Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The objective of this study is to determine whether pergolide therapy is an effective modality for the de novo treatment of patients with macroprolactinomas. Twenty-two consecutive patients with macroprolactinomas were included in the study and followed prospectively. These included 16 men and 6 women in whom pregnancy was not of concern. Pergolide was administered once or twice a day depending on the patient's preference. Ten patients received 0.1 mg daily as a maintenance regimen and in the others the daily dose ranged from 0.05 to 0.5 mg. Eight patients reported minor but tolerable side effects. One patient had to be switched to cabergoline because of intolerable nausea. After a mean of 12 months (range, 3-36), mean PRL levels declined from 3,135 ng/ml (range, 126-31,513) to 50 ng/ml (3-573), representing a mean PRL suppression of 88% (range, 0-99). PRL levels became normal in 15 patients and decreased to 25-40 ng/ml in 3 others. The mean tumor volume shrinkage was 25% or greater in 19 patients (86%), 50% or greater in 17 patients (77%), and 75% or greater in 10 patients (45%). Visual abnormalities were reversible after pergolide therapy in all but 1 of 12 patients with initially abnormal formal visual testing. Two out of 4 premenopausal women did not normalize PRL levels and had persistent oligomenorrhea. Testosterone was low in 14 men at presentation and normalized in 3 with pergolide therapy. We conclude that pergolide is a safe, inexpensive, and generally well-tolerated dopamine agonist for the treatment of macroprolactinomas in men and women in whom pregnancy is not of concern. In these specific populations, pergolide may become the first-line therapy for treatment of macroprolactinomas.
Pituitary 2000 Dec
PMID:Pergolide as primary therapy for macroprolactinomas. 1178 13

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

The authors report on a 44-year-old female hemodialysis (HD) patient who presented with hypercalcemia secondary to isolated adrenocorticotropic hormone (ACTH) deficiency. She had been suffering from nausea and abdominal pain caused by recurrent esophageal ulcer. Blood calcium (Ca) adjusted for serum albumin concentration was increased to 14.9 mg/dL (3.72 mmol/L) concurrently with fever and hypotension. Serum intact parathyroid hormone (PTH)-related peptide was not elevated, but serum intact PTH and 1,25-(OH)2 vitamin D3 were decreased to 31 pg/mL (ng/L) and 8.1 pg/mL (2.6 pmol/L), respectively. Endocrinologic examination found that plasma ACTH was reduced below 5.0 pg/mL (0.22 pmol/L). A single ACTH stimulation normally increased blood cortisol, whereas a single corticotropin-releasing hormone injection failed to increase plasma ACTH and cortisol. Pituitary magnetic resonance imaging disclosed no enlargement of pituitary gland. Circulating bone formation and absorption markers were not elevated. Blood Ca was normalized shortly after pamidronate disodium administration without glucocorticoid supplementation. This case suggested that secondary adrenal insufficiency caused by isolated ACTH deficiency could be an occult cause of severe hypercalcemia in HD subjects.
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PMID:Isolated adrenocorticotropic hormone deficiency presenting with hypercalcemia in a patient on long-term hemodialysis. 1290 Aug 50

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

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

Pituitary abscess (PA) is an infrequent disease, which consists of an infection within the sella turcica that might be life-threatening. We present here two cases of this rare entity. Case 1: A 53-year-old woman was followed for an incidentally found pituitary cyst. Six years later the cyst enlarged and transsphenoidal surgery was performed. Two years later, the patient developed sudden onset of intense headache and nausea. The MRI showed a 2 by 2.5 cm sellar and suprasellar mass, that enhanced peripherally with gadolinium contrast and became hyperintense in T2-weighted images, suggesting a new-onset cystic lesion. During transsphenoidal surgery, large amounts of purulent material were drained from the sella. The cultures were positive for Klebsiella Ozaenae. Case 2: A 63-year-old woman, 4 years after transsphenoidal resection of a GH-secreting macroadenoma, developed a new sellar 2.6 cm cystic mass. On re-operation, purulent material was drained from the sella. The lesion persisted on the MRI and visual acuity worsened so a repeat pituitary decompression was carried out 6 months later, obtaining the same pathological results. Three years later, the MRI still shows the same mass. She feels well and her physical examination and clinical history are unremarkable. These cases illustrate the difficulties in the diagnosis and management of this rare entity.
Pituitary 2008
PMID:Pituitary abscess: a report of two cases. 1745 3


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