Error message

Deprecated function: The each() function is deprecated. This message will be suppressed on further calls in book_prev() (line 775 of /home/pathwa23/public_html/modules/book/book.module).

Pituitary Adenoma

  • Neoplasms of the hormone-secreting cells of the anterior pituitary are relatively common and account for nearly 15% of all brain tumors. The majority of such neoplasms are functional and thus secrete endocrinologically-active hormones that result in characteristic syndromes depending on which hormone is excessively released. In addition, growth of the tumors can impinge on local structures resulting in symptoms associated with local mass effects.
  • Neoplasias of the anterior pituitary are monoclonal in origin and thus involve excessive growth of a particular anterior pituitary cell type, such as lactotrophs, somatotrophs, and corticotrophs, gonadotrophs, or thyrotrophs. In general, the neoplastic cells continue to secrete only their respective hormone although in some cases they may gain additional synthetic functionality resulting in multiple hormone synthesis. The most common mixed-synthetic neoplasias are those which secrete both prolactin and growth hormone. Pituitary adenomas are almost always benign and slow-growing although with time they can locally invade adjacent structures. In general, these tumors remain well-circumscribed and contain well-differentiated cells which almost never undergo metastasis.
Clinical Consequences
  • Overview
    • As mentioned, the clinical consequences of pituitary adenomas depend on whether the tumors are functional and if so what particular hormones they synthesize. If functional, neoplastic cells secrete their respective hormones in the absence of physiological feedback mechanisms thus resulting syndromes associated with particular hormone excess. In addition, tumors may manifest due to their local mass effects although this is more common in non-functional adenomas which do not secrete hormones and thus do not present early as a result of endocrine clinical consequences.
  • Endocrine Consequences
    • Prolactin-secreting Adenomas: These are tumors of lactotrophs are termed "Prolactinomas" and result in the clinical syndrome of hyperprolactinemia
    • Growth Hormone-secreting Adenomas: These are tumors of somatotrophs and result in the clinical syndromes of Growth Hormone Excess, either gigantism or acromegaly depending on the age of onset. A large subset of these tumors also synthesize prolactin and thus manifest with signs of hyperprolactinemia
    • ACTH-secreting Adenomas: These are tumors of corticotrophs and result in excess production of endogenous cortisol which leads to Cushing Syndrome
    • LH and FSH-secreting Adenomas: These tumors of gonadotrophs may cause decreased libido but often are clinically silent
    • TSH-secreting Adenomas: These relatively rare tumors of thyrotrophs result in hyperthyroidism
  • Local Mass Effects
    • Given the relatively tight anatomic quarters of the sella turcica, growth of pituitary adenomas can impinge on important local structures resulting in particular clinical consequences depending on how the tumor expands. These local mass effects are often the only clinical consequences of non-functional pituitary adenomas although functional neoplasms also frequently give rise to these signs and symptoms
    • In most cases, the rise in intracranial pressure will lead to headaches. Pressure on the optic chiasm can lead to bilateral hemianopia although in some cases direct invasion of the optic nerve can manifest as visual impairment.
    • In certain cases, expansion of the adenoma will destroy normal anterior pituitary tissue leading to signs and symptoms associated with hypopituitarism. Finally, in some patients the expanding neoplasm places pressure on the hypothalamic-pituitary portal vessels and thus eliminates the capacity of the hypothalamus to control anterior pituitary hormone secretion (See: Basic Hypothalamic-Pituitary Coordination). This "Stalk Effect" results in deficient release of most anterior pituitary hormones causing hypopituitarism. However, because pituitary release of prolactin is controlled through inhibition by hypothalamic dopamine, the stalk effect will cause mild hyperprolactinemia.