The pituitary gland lies in the pituitary fossa (sella turcica), which is situated in the middle cranial fossa at the base of the brain. It is linked functionally to the hypothalamus by the pituitary stalk. The hypothalamus lies in a superior position to the pituitary gland, and the link between the two organs is critical for normal pituitary gland function.
The anterior pituitary secretes growth hormone, thyrotropin or thyroid-stimulating hormone, corticotropin or adrenocorticotropic hormone, follicle-stimulating hormone, luteinizing hormone, and prolactin. The posterior lobe secretes arginine vasopressin (also called antidiuretic hormone) and oxytocin.
Pituitary masses may be classified based on their underlying etiology: for example, pituitary adenoma, pituitary hyperplasia, nonadenomatous tumors, and vascular, inflammatory, or infective lesions.
Most pituitary masses are caused by a pituitary adenoma; these are benign tumors arising from the anterior pituitary gland. Pituitary adenomas are classified as functional (hormone secreting) or nonfunctional, and can be further categorized by cell type or size, for example, microadenomas (<10 mm) or macroadenomas (>10 mm).
Pituitary masses may present with a clinical syndrome resulting from hypersecretion of ≥1 anterior pituitary hormones (e.g., Cushing disease, acromegaly). Alternatively, they may present more insidiously with mass effect or with tumor expansion leading to compression of surrounding structures, including normal pituitary tissue, resulting in hypopituitarism. Functional pituitary tumors can produce a complex picture of combined hormonal excess and/or deficiencies.
Analyses using autopsy and radiologic data suggest primary adenoma prevalence rates of 14.4% and 22.5%, respectively (yielding an overall estimated prevalence rate of 16.7%). Almost all of these are clinically silent microadenomas. The prevalence increases with age, and detection is more likely using high-resolution MRI sequences.
- Nonfunctional adenoma
- Gonadotropin-secreting adenoma
- Lactotroph hyperplasia
- Adrenocorticotropic hormone (ACTH)-secreting adenoma
- Growth hormone (GH)-secreting adenoma
- Thyroid-stimulating hormone (TSH)-secreting adenoma
- Thyrotroph hyperplasia
- Gonadotroph hyperplasia
- Somatotroph hyperplasia
- Corticotroph hyperplasia
- Germ cell tumors
- Metastatic disease
- Lymphocytic hypophysitis
- Drug therapy-induced hypophysitis
- Pituitary abscess
- Pituitary apoplexy
- Cerebral aneurysm
- Rathke cleft cyst
- Empty sella syndrome
- Pituitary carcinoma
Joe M. Chehade, MD
Professor of Medicine
Division of Endocrinology
University of Florida
JMC declares that he has no competing interests.
Dr Joe M. Chehade would like to gratefully acknowledge Dr Senan Sultan, a previous contributor to this topic. SS declares that he has no competing interests.
Federico Roncaroli, MD
Reader in Neuropathology and Honorary Consultant in Neuropathology
Department of Clinical Neuroscience
Division of Neuroscience and Mental Health
Faculty of Medicine
FR declares that he has no competing interests.
Tony Heaney, MD, PhD
Pituitary Tumor and Neuroendocrine Program
Medicine and Neurosurgery
David Geffen School of Medicine at UCLA
TH declares that he has no competing interests.
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