Description

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

• Pituitary adenomas have been identified as the 3rd most frequent intracranial tumor; accounts for 10–25%.
• Autopsy and radiologic data suggest that 1/6 have pituitary “incidentalomas.”
• Subtypes (hormonal): Prolactinoma (PRL) 50%, nonfunctioning pituitary adenomas 30%, somatotroph adenoma (growth hormone [GH]) 15–20%, corticotroph adenoma (adrenocorticotrophic hormone [ACTH]) 5–10%, thyrotroph adenoma (thyroid-stimulating hormone [TSH]) <1%, gonadotropinoma (luteinizing hormone/follicle-stimulating hormone [LH/FSH]), mixed
• 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.
• Clinically apparent pituitary tumors are seen in 18/100,000 persons.

Risk Factors

Multiple endocrine neoplasia I

• 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.
• McCune-Albright syndrome
• Multiple endocrine neoplasia type 1 (MEN-1)-like phenotype (MEN-4): Germline mutation in the cyclin-dependent kinase inhibitor 1B (CDKN1B)

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