Endometrial hyperplasia classification: Difference between revisions
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==Overview== | ==Overview== | ||
==Classification== | |||
Like other [[hyperplasia|hyperplastic]] disorders, endometrial hyperplasia initially represents a [[physiology|physiological]] response of endometrial tissue to the growth-promoting actions of [[estrogen]]. However, the gland-forming cells of a hyperplastic endometrium may also undergo changes over time which predispose them to [[cancer]]ous transformation. Several [[microscopic|histopathology]] subtypes of endometrial hyperplasia are recognisable to the [[pathology|pathologist]], with different therapeutic and [[prognosis|prognostic]] implications.<ref name="Weidner's">{{cite book |author=Richard Cote, Saul Suster, Lawrence Weiss, Noel Weidner (Editor) |title=Modern Surgical Pathology (2 Volume Set) |publisher=W B Saunders |location=London |year= |pages= |isbn=0-7216-7253-1 |oclc= |doi=}}</ref> | |||
*Endometrial hyperplasia (simple or complex) - Irregularity and cystic expansion of glands (simple) or crowding and budding of glands (complex) without worrisome changes in the appearance of individual gland cells. In one study, 1.6% of patients diagnosed with these abnormalities eventually developed endometrial cancer.<ref name="Kurman">{{cite journal |author=Kurman RJ, Kaminski PF, Norris HJ |title=The behavior of endometrial hyperplasia. A long-term study of "untreated" hyperplasia in 170 patients |journal=Cancer |volume=56 |issue=2 |pages=403-12 |year=1985 |pmid=4005805 |doi=}}</ref> | |||
*Atypical endometrial hyperplasia (simple or complex) - Simple or complex architectural changes, with worrisome (''atypical'') changes in gland cells, including cell stratification, tufting, loss of nuclear polarity, enlarged nuclei, and an increase in [[mitosis|mitotic activity]]. These changes are similar to those seen in true cancer cells, but atypical hyperplasia does not show invasion into the connective tissues, the defining characteristic of cancer. The previously mentioned study found that 22% of patients with atypical hyperplasia eventually developed cancer.<ref name="Kurman">{{cite journal |author=Kurman RJ, Kaminski PF, Norris HJ |title=The behavior of endometrial hyperplasia. A long-term study of "untreated" hyperplasia in 170 patients |journal=Cancer |volume=56 |issue=2 |pages=403-12 |year=1985 |pmid=4005805 |doi=}}</ref> | |||
==References== | ==References== |
Revision as of 20:32, 20 January 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Classification
Like other hyperplastic disorders, endometrial hyperplasia initially represents a physiological response of endometrial tissue to the growth-promoting actions of estrogen. However, the gland-forming cells of a hyperplastic endometrium may also undergo changes over time which predispose them to cancerous transformation. Several histopathology subtypes of endometrial hyperplasia are recognisable to the pathologist, with different therapeutic and prognostic implications.[1]
- Endometrial hyperplasia (simple or complex) - Irregularity and cystic expansion of glands (simple) or crowding and budding of glands (complex) without worrisome changes in the appearance of individual gland cells. In one study, 1.6% of patients diagnosed with these abnormalities eventually developed endometrial cancer.[2]
- Atypical endometrial hyperplasia (simple or complex) - Simple or complex architectural changes, with worrisome (atypical) changes in gland cells, including cell stratification, tufting, loss of nuclear polarity, enlarged nuclei, and an increase in mitotic activity. These changes are similar to those seen in true cancer cells, but atypical hyperplasia does not show invasion into the connective tissues, the defining characteristic of cancer. The previously mentioned study found that 22% of patients with atypical hyperplasia eventually developed cancer.[2]
References
- ↑ Richard Cote, Saul Suster, Lawrence Weiss, Noel Weidner (Editor). Modern Surgical Pathology (2 Volume Set). London: W B Saunders. ISBN 0-7216-7253-1.
- ↑ 2.0 2.1 Kurman RJ, Kaminski PF, Norris HJ (1985). "The behavior of endometrial hyperplasia. A long-term study of "untreated" hyperplasia in 170 patients". Cancer. 56 (2): 403–12. PMID 4005805.