Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 17-year-old women received 12,000 rads of alpha-particle radiation for the treatment of Cushing's disease. One day after the completion of therapy, the patient developed nausea, vomiting, headache, and postural hypotension. Laboratory evaluation demonstrated a marked fall of the previously elevated urinary 17-hydroxycorticosteroids (17-OHCS) and undetectable plasma cortisols. The urinary 17-OHCS transiently returned to supranormal levels but over a 2 1/2-week period decreased and then remained low. The patient also demonstrated a subnormal urinary aldosterone excretion in relation to plasma renin activity (PRA) during 10 mEq/24 h sodium restriction. The remainder of the endocrine evaluation was normal, suggesting that pituitary function otherwise remained intact. One and one-half years after alpha-particle therapy, the patients's urinary 17-OHCS were normal and responded normally to metyrapone. The relationship between urinary aldosterone excretion and PRA also was normal. It is postulated that there was an infarction of an ACTH secreting pituitary tumor leaving the remainder of the pituitary intact. Achronically elevated circulating level of ACTH with sudden loss of ACTH secretion appeared to have been responsible for the initial low urinary aldosterone as well as the low urinary 17-OHCS. This is the first reported case of a presumed pituitary tumor infarction in association with alpha-particle pituitary radiation.
 ...
PMID:Rapid appearance of transient secondary adrenocortical insufficiency after alpha-particle radiation therapy for Cushing's disease. 18 95

The most common cause of hypoadrenocorticism in dogs is idiopathic immune-mediated destruction of the adrenal cortex. Other causes include anterior pituitary insufficiency, pituitary or adrenal neoplasia, acute withdrawal of exogenous corticosteroids, and mitotane toxicity. Females are affected more often than males; only 1 feline case has been documented. Animals 2-5 years old are most commonly affected. Clinical signs include lethargy, weakness, weight loss, anorexia, vomiting, diarrhea and bradycardia. Hematologic and biochemical changes can include eosinophilia, lymphocytosis, anemia, hyperkalemia, hyponatremia and hypercalcemia. Diagnosis is by finding negligible resting levels of plasma cortisol and no response to ACTH administration, and a serum Na:K ratio of 20:1 or less. Treatment involves restoring fluid volume, correcting acidosis, and supplementing salt and glucocorticoids. Daily oral use of prednisone at 0.05 mg/kg can safely maintain most affected dogs. Some dogs only require glucocorticoids in stressful situations. Iatrogenic secondary adrenocortical insufficiency (iatrogenic Cushing's disease) may result from a single injection of long-acting glucocorticoids or from long-term use. Clinical signs are the same as for natural hyperadrenocorticism, but endogenous cortisol release is suppressed. Treatment is gradual withdrawal of the offending glucocorticoid and elimination of the cause that initially prompted glucocorticoid therapy.
 ...
PMID:Diseases of the adrenal cortex of dogs and cats. 674 17

A retrospective analysis was performed to study the fluid and sodium status of patients undergoing transsphenoidal surgery (TS) for Cushing's disease. We evaluated the time of onset, duration, and relative incidence of isolated hyponatremia and identified possible factors associated with it. Of 58 patients that underwent TS over 1 yr, 52 without postoperative diabetes insipidus or volume depletion were studied. Isolated hyponatremia after TS for Cushing's disease occurred in 21%, and symptomatic hyponatremia (plasma sodium, < or = 125 mmol/L) with new onset headache, nausea, and emesis occurred in 7.0% of all operated. These later patients escaped monitoring and intervention for 24 h. The development of hyponatremia began early in the postoperative period and progressed slowly over 7 days. Maximum antidiuresis occurred on postoperative day 7. Vasopressin levels measured in two patients while hypoosmolar suggested that unregulated vasopressin release contributed to the hyponatremia. Cortisol levels, glucocorticoid replacement, and pituitary adenoma size were similar in normonatremic and hyponatremic patients. Patients combining a history of an estrogenic milieu and documented posterior pituitary trauma at surgery experienced lower nadir plasma sodium. All hyponatremic patients were fluid restricted, and none developed progressive neurological symptoms, morbidity, or mortality. We speculate that the mild degree and slow rate of development of hyponatremia and/or active monitoring and intervention contributed to the good outcome.
 ...
PMID:Isolated hyponatremia after transsphenoidal pituitary surgery. 782 44

Pituitary apoplexy is rare and endocrine remission in patients with apopletic secreting pituitary adenomas is even rarer. This study reports on two patients with pituitary macroadenomas (one with Cushing's disease and the other with acromegaly) in whom endocrine remission occurred after apoplexy. The first patient had Cushing's disease and had an ictus of headache and vomiting after which she started a progressive remission of hypercortisolism. A post-apoplexy MRI disclosed persistence of a sellar and supra-sellar mass. She was submitted to transesphenoidal surgery. An hypertensive hemorrhagic cyst was found with no tumor. The second patient had acromegaly. While performing a LHRH-stimulation test he had an ictus of headache, vomiting, no visual loss and appearance of diabetes insipidus. A CT scan disclosed an intrasellar hematoma. Despite the size of the tumor and since there was no visual impairment, this patient was followed up without surgery. Imaging follow-up showed a progressive shrinkage and disappearance of the mass, which was corroborated by endocrine remission. A high rate of recurrence is reported in such patients in the literature. Both patients are being currently followed-up on a long-term basis.
 ...
PMID:[Pituitary apoplexy followed by endocrine remission. Report of two cases]. 975 27

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.
 ...
PMID:An unusual presentation of Nelson's syndrome with apoplexy and subarachnoid hemorrhage. 1455 76

Pituitary apoplexy indicates pituitary adenoma hemorrhage, which could result in acute pituitary insufficiency and mortality. The typical symptoms are headache, visual disturbance, nausea, vomiting, altered mental status, and panhypopituitarism. However, cortisol-induced hyperglycemia and acute delirium could be an initial presentation of a pituitary adenoma hemorrhage with stormy release of the adrenocorticotrophic hormone. A 28-year-old woman presented with severe vomiting, irritable state, and delusion. She had medical history of irregular menstrual cycles and marked body weight gain after her second childbirth 8 years ago. She was diagnosed of diabetic ketoacidosis 2 days before this visiting at local medical department. On physical examination, Cushing appearance without definite neurological deficit was disclosed. Further blood tests revealed high blood sugar, cortisol, and adrenocorticotrophic hormone levels without evidence of diabetic ketoacidosis. The brain computed tomography and magnetic resonance imaging showed pituitary macroadenoma and pituitary hemorrhage. Cushing disease with pituitary apoplexy was then diagnosed. Conservative management with delayed neurosurgery was applied. The patient became clear with normalized cortisol and blood sugar levels soon after. Follow-up computed tomography scan of the brain revealed no progression of tumor bleeding or mass effect. To our knowledge, pituitary apoplexy associated with cortisol-induced hyperglycemia and acute delirium has never been reported before. This case reminds us of pituitary apoplexy and its rare manifestations.
 ...
PMID:Pituitary apoplexy associated with cortisol-induced hyperglycemia and acute delirium. 1909 Dec 87

Benign intracranial hypertension (Pseudotumor cerebri) has been described as related to the reduction in steroid levels in Cushing's disease (CD), especially after surgical remission. Ketoconazole is a common and effective adjuvant therapy for hypercortisolism, but the major concern is liver enzyme dysfunction. We describe here the case of a 12-year old girl with CD who developed benign intracranial hypertension during treatment with ketoconazole. She presented headache, vomiting, a black spot on her right temporal visual field, and signs of elevated intracranial pressure. Pituitary image was normal on magnetic resonance image (MRI), and all symptoms improved after treatment with acetazolamide. We call attention to the diagnosis of this disorder in CD patients, especially children on ketoconazole treatment, because it could be confounded with adrenal insufficiency and lead to definitive severe visual impairment.
 ...
PMID:Pseudotumor cerebri during Cushing's disease treatment with ketoconazole. 2177 32

Pituitary apoplexy in patients with adrenocorticotropic hormone (ACTH) producing tumors is a rare occurrence. We report four patients with Cushing's disease harboring ACTH-secreting macroadenomas who presented with pituitary apoplexy. We report the endocrinologic and visual outcomes of these patients after emergent transsphenoidal surgery. A retrospective chart review was performed in 4 patients who presented with pituitary apoplexy from hemorrhage into an ACTH-secreting pituitary adenoma. The patient charts were reviewed for clinical presentation, neuroimaging findings, intraoperative surgical findings, pathologic findings, and postoperative endocrinologic and visual outcomes. All patients presented with acute headaches, nausea, vomiting, and visual loss from optic compression. MR imaging demonstrated a hemorrhagic macroadenoma that was confirmed at surgery. All patients underwent emergent transsphenoidal decompression (within 24 h of presentation). One of these underwent an additional craniotomy to resect residual tumor. Postoperatively, all patients showed significant improvement in visual acuity and visual fields with biochemical remission confirmed on laboratory testing. Significant weight loss as well as resolution of diabetes and hypertension was noted in all cases. All four patients remained in biochemical remission at their most recent follow-up visit (mean 40 months, range: 24-72 months). Excellent endocrine and visual outcomes can be achieved after emergent transsphenoidal surgery in patients with Cushing's disease presenting with pituitary apoplexy. Although the cure rates of non-apoplectic ACTH macroadenomas are generally poor, higher rates of remission can be achieved in cases of pituitary apoplexy. This may be partly due to the effects of tumor infarction.
 ...
PMID:Pituitary tumor apoplexy in patients with Cushing's disease: endocrinologic and visual outcomes after transsphenoidal surgery. 2192 87

The clinical syndrome idiopathic intracranial hypertension (IIH), also termed pseudotumor cerebri, consists of symptoms of headache, nausea, vomiting and visual field defects in combination with findings of papilledema. IIH is more commonly seen in overweight women where the rise in intracranial pressure is putatively a consequence of an endocrine-based disturbance of electrolytes. Less frequently, it can also occur in men and in the pediatric age group. Associated risk factors include primary and secondary aldosteronism, pregnancy, recombinant growth hormone (r-GH) therapy, oral contraceptives, obesity, vitamin A intoxication or deficiency, Addison disease, corticosteroid therapy or acute withdrawal of steroid therapy and Cushing disease. Herein, we review the association between these conditions and IIH working toward its having a unifying neuroendocrine hypothesis.
 ...
PMID:Idiopathic intracranial hypertension: a unifying neuroendocrine hypothesis through the adrenal-brain axis. 2316 Feb 27

An 18-year-old male with Cushing's disease presented with generalised skin eruptions and backache. He was diagnosed with varicella infection. During the course of the illness, he developed persistent vomiting. Hormonal evaluation suggested adrenal insufficiency. MRI of brain showed features of pituitary apoplexy. Initially, he required hydrocortisone replacement. Later on his hypothalamic-pituitary-adrenal axis recovered and he is currently asymptomatic without any treatment.
 ...
PMID:Varicella causing remission of Cushing's disease. 3024 30


1 2 Next >>