Pituitary Adenoma

Description

Typically benign, slow-growing tumors that arise from cells in the pituitary gland

• Pituitary adenomas have been identified as the third most frequent intracranial tumor; accounts for 10–25%
• Subtypes (hormonal): prolactinoma (PRL) 25–40%, nonfunctioning pituitary adenomas 30%, somatotroph adenoma (growth hormone [GH]) 15–20%, corticotroph adenoma (adrenocorticotropic hormone [ACTH]) 5–10%, thyrotroph adenoma (thyroid-stimulating hormone [TSH]) <1%, gonadotropinoma (luteinizing hormone/follicle-stimulating hormone [LH/FSH]), mixed (1)[A]
• Defined as microadenoma <10 mm and macroadenoma ≥10 mm
• May secrete hormones and/or cause mass effects

Epidemiology

• Predominant age: Age increases incidence.
• Predominant sex: female > male (3:2) for microadenomas (often delayed diagnosis in men)

• Autopsy studies have found microadenomas in 3–27% and macroadenomas in <0.5% of people without any pituitary disorders.
• MRI scans illustrate abnormalities consistent with pituitary adenoma in 1/10 persons.
• Clinically apparent pituitary tumors are seen in 18/100,000 persons.

Etiology and Pathophysiology

• Monoclonal adenohypophysial cell growth
• Hormonal effects of functional microadenomas often prompt diagnosis before mass effect.
• Prolactin increased by functional prolactinomas or inhibited dopaminergic suppression by stalk effect

• Carney complex
• Familial isolated pituitary adenomas: ~15% have mutations in the aryl hydrocarbon receptor–interacting protein gene (AIP); present at a younger age and are larger in size (2)
• McCune-Albright syndrome
• Multiple endocrine neoplasia type 1 (MEN1)–like phenotype (MEN4): germline mutation in the cyclin-dependent kinase inhibitor 1B (CDKN1B) (2)

Risk Factors

Multiple endocrine neoplasias