Imaging description

The adenoma arises from the hypophyseal cells in the anterior pituitary, and when more than 1cm in diameter it is considered a macroadenoma. More than 30% of patients with macroadenoma have one or more hormone deficiencies at the time of presentation, most commonly growth hormone (GH) deficiency. The following laboratory studies are routinely performed: ACTH, free cortisol, thyrotroponin, thyroxine, prolactin, GH, IGF-1, testosterone, LH, FSH, and estradiol [1].

Histologically, pituitary adenomas are benign in nature, but they may enlarge and invade surrounding structures. They may be diagnosed early when they are endocrinologically active [1], but neurologically silent pituitary macroadenomas can extend into the suprasellar region (Fig. 35.1), invade surrounding structures, encase the internal carotid artery (ICA) (Fig. 35.2), invade the cavernous sinus, and extend into the sphenoidal sinuses (Fig. 35.3). Recently, two potential molecular markers, EMMPRIN and galectin-3, were found to be associated with aggressiveness and invasion by pituitary adenoma [2].

The presence of symptomatic pituitary adenoma is estimated to be close to 94 cases per 100 000 population. The pituitary adenomas represent about 10% of all intracranial neoplasms [3]. MRI is currently the diagnostic imaging modality of choice for pituitary macroadenomas, allowing for superior soft tissue differentiation and the ability to evaluate possible invasion of surrounding structures. The pituitary macroadenomas appear to be hypo- to isointense to gray matter, while on T2-weighted images they most commonly appear isointense to gray matter (Fig. 35.1). Some of the GH-producing adenomas display hypointense T2 signal. Postcontrast enhancement is generally strong but heterogeneous. Depending on the possibility of cystic degeneration and intratumoral hemorrhage, there may be small areas of fluid-fluid levels (Fig. 35.1E) or pituitary apoplexy within the macroadenoma (Fig. 35.4) [3,4].