Pituitary Adenomas
What is it?
Pituitary adenomas (PA) are benign tumors affecting the pituitary gland. The pituitary gland is an endocrine gland located in a bony cavity in sphenoid bone in the middle cranial fossa, called sella turcica, and it measures approximately 9 mm, being bigger in puberty and pregnancy and smaller in children and older adults. It lies immediately below the hypothalamus and optic chiasm and it is usually divided into anterior and posterior part, the anterior pituitary and the posterior pituitary or neurohypophysis which is a protrusion of the hypothalamus. It is surrounded by a dural fold called diaphragma sellae with an opening for the infundibular stalk.
Pituitary gland produces hormones and regulates hormone secretion by other endocrine glands, acting as a “control panel” for many vital body functions including growth, blood pressure, metabolism and reproduction. Hormones secreted by pituitary include growth hormone or somatotropin (GH), thyroid stimulating hormone (TSH), adenocorticotropic hormone (ACTH), follicular stimulating hormone (FSH), luteinizing hormone (LH) and prolactin. Their release is controlled by releasing hormone produced by the hypothalamus with the exception of prolactin, whose production is tonically inhibited by dopamine.
PA are the third most common brain tumor accounting for 10-15% of all CNS neoplasms. The peak incidence of pituitary adenomas occurs between the ages of 30 and 60 years, and occurs earlier in women (20-45 years) than in men (35-60 years) owing to the greater frequency of prolactinomas in young women.
They are generally classified by size distinguishing microadenomas (up to 10 mm in diameter) and macroadenomas. Microadenomas are diagnosed if hormone hypersecretion causes symptoms or incidentally, in these cases treatment aims at remission of hormone hypersecretion, preservation of normal pituitary function. In macroadenomas treatment aims also at nervous structures decompression and tumor control.
Which are the symptoms?
PA may also be classified by clinical behavior in non-functioning and functioning.
In non-functioning PA symptoms are related to mass-effect and compression of surrounding tissues: visual field loss (usually bitemporal) for optic chiasm compression, loss of visual acuity or inability to perceive colors in optic nerve compression, headache, hypopituitarism for normal gland compression, hydrocephalus for growth into the third ventricle, facial pain and paresthesia from involvement of cranial nerves.
Functioning PA produces symptoms according to hormone secretion:
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GH producing – acromegaly. The syndrome includes acral growth, hyperidrosis, asthenia, arthralgia, glucose intolerance and diabetes, hypertension and organ damage, carpal tunnel syndrome. The disease is often diagnoses when it causes changes in external features and at this point it has already caused organ damage. If untreated, GH-producing PA may also cause visual problems.
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PRL producing (prolactinomas). They cause secondary amenorrhea or oligomenorrhea, galactorrhea, and gynecomastia. In men the presenting symptoms are loss of libido and impotence with decreased sperm count.
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ACTH-producing – Cushing disease. The disease is more frequent in female and has a poor prognosis, it presents with centripetal obesity, plethoric moon-shaped face, hirsutism, hypertension, muscle weakness, mental disorders, amenorrhea and strie rubrae.
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TSH-producing. It causes hyperthyroidism: increased perspiration, hand tremors, difficulty in sleeping, thinning of the skin and fine and brittle hair, muscular weakness, more frequent bowel movements and weight loss. A thyroid storm is a rare but severe complication of hyperthyroidism occurring when a thyrotoxic patient becomes very sick or physically stressed; it present with an increase in body temperature to over 40 degrees Celsius, tachycardia, vomiting and diarrhea and dehydration.
How is it diagnosed?
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Blood sample for hormone testing
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CT scan. Computed tomography (CT) with intravenous contrast enhancement is less effective than MRI in diagnosing small adenomas and in defining the extension of large tumors, but may be used if MRI is unavailable or contraindicated.
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Brain MRI. The preferred imaging study is MRI of the sellar region which can provide details of the tumor location, size, extent, and relation to surrounding structures such as the optic chiasm and cavernous sinuses.
Suggested exams
How is it treated?
Surgery. The choice is made according to tumor size and characteristics.
- Transsphenoidal. The patient is under general anesthesia and a 2-cm incision is made at the buccogingival junction crossing the midline symmetrically, the nasal spina is exposed and dissection starts, developing a septal submucosal unilateral tunnel to reach the rostrum sphenoidale. A large piece of the upper bony septum is removed and preserved in antibiotic solution for the sellar closure. The anterior wall of the sphenoid is opened and the sellar wall identified, the sellar floor and the dura are opened to reach the pituitary adenoma. After tumor removal, a dural patch is employed and a fragment of bone from the nasal septum is placed superficially with fibrin glue. An antibiotic solution of rifamycin is left in the sphenoid sinus after washing with peroxide and saline solution. Bilateral anterior nasal packing is performed with two standard dressings, having pushed the septal mucosa medially to cover the residual bony and cartilaginous septum. The sublabial wound then is sutured with absorbable thread and the patient is awakened immediately.
- Craniotomy (frontotemporal-orbitozygomatic approach)
Medical treatment
- Somatostatin analogs for acromegaly
- Dopamine agonists such as bromocriptine and cabergoline for prolactinomas
- Anti-thyroid drugs for TSHomas
Radiation treatment. It can be employed as a first-line treatment or perfomed after surgery.
Where do we treat it?
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