Pituitary Adenoma

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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


  • 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.
  • PRL 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

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