Pituitary tumor apoplexy associated with extrapontine myelinolysis during pregnancy: A case report.

RATIONALE: Pituitary tumor apoplexy (PTA) is a rare clinical syndrome which requires urgent diagnosis and treatment due to its life-threatening consequences. Management of undiagnosed pituitary tumor before pregnancy is a problem during pregnancy. PATIENT CONCERNS: We reported a case with PTA which was not diagnosed before pregnancy presenting with vomiting associated with hyponatremia during the third trimester. After supplying the sodium the patient presented with dysarthria and hemiplegia. DIAGNOSES: MRI examination showed PTA accompanied with extrapontine myelinolysis (EPM). INTERVENTIONS: The patient was given hydrocortisone according to the symptoms gradually to taper off dose, at the same times oral levothyroxine therapy (25µg/day) was given. OUTCOMES: The patient delivered a healthy baby via cesarean section at hospital at 38 + 1 week of gestation. We performed MRI examination regularly and the tumor regressed significantly 8 months postpartum. LESSONS: We reported a case as PTA associated with EPM. Headache during pregnancy is often nonspecific, so careful medical history inquiry is very important.

An unusual case of hypopituitarism and transient thyrotoxicosis following asymptomatic pituitary apoplexy.

Although pituitary function is often impaired in pituitary apoplexy, the development of thyrotoxicosis is rare. We describe an unusual case of hypopituitarism due to pituitary apoplexy coexisting with transient hyperthyroidism. A 74-year-old woman presented with severe fatigue, palpitation, appetite loss, hypotension, and hyponatremia. Endocrine studies showed hyperthyroidism and anterior pituitary hormone deficiencies. A magnetic resonance imaging suggested recent-onset pituitary apoplexy in a pituitary tumor, although the patient had no apoplectic symptoms such as headache and visual disturbance. Thyrotoxicosis and adrenal insufficiency worsened her general condition. Glucocorticoid supplementation improved her clinical symptoms and hyponatremia. Serum anti-thyrotropin receptor and thyroid-stimulating antibody titers were negative, and her thyroid function was spontaneously normalized without antithyroid medication, suggesting painless thyroiditis. Thereafter, her thyroid function decreased because of central hypothyroidism and 75 µg of levothyroxine was needed to maintain thyroid function at the euthyroid stage. The pituitary mass was surgically removed and an old hematoma was detected in the specimen. Considering that painless thyroiditis develops as a result of an autoimmune process, an immune rebound mechanism due to adrenal insufficiency probably caused painless thyroiditis. Although the most common type of thyroid disorder in pituitary apoplexy is central hypothyroidism, thyrotoxicosis caused by painless thyroiditis should be considered even if the patient has pituitary deficiencies. Because thyrotoxicosis with adrenal insufficiency poses a high risk for a life-threatening adrenal crisis, prompt diagnosis and treatment are critical.

Hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome with pituitary apoplexy.

After hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome was diagnosed in a 35-year-old woman at 39 weeks' gestation, magnetic resonance imaging and hormone examination revealed pituitary apoplexy with panhypopituitarism and diabetes insipidus. Evaluation of pituitary function should be considered in patients with HELLP syndrome.

SIADH following pituitary adenoma apoplexy.

The rare case of a patient with SIADH following pituitary adenoma apoplexy is reported. Since apoplexy did not exert any mass effect on surrounding structures, the patient was treated conservatively and the anterior pituitary gland insufficiency has been substituted adequately. Seven days after the apoplexy the patient again showed low serum-Na(+) levels despite cortisol substitution. Diagnosis of SIADH was made. It is essential to be aware of this rare syndrome in patients with pituitary adenoma apoplexy.

Hyponatremia associated coma due to pituitary apoplexy in early pregnancy: a case report.

Pituitary apoplexy in pregnancy is rare. Its clinical features may range from unspecific complaints to panhypopituitarism resulting even in coma and death. Therefore, alertness to signs and symptoms of acute loss of pituitary function in pregnancy is mandatory. We report a woman in her 7th week of her first gestation presenting with sudden coma due to severe hyponatremia. Secondary adrenal insufficiency could be identified as the underlying cause. Panhypopituitarism including central diabetes insipidus and spontaneous abortion developed during the follow-up. Magnetic resonance imaging showed pituitary apoplexy without a pre-existing pituitary mass. The clinical course was notable for severe complications, including neurological deficits through cerebral ischemia, but eventual recovery could be achieved. We discuss the diagnostic difficulties in the evaluation of pituitary disease in pregnancy.

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Pituitary adenoma apoplexy with initial presentation mimicking bacterial meningoencephalitis: a case report.

Pituitary apoplexy is a rare but life-threatening disorder. Clinical presentation of this condition includes severe headache, impaired consciousness, fever, visual disturbance, and variable ocular paresis. Signs of meningeal irritation are very rare. However, if present and associated with headache, fever, and pleocytosis, meningeal irritation may lead to misinterpretation as infectious meningoencephalitis. To the best of our knowledge, pituitary apoplexy with an initial presentation mimicking infectious meningoencephalitis had rarely been reported in the literature. Here, we report a 57-year-old man who had acute severe headache, high fever, neck stiffness, disturbance in consciousness, and left ocular paresis. Laboratory data showed leukocytosis, an elevated C-reactive protein level, and neutrophilic pleocytosis in the cerebrospinal fluid. Because bacterial meningoencephalitis was suspected, empiric antibiotic therapy was administered but in vain. Further examinations indicated a diagnosis of pituitary adenoma with apoplexy. After the immediate administration of intravenous corticosteroid supplement and surgical decompression, the patient recovered.

Pituitary apoplexy within a macroprolactinoma.

BACKGROUND: A 61-year-old lady was admitted to hospital with sepsis due to a urinary tract infection. Three days after admission, she suddenly started to have severe headache with visual disturbance and right third nerve palsy. Urgent magnetic resonance angiography excluded internal carotid artery aneurysm but showed a large lesion extending superiorly from the clivus towards the right cerebral peduncle, which was confirmed by a CT scan of the brain. The lesion was initially thought to be a primary or a metastatic brain tumor. CT scans of the thorax, abdomen and pelvis showed no evidence of metastatic disease. MRI scan revealed a huge pituitary adenoma containing hemorrhage. Subsequent pituitary function tests indicated a grossly elevated serum prolactin level and hypopituitarism. INVESTIGATIONS: Magnetic resonance angiography of the head; CT scans of the brain, thorax, abdomen and pelvis; MRI scan of the pituitary gland; and baseline and dynamic anterior pituitary function testing. DIAGNOSIS: Pituitary apoplexy within a macroprolactinoma. MANAGEMENT: Steroid replacement, careful control of fluid and electrolyte balance and conservative nonsurgical management with the dopamine agonist cabergoline resulted in resolution of the patient's headache, improvement of the third nerve palsy and subsequent normalization of the prolactin level, with reduction in size of the prolactinoma on MRI scan.

Guía clínica del diagnóstico y tratamiento de la apoplejía hipofisaria / Clinical practice guideline for the diagnosis and treatment of pituitary apoplexy

La apoplejía hipofisaria (AH) es un fenómeno isquémico o hemorrágico que aparece generalmente en un adenoma hipofisario. La AH se produce como consecuencia de un infarto con aparición posterior de hemorragia y edema del tumor. La forma aguda se considera una urgencia neuroendocrinológica, ocurre de forma brusca y se caracteriza por un cuadro de cefalea brusca, junto con náuseas, vómitos, alteraciones del campo visual y afección de pares craneales. La forma subclínica es más frecuente y es silente. El diagnóstico de la AH se basa en un cuadro clínico típico en el contexto de un tumor hipofisario. La AH puede provocar cualquier deficiencia hormonal hipofisaria transitoria o permanente. El déficit brusco de corticotropina y de cortisol es el más importante, por el riesgo vital que conlleva. En el momento de la sospecha diagnóstica se debe llevar a cabo una evaluación endocrinológica con determinación de las hormonas basales hipofisarias y las correspondientes periféricas. Posteriormente, se realizará una valoración endocrinológica en la fase de estabilización encaminada a evaluar el funcionamiento remanente de la hipersecreción hormonal, en el caso de tumores funcionantes previos, y al diagnóstico de un posible hipopituitarismo permanente como secuela de la AH. Para la confirmación de la sospecha diagnóstica clínica se debe realizar una prueba de neuroimagen, una tomografía computarizada o una resonancia magnética hipofisarias. No existe un consenso sobre el tratamiento óptimo de la AH. Clásicamente, dado que el determinante de la lesión por AH es el aumento de la presión intraparaselar, la cirugía descompresiva se consideraba el tratamiento de elección. Sin embargo, en los últimos años se ha utilizado el tratamiento médico conservador con esteroides, especialmente si no existen déficit visuales

Pituitary apoplexy (PA) is an ischemic or hemorrhagic phenomenon that is usually found in the context of a pituitary adenoma. PA is produced as a result of an infarction with subsequent hemorrhage and edema of the tumor. The acute form is considered a neuroendocrinological emergency. Onset is abrupt and this form is characterized by thunderclap headache together with nausea, vomiting, visual disturbances and cranial nerve involvement. The more frequent subclinical form is clinically silent. The diagnosis of PA is based on typical clinical findings in the context of a pituitary tumor. PA can provoke any type of transitory or permanent pituitary hormone deficiency. The most important of these is abrupt ACTH and cortisol deficiency as it can be life-threatening. When AP is suspected, endocrinological evaluation should be performed with baseline and peripheral pituitary hormone determinations. Subsequently endocrinological evaluation should be performed in the stabilization phase to evaluate remaining hormonal hypersecretion in the case of prior functioning tumors and diagnosis of possible permanent hypopituitarism as a sequel of PA. To confirm clinical diagnostic suspicion, a neuroimaging test ­computerized axial tomography or magnetic resonance imaging of the pituitary­ should be performed. Consensus on the optimal treatment of PA is lacking. Classically, given that the determining feature of AP is increased intra-parasellar pressure, decompressive surgery used to be considered the treatment of choice. However, in the last few years, conservative medical treatment with steroids has been used, especially when visual impairment is absent

Elevated soluble epidermal growth factor receptor level in pituitary adenoma and carcinoma.

OBJECTIVE: To investigate effect of the soluble epidermal growth factor receptor (sEGFR/sErbB1) level in the peripheral blood in development, invasiveness, apoplexy of each type of pituitary tumor. METHODS: The sEGFR level was determined in peripheral serum from 190 patients with pituitary diseases by enzyme linked immunosorbent assay. The sEGFR levels were measured in 10 pituitary Rathke's pouch, 18 pituitary hyperplasia, 161 pituitary adenomas including 30 microadenomas, 83 large adenomas, 48 giant adenomas, 1 pituitary carcinoma, and 28 healthy controls. RESULTS: In the patients with pituitary hyperplasia, microadenoma, large adenoma, giant adenoma, and pituitary carcinoma, the sEGFR level was 188.92 +/- 32.62, 209.83 +/- 19.01, 333.20 +/- 69.33, 405.85 +/- 37.38, and 617.45 fmol/mL independently. They were all significantly higher than patients with pituitary Rathke's pouch (156.78 +/- 18.24 fmol/mL, P < 0.001) and healthy control group (159.11 +/- 40.50 fmol/mL, P < 0.05). The sEGFR level in pituitary carcinoma was higher than pituitary adenoma. In patients with pituitary adenoma, the sEGFR level was positive correlated to the size of pituitary adenomas (r=0.998), the significant difference was observed for the sEGFR level in each group of the patients with pituitary adenomas (P < 0.001). Furthermore, in patients with pituitary ACTH-secreting microadenomas, the serum sEGFR levels in invasiveness (295.00 +/- 77.80 fmol/mL) was higher than that in non-invasiveness (210.60 +/- 16.4 fmol/mL, P < 0.05). In patients with pituitary ACTH-secreting, PRL-secreting, GH-secreting, and non-functioning large adenomas, the serum sEGFR levels in invasiveness (407.86 +/- 28.50, 399.25 +/- 30.10, 386.00 +/- 13.08, and 369.25 +/- 36.70 fmol/mL) was higher than that in non-invasiveness (335.25 +/- 63.49, 300.64 +/- 47.57, 297.00 +/- 61.93, and 269.30 +/- 25.68 fmol/mL) respectively (P < 0.05). In patients with invasive pituitary PRL-secreting, GH-secreting, and non-functioning giant adenomas, the serum sEGFR levels not significantly different in between invasiveness (417.50 +/- 35.94, 409.50 +/- 69.14, and 417.50 +/- 44.13 fmol/mL) and non-invasiveness (386.00 +/- 49.64, 417.50 +/- 44.03, and 409.51 +/- 35.17 fmol/mL) (P > 0.05). In patients with pituitary large adenomas, the sEGFR levels in pituitary apoplexy (377.48 +/- 39.18 fmol/mL) was higher than that in non-pituitary apoplexy (343.18 +/- 68.17 fmol/mL, P > 0.05). CONCLUSIONS: The increased level of peripheral serum sEGFR is concomitant with development, proliferous size of the adenomas in patients with pituitary adenomas. In addition, the elevated levels of serum sEGFR occur in pituitary apoplexy as clinical active tumors, and the non-invasive ACTH secreting adenomas. The sEGFR levels could be differentiated helpfully between pituitary adenomas and non-pituitary adenomas. These data suggest that serum sEGFR could be as a referable marker of the size and activation of proliferation in pituitary adenoma.

Pituitary apoplexy caused by luteinizing hormone-releasing hormone in prolactin-producing adenoma.

We report a case in which pituitary apoplexy developed shortly after an intravenous (i.v.) injection of luteinizing hormone-releasing hormone (LH-RH). A 56-year-old man with prolactin-producing pituitary tumor complained of severe headache, visual field loss and facial nerve palsy shortly after LH-RH test. Magnetic resonance image (MRI) revealed a hemorrhage in the pituitary adenoma. He showed dramatic improvement in his symptoms after decompression surgery. These findings suggest a causal relationship between the i.v. injection of LH-RH and pituitary apoplexy. Possible pituitary apoplexy should be kept in mind during pituitary testing.

Transient diabetes insipidus and hypopituitarism after pituitary apoplexy: a rare association with pericardial effusion and painless thyroiditis.

Pituitary apoplexy in a 38-year-old male patient with acromegaly who presented with pericardial effusion, anterior pituitary dysfunction, and diabetes insipidus is described. With corticosteroid therapy, there was good initial recovery of pituitary function and regression of pericardial effusion. On withdrawal of corticosteroids, he developed painless thyroiditis, with transient thyrotoxicosis. Subsequently, the pituitary function tests remained normal for a year, but later he gradually developed hypogonadotropic hypogonadism, hypocortisolism, growth hormone deficiency, and progressive pituitary atrophy, resulting in empty sella syndrome.

Vascular complications of transsphenoidal surgery.

Vascular complication of transsphenoidal surgery can lead to mortality and serious morbidity. In a series of 3,061 transsphenoidal operations for pituitary disease, 24 such complications were encountered, seven of which were fatal. The anatomic substrate for such complications is discussed, along with technical aspects of surgery and other methods for the avoidance of vascular complications.

[Partial remission of hypercortisolism in Cushing disease after pituitary apoplexy. A case report]. / Remisión parcial del hipercortisolismo en una enfermedad de Cushing posterior a una apoplejía hipofisiaria. Caso clínico.

ACTH secreting macroadenomas and pituitary apoplexy are unusual in Cushing disease. In the few cases reported in the literature, they have been found in long term hypercortisolism. We communicate a 43 yr old woman with a 4 year evolution Cushing syndrome, who developed sudden cephalea and oftalmoplejia. A Computed Tomography of the pituitary fossa disclosed a macroadenoma with intracapsular hemorrhage and suprasellar expansion. In the functional tests, serum cortisol was suppressed with dexamethasone in a dose of 1 and 8 mg and responded to the desmopressin stimulus. Nevertheless, cortisol levels were lower than those observed in Cushing syndrome of similar magnitude. The tumor was resected by transphenoidal surgery and immunohistochemistry to ACTH was positive. In this case, the laboratory results suggest a partial remission of the hypercortisolism after pituitary apoplexy.

Pituitary apoplexy with spontaneous cure of acromegaly and its possible relation to Gd-DTPA-administration.

A case of pituitary apoplexy occurring after Gd-DTPA-administration for contrast enhanced MRI in a patient with an hGH-producing macro-adenoma is presented. Within days the initially increased hGH level fell to the normal range, the oral glucose tolerance test (OGTT) showed a normal suppression of hGH and complete anterior pituitary insufficiency developed. At this time repeated MRI suggested a haemorrhagic infarction of the macro-adenoma. Fourteen months later re-examination confirmed spontaneous cure of the acromegaly, improvement of adenopituitary function and shrinkage of the sellar content. The causal linkage between the pituitary adenoma apoplexy and Gd-DTPA-administration is unclear. It might be due to contrast induced blood pressure and endothelial permeability changes, possibly promoted by pre-existing diabetes mellitus associated vasculopathy.

[Pituitary apoplexy: analysis of endocrine function in 17 cases]. / Apoplejía hipofisaria: análisis de la función endocrina en 17 casos.

BACKGROUND: From a neurological standpoint, pituitary apoplexy (PA) is a well defined syndrome. There are few systematic studies addressing pituitary hormone secretion after a PA episode. The aim of the present study was to assess the frequency and degree of endocrine dysfunction due to PA. METHODS: In 17 consecutive patients, the secretion of growth hormone (GH), the pituitary-adrenal axis status, thyrotropin (TSH), prolactin and gonadotropins (LH, FSH) were evaluated after the administration of insulin, thyrotropin releasing hormone (TRH) and gonadotropin-releasing hormone (LHRH) after an episode of PA. 20-90 days after surgery the measurements were repeated. Antidiuretic hormone (ADH) was measured by plasma/urine osmolality after water deprivation and, in some cases, by administration of hypertonic saline. RESULTS: The most commonly found deficiency was that of GH (84%), which in two cases resulted in cure of acromegaly, followed by that of LH (78%). Pituitary-adrenal dysfunction was improved in two patients after surgery. In all cases except one there was a reduced secretion of at least two hormones. If serum prolactin was reduced, the rest of pituitary function was usually impaired. In one case, permanent diabetes insipidus developed after PA. The prevalence of PA in pituitary adenomas was 9%. CONCLUSIONS: Pituitary hormone secretion after a PA episode is almost invariably impaired. This impairment may be reversed after surgery. Hypoprolactinemia is an indicator of pituitary hypofunction.