Pituitary adenoma are primary tumours than occur in the pituitary gland and are one of the most common intracranial neoplasms.
Depending on their size they are broadly classified into:
- pituitary microadenoma : less than 10 mm in size
- pituitary macroadenoma : greater than 10 mm in size
Although this distinction is largely arbitrary, it is commonly used and does highlight an important fact: small intra-pituitary lesions (microadenomas) present differently and have different surgical and imaging challenges than larger lesions (macroadenomas) which extend into the suprasellar region. As such it is not unreasonable to discuss them separately. Below is general overview.
Pituitary adenomas are common, with rates varying widely depending on definition: population prevalence ~ 0.1 %; autopsy prevalence ~ 15 % 2. They account for approximately 10% of all intracranial neoplasms and 30-50% of all pituitary region masses 3.
Pituitary macroadenomas are approximately twice as common as microadenomas 3.
A minority of tumours are associated with multiple endocrine neoplasia type I (MEN I).
Pituitary adenomas present either due to hormal imbalance (both microadenomas and macroadenomas) or mass effect on adjacent structures (macroadenomas), classically the optic chiasm. Rarely presentation can be catastrophic, due to pituitary apoplexy.
Over half of all adenomas are secretory 2, although even when this is the case this may not be the cause of presentation. A lack of libido or even galactorhhea may not lead to presentation, and as such many secreting tumours are only diagnosed when mass effect occur (see below).
Hormones secreted include:
- secretory : ~ 65 %
- prolactin : ~ 48 %
- growth hormone (GH) : 10 %
- adrenocorticotropin (ACTH) : 6 %
- thyrotropin (TSH) : 1 %
- mixed :
- non secretory : ~ 35 % most tend to be macrodenomas
It is also important to note that larger tumours can lead to hormonal imbalance due to mass effect rather than secretion. Hypopituitarism or moderately elevated prolactin are both seen, the later due to so-called stalk effect; prolactin release (unlike other pituitary hormones) is tonically inhibited by prolactin inhibitory hormone (aka dopamine) and as such compression of the pituitary infundibulum can result in elevation of systemic prolactin levels due to interruption of normal inhibition.
Most of the cases presenting due to mass effect are due to non-secreting macroadenomas 3 and the most common structure to be compressed by a macroadenoma is the optic chiasm. Invasion into the cavernous sinus is also encountered, with occasional compression of the oculomotor (CN III) or less frequently abducens (CN VI) nerves. Uncommonly large tumours may result in hydrocephalus (by compressing the midbrain or distorting the third ventricle), orbital or sinonasal symptoms.
Radiographic features are discussed separately:
Treatment and prognosis
Treatment of pituitary adenomas depends on a number of factors:
- size and presence of symptoms related to mass effect - these will often necessitate surgical decompression regardless of cell type
- cell type - prolactin and growth hormone secreting tumours can often be treated medically
The most commonly employed approach to pituitary masses is transphenoidally, whereby the floor of the pituitary fossa is accessed via the nasal cavity. In large tumours other approaches may be necessary (e.g. craniotomy).
Medical management of prolactinomas relies on administering a dopamine agonist (e.g. bromocriptine). Although it can dramatically reduce the size of a macroadenoma, it has been associated with increased incidence of haemorrhage into the tumour 4.
Growth hormone secreting tumours are usually surgically resected, however in recurrent cases or in patients who are not able to undergo surgery they can be treated with octreotide (a long-acting somatostatin analogue) . This can result in both reduction of the size of the tumour and reduction in the serum levels of growth hormone 4-5.
Radiosurgery is also occasionally used. Its main complications are hypopituitarism (seen in up to 70% of cases). Less common complications include damage to the optic apparatus (optic nerves, chiasm, tracts), cranial nerves and internal carotid arteries 7.
Recurrent symptoms requiring further intervention is relatively common, with 18% of patients with non-functioning tumours and 25% of patients with prolactinomas eventually needing further treatment 6.
- 1. Davis PC, Hoffman JC, Spencer T et-al. MR imaging of pituitary adenoma: CT, clinical, and surgical correlation. AJR Am J Roentgenol. 1987;148 (4): 797-802. AJR Am J Roentgenol (abstract) - Pubmed citation
- 2. Gutenberg A, Larsen J, Lupi I et-al. A radiologic score to distinguish autoimmune hypophysitis from nonsecreting pituitary adenoma preoperatively. AJNR Am J Neuroradiol. 2009;30 (9): 1766-72. doi:10.3174/ajnr.A1714 - Pubmed citation
- 3. Pisaneschi M, Kapoor G. Imaging the sella and parasellar region. Neuroimaging Clin. N. Am. 2005;15 (1): 203-19. doi:10.1016/j.nic.2005.02.007 - Pubmed citation
- 4. Newton HB, Jolesz FA. Handbook of neuro-oncology neuroimaging. Academic Pr. (2008) ISBN:012370863X. Read it at Google Books - Find it at Amazon
- 5. Lundin P, Edén engström B, Karlsson FA et-al. Long-term octreotide therapy in growth hormone-secreting pituitary adenomas: evaluation with serial MR. AJNR Am J Neuroradiol. 1997;18 (4): 765-72. AJNR Am J Neuroradiol (abstract) - Pubmed citation
- 6. Thapar K. Diagnosis and management of pituitary tumors. Humana Pr Inc. (2001) ISBN:0896034038. Read it at Google Books - Find it at Amazon
- 7. Lunsford LD, Sheehan JP. Intracranial Stereotactic Radiosurgery. Thieme Medical Pub. (2009) ISBN:1604062002. Read it at Google Books - Find it at Amazon
Synonyms & Alternative Spellings
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|Adenoma of pituitary gland||✗|
|Adenoma of pituitary||✗|