Pituitary apoplexy pathophysiology: Difference between revisions
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==Genetics== | ==Genetics== | ||
* | *Gene involved in the pathogenesis of pituitary apoplexy include mutation in AIP gene, which is located on chromosome 11q13.2 | ||
*The most common mutation site in AIP gene is p.R304 locus. | *The most common mutation site in AIP gene is p.R304 locus. | ||
*Mutated AIP loses its activity as a tumor supressor gene and leads to increased proliferation. | *Mutated AIP loses its activity as a tumor supressor gene and leads to increased proliferation. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]
Overview
Pathophysiology
Pituitary apoplexy is caused by bleeding into pituitary gland.
- Most often, pituitary apoplexy is seen with a pituitary adenoma.
- These adenomas have decreased blood supply, angiogenesis and have fenestrated endothelium surrounded by a variable number of smooth muscle cells, which are not found in normal pituitary gland.[1][2][3]
- In addition, the pituitary adenomas can outgrow their blood supply making them susceptible to bleeding and infarction. The bleeding may lead to increase in intrasellar pressure.
- The increased intrasellar pressure can compress the adjoining structures and lead to clinical symptoms of pituitary apoplexy.[4]
Genetics
- Gene involved in the pathogenesis of pituitary apoplexy include mutation in AIP gene, which is located on chromosome 11q13.2
- The most common mutation site in AIP gene is p.R304 locus.
- Mutated AIP loses its activity as a tumor supressor gene and leads to increased proliferation.
- The penetration of AIP postive carriers is 12-30%.
Associated conditions
Pituitary apoplexy is seen with 0.6 to 10% of pituitary adenomas.
Gross pathology
References
- ↑ Oldfield EH, Merrill MJ (2015). "Apoplexy of pituitary adenomas: the perfect storm". J Neurosurg. 122 (6): 1444–9. doi:10.3171/2014.10.JNS141720. PMID 25859802.
- ↑ Schechter J (1972). "Ultrastructural changes in the capillary bed of human pituitary tumors". Am J Pathol. 67 (1): 109–26. PMC 2032586. PMID 5055626.
- ↑ Schechter J, Goldsmith P, Wilson C, Weiner R (1988). "Morphological evidence for the presence of arteries in human prolactinomas". J Clin Endocrinol Metab. 67 (4): 713–9. doi:10.1210/jcem-67-4-713. PMID 3417848.
- ↑ Zayour DH, Selman WR, Arafah BM (2004). "Extreme elevation of intrasellar pressure in patients with pituitary tumor apoplexy: relation to pituitary function". J Clin Endocrinol Metab. 89 (11): 5649–54. doi:10.1210/jc.2004-0884. PMID 15531524.