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%, at times identified incidentally on magnetic resonance imaging (MRI)
• 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, or visual changes

Epidemiology

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

Incidence

• 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.
• PRL increased by functional prolactinomas or inhibited dopaminergic suppression by stalk effect

Genetics

• 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)
• MEN1-like phenotype (MEN4): germline mutation in the cyclin-dependent kinase inhibitor 1B (CDKN1B) (2)
• Gs-alpha (G_sα): an activating mutation of the guanine nucleotide stimulatory protein (G_sα) gene found in ~40% of somatotroph adenomas (3)

Risk Factors

Multiple endocrine neoplasias