Cases reported "Prolactinoma"

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1/77. Rapid enlargement and recurrence of a preexisting intrasellar craniopharyngioma during the course of two pregnancies. Case report.

    Enlargement of preexisting pituitary adenomas during pregnancy is well documented, but this phenomenon is unusual for nonendocrine pituitary tumors such as craniopharyngiomas. Only six cases of craniopharyngioma have been reported as presenting during pregnancy. The authors describe a 19-year-old woman who presented with amenorrhea and galactorrhea caused by an intrasellar mass. Seven months later, when she was 20 weeks pregnant, the patient developed sudden visual dysfunction. Emergency transsphenoidal surgery was performed to restore visual function, and the tumor was found to be a craniopharyngioma. The patient had spontaneous labor and delivered a healthy infant at term. The tumor recurred 4 years later, during her second pregnancy, and was again entirely removed via a second transsphenoidal approach. She again had a normal term delivery. During the 5-year follow-up period she has demonstrated no endocrinological or visual dysfunction. Control magnetic resonance images have revealed no recurrence of the tumor. The transsphenoidal approach seems to be the safest procedure to use during pregnancy to achieve an immediate optic nerve decompression and to preserve pituitary function.
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2/77. Pituitary adenoma with neuronal choristoma: a report of two rare cases.

    Two rare cases of pituitary adenoma with neuronal choristoma are described. Both patients were female and presented with features of acromegaly with elevated growth hormone and prolactin levels. Radiologically, both lesions were predominantly intrasellar in location with extension into suprasellar region, but hypothalamus was not involved. Histopathological examination revealed a mixture of chromophobe pituitary adenoma cells and neuronal cells. In both cases, the adenoma component was positive for growth hormone and prolactin. Interestingly, immunopositivity for alpha-subunit, cytokeratin and prolactin was seen in the adenoma and neuronal cells in one case. Our findings support the hypothesis that the neuronal cells possibly arise from adenoma cells as a result of metaplasia.
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3/77. pituitary apoplexy following metastasis of bronchogenic adenocarcinoma to a prolactinoma.

    A 42-year-old house wife presented with worsening headaches over 6 months in the absence of visual symptoms or symptoms suggestive of focal neurology. She was a life-long smoker. Systems review was unremarkable apart from secondary amenorrhoea and galactorrhoea of 6 months duration. Her serum prolactin was found to be 620 mU/l (60-400), FT4 12.6 nmol/l (9.8-23.1), TSH 1.38 mU/l (0.35-5.5), oestradiol < 73 pmol/l, LH and FSH of 4.4 and 12.6 mIU/l, respectively. She was on bromocriptine. A presumptive diagnosis of pneumonia, based on pyrexia and CXR findings, was made and she was started on IV antibiotics. Two days later she developed meningism and deterioration of conscious level. (Lumbar puncture results: no organisms, 312 neutrophils and 164 lymphocytes). CT scan revealed a 2.5-cm pituitary adenoma, with suprasellar extension. A repeat hormonal profile revealed FSH 1.4, LH < 0.3 mU/l, oestradiol < 73 pmol/l, prolactin 488 mU/l (60-400), and low random cortisol at 29 nmol/l. T1-weighted MRI revealed a large pituitary mass with evidence of haemorrhage. The patient subsequently underwent a transsphenoidal exploration with resection of the pituitary lesion. Whilst awaiting the histopathology results, CT of chest revealed a 1. 5-cm diameter rounded well defined density in the right lower lobe associated with hilar, pre- and right para-tracheal lymphadenopathy. The histopathology of the pituitary lesion, obtained piecemeal, revealed fragments of fibrous tissue infiltrated by sheets of acidophilic prolactin-positive cells, in keeping with a prolactinoma. In addition, other fragments with blood clot included highly atypical epithelial cells with mitotic figures. These were negative for prolactin but showed HMFG-and CEA-positivity, excluding them from a pituitary lineage. Transbronchial biopsy revealed moderately differentiated adenocarcinoma, with evidence of lymphatic spread. The overall conclusion was of bronchogenic adenocarcinoma, metastasizing to a prolactinoma and complicated by apoplexy.
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4/77. Gangliocytoma masquerading as a prolactinoma. Case report.

    The authors describe the case of a 36-year-old man who presented with bitemporal hemianopsia and a serum prolactin concentration of 1440 ng/ml. magnetic resonance imaging of the pituitary revealed a presumed macroadenoma with suprasellar and temporal lobe extension. Although the patient's prolactin level was lowered to 55 ng/ml by bromocriptine therapy, no tumor shrinkage occurred. Fourteen months later, progression of visual field defects necessitated transsphenoidal resection, which was incomplete. Immunocytochemical analysis of the biopsy tissue was positive for prolactin and, in view of the clinical picture, more detailed analysis was not performed. External-beam radiotherapy was given 2 years later because of enlargement of residual tumor. Subsequently, despite a fall in the serum prolactin concentration to less than 20 ng/ml in response to the course of bromocriptine, the mass displayed further extension into the temporal lobe. Nine years after the patient's initial presentation, he underwent transfrontal craniotomy for sudden deterioration in visual acuity caused by hemorrhage into the mass. No adenohypophyseal tissue was identified in the resected tissue. The mass was composed of dysplastic neurons that were strongly immunoreactive for synaptophysin and neurofilament (indicating neural differentiation) and prolactin. review of the original biopsy specimen indicated that the prolactin-positive cells had striking neuronal morphological characteristics. The final diagnosis in this case is prolactin-secreting gangliocytoma. Although exceedingly rare, this disease must be added to the differential diagnosis in cases of "prolactinoma" when bromocriptine therapy is followed by a marked decline in serum prolactin that is not accompanied by significant tumor shrinkage. Furthermore, in such instances, consideration should be given to "obtaining a biopsy sample prior to electing for radiotherapy.
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5/77. mucocele-like formation leading to neurological symptoms in prolactin-secreting pituitary adenomas under dopamine agonist therapy.

    BACKGROUND: mucocele-like formation associated with pituitary adenomas, to the best of our knowledge, has been paid little attention. We report three adult male patients with a mucocele-like formation that developed behind the tumor and led to neurological symptoms in prolactin-secreting pituitary adenomas (prolactinomas) under dopamine agonist therapy. CLINICAL PRESENTATION: Three adult male patients with prolactinomas developed hyperprolactinemia and new neurological symptoms during dopamine agonist treatment. In each case, the pathogenesis of these symptoms was due in part to a mass enlargement with development of a mucocele-like formation behind a prolactinoma. In our patients, a prolactinoma with a suprasellar extension originally filled the sphenoid sinus. When dopamine agonist therapy became ineffective, new symptoms, such as progressive visual impairment other than typical hemianopsia or headache, developed and mass enlargement was found on MRI. MRI demonstrated two different components: an enhancing prolactinoma and a nonenhancing mucocele-like formation behind the tumor. Two patients had compression of the optic nerves by a mass. Transnasal removal of mucoceles and adenomas led to resolution of the neurological symptoms. CONCLUSION: Early suspicion of a mucocele-like formation under dopamine agonist therapy for prolactinomas is important in order to avoid a delay in surgery, because a change in medical treatment will be ineffective.
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6/77. Giant prolactinoma presented as unilateral exophthalmos in a prepubertal boy: response to cabergoline.

    We report the case of a giant prolactinoma in a 7-year-old boy, which was complicated by unilateral exophthalmos. The initial levels of prolactin (PRL) were about 80,000 microU/ml. Treatment with cabergoline (CAB) resulted in rapid normalization of serum PRL (6 weeks after initiation of treatment) and reduction of tumor size. In particular, magnetic resonance imaging (MRI), which was done 2.5 months after the patient was put on CAB, revealed tremendous improvement with a decrease in the size of the tumor which now showed no extrasellar extension. Subsequent MRI studies demonstrated further improvement. exophthalmos, anisocoria and visual fields improved. In summary, this patient represents the first report of the therapeutic use of CAB as the primary mode of treatment in a 7-year-old boy with infiltrative giant prolactinoma complicated by unilateral exophthalmos. It is a noninvasive treatment that can preserve and restore vision, as well as pituitary function, and is preferable to surgery or radiation in the treatment of prolactin-secreting macroadenoma in childhood and adolescence.
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7/77. Osteopenia in children and adolescents with hyperprolactinemia.

    Three patients with hyperprolactinemia due to pituitary adenomas (two patients) or empty sella (one patient) and osteopenia are described. Their ages at presentation ranged from 8 to 17 years. Each patient was treated with cabergoline. serum prolactin levels became normal in all patients within one month. bone density and pubertal stage improved after 12 months of treatment.
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8/77. From macroprolactinoma to concomitant ACTH-PRL hypersecretion with Cushing's disease.

    Multiple pituitary hormone hypersecretions have been already described, but the combination of PRL and ACTH excess is rare. This report deals with a 42-yr-old woman affected by macroprolactinoma (PRL 12,720 microg/l, huge tumor with extrasellar extension at imaging). After one year on dopaminergic treatment causing PRL normalization and tumor shrinkage, she developed hypercortisolism (UFC 1,000 microg/24 h, ACTH 200 ng/l). Cushing's disease was diagnosed. After neurosurgery (at immunocytochemistry mixed ACTH-PRL adenoma was shown) hypercortisolism remitted, whereas pathological hyperprolactinemia with tumor remnant in cavernous sinus persisted and hypopituitarism developed. The patient reported seems atypical for the following reasons: 1) the concomitant PRL and ACTH hypersecretions; 2) the clinical presentation with hypercortisolism following hyperprolactinemia; 3) the surgical cure of hypercortisolism with persisting hyperprolactinemia.
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9/77. Endoscopic endonasal hemisphenoidotomy for resection of pituitary lesions confined to the sella: report of 3 cases and technical note.

    The authors report use of a minimally invasive endoscopic procedure, unilateral endonasal hemisphenoidotomy, for removal of lesions contained in the sella. The entire procedure was performed through a single nostril with the use of an endoscope. A unilateral endonasal hemisphenoidotomy (1.5 cm x 1.5 cm) was performed and was sufficient to expose the sellar floor for successful removal of adenomas confined to the sella in three patients. Neither outfracturing the midline septum nor exposure of the opposite sphenoid ostium was necessary for adequate visualization, tumor exposure, or instrument maneuverability. There was, however, a learning curve required in order to become facile and efficient with the equipment. All lesions were completely resected. When compared to a bilateral endoscopic endonasal sphenoidotomy as practiced by us, the operative time was reduced and the length of stay was 1-2 days. There was less operative trauma, patients appeared to experience less pain immediately postoperatively, and their satisfaction was very high. In conclusion, for resection of this group of intrasellar tumors, the hemisphenoidotomy procedure proved to be less invasive and traumatic, more simple, and faster than the standard bilateral endoscopic sphenoidotomy.
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10/77. cerebrospinal fluid rhinorrhea associated with untreated prolactinoma--case report.

    An 80-year-old female presented with non-traumatic cerebrospinal fluid (CSF) rhinorrhea due to untreated prolactinoma, with simultaneous development of bilateral leg pains and gait disturbance due to lumbar canal stenosis. neuroimaging showed an intrasellar mass extending into the sphenoid sinus, right cavernous sinus, and suprasellar cistern. Computed tomography cisternography clearly showed the CSF pathway through the tumor. Subtotal removal of the tumor and reconstruction of the sellar floor via a transsphenoidal approach resulted in resolution of the CSF rhinorrhea. Both the invasive features and/or spontaneous shrinkage of the tumor might have created the abnormal CSF pathway. The clinical manifestation of lumbar canal stenosis might be triggered by such profound CSF leakage.
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