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-Pituitary tumor apoplexy is a medical emergency due to acute infarction or hemorrhage in the pituitary gland. In this review, the authors discuss the sellar anatomy, the pituitary gland and adenomas' vascularization and the general aspects of the syndrome such as its ethiopatogenesis, predisposing factors, clinical features, treatment and prognosis.Key words: pituitary tumor apoplexy, pituitary, pituitary adenomas. apoplexia em tumor hipofisário resumo -A apoplexia em tumor hipofisário é uma emergência médica decorrente do infarto agudo ou hemorrágico na glândula hipófise. Nesta revisão os autores discutem a anatomia da região selar, a vascularização da hipófise e adenomas hipofisários, e demais aspectos da síndrome como etiopatogenia, fatores predisponentes, quadro clínico, tratamento e prognóstico.PAlAvrAs-chAve: apoplexia hipofisária, hipófise, adenoma hipofisário.

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Hemichorea-hemiballism (HCHB) can be the solely presentation of a wide range of non-neurological clinical pictures, such as metabolic or hydro-electrolyte derangements. HCHB as the first presentation of type 2 diabetes mellitus has been rarely described [1][2][3] . The case depicted herein reinforces this association highlighting that especially in elder patients with newly diagnosed HCHB, non-ketotic hyperglycemia should promptly be recognized. caseA 70-year-old white man presented with one month history of involuntary movements of the left upper and lower limbs. He also noticed polyuria and polydipsia for the last 2 months and lost 10 kg within this period. His past medical history included controlled hypertension and a heart attack three years before. He used to take on a regular basis and at the time of presentation to our emergency department captopril 50 mg per day, hydrochlorothiazide 25 mg per day, propranolol 120 mg per day, aspirin 200 mg per day, and digoxin 0.25 mg per day. He used to be a heavy drinker (stopped 15 years ago) and smoker (stopped 3 years ago). There was no history of diabetes mellitus, other diseases or exposure to neuroleptic medication. No family history of movement disorders was obtained.On admission, he was fully alerted and oriented. He had HCHB involving his left upper and lower limb with normal muscle strength, but mild hypotonia. The movements were almost continuous during wakefulness, and disappeared during sleep. Fasting blood glucose was obtained (560 mg/dL) and type 2 diabetes mellitus was diagnosed. Glycosylated hemoglobin A1c was 6.6%. No ketones were detected in urinalysis and urine pH was normal. Corrected sodium concentration was 140 mmol/L, and estimated serum osmolality was 332 mOsm/L. Other routine blood tests including calcium, potassium, magnesium, and phosphate concentrations, and thyroid and parathyroid hormone tests were normal as well liver and kidney functional status. A brain computer tomography (CT) showed a slight hyperdense lesion on the right putamen. T1-weighted brain magnetic resonance imaging (MRI) showed a right hyperintense lesion on putamen with iso-signal intensity on T2-weighted and Flair images.With the administration of haloperidol (10 mg per day) and glycemia control (10 IU bed time NPH insulin) and 6 mg per day glimepiride his movement disorder decreased in severity and completely disappeared 15 days after the first medical appointment. A nine-month re-scan with MRI showed a normal putamen without the previously seen hyperintense lesion (Figure).The patient signed an informed consent to allow his data publication. discussionThe underlying mechanisms of brain alterations in patients with non-ketotic hyperglycemia-induced HCHB are not known yet, but they have been attributed to base ganglia cerebral blood flow reduction, petechial hemorrhage, depletion of both GABA and acetylcholine, or metabolic acidosis 4 . Interestingly, among neuronal subtypes, striatal medium spiny neurones are highly vulnerable to energy depletion and this might explain ...

Background/Aims: Although craniopharyngioma (CP) is histologically benign, it is a pituitary tumour that grows rapidly and often recurs. Adamantinomatous CP (ACP) was associated with an activating mutation in β-catenin, and it has been postulated that pituitary stem cells might play a role in oncogenesis in human ACP. Stem cells have also been identified in pituitary adenoma. Our aim was to characterize the expression pattern of ABCG2, CD44, DLL4, NANOG, NOTCH2, POU5F1/OCT4, SOX2, and SOX9 stem cell markers in human ACP and pituitary adenoma. Methods and Results: We studied 33 patients (9 ACP and 24 adenoma) using real-time quantitative PCR (RT-qPCR) and immunohistochemistry. SOX9 was up-regulated in ACP, exhibiting positive immunostaining in the epithelium and stroma, with the highest expression in patients with recurrence. CD44 was overexpressed in ACP as confirmed by immunohistochemistry. SOX2 did not significantly differ among the tumour types. The RT-qPCR array showed an increased expression of MKI67,OCT4/POU5F1, and DLL4 in all tumours. NANOG was decreased in ACP. ABCG2 was down-regulated in most of the tumours. NOTCH2 was significantly decreased in the adenomas. Conclusion: Our results confirm the presence of stem cell markers in human pituitary tumours as well as the different expression patterns of ACP and adenoma. These findings suggest that ACP may originate from a more undifferentiated cell cluster. Additionally, SOX9 immunodetection in the stroma and the highest expression levels related to the relapse of patients suggest a contribution to the aggressive behaviour and high recurrence of this tumour type.