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Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

Pituitary apoplexy is the most serious and life-threatening complication of pituitary adenomas. Most of the cases occur spontaneously but it may occur also after a number of events such as the pituitary stimulation tests. We report a case of acromegaly due to a giant pituitary adenoma in which pituitary apoplexy developed 88 hours after TRH/GnRH stimulation test. The patient had severe headaches, nausea, vomiting, visual disturbance and mental alteration and the computed tomography (CT) scans revealed intratumoral and intraventricular bleeding. The pituitary mass was removed by transsphenoidal approach. The patient developed pneumonia and died on the 9th postoperative day. Pituitary apoplexy was confirmed at surgery and on histological examination. Immunohistochemical staining was positive for GH and PRL. This case indicates that pituitary apoplexy may develop several days after TRH/GnRH stimulation test.
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PMID:Pituitary apoplexy probably due to TRH and GnRH stimulation tests in a patient with acromegaly. 1090 71

Pituitary apoplexy has been reported as a rare complication of dynamic testing used for the study of pituitary functional reserve. In 1993, a diagnosis of non-secreting macroadenoma with moderate functional hyperprolactinaemia was made in a 43-year-old woman. Soon after the start of therapy with bromocriptine up to 5 mg/die, the patient complained of nausea and postural hypotension. As the symptoms persisted even when the dose was reduced to 2.5 mg/die, the patient was transferred to therapy with quinagolide at the dosage of 37.5 microg/die. PRL levels quickly normalized (range 1.4-5.7 ng/ml) as well as menstrual cycles, and no side-effect was reported. In 1995 a sellar magnetic resonance imaging (MRI) showed no shrinkage of the known macroadenoma. In 1996, few hours after a gonadotropin-releasing-hormone (GnRH) test, which showed normal LH and FSH response and with baseline PRL levels in the normal range, the patient started complaining of severe frontal headache, nausea and vomiting. No gross visual defects were present. An emergency computed tomography (CT) showed no evident hemorrhagic infarction in the macroadenoma. The symptoms completely resolved in few days with steroidal and antiemetic therapy. A new MRI performed in 1998 showed a partial empty sella and PRL levels were in the normal range under dopaminergic treatment. The pituitary functional reserve proved normal on dynamic testing. The temporal association between the onset of symptoms and the GnRH test strongly suggests an association between the two events. No evident signs of pituitary apoplexy (either on emergency CT or hormonal evaluation) were detected. The authors suggest that GnRH can cause severe side-effects that mimic pituitary apoplexy without related morphological evidence and that, in our particular case, it can have caused the gradual disappearance of the non-secreting macroadenoma. Moreover, a causal role of the chronic dopaminergic treatment cannot be completely ruled out.
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PMID:Gonadotropin-releasing hormone-induced partial empty sella clinically mimicking pituitary apoplexy in a woman with a suspected non-secreting macroadenoma. 1080 Jul 66

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.
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PMID:Pituitary apoplexy in a patient with acute myeloid leukemia and thrombocytopenia. 1114 94

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.
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PMID:Pituitary apoplexy after leuprolide. 1683 87

Pituitary apoplexy (PA), which is one of the most serious life-threatening complications of pituitary adenoma, is characterized by abrupt onset of headache, nausea, vomiting, visual disturbances and oculomotor paresis. Combination of oculomotor cranial nerve paralysis with normal visual fields is very rare in PA. We report a 60-year-old acromegalic man presented with panhypopituitarism and bilateral total opthalmoplegia without a visual field defect. At initial evaluation his clinical findings were compatible with adrenal crisis and eye examination revealed total opthalmoplegia, bilateral ptosis and normal vision. MRI showed a large heterogeneous mass in the pituitary fossa. Although clinical findings due to adrenal crisis improved after glucocorticoid therapy there was no improvement in opthalmoplegia and ptosis. The patient underwent transsphenoidal excision of the pituitary mass. Histological examination revealed an adenoma with large areas of hemorrhagic infarction and most of the cells were positive for GH in immunohistochemical analysis. Although opthalmoplegia was severe at presentation, total recovery was achieved 3 months after transsphenoidal surgery. Therefore the presented case clearly demonstrates that opthalmoplegia without a visual field defect due to PA has a good prognosis and early diagnosis and treatment including surgical decompression are crucially important.
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PMID:Complete surgical resolution of bilateral total opthalmoplegia without visual field defect in an acromegalic patient presented with pituitary apoplexy. 1778 21

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.
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PMID:Pituitary apoplexy associated with cortisol-induced hyperglycemia and acute delirium. 1909 Dec 87

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.
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PMID:Pituitary tumor apoplexy in patients with Cushing's disease: endocrinologic and visual outcomes after transsphenoidal surgery. 2192 87

Pituitary apoplexy is defined as a sudden loss of blood supply to the pituitary gland, leading to tissue necrosis and hemorrhage. Its clinical symptoms are characterized by sudden onset of headache, nausea, vomiting, ophthalmic symptoms and hormonal dysfunction. A 65-year-old woman presented with left-sided ptosis and blurred vision. These ophthalmic symptoms gradually worsened for one month without headache, visual acuity and field deficit. Neuro-ophthalmic examination revealed left oculomotor nerve palsy. Magnetic resonance imaging (MRI) revealed a round mass lesion in the left cavernous sinus, which was initially suspected as thrombosed cerebral aneurysm or hemorrhagic Rathke's cleft cyst. The mass lesion was finally diagnosed as pituitary apoplexy. The patient underwent trans-sphenoidal surgery and oculomotor nerve palsy improved after the surgery. Early diagnosis and treatment including surgical decompression are crucially important in patients with oculomotor nerve palsy in pituitary apoplexy, but the symptoms of pituitary apoplexy may slowly progress. It should be noted that pituitary apoplexy could be misdiagnosed as cerebral aneurysm or Rathke's cleft cyst.
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PMID:Pituitary apoplexy presenting atypical time course of ophthalmic symptoms. 2257 5

Pituitary apoplexy (PA) is a rare, potentially life-threatening medical condition due to acute ischaemia or haemorrhage of the pituitary gland. The main clinical features are: abrupt onset of severe headache, nausea, vomiting, deteriorating level of consciousness, visual impairment and/or endocrine deficiency. Correct and prompt diagnosis is essential for effective therapy, but there are no randomised studies or strict recommendations defining treatment modalities. We present the case of a 59 year-old woman with pituitary tumour apoplexy, presenting with severe headache, vomiting and visual field deterioration. The patient was treated conservatively because of her refusal of surgery and was followed-up for five years. In the course of treatment, recovery of the visual field defects, as well as right sixth cranial nerve paresis, was observed. Repeated magnetic resonance imaging (MRI) revealed regression of the tumour without signs of its re-growth. We discuss therapeutic modalities with particular emphasis on morbidity and review the literature relating to the management of pituitary tumour apoplexy.
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PMID:Spontaneous regression of non-functioning pituitary adenoma due to pituitary apoplexy following anticoagulation treatment - a case report and review of the literature. 2345 Apr 48


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