Endometrial hyperplasia pathophysiology
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Endometrial hyperplasia Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Soujanya Thummathati, MBBS [2]
Overview
Endometrial hyperplasia is a condition of excessive proliferation of the endometrial cells (inner lining of the uterus) associated with an increased gland to stroma ratio. The majority of cases of endometrial hyperplasia result from high concentrations of estrogen combined with insufficient concentration of the progesterone-like hormones which normally counteract the proliferative effects of estrogen on the endometrial tissue.[1] Anovulation results in the prolonged release of estrogen and the relative lack of progesterone resulting in excessive stimulation of the endometrium. Unopposed oestrogen stimulation may be either from an endogenous or exogenous source.[1][2]
Pathophysiology
Pathogenesis
- Endometrial hyperplasia is a condition of excessive proliferation of the endometrial cells (inner lining of the uterus) associated with an increased gland to stroma ratio.
- The majority of cases of endometrial hyperplasia result from high concentrations of estrogen combined with insufficient concentration of the progesterone-like hormones which normally counteract the proliferative effects of estrogen on the endometrial tissue.[1]
- Normal endometrial changes during menstrual cycle:[3]
- The proliferative phase is the second phase in normal mentrual cycle when estrogen causes the lining of the uterus to proliferate. As the ovarian follicles mature, they begin to secrete increasing amounts of estradiol and estrogen. The estrogens initiate the formation of a new layer of endometrium in the uterus, histologically identified as the proliferative endometrium.
- After ovulation, the remains of the dominant follicle in the ovary become a corpus luteum which produces large amounts of progesterone.
- Anovulation results in the prolonged release of estrogen and the relative lack of progesterone resulting in excessive stimulation of the endometrium.
- Unopposed estrogen stimulation may be either from an endogenous or exogenous source.[2][1]
- Excessive endogenous estrogen in pre or perimenopausal women may result from chronic anovulation caused by obesity, polycystic ovary disease, and estrogen producing tumors (e.g. granulosa cell tumor).
- Excessive exogenous estrogen may result from hormone replacement therapy or non-prescription herbal medications.
- Tamoxifen therapy in breast cancer patients results in an endometrial lesion within 6-36 months of therapy.[4]
- Tamoxifen is a non-steroidal anti-estrogen that binds to the estrogen receptor and is used primarily for adjuvant therapy in breast cancer
- Tamoxifen may also act as an estrogen agonist in a low estradiol environment
- Any patient who develops bleeding while on tamoxifen needs evaluation
- Endometrial hyperplasia may rarely result from the peripheral conversion of androgens to estrogens in androgen-secreting tumors of the adrenal cortex.[5]
Microscopic Pathology
- Prolonged estrogenic stimulation results in larger, more complex, and proliferating endometrial glands.[2]
- On microscopic histopathological analysis, the proliferating endometrium is characterized by the following:[6]
| Character | Simple hyperplasia | Complex hyperplasia |
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Gland to stroma ratio |
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Endometrium |
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Mitoses |
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Nuclear atypia |
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Gallery
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![Diagram illustrating how the uterus lining builds up and breaks down during the menstrual cycle[7]](/images/9/9f/Lining_of_Uterine_Wall.jpg)
Diagram illustrating how the uterus lining builds up and breaks down during the menstrual cycle[7]
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![Low magnification micrograph of simple endometrial hyperplasia without nuclear atypia. Normal gland-to-stroma ratio (~1:3); proliferating pseudostratified glandular epithelium; irregular endometrial glands: dilated glands or glands with variable size; non-ovoid/non-circular glands[8]](/images/3/3d/Simple_endometrial_hyperplasia_-_low_mag_%281%29.jpg)
Low magnification micrograph of simple endometrial hyperplasia without nuclear atypia. Normal gland-to-stroma ratio (~1:3); proliferating pseudostratified glandular epithelium; irregular endometrial glands: dilated glands or glands with variable size; non-ovoid/non-circular glands[8]
![Diagram illustrating how the uterus lining builds up and breaks down during the menstrual cycle[7]](/index.php/File:Lining_of_Uterine_Wall.jpg)
![Low magnification micrograph of simple endometrial hyperplasia without nuclear atypia. Normal gland-to-stroma ratio (~1:3); proliferating pseudostratified glandular epithelium; irregular endometrial glands: dilated glands or glands with variable size; non-ovoid/non-circular glands[8]](/index.php/File:Simple_endometrial_hyperplasia_-_low_mag_(1).jpg)
References
- ↑ 1.0 1.1 1.2 1.3 Endometrial hyperplasia. Wikipedia. https://en.wikipedia.org/wiki/Endometrial_hyperplasia Accessed on March 7, 2016.
- ↑ 2.0 2.1 2.2 Owings RA, Quick CM (2014). "Endometrial intraepithelial neoplasia". Arch Pathol Lab Med. 138 (4): 484–91. doi:10.5858/arpa.2012-0709-RA. PMID 24678678.
- ↑ Menstrual cycle. Wikipedia. https://en.wikipedia.org/wiki/Menstrual_cycle Accessed on March 7, 2016
- ↑ Tamoxifen associated endometrial changes. Radiopedia. http://radiopaedia.org/articles/tamoxifen-associated-endometrial-changes Accessed on March 10, 2016
- ↑ Endometrial hyperplasia. Wiley Online Library.http://onlinelibrary.wiley.com/doi/10.1576/toag.10.4.211.27436/full Accessed on March 7, 2016
- ↑ McCluggage WG (2006). "My approach to the interpretation of endometrial biopsies and curettings". J Clin Pathol. 59 (8): 801–12. doi:10.1136/jcp.2005.029702. PMC 1860448. PMID 16873562.
- ↑ Menstrual cycle. Wikipedia. https://en.wikipedia.org/wiki/Menstrual_cycle Accessed on March 7, 2016
- ↑ Endometrial hyperplasia. Wikipedia. https://en.wikipedia.org/wiki/Endometrial_hyperplasia#/media/File:Simple_endometrial_hyperplasia_-_low_mag.jpg Accessed on March 7, 2016
