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Pituitary adenomas are present in 20-25% of "normal" adults, as shown by MRI. Clinically significant adenomas appear most often from the thirties to fifties.
Pituitary adenomas account for about 10% of intracranial neoplasms and are discovered incidentally in up to 25% of routine autopsies.
The most common cause of hyperpituitarism is an adenoma arising in the anterior lobe.
Prolactinomas are the most common type of functioning adenoma, accounting for up to 30% of all clinically recognized tumours.
Tumours under 1 cm are termed microadenomas, while those over 1 cm are called macroadenomas.
a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.
About 3% of pituitary adenomas are associated with multiple endocrine neoplasia (MEN) type I, though most are isolated lesions.
G-protein mutations are the best-characterized molecular abnormalities. G proteins play a critical role in hormonal signal transduction. Ras and MYC mutations confer a more aggressive phenotype.
Pituitary adenomas are usually composed of a single cell type and produce a single hormone, though some can secrete more than one.
Pituitary adenomas can be functional, producing excess hormones, or silent, not causing any noticable effects.
Adenomas of various types produce mass effects, including:
Prolactinomas have a tendency to calcify. Increased prolactin levels (hyperprolactinemia) cause amenorrhea, galactorrhea, loss of libido, and infertility.
30-35% of all pituitary tumours are non-functional, with most of these producing LH or FSH.
With microadenomas, hormone control is important.
For prolactinomas, dopamine agonists such as bromocriptine or cabergoline can be used. About 20% of people are resistant to dopamine agonists.
Surgery can be done for macroadenomas.
Stereotactic radiosurgery can be done as well.
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