World Neurosurg
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Case Reports
Prolactin-Secreting Pituitary Carcinoma with Dural Metastasis: Diagnosis, Treatment, and Future Directions.
Pituitary carcinoma is extremely rare, representing approximately 0.2% of all surgically resected pituitary neoplasms. It is thought to arise from World Health Organization grade II (atypical) pituitary adenomas. Pituitary carcinoma is defined by metastasis; it is otherwise indistinguishable from atypical pituitary adenomas, which can be considered carcinoma in situ. Pituitary carcinoma is difficult to diagnose and treat and is associated with poor long-term outcomes. ⋯ Long-term surveillance using serum prolactin as a tumor biomarker and correlation to imaging studies were critical for the diagnosis and interval screening for recurrence. This technique can be applied to all secretory atypical pituitary adenomas to improve early detection of potential metastasis. Further research, especially of genetic and epigenetic characteristics, could readily improve the diagnosis and treatment of pituitary carcinomas.
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The 2 paired arteries-the posterior communicating arteries (PCoAs) and the precommunicating parts of the posterior cerebral arteries-form the so-called posterior segment of the cerebral arterial circle on the base of the brain. A number of (ab)normal morphologic features were described in the literature (e.g., unusual kinking, or extreme elongations, hypoplasia, duplications, fenestrations, the infundibular widening, or aplasia of the PCoA in the prenatal and/or postnatal periods). The aim of this study was to analyze an incidence of various fenestrations and duplications of the PCoA, and describe their general features and their association with other vascular abnormalities. ⋯ After thorough examination, the fenestrations and duplications of the PCoA are distinguished as 2 special forms of vascular abnormalities, and the PCoA duplications are characterized as partial and total. Furthermore, whereas the low incidence of a fenestration of the PCoA suggests it to be a sufficiently rare phenomenon, the duplications of the PCoA trunk are fairly frequent, especially concerning its terminal segment.
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Primary hypothyroidism can cause both hyperprolactinemia and pituitary hyperplasia. The degree of hyperprolactinemia is generally modest, and rarely do prolactin concentrations exceed 100 ng/mL (4.34 nmol/L). This combination of hyperprolactinemia and pituitary gland enlargement might raise suspicion for a prolactinoma or a nonfunctioning adenoma limiting the ability of hypothalamic dopamine to inhibit prolactin production, the so-called "stalk effect." ⋯ Primary hypothyroidism can cause hyperprolactinemia, and prolonged disease may lead to pituitary hyperplasia. However, a marked elevation of prolactin should raise suspicion to investigate additional etiologies for hyperprolactinemia. Our case exemplifies a dual etiology for hyperprolactinemia and pituitary hyperplasia caused by both hypothyroidism and macroprolactin. This knowledge is invaluable for clinicians to avoid unnecessary management with dopamine agonists and/or surgery. This patient's prolactin was 323 ng/mL (14.06 nmol/L). Before our case, the highest prolactin in a hypothyroid patient reported in the literature was 253 ng/mL (11.0 nmol/L).