Endometrial hyperplasia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Badria Munir M.B.B.S.[2] , Soujanya Thummathati, MBBS [3]

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.

Pathophysiology

Pathogenesis

Genetics

It is assumed that there is association between endometrial hyperplasia and DNA repair gene (XPD, XRCC4, and XRCC1) polymorphisms. After experiments, it became evident the DNA repair gene XPD and XRCC4 polymorphisms had a role in the pathophysiology of endometrial hyperplasia.[7]

Other Genes involved

  • Oncogene bcl-2 in complex hyperplasia[8][9]
  • Fas/FasL gene also has been investigated recently in the development of endometrial hyperplasia

Mtor Signallin pathway

Gross pathology

Endometrial hyperplasia typically represents as: [14]

Microscopic Pathology

  • Prolonged estrogenic stimulation results in larger, more complex, and proliferating endometrial glands.[3]
  • On microscopic histopathological analysis, the proliferating endometrium is characterized by the following:[15]
Character Simple hyperplasia Complex hyperplasia

Gland to stroma ratio

  • Normal or slightly increased
  • Increased

Endometrium

  • Irregularly dilated cystic glands
  • Out‐pouching, infoldings, and budding of the glands may be present
  • Glandular crowding
  • Luminal outpouching of glands

Mitoses

  • May or may not be present
  • Typically present

Location

  • Generalized
  • Focal

Nuclear atypia

  • Not seen
  • Not seen
  • Endometrial hyperplasia is morphologically defined as proliferating endometrium with architectural abnormalities.
  • These architectural changes range as :
    • Cystic dilatation
    • Budding and branching
    • Papillary infoldings
    • Villous and villoglandular growths
    • Cribriform structures.
  • In addition to abnormal architecture, a diagnosis of hyperplasia usually requires increased glandular density with a gland-to-stroma ratio of ∼3:1.
  • Luminal spaces and villoglandular structures are also included in the glandular component for this calculation.
  • If the gland-to-stroma ratio fails to meet the required cut-off, a lesion is probably best classified as disordered proliferative endometrium rather than hyperplasia.
  • Although hyperplastic endometrium might have cytologic atypia, this criterion is neither required nor sufficient for this diagnosis.
  • The assessment of cytologic atypia is poorly understood, but the various criteria include:
    • Nuclear rounding and enlargement
    • Nuclear pleomorphism
    • Loss of polarity
    • Increased nuclear-to-cytoplasm ratio
    • Prominent nucleoli
    • Irregular nuclear borders
    • Vesicular chromatin
    • Clumped chromatin
    • Atypical cells may show tufting and focal stratification

World Health Organization classification of endometrial hyperplasia

    • Simple hyperplasia without atypia
    • Simple hyperplasia is characterized by:
      • Densely packed, cystically dilated, variable sized glands separated by normal intervening stroma ( Figure 10 ). Although
      • 3:1 gland-to-stroma ratio.
      • Ciliated cells
      • squamous morular metaplasia
    • Complex hyperplasia without atypia
    • Complex hyperplasia without atypia is defined as:
      • Glands with abnormal, irregular architecture set in a background of scant intervening stroma
      • Some stroma must be present,
      • Basement membrane lining individual glands and a rim of intervening endometrial-type stroma between them. In addition to back-to-back and cribriform-like arrangements, other glandular architectural abnormalities warranting designation of complex hyperplasia include
      • Outpouchings,
      • Infoldings, and budding
      • Squamous or morular metaplasia
      • Eosinophilic and ciliated cell changes
    • Simple hyperplasia with atypia
    • Complex hyperplasia with atypia
      • Increased gland-to-stroma ratio (≥3:1)
      • Gland complexity—caused by:
        • Branching
        • Outward budding
        • Internal papillary infoldings
        • Internal bridge

Gallery

References

  1. 1.0 1.1 Endometrial hyperplasia. Wikipedia. https://en.wikipedia.org/wiki/Endometrial_hyperplasia Accessed on March 7, 2016.
  2. Menstrual cycle. Wikipedia. https://en.wikipedia.org/wiki/Menstrual_cycle Accessed on March 7, 2016
  3. 3.0 3.1 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.
  4. Tamoxifen associated endometrial changes. Radiopedia. http://radiopaedia.org/articles/tamoxifen-associated-endometrial-changes Accessed on March 10, 2016
  5. Endometrial hyperplasia. Wiley Online Library.http://onlinelibrary.wiley.com/doi/10.1576/toag.10.4.211.27436/full Accessed on March 7, 2016
  6. Wang S, Pudney J, Song J, Mor G, Schwartz PE, Zheng W (February 2003). "Mechanisms involved in the evolution of progestin resistance in human endometrial hyperplasia--precursor of endometrial cancer". Gynecol. Oncol. 88 (2): 108–17. PMID 12586588.
  7. Öztürk E, Pehlivan S, Balat O, Ugur MG, Ozcan HC, Erkılıç S (October 2018). "DNA Repair Gene (XPD, XRCC4, and XRCC1) Polymorphisms in Patients with Endometrial Hyperplasia: A Pilot Study". Med Sci Monit Basic Res. 24: 146–150. doi:10.12659/MSMBR.911041. PMID 30275440.
  8. McDonnell TJ, Troncoso P, Brisbay SM, Logothetis C, Chung LW, Hsieh JT, Tu SM, Campbell ML (December 1992). "Expression of the protooncogene bcl-2 in the prostate and its association with emergence of androgen-independent prostate cancer". Cancer Res. 52 (24): 6940–4. PMID 1458483.
  9. . doi:10.1002/1097-0142(19950501)75:9<2209. Missing or empty |title= (help)
  10. Lu QL, Abel P, Foster CS, Lalani EN (February 1996). "bcl-2: role in epithelial differentiation and oncogenesis". Hum. Pathol. 27 (2): 102–10. PMID 8617450.
  11. Tanaka Y, Park JH, Tanwar PS, Kaneko-Tarui T, Mittal S, Lee HJ, Teixeira JM (January 2012). "Deletion of tuberous sclerosis 1 in somatic cells of the murine reproductive tract causes female infertility". Endocrinology. 153 (1): 404–16. doi:10.1210/en.2011-1191. PMC 3249683. PMID 22128018.
  12. Wang Y, Zhu L, Kuokkanen S, Pollard JW (March 2015). "Activation of protein synthesis in mouse uterine epithelial cells by estradiol-17β is mediated by a PKC-ERK1/2-mTOR signaling pathway". Proc. Natl. Acad. Sci. U.S.A. 112 (11): E1382–91. doi:10.1073/pnas.1418973112. PMC 4371960. PMID 25733860.
  13. Blagosklonny MV (May 2010). "Why men age faster but reproduce longer than women: mTOR and evolutionary perspectives". Aging (Albany NY). 2 (5): 265–73. doi:10.18632/aging.100149. PMC 2898017. PMID 20519781.
  14. Lacey, J V; Ioffe, O B; Ronnett, B M; Rush, B B; Richesson, D A; Chatterjee, N; Langholz, B; Glass, A G; Sherman, M E (2007). "Endometrial carcinoma risk among women diagnosed with endometrial hyperplasia: the 34-year experience in a large health plan". British Journal of Cancer. 98 (1): 45–53. doi:10.1038/sj.bjc.6604102. ISSN 0007-0920.
  15. 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.
  16. Menstrual cycle. Wikipedia. https://en.wikipedia.org/wiki/Menstrual_cycle Accessed on March 7, 2016
  17. Endometrial hyperplasia. Wikipedia. https://en.wikipedia.org/wiki/Endometrial_hyperplasia#/media/File:Simple_endometrial_hyperplasia_-_low_mag.jpg Accessed on March 7, 2016

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