocriptine for 3 months. Hyperprolactinemia was detected in three patients only (3%), with no findings of pituitary tumors. Treatment with bromocriptine markedly reduced the level of serum prolactin together with improvement of sexual libido and potency. The mere presence of 3 cases only with hyperprolactinemia among 100 impotent subjects suggested that hyperprolactinemia is not one of the main causes of impotence.     

Hyperprolactinemia in patients with renal insufficiency and chronic renal failure requiring hemodialysis or chronic ambulatory peritoneal dialysis

Hyperprolactinemia is common in patients with renal failure. Because radiographic contrast material given during a computed tomographic (CT) scan of the sella as part of the evaluation for prolactinoma worsens renal insufficiency, we attempted to define the point at which hyperprolactinemia becomes an expected finding in patients with renal insufficiency in this study. Of 59 patients with serum creatinine levels of 1.5 to 12 mg/dL, 16 (27.1%) were hyperprolactinemic. Of these 16, nine were not taking medications known to raise prolactin levels and their prolactin levels were less than 100 ng/mL. In the eight patients taking medications prolactin levels were much higher. In one patient the prolactin level fell from 2,210 to 100 ng/mL when methyldopa was discontinued. In patients with chronic renal failure prolactin levels were similar regardless of the method of dialysis. We conclude that in the absence of medications known to affect prolactin secretion, hyperprolactinemia occurs infrequently (18.3%) and, when it occurs, is mild (less than 100 ng/mL). Marked hyperprolactinemia may occur in patients taking such medications. These should be stopped and the prolactin level rechecked before a CT scan is performed.     

Concomitant occurrence of macroprolactin, exercise-induced amenorrhea, and a pituitary lesion: a diagnostic pitfall. Case report.

The authors report the case of a 37-year-old woman who presented with amenorrhea and an increased level of serum prolactin. Magnetic resonance images of the pituitary revealed a lesion with characteristics consistent with those of a microadenoma. Transsphenoidal exploration was performed, but a prolactinoma was not found. After endocrinological review, the patient's hyperprolactinemia was found to be caused by the presence of macroprolactin and her amenorrhea was due to intense exercise and low body weight. Macroprolactin is an isoform of prolactin that is variably reactive in assays for prolactin, but displays minimum bioactivity in vivo. Patients with macroprolactin are mostly asymptomatic. This phenomenon may cause elevated prolactin values, which the authors view as apparent hyperprolactinemia. The presence of macroprolactin is an underrecognized problem, occurring in as many as 15 to 20% of patients with elevated prolactin values and often leading to unnecessary, expensive diagnostic procedures and inappropriate treatment. The presence of macroprolactin should always be suspected when the patient's clinical history or clinical or radiological data are incompatible with the prolactin value. Physicians dealing with diagnosis and treatment of hyperprolactinemia (general practitioners, gynecologists, neurosurgeons, endocrinologists, and biochemists) should be aware of the potentially misleading nature of macroprolactin.     

Hyperprolactinemia and impotence: why, when and how to investigate

The contribution of hyperprolactinemia to erectile disorders has not been clarified. Modest elevations of serum prolactin occur after administration of drugs that by themselves affect erectile function. Prolactinomas produce marked elevations of the hormone and invariably are accompanied by hypogonadotropic hypogonadism. Among 1,236 consecutive impotent patients investigated at our center 5.3% had serum levels of prolactin greater than normal. Only 34 of the 66 hyperprolactinemic patients were available for analysis. The etiology of the hyperprolactinemia in this group was pituitary adenoma in 14.7%, drug-induced in 29%, chronic renal failure in 6%, laboratory error in 2.9% and idiopathic in 47.1%. Medical management has a high degree of success but simply lowering the levels of prolactin is not invariably accompanied by restoration of function.     

Association between Hyperprolactinemia and Granulomatous Mastitis

Granulomatous mastitis (GM) is a relatively uncommon inflammatory breast lesion with multiple suggested etiologies. Although most GM cases show association with lactation and pregnancy, a minority of cases have been linked to hyperprolactinemia caused by either dopamine antagonist medications or with intracranial lesions, such as pituitary adenoma. The goal of this study is to review the GM cases reported in the literature with a specific emphasis on those cases associated with hyperprolactinemia and prolactinomas and to identify cases of GM seen at the Cleveland Clinic Florida which demonstrate co‐occurrences of GM and intracranial lesions. CoPath and Epic data bases at Cleveland Clinic Florida were searched for cases describing inflammatory breast lesions in patients with pituitary pathology. Chart reviews were conducted and pertinent medical history was extracted for case reports. H&E‐stained paraffin‐embedded sections retrieved from Cleveland Clinic Florida pathology storage were evaluated by light microscopy. Four cases showing a co‐occurrence of GM and hyperprolactinemia were consequently identified. A prolactin‐secreting pituitary adenoma was present in two of the three GM cases. The third case demonstrated a concomitant craniopharyngioma, which was also associated with a rise in serum prolactin. This phenomenon was presumably attributable to compression, resulting in compromised transport of dopamine to the adenohypophysis and subsequent disinhibition of prolactin secretion by lactotrophs. The fourth patient with GM had a similar history of elevated prolactin. Classical histopathological features of GM were found in all four cases, including noncaseating granulomas, multinucleated giant cells, epithelioid histiocytes, and chronic inflammation. Intriguingly, complete resolution of inflammatory breast lesions along with normalization of prolactin levels occurred following the surgical excision of the craniopharyngioma, suggesting that intracranial lesion–induced hyperprolactinemia might be directly causal in GM. Therefore, the authors would suggest screening for pituitary tumors and evaluate prolactin levels in the workup of GM patients without a recent history of lactation and pregnancy and no other identified etiology.     

Serum prolactin concentration in impotent African males

Serum prolactin concentration, measured by radioimmunoassay, was significantly higher (p less than 0.005) in 49 patients with impotence than in a control population of 16 normal subjects. 26.5% of the impotent patients had hyperprolactinemia. Their serum testosterone was also significantly lower (p less than 0.05). Bromocriptine suppressed the raised prolactin, normalised testosterone in seven treated hyperprolactinemic patients, and restored potency in five of them. These results suggest a possible role for hyperprolactinemia in a substantial proportion of African patients with impotence. Further studies in more affected patients are in order.     

Role of serum prolactin determination in evaluation of impotent patient

Hyperprolactinemia is a recognized cause of impotence. The discovery of elevated prolactin levels in impotent men is very important since pharmacotherapy in this instance is highly successful. We review our experience with prolactin determinations in impotent men, and a population is defined that may benefit from routine prolactin determination. In our experience, the predominant symptom associated with hyperprolactinemia in men is loss of libido.     

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.     

Prolactin gene expression in human growth hormone-secreting pituitary adenomas

To elucidate the mechanism of hyperprolactinemia often observed in patients with growth hormone (GH)-secreting pituitary adenomas, the presence of immunoreactive prolactin (ir-PRL) and prolactin (PRL) messenger ribonucleic acid (mRNA) in the tumor tissue was examined by immunohistochemistry and cytoplasmic dot hybridization. Hyperprolactinemia was observed in three of 18 patients with GH-secreting adenoma. The tumor tissue was demonstrated to contain ir-PRL in nine patients and PRL mRNA in 13. The presence of ir-PRL in the tumor tissue was always associated with positive PRL mRNA, indicating production of PRL in GH-secreting tumors. Among the three patients with hyperprolactinemia, both ir-PRL and PRL mRNA was revealed in the tumor tissue of one, PRL mRNA but not ir-PRL was detected in the adenoma tissue of another, and neither PRL mRNA nor ir-PRL was found in the tumor tissue of the third. The association of hyperprolactinemia with the presence of both ir-PRL and PRL mRNA or PRL mRNA alone is indicative of PRL production and secretion. However, the absence of ir-PRL and PRL mRNA in the tumor tissue may indicate that hyperprolactinemia is caused by the suppression of PRL inhibitory factor due to hypothalamic dysfunction by the tumor mass. Thus, the study of PRL gene expression and immunohistochemistry in GH-secreting adenomas is valuable to understanding the pathophysiology of pituitary tumors.     

Hyperprolactinemia and pregnancy

Prolactin is a polipeptidic hormone secreted by the anterior pituitary gland, whose main role consists in the stimulation of lactation in the postpartum period. The increasing of prolactin secretion can be physiological (pregnancy and lactation) or pathological (hypothalamic and pituitary diseases, iatrogenic, etc.). The suppression of the hypothalamic-pituitary-gonadal axis and the resistivity of the ovary and gonadotropin action are induced in hyperprolactinemia, the amenorrhea and lack of ovulation being the result. Infertility associated with hyperprolactinemia is reversible with treatment, irrespectively to the type of treatment (radical or medical). Lowering of prolactin levels to normal or near normal is often necessary to permit ovulation. Dopamine-like drogs, as bromocriptine, appear to be safe for the developing fetus, at lest when the treatment is interrupted in the first trimester of pregnancy.     

Sexual dysfunction in women with hyperprolactinemia: a pilot study report

PURPOSE: Hyperprolactinemia is a common hormonal disorder in women that may affect the phases of female sexual function (FSD). We investigated sexual function in patients with hyperprolactinemia. MATERIAL AND METHODS: A total of 25 women with primary hyperprolactinemia and 16 age matched voluntary healthy women who served as the as control group were evaluated with a detailed medical and sexual history, including a female sexual function index (FSFI) questionnaire and the Beck Depression Inventory. Serum prolactin, dehydroepiandrosterone sulfate, free testosterone, androstenedione, 17alpha-hydroxyprogesterone, estradiol, free thyroxin and thyrotropin were measured. These variables were compared statistically between the 2 groups. RESULTS: Except for prolactin serum hormone levels in women with hyperprolactinemia were not different from those in the control group. The median total FSFI score was 23.40 (IQR 17.70 to 27.30) in the hyperprolactinemic group, whereas healthy women had a median total FSFI score of 31.10 (IQR 27.55 to 32.88, p < 0.0001). FSD was diagnosed in 22 of 25 patients (88%), while 4 of 16 healthy women (25%) had FSD (p = 0.03). Desire (p = 0.001), arousal (p < 0.0001), lubrication (p = 0.001), orgasm (p = 0.001), satisfaction (p = 0.07) and pain (p = 0.003) domain scores were also significantly lower in women with hyperprolactinemia. Total FSFI (p = 0.009, r = -0.405), desire (p = 0.001, r = -0.512), arousal (p = 0.002, r = -0.466), orgasm (p = 0.026, r = 0.348) and satisfaction (p = 0.041, r = -0.320) scores negatively correlated with mean prolactin but not with the other hormones measured. CONCLUSIONS: A significant percent of women with hyperprolactinemia whom we evaluated had sexual dysfunction. No hormonal changes other than prolactin and no depression was found as a cause of FSD.     

Effect of Chronic Hyperprolactinemia Induced by Sulpiride on Plasma Dehydroepiandrosterone (DHA) in Normal Men

In order to elucidate the relationship between plasma dehydroepiandrosterone (DHA) and sulpiride-induced hyperprolactinemia (of 60 day duration) in normal men, five normal men (aged 27-46) were administered daily 300 mg of sulpiride orally for 60 days to induce hyperprolactinemia. Plasma levels of prolactin, DHA and cortisol were measured by radioimmunoassay before sulpiride treatment, at day 14 and day 60 after initiation of the treatment. Plasma levels of prolactin after the administration rose significantly (P less than 0.001) to 71.6-95.3 ng/ml in four out of the five subjects compared with those of the controls. In the same four subjects the mean DHA values in plasma were elevated significantly (P less than 0.05) to 877 +/- 160 ng/dl from the mean baseline values (669 +/- 91 ng/dl). The elevated values remained during sulpiride treatment. Plasma levels of cortisol did not change significantly during sulpiride administration in all subjects. Our results suggest that sulpiride-induced hyperprolactinemia sustained at least 14-60 days in normal men stimulates the adrenal cortex to secrete DHA.     

Prolactin secretion in women after plastic breast augmentation and reduction

Prolactin secretion in women undergoing augmentation and reduction mammaplasties was studied by determining serum prolactin concentrations preoperatively, intraoperatively, and for one year postoperatively. Thyrotropin-releasing hormone tests for prolactin secretion were performed in a small subgroup of these patients. The subjects were 7 women undergoing reduction mammaplasty, 13 women undergoing augmentation mammaplasty, and 14 normal control women. Short-term (up to three days postoperatively) but not long-term changes in prolactin secretion were identified. Persistent hyperprolactinemia does not appear to be a common complication of plastic breast operations.     

Prolactin levels during short‐ and long‐term cross‐sex hormone treatment: an observational study in transgender persons

The cause of prolactin alterations in transgender persons is often assigned to oestrogens, but the precise cause and time course during different phases of cross‐sex hormone treatment (CHT) remain unclear. In this study, we prospectively examined prolactin levels in 55 female‐to‐males (FtMs) and 61 male‐to‐females (MtFs) during the first year of CHT. Because long‐term prolactin data were not available in this population, we studied these levels in a retrospective population of 25 FtMs and 38 MtFs who underwent gonadectomy. FtMs were treated with testosterone and MtFs with estradiol, with or without the anti‐androgen cyproterone acetate (CPA) (after gonadectomy CPA is cessated). During the first year of CHT, prolactin decreased with 25% (95CI: ?33%, ?12%) in FtMs and increased with 193% (95CI: 156%, 219%) in MtFs. Eighteen MtFs developed hyperprolactinemia (≥0.6 IU L^?1). In the retrospective population, post‐gonadectomy levels in FtMs were lower than baseline levels (?39%; 95CI: ?51%, ?20%) while in MtFs post‐gonadectomy levels and baseline levels were comparable (?6%; 95CI: ?24%, 15%). No hyperprolactinemia was found after gonadectomy. In conclusion, in FtMs, prolactin decreased consistently during CHT and in MtFs, prolactin increased during pre‐surgical CHT but normalised after gonadectomy. It is likely that CPA induces increasing prolactin levels in MtFs.     

Amenorrhea-galactorrhea and craniopharyngioma

A 40-year-old woman had a 1-year history of amenorrhea-galactorrhea. She was found to have an intrasellar tumor with suprasellar extension and a prolactin level of 98.1 ng/mL. Subtotal resection of the tumor resulted in a return of the prolactin level to normal within 4 days of the operation and of the prolactin response to thyrotropin releasing hormone, accompanied by the disappearance of the galactorrhea. Histologic examination revealed a typical craniopharyngioma. These observations indicate that one important mechanism of hyperprolactinemia in patients with craniopharyngioma is direct encroachment on the hypothalamus and/or pituitary stalk by the tumor and interruption of prolactin inhibiting factor.     

Endocrine contribution to the sexual dysfunction in patients with advanced chronic kidney disease and the role of hyperprolactinemia

In this study, we investigated the prevalence of sexual dysfunction among males with advanced chronic kidney disease and the effect of treating hyperprolactinemia among these patients. In this prospective study, patients were assessed with history, physical examination, hormonal assessment, and two questionnaires, IIEF and AIPE. Patients with hyperprolactinemia received treatment with cabergoline 0.5 mg once per week for 6 months and were re-evaluated. A total of 102 patients were included in this study, 75 (73.53%) were on hemodialysis, 13 (12.75%) on peritoneal dialysis and 14 (13.73%) on medical treatment alone. Ninety (88.24%) patients had premature ejaculation, 85 (83.33%) had anything from mild-to-moderate-to-severe erectile dysfunction. The incidence of hypogonadism and hyperprolactinemia was 34.4%. Patients treated with cabergoline (n = 26) showed a significant increase in LH levels (p = .003) and a significant decrease in prolactin levels (p = .003). Testosterone levels and the incidence of erectile dysfunction or premature ejaculation did not improve significantly. There is a high incidence of sexual dysfunction among patients. Treatment of hyperprolactinemia is effective in correcting prolactin levels, but does not improve erectile dysfunction or premature ejaculation. Therefore, treating hyperprolactinemia is not an overall effective treatment for erectile dysfunction in these patients.     

Breast cancer in a patient with prolactinoma

Although the role of prolactin in the initiation and promotion of mammary carcinoma has been proved in animal experiments, a similar effect of hormone in the development of human mammary tumor has not been clearly demonstrated. If hyperprolactinemia is a significant factor in the initiation and promotion of human breast carcinoma, the incidence of mammary carcinoma in patients with hyperprolactinemia, with or without prolactinomas, might be higher than in control populations, but this relationship has never been documented. We present this case to stimulate awareness of the possibility so the condition will be investigated further.     

Relapse of hyperprolactinemia after transsphenoidal surgery for microprolactinoma: lessons from long-term follow-up

OBJECTIVE: The long-term results of transsphenoidal surgery for microprolactinoma, with particular reference to the question of permanence of relapse of hyperprolactinemia after biochemical cure, are examined. METHODS: Patients whose operations were performed in the city of Glasgow, Scotland, by one neurosurgeon (GMT) have been followed up for between 15 and 21 years after surgery was performed. RESULTS: Of a cohort of 44 patients with confirmed microprolactinoma at the time of surgery, 8 patients (18.2%) who experienced recurrent hyperprolactinemia postoperatively continued to be monitored. Selective hypophysectomy resulted in normal prolactin levels in all patients initially. Relapse occurred at 2 to 10 years (mean, 5.3 yr) postoperatively, but was permanent in only two patients (4.5%). Of the remaining six patients (13.6%), four (9.1%) became normoprolactinemic after 6 or 7 years' recurrence, and two (4.5%) are now only marginally hyperprolactinemic (prolactin >500 but <700 mU/L) at 15 and 18 years after transsphenoidal hypophysectomy. CONCLUSION: The recurrence of hyperprolactinemia after transsphenoidal surgery for microprolactinoma is not necessarily a permanent feature and does not inevitably indicate operative failure.