Pituitary Apoplexy Following Systemic Anticoagulation.

Pituitary apoplexy is a rare medico-surgical emergency that stems from an acute expansion of a pituitary adenoma from infarction or haemorrhage and where the treatment strategy is still controversial. Clinical presentation is highly variable and a high index of suspicion is needed to make the diagnosis. Furthermore, in less than half of cases, a precipitating event is identified. We report a case of a 74-year-old female who, after introduction of anticoagulation for pulmonary thromboembolism, presented with pituitary apoplexy heralded by acute adrenal insufficiency, headaches, visual symptoms and hypogonadotropic hypogonadism. Timely initiation of corticosteroids was crucial, and after stabilisation, a conservative treatment strategy was favoured with good long-term prognosis. Long-term follow-up of pituitary function also revealed new growth hormone deficiency. LEARNING POINTS: Corticosteroid therapy may be crucial in the emergency setting, and it is recommended for all patients with suspected pituitary apoplexy (PA).Early recognition of PA and its predisposing factors is crucial for the best outcome for the patient.Initial conservative treatment strategies are gaining popularity but close clinical monitoring is fundamental to recognise the need for sellar decompression.

Paraganglioma or pheochromocytoma? A peculiar diagnosis.

Paragangliomas and pheochromocytomas are rare catecholamine secreting neoplasms that arise in the extra-adrenal autonomic paraganglia and adrenal medulla, respectively. Although typically presenting with paroxysms of headaches, palpitations, diaphoresis and hypertension, a broad spectrum of clinical manifestations may occur. Diagnosis relies on biochemical studies followed by adequate imaging investigation. Cross sectional morphological and functional imaging modalities have improved diagnostic accuracy and are crucial in the surgical planning. The authors report on a case of a 64-year-old female that presented with severe hypertension, palpitations and fatigue as the manifestations of a catecholamine secreting neoplasm. Abdominal contrast enhanced computer tomography revealed a right sided 78 mm adrenal medullary tumor suggestive of a pheochromocytoma. Standard therapeutical strategies were initially unsuccessful, and additional investigation and therapy were required to cure the patient. The challenges faced by the multidisciplinary team in the pre-operative evaluation, medical management and surgical treatment are reported.

Granular cell tumour of the neurohypophysis: an unusual cause of hypopituitarism.

Granular cell tumours (GCT) are rare, slow-growing, benign neoplasms that are usually located in the head and neck. They are more frequent in the female gender and typically have an asymptomatic clinical course, being diagnosed only at autopsy. Symptomatic GCT of the neurohypophysis are exceedingly rare, being less than 70 cases described so far. The authors report on a case of a 28-year-old male that presented to the Endocrinology clinic with clinical and biochemical evidence of hypogonadism. He also reported minor headaches without any major visual symptoms. Further laboratory tests confirmed hypopituitarism (hypogonadotrophic hypogonadism, central hypothyroidism and hypocortisolism) and central nervous system imaging revealed a pituitary macroadenoma. The patient underwent transcranial pituitary adenoma resection and the pathology report described a GCT of the neurohypophysis with low mitotic index. The reported case is noteworthy for the rarity of the clinicopathological entity. LEARNING POINTS: Symptomatic GCTs are rare CNS tumours whose cell of origin is not well defined that usually give rise to visual symptoms, headache and endocrine dysfunction.Imaging is quite unspecific and diagnosis is difficult to establish preoperatively.Surgical excision is challenging due to lesion's high vascularity and propensity to adhere to adjacent structures.The reported case is noteworthy for the rarity of the clinicopathological entity.

Thyrotoxicosis leading to adrenal crises reveals primary bilateral adrenal lymphoma.

Primary adrenal lymphoma is a rare malignancy. It frequently presents bilaterally and with symptoms of adrenal insufficiency. Amiodarone may induce secondary organ dysfunction, and thyrotoxicosis develops in 15% of cases. The symptomatology of both conditions is nonspecific, especially in the elderly, and a high suspicion index is necessary for appropriate diagnosis. A 78-year-old female presented to the emergency department with confusion, nausea and vomiting. She had recently been to the emergency department with urinary tract infection, vomiting and acute hypochloremic hyponatremia. Upon re-evaluation, the leukocyturia persisted and because of TSH 0.01 µU/mL and free-T4 68 (10-18) pmol/L, she was admitted to the Endocrinology ward. Further evaluation supported amiodarone-induced thyroiditis type 2. Sepsis ensued, in the setting of nosocomial pneumonia. Hemodynamic instability, hyponatremia, hypoglycemia and vomiting raised the suspicion of adrenocortical insufficiency. Fluid resuscitation and hydrocortisone led to clinical improvement, and adrenal insufficiency was admitted. The thoracoabdominal tomography suggested an endobronchic primary lesion with hepatic and adrenal secondary deposits (6.6 and 7 cm), but this was confirmed neither on pleural effusion nor on bronchofibroscopic fluid analyses. The adrenals were not accessible for biopsy. Despite high-dose hydrocortisone maintenance, the patient died before definite diagnosis. The autopsy confirmed primary non-Hodgkin lymphoma. LEARNING POINTS: Primary adrenal lymphoma is a rare cause of adrenal insufficiency, but progression can be fast and fatal.Hyperpigmentation is frequently absent.The presenting symptoms are nonspecific and might mimic infection. Disproportion of the general state with signs of specific organ symptomatology is a diagnostic clue.Infection may precipitate adrenal crisis and worsen thyroid function with further adrenal insufficiency exacerbation.In the context of thyrotoxicosis, there may be little clinical response to a therapeutic trial with standard dose glucocorticoids.High-dose glucocorticoid substitution may be required to achieve clinical stability in thyrotoxic patients.