Cases reported "Hyperprolactinemia"

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1/7. Secondary infertility as early symptom in a man with multiple endocrine neoplasia-type 1.

    multiple endocrine neoplasia-type 1 (MEN1) is an autosomal dominant familial cancer syndrome characterized by parathyroid hyperplasia, pancreatic endocrine tumours and pituitary adenomas. Here, we report a patient with a history of insulinoma who developed secondary infertility as a further symptom of the disease. When he was first examined at the age of 36 years, he complained of weakness, reduced libido and impotence. Laboratory evaluation revealed non-obstructive azoospermia and hyperprolactinaemia. In contrast to sexual activity and serum prolactin, semen quality did not significantly respond to bromocriptine therapy. During follow-up, a growing pituitary adenoma caused acromegaly with elevated serum concentrations of growth hormone, insulin-like growth factor 1 (IGF-1), and prolactin. After microsurgery of the tumour at the age of 44 years, sperm concentration persistently increased up to 5.6 x 10(6)/ml. In accordance with the clinical diagnosis of MEN1, dna sequencing revealed a mutation in exon 2 of the menin gene which results in a truncated, inactive protein product. In conclusion, MEN1 with pituitary lesions may cause severe hypogonadism and infertility. Both hyperprolactinaemia and overproduction of growth hormone and IGF-1 seem to be involved in testicular dysfunction in the present case. The possible role of menin in the testis, however, remains to be elucidated.
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2/7. Severe erectile dysfunction is a marker for hyperprolactinemia.

    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. In addition, it is widely thought that sexual desire problems are a good clinical marker for HP and/or low testosterone in men with ED. Within a 15-month period, 844 consecutive PRL and sexual hormone determinations were conducted in men at the Kingston General Hospital. Of these patients, 138 were comprehensively evaluated at the first visit for ED and completed the International Index of Erectile Function (IIEF). In the 138 patients, 2.2% had severe hyperprolactinemia (>35 ng/ml), within the range of 1-5% previously reported. No correlation between initial prolactin value and the sexual desire domain or the erectile function domain (EFD) of the IIEF was found for this population. However, all cases of severe HP were found to occur in men who scored less than 10 in the EFD of the IIEF. Low libido is widely accepted as a marker of HP. In this study, HP was found in patients not reporting major problems with a desire disorder. Clinically significant HP may be reliably found with routine biochemical evaluation and in this series was not detected in patients with EFD scores above 10. A routine PRL measurement is inexpensive and early detection of a serious and treatable disease may afford greater therapeutic success.
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3/7. Switch to quetiapine in antipsychotic agent-related hyperprolactinemia.

    Novel antipsychotics (clozapine, risperidone, olanzapine, quetiapine) are effective in treating psychotic symptoms, also in neurological disease. hyperprolactinemia is a side effect related to antipsychotics that can cause galactorrhea, gynecomastia, amenorrhea, anovulation, impaired spermatogenesis, decreased libido and sexual arousal, impotence, and anorgasmia, consequent to removal of tonic dopaminergic inhibition of prolactin secretion via hypothalamic dopaminergic receptor blockade in the tuberoinfundibolar tract. hyperprolactinemia occurs more frequently during treatment with risperidone and olanzapine compared with clozapine and quetiapine. The therapeutic algorithm to antipsychotic-relatedhyperprolactinemia is the following: reduction in antipsychotic dose, addition of cabergoline, bromocriptine, amantadine, and/or switch to another antipsychotic. We propose switching to quetiapine in symptomatic hyperprolactinemia related to antipsychotics and describe five cases.
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4/7. testosterone replacement-induced hyperprolactinaemia: case report and review of the literature.

    Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement. However, very little is known about the effect of testosterone on prolactinomas. We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma. On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095). Furthermore, imaging studies suggested the possibility of tumour re-growth after testosterone therapy. We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary. This was supported by the increase in oestradiol levels after testosterone replacement, although statistical significance was not achieved due to the availability of only a few data points. This case highlights the need to be aware of testosterone-replacement-induced hyperprolactinaemia, an under-recognized complication of androgen replacement in this setting. The use of aromatase inhibitors together with testosterone-replacement therapy or the use of non-aromatizable androgens might be indicated in such patients. Taken together, this report and previous studies show that dopamine agonists apparently do not suppress the hyperprolactinaemia induced by testosterone replacement.
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5/7. 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.
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6/7. amantadine in the treatment of neuroendocrine side effects of neuroleptics.

    An open-label reversal drug study was undertaken on 10 neuroleptic-treated schizophrenic inpatients to assess the impact of amantadine hydrochloride on presumed prolactin-mediated neuroendocrine side effects. Measures were conducted across 7 weeks, including a 2-week neuroleptic baseline, a 3-week neuroleptic-plus-amantadine phase, and a 2-week return to the baseline regimen. Significant reduction with amantadine was observed on all six indices of neuroendocrine side effects: serum prolactin levels, body weight, gynecomastia/galactorrhea, breast tenderness, decreased libido, and amenorrhea. Improvement on these parameters was noted for as many as nine or all 10 patients, while in no cases was there worsening. In terms of motor and clinical effects, significant diminution of extrapyramidal and psycho-pathological symptoms was also achieved during this phase. The results suggested that amantadine may be beneficial for the treatment of neuro-endocrine side effects of antipsychotic medication owing to its ability to reverse neuroleptic-induced hyperprolactinemia.
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7/7. Sexual dysfunction secondary to cocaine abuse in two patients.

    hyperprolactinemia and sexual dysfunction occurred in 7 of 10 chronic cocaine users. Two of these 7 patients who underwent rehabilitation for cocaine abuse and developed hyperprolactinemia and decreased libido are described. One patient developed galactorrhea. These adverse effects were reversed by bromocriptine. The pathophysiology of cocaine abuse and the central dopaminergic influence on sexual function are discussed.
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