Pituitary adenoma

Epidemiology
3rd most common brain tumor after glioma, meningioma
Many tumors are clinically silent; ~10% of patients in autopsy series have occult pituitary adenoma (PMID 15760793)
More common in women

Risk Factors
Only known genetic association is MEN1 (mutation on 11q13; parathyroid tumors, pancreatic islet cell tumor, pituitary adenoma)

Anatomy/Physiology
Adenohypophysis: secretes GH, prolactin, TSH, ACTH, gonadotropins (FSH/LH); source of nearly all pituitary tumors
Neurohypophysis: secretes ADH, oxytocin

Clinical
Up to 70% are endocrinologically active although this percentage is decreasing as the proportion of tumors found incidentally on imaging has increased

Endocrinopathies (most to least common): prolactinoma, acromegaly (GH), Cushing's disease (ACTH), hyperthyroidism (TRH), hypergonadotropism (FSH/LH)...last two are quite rare

Hyperprolactinemia can occur with any sellar mass due to compression of the stalk (stops dopamine from reaching the pituitary and suppressing prolactin secretion).  This syndrome is usually associated with serum prolactin < ~150ng/mL.

Headache

Bitemporal hemianopsia 

Cavernous sinus extension (cranial nerve palsies III, IV, V-1, V-2, VI)

Treatment
Surgery is the mainstay

Indications for XRT
Residual or recurrent macroadenoma
Refractory endocrinopathy

RT: techniques and side effects
Nonfunctional macroadenoma gets 16Gy to 50% line (50.4-54Gy for fractionated RT)

Functioning tumors may need higher doses for control but control rates for secretory tumors are difficult to judge given wildly varying definitions of endocrinologic control in the literature (PMID 15871511)

Endocrinologic control is less likely than tumor growth control: 80-90% of non-secretory macroadenomas are controlled; ~70% of prolactinomas; 50-60% of GH, ACTH secreting tumors

SRS is contraindicated if anticipated dose to chiasm/optic N. is > 8Gy (usually corresponds to 5mm separation)

Post-treatment hypopituitarism is the most important complication