Endometrial hyperplasia: Difference between revisions
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Revision as of 03:08, 7 March 2010
| Endometrial hyperplasia | |
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| Specialty | Gynaecology  |
Endometrial hyperplasia is a condition of excessive proliferation of the cells of the endometrium, or inner lining of the uterus.
Most cases of endometrial hyperplasia result from high levels of estrogens, combined with insufficient levels of the progesterone-like hormones which ordinarily counteract estrogen's proliferative effects on this tissue. This may occur in a number of settings, including polycystic ovary syndrome, estrogen producing tumours (e.g. granulosa cell tumour) and certain formulations of estrogen replacement therapy. Endometrial hyperplasia is a significant risk factor for the development of endometrial cancer so careful monitoring and treatment of women with this disorder is essential.
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]
Diagnosis
Diagnosis of endometrial hyperplasia is typically performed though curettage of the uterine cavity to obtain endometrial tissue for histopathologic analysis. A workup for endometrial disease may be prompted by abnormal uterine bleeding, or the presence of atypical glandular cells on a pap smear.[3]
Treatment
Treatment of endometrial hyperplasia is individualized, and may include hormonal therapy, such as cyclic or continuous progestin therapy, or hysterectomy.[3]
References
- ^ Richard Cote, Saul Suster, Lawrence Weiss, Noel Weidner (Editor) (2002). Modern Surgical Pathology (2 Volume Set). London: W B Saunders. ISBN 0-7216-7253-1.
{{cite book}}:|author=has generic name (help)CS1 maint: multiple names: authors list (link) - ^ a b 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. doi:10.1002/1097-0142(19850715)56:2<403::AID-CNCR2820560233>3.0.CO;2-X. PMID 4005805.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ a b Howard A Zacur, Robert L Giuntoli, II, Marcus Jurema, Endometrial Hyperplasia, UpToDate Online (subscription required), retrieved 2007-05-26
{{citation}}: CS1 maint: multiple names: authors list (link)