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Pituitary Adenomas

Elaine Sunderlin, MD

PGY-2

Morning Report

March 19, 2010

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Laboratory Evaluation

Microadenoma Evaluation for hormonal hypersecretion (prolactin,

IGF-1, 24hr urine cortisol/overnight dexamethasonesuppression test)

Informal visual field evaluation Macroadenoma

Evaluation for hormonal hypersecretion (prolactin,IGF-1, 24hr urine cortisol/overnight dexamethasone

suppression test) Evaluation for hormonal hyposecretion (LH, FSH,

testosterone)

Formal visual fields

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Imaging Evaluation

Nonfunctioning microadenoma (2-4mm)

Likely need no further imaging

Nonfunctioning microadenoma (5-9mm)

MRI can be done once or twice over the subsequent 2yrs; if stable, frequency can be decreased

Nonfunctioning macroadenoma (< 20mm w/oneurologic abnormalities)

Monitor for adenoma size, visual changes, andhormonal hypersecretion in 6 and 12 months, thenannually for a few years

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Prolactinoma

Most common hormone-secreting pituitary tumors,approximately 40% of all pituitary tumors

Microprolactinomas more common

Prolactin (PRL) > 200 ng/mL. Levels between 20-200 could

be due to a prolactinoma or any other sellar mass Occur most frequently in females aged 20-50 years, gender

ratio of 10:1

Men: decreased libido, galactorrhea

Women: amenorrhea, galactorrhea

Occasionally prolactin is co-secreted with GH causingclinical syndrome of both prolactinemia and acromegaly

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Treatment of Prolactinomas

Regardless of size, medical therapy is first line toobtain normalization of prolactin levels

Dopamine agonists (DA) Bromocriptine (D2 receptor agonist, D1 antagonist)

2.5-15mg/day divided into 2-3 doses. Occasionallyrequires doses as high as 20-30mg/day Normalizes PRL levels, restores gonadal function, and

decreases tumor size in 80-90% of microadenomas and 70%of macroadenomas

Cabergoline (D2 selective agonist) 0.5-1mg/week Works in 95% of microadenomas and 80% of

macroadenomas

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Surgery

Surgical indications for prolactinomas

Sudden vision disturbance, associated w/ severeHA, altered consciousness and vascular collapse

2/2 apoplexy Failure of medical therapy (inadequate PRL

reduction on high doses of Das or tumorenlargement)

Expanding prolactinomas associated w/ unstableneurological and ophthalmologic deficitsunresponding to DAs

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Pituitary Apoplexy

Acute infarction or hemorrhage into the pituitary gland

Usually life-threatening emergency

Severe headaches, visual loss, altered consciousness,

and impaired pituitary function Predisposing factors: closed head trauma, blood

pressure alterations, h/o pituitary irradiation, cardiacsurgery, anticoagulation, treatment with DAs, andpregnancy

The majority of patients present with, at least, partialhypopituitarism. Deficit in ACTH leads to acuteglucocorticoid deficiency

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Acromegaly Symptoms

Sweaty, oily skin; skin tags; macroglossia

Broadened hands and feets

Jaw thickening, teeth separation, nasal bone

hypertrophy

Carpal tunnel syndrome, ulnar nerve neuropathy

Headache

Arthralgias and myalgias

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References

UpToDate

Colao, Annamaria. The Prolactinoma, Best Practice &Research Clinical Endocrinology & Metabolism;23, 2009;575-596.

Chanson MD, Phillipe, et.al. Acromegaly, Best Practice &Research Clinical Endocrinology & Metabolism;23, 2009;555-574

Murad-Kejbou S, Eggenberg E. Pituitary apoplexy: evaluation,management, and prognosis, Curr Opin Ophthalmol.2009,Nov;20(6);456-61

Chang, Claudia, et.al. Pituitary tumor apoplexy. Arq. Neuro-Psiquiatr. vol.67 no.2a So Paulo June 2009