Abstract
To analyze the clinical, laboratory, and radiological findings and management of patients with clinical pituitary apoplexy and to screen for aryl hydrocarbon receptor-interacting protein (AIP) mutations. The clinical findings were collected from the medical records of consecutive sporadic pituitary adenoma patients with clinical apoplexy. Possible precipitating factors, laboratory data, magnetic resonance imaging (MRI) findings and treatment were also analyzed. Peripheral blood samples were obtained for DNA extraction from leukocytes, and the entire AIP coding region was sequenced. Thirty-five patients with pituitary adenoma were included, and 23 (67%) had non-functioning pituitary adenomas. Headache was observed in 31 (89%) patients. No clear precipitating factor was identified. Hypopituitarism was observed in 14 (40%) patients. MRI from 20 patients was analyzed, and 10 (50%) maintained a hyperintense signal in MRI performed more than three weeks after pituitary apoplexy (PA). Surgery was performed in ten (28%) patients, and 25 (72%) were treated conservatively with good outcomes. No AIP mutation was found in this cohort. Patients with stable neuroophthalmological impairments can be treated conservatively if no significant visual loss is present. Our radiological findings suggest that hematoma absorption lasts more than that observed in other parts of the brain. Additionally, our study suggests no benefits of AIP mutation screening in sporadic patients with apoplexy.
Highlights
Pituitary apoplexy (PA) is an acute event associated with hemorrhage or infarction and occurs in approximately 2% to 12% of those with a preexisting pituitary adenoma [1,2,3,4]
We evaluated the frequency of AIP mutations (AIPmuts) in these apparently sporadic pituitary adenoma patients
Non-functioning pituitary adenomas were present in 23 patients (66%), seven (20%) harbored somatotropinomas, and five (14%) harbored prolactinomas
Summary
Pituitary apoplexy (PA) is an acute event associated with hemorrhage or infarction and occurs in approximately 2% to 12% of those with a preexisting pituitary adenoma [1,2,3,4]. The pathophysiology of apoplexy involves changes in the pituitary blood supply and can be related to rapid tumor enlargement that increases metabolic demand and intrasellar pressure, leading to the compression of adjacent structures [7]. Nonfunctioning pituitary adenomas (NFPAs) are the most prevalent in a series of apoplexy, likely related to silent growth, identified only after the development of a mass effect [3,9,11].
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