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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine cases of symptomatic Rathke's cleft cyst are reported. Their most frequent signs and symptoms included headache, chiasmal syndrome and hypopituitarism, while one of the cases developed a sudden onset of headache and vomiting following diabetes insipidus. Endocrinological findings showed a decreased ACTH, gonadotropin and growth hormone more frequently while there were 2 cases of hyperprolactinemia and 1 case of diabetes insipidus. In a neuroradiological examination, a plain skull X-ray showed 5 cases of ballooning of the sella turcica, and a CT scan demonstrated a low to high density of the cyst and 2 cases of marginal enhancement of the cyst. MRI mostly demonstrated a well delineated mass at the sella extending mostly into the suprasellar region and a low to high intensity of the cyst in the T1-weighted image. Two cases were marginally enhanced after gadolinium DTPA administration. The pathological examination, done on 6 cases, showed either single or multiple layers of the epithelium which were mostly ciliated. The epithelium was positive in PAS and Alcian blue in all cases and a histochemical examination showed 3 cases to be positive in EMA and 2 cases positive in CEA. A resection of the cyst wall and an opening of the cyst is thus recommended in symptomatic cases. Therefore, the transsphenoidal approach should be the choice of treatment in an intra- and suprasellar extension of the cysts with sellar enlargement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Symptomatic Rathke's cleft cyst: a clinicopathologic study of 9 cases]. 816 47

38 women aged between 23 and 42 years had secondary amenorrhea and clinical hypoesterogenism as assessed by the failure to have a withdrawal bleed in response to a progestin. All women were initially treated with up to 7.5 mg bromocriptine but it was discontinued because of failure to lower serum prolactin (PRL) or intolerance. Each woman had a basal computerized tomography (CT) scan before estrogen (E) replacement therapy, which was repeated after 6 months, and then yearly. The clinical course was monitored at 3-month intervals for the first year and the yearly. The patients were classified by CT scan as having either idiopathic hyperprolactinemia (19 patients), microadenoma (18 patients), or macroadenoma (1 patient). All patients have been followed with continuous exogenous E therapy for 2 to 6 years. The serum PRL was measured as a single random value by a double antibody homologous radioimmunoassay. 29 received physiological replacement with conjugated E (.625 mg, Premarin) from days 1 to 25 of each month, and added medroxyprogesterone acetate (10 mg, Provera) from days 16 to 25 of each month for 4.0 +or- 1.2 years. There was a significant decrease of serum PRL, and monthly withdrawal bleeding occurred in all women with alleviation of E-deficiency symptoms. 9 patients were treated with OCs for 2.0 +or- .8 years. There was a downward trend in the serum PRL without statistical significance. With abnormal CT scans, 6 patients with microadenomas had a decrease in size, whereas the remainder were unchanged. The patient with the macroadenoma (patient 29) had an onset of headaches after 4 months of therapy, but there was no change in the size of the tumor. The patients with normal CT scans did not show any change. The microadenomas in 2 of 3 women decreased in size. In summary, E-replacement therapy may be given to women with E deficiency, despite the presence of pathological hyperprolactinemia, as the induction of rapid growth of an underlying pituitary adenoma was not confirmed.
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PMID:The safety of physiological estrogen plus progestin replacement therapy and with oral contraceptive therapy in women with pathological hyperprolactinemia. 845 75

Granular cell tumours of neurohypophysis are rare. These tumours are more often encountered as incidental autopsy findings seen in up to 17% of unselected adult autopsy cases. There are few reports of parasellar granular cell tumours large enough to cause symptoms. We present three cases of neurohypophysis granular cell tumour and a review of the literature. In one patient, the asymptomatic granular cell tumour was incidentally discovered at surgical removal of a corticotroph microadenoma. The remaining 2 patients had a symptomatic tumour which caused neurological symptoms such as visual disturbance and headaches and endocrine disorders such as hypopituitarism or hyperprolactinaemia. In these 2 cases, computerized tomography showed a well-circumscribed, contrast-enhanced, intrasellar and suprasellar mass. Magnetic resonance imaging demonstrated an isointense gadolinium-enhanced mass in T1-weighted images. Transsphenoidal partial resection was performed and histology was interpreted as a granular cell tumour. The immunohistochemical study was positive for glial fibrillary acidic protein (GFAP) and neuron specific enolase (NSE) in 1 of the 2 tumours and positive for S100 protein and vimentin in both tumours but negative for CD68. The histogenesis of neurohypophysis granular cell tumours is still controversial but ultrastructural and immunohistochemical studies support the theory that they may arise from pituicytes, the glial cells of neurohypophysis. Management of these benign, slow-growing, tumours is based mainly on neurosurgical resection. Data from the literature do not support a beneficial effect of postoperative radiation therapy on postoperative recurrences.
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PMID:[Granular cell tumors. Rare tumors of the neurohypophysis]. 854 14

A case of pituitary adenoma which had progressed from subclinical pituitary apoplexy to subacute pituitary apoplexy on the occasion of cerebral angiography is reported. A 29-year-old man, complaining of bitemporal hemianopsia, was admitted to our department. Plain skull X-p revealed enlargement and double floor of the sella turcica. No abnormal calcification was revealed. CT demonstrated an isodensity mass with a diameter of 4 x 4 cm, and with ring enhancement in the suprasellar region. The mass extended from the intrasellar region to the suprasellar region and had a signal of high intensity on T1-weighted images. Endocrinological examination revealed hyperprolactinemia with a serum level of 422 ng/ml and normal reaction of anterior pituitary hormones. On 3rd March, digital subtraction angiography with 5F catheter was performed with the patient under sedation. The contrast medium was ioxaglic acid (Hexabrix 320). A volume of 6 ml with a speed of 4 ml per second was injected for the internal carotid angiogram. A total volume of 60 ml was used. Serum saline with 10 unit per ml of heparin sodium was also used for flushing. During angiography, the patient's blood pressure was 125/60-115/60mm Hg. DSA revealed upward displacement of the proximal portion of the anterior cerebral artery, pocket formation, and staining of the tumor capsule. Six hours later, he complained of retroorbital headache. Next morning, he noticed complete lack of left visual acuity. On 7th March, right visual acuity degenerated to blindness. CT revealed that the mass had increased its density. With bifrontal osteoplastic craniotomy, the tumor with marked intratumoral hemorrhage was resected. Its histology was chromophobe adenoma. The patient's right visual acuity improved rapidly. On the occasion of cerebral angiography, we could observe that subclinical pituitary apoplexy deteriorated to subacute pituitary apoplexy. Rosenbaum postulated that injection of contrast media increased intravascular pressure leading to pituitary apoplexy. At present, we cannot postulate increased intravascular pressure with 5F catheter and DSA. We cannot rule out that, with underlying subclinical pituitary apoplexy, hemorrhagic infarction due to contrast media and the anti-coagulate effect of heparin sodium accelerated the intratumoral bleeding. Subclinical pituitary apoplexy is a vulnerable state because of its aggravation to symptomatic apoplexy under mild stress. We emphasize that an operation should be performed as early as possible in the case of subclinical pituitary apoplexy.
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PMID:[A case of pituitary adenoma progressing to pituitary apoplexy on the occasion of cerebral angiography]. 869 76

We report the case of a patient with Klinefelter's syndrome who developed a prolactin (PRL)-secreting tumor. The patient developed headaches, visual alterations and also symptoms of hypogonadism despite appropriate testosterone (T) replacement therapy. The diagnosis of hyperprolactinemia was then suspected. The laboratory findings confirmed the hypothesis, showing high levels of serum PRL. The patient was initially treated with oral bromocriptine, and afterwards with the injectable form. There was a marked decrease in PRL levels and in tumor size. Although some neoplasms, like breast carcinoma and germ cell tumors, are known to occur more frequently in patients with Klinefelter's syndrome, an association with PRL-secreting tumor has not been reported yet. In conclusion, symptoms of hypogonadism in patients with Klinefelter's syndrome receiving appropriate T replacement therapy can suggest the presence of hyperprolactinemia.
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PMID:A prolactin-secreting tumor in a patient with Klinefelter's syndrome: a case report. 886 6

Prolactinoma, a benign tumor originating from the lactotroph cells of the anterior pituitary, is responsible for signs and symptoms related to both hypersecretion of prolactin and tumor mass. Hyperprolactinemia frequently causes menstrual cycle disturbances, galactorrhea and infertility in women, sexual disorders in men. Microadenomas, characterized by a largest diameter less than 10 mm, may induce frontal headaches, and macroadenomas (more than 10 mm in diameter) may also impair visual function through chiasma compression. Treatment modalities include dopamine agonist therapy such as bromocriptine which allows normalization of prolactin levels, restoration of gonadal functions and tumor shrinkage in most cases. In microadenomas a definitive cure may be achieved by transsphenoidal total selective adenomectomy.
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PMID:[Prolactin-secreting adenoma]. 888 Nov 62

Two cases of hyperprolactinaemia and one case of depression caused by oxetorone are described. These rare side effects are probably related to the pharmacological properties of the drug.
Cephalalgia 1996 Dec
PMID:Hyperprolactinaemia and depression induced by oxetorone. 898 Aug 59

This study was aimed at investigating the absorption of nasally administered bromocriptine and its effect on serum prolactin level. Fifteen physiologically hyperprolactinemia women who had asked to discontinue breast feeding received a single nasal spray administration of 0.8 mg bromocriptine. Serum prolactin levels were measured by radioimmunoassay at 30 and 15 min before drug administration, at the time of administration and at 15, 30, 60, 120, 240, 480 and 720 min after administration; bromocriptine was radioimmunoassayed in only five of the patients from time 0 to 720 min after administration. Serum bromocriptine levels increased rapidly after administration, reached a maximum at 120 min and thereafter declined slowly over the subsequent 10 h. As the bromocriptine level increased there was a decline in the serum prolactin level. The first significant decline in serum prolactin level compared with the baseline level occurred at 30 min after administration and the level continued to decrease significantly until time 120 min. Four hours after administration the mean serum prolactin level was within the normal assay range. The maximum decline in serum prolactin level was reached at 720 min after administration. Correlation analysis between serum bromocriptine and prolactin concentrations yielded a significant negative value between times 0 and 120 min after administration. There was no significant change in mean orthostatic systolic or diastolic blood pressure or in mean heart rate. Only one patient complained of headache and dizziness; another experienced mild transient nausea, and none had vomiting. Ten patients (66.67%) reported light endonasal burning and an unpleasant taste which subsided after a few minutes; no patient showed nasal irritation at nasal examination. In conclusion, nasal administration of 0.8 mg bromocriptine was effective in reducing the serum prolactin level for more than 12 h after administration without inducing significant side-effects.
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PMID:Nasal spray administration of bromocriptine: pharmacology and effect on serum prolactin level in puerperal women. 903 65

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.
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PMID:A study of the clinical differences between women and men with hyperprolactinemia. 903 66

Cabergoline (CAB), a new, potent, and long-lasting PRL-lowering agent, was shown to be effective in tumoral hyperprolactinemia. The aim of this study was to investigate the effectiveness of CAB in patients with prolactinoma proven to be resistant to bromocriptine (BRC) and quinagolide (CV 205-502). Twenty-seven patients (19 macro- and 8 microprolactinomas) were treated with CAB at a weekly dose of 0.5-3 mg for 3-22 months. All patients were previously shown to be resistant to BRC, and 20 of them were resistant to CV 205-502 as well. Basal serum PRL levels before CAB treatment ranged from 108-3500 micrograms/L in macroprolactinomas and from 64-205 micrograms/L in microprolactinomas. Gonadal failure was present in all patients, whereas symptoms of tumor expansion, such as visual field defects and headache, were present in 10 of 27 patients. Eight macroprolactinomas had previously undergone surgery and/or radiotherapy. CAB treatment normalized serum PRL levels in 15 of 19 macroprolactinomas and in all 8 microprolactinomas. In 3 of the remaining 4 patients it caused a notable decrease in prolactinemia (89%, 80.5%, and 68.7% of the baseline). Only 1 patient was withdrawn from CAB therapy after 3 months at the weekly dose of 2 mg due to the absence of any significant clinical, hormonal, or radiological improvement. Gonadal function was restored in 18 of 27 patients, galactorrhea disappeared in 5 of 6 women, and headache improved in 7 of 8 patients. A significant tumor shrinkage was detected by computed tomography and/or magnetic resonance imaging in 9 macroprolactinomas and 4 microprolactinomas. CAB was well tolerated by all patients, except 6 who referred slight and short-lasting nausea, postural hypotension, abdominal pain, dizziness, and sleepiness at the beginning of treatment. In particular, CAB was well tolerated by 19 patients previously shown to be poorly tolerant to BRC and CV 205-502. In conclusion, CAB may represent, at the moment, the only successful therapy for prolactinoma-bearing patients resistant to BRC and CV 205-502, as it normalized PRL levels in 22 of 27 patients, reduced tumor size in 13 of 27 patients, and improved clinical symptoms in 25 of 27 patients in the present study.
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PMID:Prolactinomas resistant to standard dopamine agonists respond to chronic cabergoline treatment. 925 67


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