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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pituitary stimulation tests are widely used to explore hypophyseal adenomas. There are few disadvantages, although a few cases of pituitary necrosis have been published. We report a new case with a dramatic outcome. A 30-year-old man with clinical signs of acromegalia and major visual disorders was found to have a voluminous macro-adenoma of the pituitary gland. Thirty minutes after beginning the stimulation test, the patient complained of major headache and experienced persistant vomiting for several hours. Brain magnetic resonance imaging the next day did not reveal evidence of pituitary necrosis. Sudden onset coma occurred one hour later. The CT scan demonstrated hemorrhagic necrosis of the adenoma. The patient died despite emergency surgery. Due to the risk of hemorrhagic necrosis of a pituitary adenoma, baseline assays may be sufficient for diagnosis in patients with clinical signs highly suggestive of pituitary oversecretion, especially when a voluminous tumor is involved. Rigorous clinical surveillance is required after stimulation tests.
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PMID:[Fatal hemorrhagic necrosis of pituitary macro-adenoma after a stimulation test]. 895 74

We describe a 72-year-old woman with a history of acute myeloid leukemia who developed pituitary apoplexy associated with thrombocytopenia secondary to chemotherapy. She presented with new onset severe headache, nausea, vomiting and blurred vision. Initial physical examination was unremarkable. CT scan of the head was initially negative. Upon admission for further work up, She developed a high-grade fever, hypotension and obtundation. Subsequent physical examination revealed bitemporal visual fields defects and decreased visual acuity. Repeat imaging of head revealed a hemorrhagic pituitary mass compressing the optic chiasm. Laboratory results were compatible with the diagnosis of pan-hypopituitary syndrome. She received high dose steroids and was transferred for transnasal sphenoidotomy decompression surgery. The visual defects improved postoperatively. A literature review of Pituitary apoplexy is presented. Pituitary apoplexy secondary to thrombocytopenia has never been reported.
Pituitary 2000 Oct
PMID:Pituitary apoplexy in a patient with acute myeloid leukemia and thrombocytopenia. 1114 94

A case of isolated ACTH deficiency who developed autoimmune-mediated hypothyroidism and still showed impaired water diuresis during glucocorticoid replacement therapy is reported. A 45-year-old woman was initially admitted for nausea, vomiting, and general malaise. Her serum sodium and plasma osmolality, ACTH and cortisol values were low, but her urine osmolality was high. Other pituitary hormone levels, thyroid hormone levels, and a computed tomogram of the pituitary gland were normal. The patient was treated with hydrocortisone and followed in the outpatient clinic; however, she was lost to follow up 18 months after admission. Three years later she presented with hypoglycemia and hyponatremia. Her serum or plasma ACTH, FT3, FT4, cortisol levels were low and her serum TSH level was high. Pituitary stimulation tests revealed a blunted response of ACTH to CRH and an exaggerated response of TSH to TRH. Plasma ADH was inappropriately high, and a water-loading test revealed impaired water diuresis and poor suppression of ADH. Although ADH was suppressed, impaired water diuresis was observed in the water loading test after hydrocortisone supplementation. Thyroxine supplementation completely normalized the water diuresis. Her outpatient clinic medical records revealed a gradual increase in TSH levels during follow up, indicating that she had developed hypothyroidism during glucocorticoid replacement therapy. The hyponatremia on the first admission was due to glucocorticoid deficiency, whereas the hyponatremia on the second admission was due to combined deficiencies of glucocorticoid and thyroid hormones.
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PMID:A case of isolated ACTH deficiency who developed autoimmune-mediated hypothyroidism and impaired water diuresis during glucocorticoid replacement therapy. 1122 40

It is widely accepted that glucagon stimulates GH, ACTH and cortisol release in humans, though the mechanisms underlying these effects are unclear. Aim of the present study was to evaluate the stimulatory effect of intramuscolar (i.m.) and intravenous (i.v.) glucagon (GLU) administration on ACTH, cortisol (F) and GH release in normal adult subjects and to compare its effect on hypothalamo-pituitary adrenal (HPA) axis with that of hCRH. To this goal, in 6 normal young women (26-32 yrs, 50-58 kg) we studied the ACTH and F responses to either i.m. or i.v. GLU (1 mg, approximately 0.017 mg/kg in subjects of 54.1 +/- 1.6 kg) administration as well as to i.v. hCRH (2.0 micrograms/kg) or placebo administration. The GH and glucose variations after GLU administration were also studied. I.v. GLU did not modify the spontaneous decrease of ACTH and cortisol levels observed after placebo. Conversely, i.m. GLU elicited clear-cut ACTH and F responses (peak vs baseline, mean +/- SEM: 53.0 +/- 15.2 vs 19.0 +/- 1.5 pg/ml, p < 0.05 and 222.3 +/- 23.8 vs 158.3 +/- 7.0 micrograms/l, p < 0.05) which were higher than those recorded after hCRH (28.1 +/- 4.6 vs 17.4 +/- 3.1 pg/ml, p < 0.02 and 182.7 +/- 22.8 vs 114.8 +/- 12.3 micrograms/l p < 0.02), though this difference did not attain statistical significance. Also GH rise was recorded after i.m. but not after i.v. GLU administration (11.6 +/- 3.4 vs 3.3 +/- 0.7 micrograms/l, p < 0.05). Thirty min after both i.v. and i.m. GLU administration glucose levels showed a similar increase followed by similar decrease. The intramuscular administration of GLU induced negligible side-effects in some subject (mild and transient nausea) which, on the contrary, were clear in all subjects after its intravenous administration (nausea, vomiting, tachycardia). In conclusion, glucagon "per se" is not an ACTH, cortisol and GH secretagogue. After intramuscular administration glucagon is a stimulus of HPA axis at least as effective as hCRH. The mechanisms underlying the ACTH, cortisol and GH responses to i.m. glucagon unlikely include glucose variations or stress.
Pituitary 2000 Nov
PMID:Glucagon is an ACTH secretagogue as effective as hCRH after intramuscolar administration while it is ineffective when given intravenously in normal subjects. 1138 81

We report a pregnant woman with a large macroprolactinoma successfully treated with cabergoline after a suboptimal response to bromocriptine. A 7 week pregnant woman with a history of a prolactinoma presented to the endocrine clinic with the complaints of headaches and nausea. She had a prolactin level of 65 microg/L 1 1/2 weeks following her last menstrual period. Bromocriptine was discontinued at 6 weeks gestation when pregnancy was confirmed. A PRL concentration was 1899 microg/L (non-pregnant normal range 1.39-24.20 microg/L, the mean peak levels during pregnancy reported from the literature are 200-210 microg/L) at 7 weeks gestation, and a repeat was 2197 microg/L. An MRI showed a 3 x 2.2 x 2.5 cm seller mass abutting the optic chiasm and displacing the optic nerves superiorly; the visual field testing was normal. Bromocriptine was reinitiated and the patient responded initially with decreasing headaches and declining PRL concentrations to 1488 microg/L at 15 weeks gestation. However, PRL increased to 1836 microg/L at 16 weeks and remained elevated despite bromocriptine 2.5 mg three times a day; in addition, she complained of severe nausea, vomiting, and persistent headaches. Cabergoline was added at 18 weeks gestation. PRL decreased dramatically from 1710 to 859 microg/L in 1 week, and to 488 microg/L within 4 weeks. A repeat MRI showed more than 30% reduction in tumor size. Bromocriptine was discontinued at 24 weeks gestation; she was maintained on cabergoline 0.5 mg twice a week without complaints. PRL levels ranged from 190 to 278 microg/L during the last 10 weeks of pregnancy. She had a C-section electively at 37 weeks gestation and delivered a healthy baby. Management options in this patient and during pregnancy are discussed.
Pituitary 2001 Aug
PMID:Successful treatment of a large macroprolactinoma with cabergoline during pregnancy. 1213 91

A thirty-eight year-old lady with a history of bilateral adrenalectomy for Cushing's disease seven years previously, presented with sudden onset of severe headache, nausea, vomiting and loss of consciousness. She was somnolent and confused. She had neck stiffness, sixth nerve palsy and mydriasis on the left side. Computerized tomography (CT) and magnetic resonance imaging (MRI) studies revealed a non-homogeneous, grade IV D pituitary mass lesion associated with hemorrhage in the chiasmatic, interhemispheric, cerebellopontine, perimesencephalic cisterns and a hematoma within the frontal lobe. Angiography showed only bilateral elevation of horizontal segments of the anterior cerebral arteries. According to this angiographic evidence, it was presumed that the subarachnoid hemorrhage and the intracerebral hematoma were linked to pituitary adenoma apoplexy. ACTH level was 450 pg/ml. The hemorrhagic lesion with suprasellar extension was totally removed by left pterional craniotomy. Histological examination revealed a necrotic, ACTH-secreting pituitary adenoma. Even though apoplexy is a well known complication of pituitary adenomas, to our knowledge subarachnoid hemorrhage and intracerebral hematoma as a result of pituitary apoplexy in the context of Nelson's syndrome has not previously been reported.
Pituitary 2002
PMID:An unusual presentation of Nelson's syndrome with apoplexy and subarachnoid hemorrhage. 1455 76

We describe two young men with cystic pituitary enlargement on magnetic resonance imaging (MRI) causing hypopituitarism. The first patient presented acutely unwell with headache and vomiting associated with anterior and posterior pituitary dysfunction. The second patient presented with hypopituitarism after a long history of hypogonadism. In both cases yellow/brown fluid was found at surgery and histological examination revealed inflammatory infiltrate with foamy histiocytes, lymphocytes and multinucleated giant cells containing cholesterol clefts. Full recovery of pituitary function occurred after surgery in the first but not the second patient. The first case is the first documented case of xanthomatous hypophysitis with recovery of pituitary function following surgery. The cases differed in duration of disease, as indicated by the long history of symptoms, the histological finding of marked fibrosis and the lack of recovery of pituitary function in the second. Xanthomatous pituitary lesions categorized in the literature as xanthomatous hypophysitis, xanthogranulomatous hypophysitis and xanthogranuloma of the sellar region have overlapping histological features. Our two cases revealed histological features that do not fit completely into any of the categories but share features of all three. These findings suggest that the various xanthomatous lesions of the sellar region may be a spectrum of a common inflammatory process rather than distinct pathological entities.
Pituitary 2003
PMID:Xanthomatous pituitary lesions: a report of two cases and review of the literature. 1497 40

Clinically unsuspected pituitary adenomas are common among adults on autopsy and MRI survey. Acute pituitary hemorrhage is far more rare. We report a case of a 61-year-old male patient with locally advanced prostate cancer who presented with an acute picture of pituitary apoplexy after his first dose of leuprolide. He developed headache and neck pain within a few hours of treatment followed by nausea, vomiting, ptosis and diplopia. Pituitary apoplexy is a potentially life threatening medical emergency. Although the pathophysiology is poorly defined, various conditions and treatments have been reported to trigger apoplexy. Apoplexy has been reported in response to pituitary stimulation by GnRH or GnRH-agonists. Initial stimulatory effects of gonadotropin releasing hormone (GnRH) analogue may induce apoplexy in patients with asymptomatic gonadotroph adenomas.
Pituitary 2006
PMID:Pituitary apoplexy after leuprolide. 1683 87

Pituitary abscess secondary to an adenoma is rare. To date, only 19 cases have been reported. This is the first report of a patient who presented with bilateral total ophthalmoplegia. A 59-year-old male patient presented with headache, nausea, vomiting, decreasing visual acuity, diplopia and bilateral ophthalmoplegia with ptosis. Magnetic resonance imaging was suggestive of a pituitary abscess with adenoma. Transphenoidal surgery was performed and, during debulking of the tumour, the abscess was seen and excised. After the operation, the patient received antibiotic therapy and his neurological condition improved. Pituitary abscess with adenoma is a serious condition that has a high mortality rate. Therefore, early diagnosis and surgical intervention with antibiotic therapy are necessary.
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PMID:Abscess formation within invasive pituitary adenoma. 1693 Oct 19

Spindle cell oncocytoma (SCO) is a rare non-functioning tumour of the pituitary which has just been formally recognized as a distinct entity by the 2007 WHO classification of brain tumours. We report a case of SCO who presented with symptoms of visual blurring, weight loss, intermittent vomiting and excessive tiredness of several months duration. Investigations revealed a bitemporal visual field defect, a panhypopituitary hormonal profile and a large pituitary tumour with suprasellar extension. He underwent a successful trans-sphenoidal resection of the pituitary tumour but it subsequently recurred twice at 9 months interval which required further two debulking procedures. A diagnosis of SCO was made based on its unique histologic and staining properties. To date there are only ten reported cases of SCO in total with only two of these cases being recurrent. Our case displayed the most aggressive clinical course despite having a low Ki-67 index contrary to the previously reported cases of recurrent SCO.
Pituitary 2011 Dec
PMID:Recurrent spindle cell oncocytoma of the pituitary, a case report and review of literature. 1924 Nov 73


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