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==Natural History==
==Natural History==
*The majority of cases of [[endometrial]] [[hyperplasia]] (except complex atypical [[hyperplasia]]) resolve spontaneously with time.<ref name="pmid9255033">{{cite journal| author=Terakawa N, Kigawa J, Taketani Y, Yoshikawa H, Yajima A, Noda K et al.| title=The behavior of endometrial hyperplasia: a prospective study. Endometrial Hyperplasia Study Group. | journal=J Obstet Gynaecol Res | year= 1997 | volume= 23 | issue= 3 | pages= 223-30 | pmid=9255033 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9255033  }} </ref><ref name="pmid9255033">{{cite journal| author=Terakawa N, Kigawa J, Taketani Y, Yoshikawa H, Yajima A, Noda K et al.| title=The behavior of endometrial hyperplasia: a prospective study. Endometrial Hyperplasia Study Group. | journal=J Obstet Gynaecol Res | year= 1997 | volume= 23 | issue= 3 | pages= 223-30 | pmid=9255033 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9255033  }} </ref> If left untreated, 30% of patients with atypical hyperplasia may progress to develop [[endometrial carcinoma]].<ref name="pmid19285814">{{cite journal| author=Lacey JV, Chia VM| title=Endometrial hyperplasia and the risk of progression to carcinoma. | journal=Maturitas | year= 2009 | volume= 63 | issue= 1 | pages= 39-44 | pmid=19285814 | doi=10.1016/j.maturitas.2009.02.005 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19285814  }} </ref> [[Malignant]] [[transformation]] into [[endometrial cancer]] is the most common [[Complication (medicine)|complication]] of [[Endometrial hyperplasia|endometrial hyperpasia]].<ref name="rc">Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 16, 2016</ref> Prognosis is generally good with treatment.
*The majority of cases of [[endometrial]] [[hyperplasia]] (except complex atypical [[hyperplasia]]) resolve spontaneously with time.<ref name="pmid9255033">{{cite journal| author=Terakawa N, Kigawa J, Taketani Y, Yoshikawa H, Yajima A, Noda K et al.| title=The behavior of endometrial hyperplasia: a prospective study. Endometrial Hyperplasia Study Group. | journal=J Obstet Gynaecol Res | year= 1997 | volume= 23 | issue= 3 | pages= 223-30 | pmid=9255033 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9255033  }} </ref><ref name="pmid9255033">{{cite journal| author=Terakawa N, Kigawa J, Taketani Y, Yoshikawa H, Yajima A, Noda K et al.| title=The behavior of endometrial hyperplasia: a prospective study. Endometrial Hyperplasia Study Group. | journal=J Obstet Gynaecol Res | year= 1997 | volume= 23 | issue= 3 | pages= 223-30 | pmid=9255033 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9255033  }} </ref>  
*If left untreated, 30% of patients with atypical hyperplasia may progress to develop [[endometrial carcinoma]].<ref name="pmid19285814">{{cite journal| author=Lacey JV, Chia VM| title=Endometrial hyperplasia and the risk of progression to carcinoma. | journal=Maturitas | year= 2009 | volume= 63 | issue= 1 | pages= 39-44 | pmid=19285814 | doi=10.1016/j.maturitas.2009.02.005 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19285814  }} </ref>
*If left untreated, 30% of patients with atypical hyperplasia may progress to develop [[endometrial carcinoma]].<ref name="pmid19285814">{{cite journal| author=Lacey JV, Chia VM| title=Endometrial hyperplasia and the risk of progression to carcinoma. | journal=Maturitas | year= 2009 | volume= 63 | issue= 1 | pages= 39-44 | pmid=19285814 | doi=10.1016/j.maturitas.2009.02.005 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19285814  }} </ref>  
*[[Malignant]] [[transformation]] into [[endometrial cancer]] is the most common [[Complication (medicine)|complication]] of [[Endometrial hyperplasia|endometrial hyperpasia]].<ref name="rc">Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 16, 2016</ref>  
*Prognosis is generally good with treatment.
*Hyperplasia without atypia tends to spontaneously regress.
*Atypical hyperplasias are more likely to progress
*Endometrial carcinoma with concomitant hyperplasia is associated with less aggressive disease.
*When an endometrial biopsy or curettage specimen is diagnosed as atypical hyperplasia, the risk of concomitant carcinoma in the same uterus has been reported as 17% to 25% (35–37).
*On the contrary, 2 recent studies have concluded that the concomitant presence of carcinoma in uteri sampled for endometrial hyperplasia is considerably higher.<ref name="WidraDunton1995">{{cite journal|last1=Widra|first1=E.A.|last2=Dunton|first2=C.J.|last3=McHugh|first3=M.|last4=Palazzo|first4=J.P.|title=Endometrial hyperplasia and the risk of carcinoma|journal=International Journal of Gynecological Cancer|volume=5|issue=3|year=1995|pages=233–235|issn=1048-891X|doi=10.1046/j.1525-1438.1995.05030233.x}}</ref>
*Adenocarcinomas arising from an atypical hyperplasia are of the endometrioid cell type, whereas those developing from an atrophic endometrium may be either endometrioid or non-endometrioid cell type.
**Endometrioid adenocarcinomas arising through the hyperplasia-neoplasia sequence are oestrogen induced. 
***Well differentiated
***Less invasive of the myometrium
***Lack lymphatic and metastatic involvement
***Excellent prognosis.
**Oestrogen-induced adenocarcinomas are also endometrioid, arising from an atrophic or a rather weakly proliferating endometrium.
***Frequently of higher histological grade
***Less favourable prognosis.  
**Finally, endometrial carcinomas of the non-endometrioid cell type, mainly serous papillary and clear cell carcinomas, are non-oestrogen induced and non-hyperplasia associated.
***Adverse aggressive histological features
***Extremely poor prognosis.<ref name="pmid23073327">{{cite journal |vauthors=Rakha E, Wong SC, Soomro I, Chaudry Z, Sharma A, Deen S, Chan S, Abu J, Nunns D, Williamson K, McGregor A, Hammond R, Brown L |title=Clinical outcome of atypical endometrial hyperplasia diagnosed on an endometrial biopsy: institutional experience and review of literature |journal=Am. J. Surg. Pathol. |volume=36 |issue=11 |pages=1683–90 |date=November 2012 |pmid=23073327 |doi=10.1097/PAS.0b013e31825dd4ff |url=}}</ref>




Hyperplasia without atypia tends to spontaneously regress.
* whereas atypical hyperplasias are more likely to progress {{cite journal |vauthors=Terakawa N, Kigawa J, Taketani Y, Yoshikawa H, Yajima A, Noda K, Okada H, Kato J, Yakushiji M, Tanizawa O, Fujimoto S, Nozawa S, Takahashi T, Hasumi K, Furuhashi N, Aono T, Sakamoto A, Furusato M |title=The behavior of endometrial hyperplasia: a prospective study. Endometrial Hyperplasia Study Group |journal=J. Obstet. Gynaecol. Res. |volume=23 |issue=3 |pages=223–30 |date=June 1997 |pmid=9255033 |doi= |url=}}
* Endometrial carcinoma with concomitant hyperplasia is associated with less aggressive disease.
When an endometrial biopsy or curettage specimen is diagnosed as atypical hyperplasia, the risk of concomitant carcinoma in the same uterus has been reported as 17% to 25% (35–37). However, 2 recent studies have concluded that the concomitant presence of carcinoma in uteri sampled for endometrial hyperplasia is considerably higher.<ref name="WidraDunton1995">{{cite journal|last1=Widra|first1=E.A.|last2=Dunton|first2=C.J.|last3=McHugh|first3=M.|last4=Palazzo|first4=J.P.|title=Endometrial hyperplasia and the risk of carcinoma|journal=International Journal of Gynecological Cancer|volume=5|issue=3|year=1995|pages=233–235|issn=1048-891X|doi=10.1046/j.1525-1438.1995.05030233.x}}</ref>


==Complications==
==Complications==
[[Malignant]] transformation  is the most common complication of endometrial hyperpasia.<ref name="rc">Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 16, 2016</ref>
*[[Malignant]] transformation  is the most common complication of endometrial hyperpasia.<ref name="rc">Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 16, 2016</ref>
Complications of untreated or poorly controlled endometrial hyperplasia can be serious. You can help minimize your risk of serious complications by following the treatment plan you and your health care professional design specifically for you. Complications of endometrial hyperplasia include:
*Complications of untreated or poorly controlled endometrial hyperplasia can be serious.
 
*To minimize risk of serious complications follow the treatment plan provided by health care professional designed specifically for patient.  
    Absenteeism from work or school
*Complications of endometrial hyperplasia include:
    Anemia (low red blood cell count)
**Absenteeism from work or school
    Cancer of the uterus
**Anemia
    Inability to participate normally in activities
**Cancer of the uterus
    Infertility
**Inability to participate normally in activities
    Menorrhagia (heavy bleeding during your menstrual period)
**Infertility
**Menorrhagia  


==Prognosis==
==Prognosis==
Prognosis is generally good with treatment for endometrial hyperplasias without atypia.
*Prognosis is generally good with treatment for endometrial hyperplasias without atypia.
Chronic anovulation, obesity, polycystic ovarian syndrome, metabolic syndrome, insulin resistance, and type 2 diabetes mellitus must be appreciated as risk factors for endometrial pathology. Providers must exert vigilance in identifying patients at risk and in initiating pre-emptive strategies. Risk reduction with lifestyle modification, weight loss, and glycemic control can improve regression and overall health. Fertility outcomes for these patients are promising, especially with assisted reproductive technology.<ref name="GresselParkash2015">{{cite journal|last1=Gressel|first1=Gregory M.|last2=Parkash|first2=Vinita|last3=Pal|first3=Lubna|title=Management options and fertility-preserving therapy for premenopausal endometrial hyperplasia and early-stage endometrial cancer|journal=International Journal of Gynecology & Obstetrics|volume=131|issue=3|year=2015|pages=234–239|issn=00207292|doi=10.1016/j.ijgo.2015.06.031}}</ref>
*Chronic anovulation, obesity, polycystic ovarian syndrome, metabolic syndrome, insulin resistance, and type 2 diabetes mellitus must be appreciated as risk factors for endometrial pathology.  
There are various forms of endometrial hyperplasia which, in terms of prognosis and therapy, can be subdivided into those having cytological atypia and those lacking this feature. The former may progress into invasive endometrial malignancy through a transitional non-invasive stage. This is a continuous process and, as a result, the distinction between an atypical hyperplasia and an intraepithelial adenocarcinoma (IEA) or an adenocarcinoma with stromal invasion is not histologically reproducible. The concept of endometrioid neoplasia, which includes the entire spectrum of the aforementioned proliferating endometrial lesions, was introduced. Adenocarcinomas arising from an atypical hyperplasia are invariably of the endometrioid cell type, whereas those developing from an atrophic endometrium may be either of the endometrioid or of the non-endometrioid cell type. Endometrioid adenocarcinomas arising through the hyperplasia-neoplasia sequence are oestrogen induced and tend to be well differentiated and less invasive of the myometrium, lack lymphatic and metastatic involvement and have an excellent prognosis. Oestrogen-induced adenocarcinomas are also endometrioid, arising from an atrophic or a rather weakly proliferating endometrium, but these neoplasms are frequently of higher histological grade and have a somewhat less favourable prognosis. Finally, endometrial carcinomas of the non-endometrioid cell type, mainly serous papillary and clear cell carcinomas, are non-oestrogen induced, non-hyperplasia associated and show adverse aggressive histological features and an extremely poor prognosis. The antigenic characteristics and the molecular events associated with the development of these forms of endometrial malignancy are distinct and allow the description of, at least, two pathogenetic types of endometrial carcinoma.<ref name="pmid23073327">{{cite journal |vauthors=Rakha E, Wong SC, Soomro I, Chaudry Z, Sharma A, Deen S, Chan S, Abu J, Nunns D, Williamson K, McGregor A, Hammond R, Brown L |title=Clinical outcome of atypical endometrial hyperplasia diagnosed on an endometrial biopsy: institutional experience and review of literature |journal=Am. J. Surg. Pathol. |volume=36 |issue=11 |pages=1683–90 |date=November 2012 |pmid=23073327 |doi=10.1097/PAS.0b013e31825dd4ff |url=}}</ref>
*Initiating pre-emptive strategies is highly important. This includes; risk reduction with lifestyle modification, weight loss, and glycemic control can improve regression and overall health.  
*Fertility outcomes for these patients are promising, especially with assisted reproductive technology.<ref name="GresselParkash2015">{{cite journal|last1=Gressel|first1=Gregory M.|last2=Parkash|first2=Vinita|last3=Pal|first3=Lubna|title=Management options and fertility-preserving therapy for premenopausal endometrial hyperplasia and early-stage endometrial cancer|journal=International Journal of Gynecology & Obstetrics|volume=131|issue=3|year=2015|pages=234–239|issn=00207292|doi=10.1016/j.ijgo.2015.06.031}}</ref>


==References==
==References==

Revision as of 13:36, 8 May 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Swathi Venkatesan, M.B.B.S.[2]

Overview

The majority of cases of endometrial hyperplasia (except complex atypical hyperplasia) resolve spontaneously with time.

Natural History

  • The majority of cases of endometrial hyperplasia (except complex atypical hyperplasia) resolve spontaneously with time.[1][1]
  • If left untreated, 30% of patients with atypical hyperplasia may progress to develop endometrial carcinoma.[2]
  • Malignant transformation into endometrial cancer is the most common complication of endometrial hyperpasia.[3]
  • Prognosis is generally good with treatment.
  • Hyperplasia without atypia tends to spontaneously regress.
  • Atypical hyperplasias are more likely to progress
  • Endometrial carcinoma with concomitant hyperplasia is associated with less aggressive disease.
  • When an endometrial biopsy or curettage specimen is diagnosed as atypical hyperplasia, the risk of concomitant carcinoma in the same uterus has been reported as 17% to 25% (35–37).
  • On the contrary, 2 recent studies have concluded that the concomitant presence of carcinoma in uteri sampled for endometrial hyperplasia is considerably higher.[4]
  • Adenocarcinomas arising from an atypical hyperplasia are of the endometrioid cell type, whereas those developing from an atrophic endometrium may be either endometrioid or non-endometrioid cell type.
    • Endometrioid adenocarcinomas arising through the hyperplasia-neoplasia sequence are oestrogen induced.
      • Well differentiated
      • Less invasive of the myometrium
      • Lack lymphatic and metastatic involvement
      • Excellent prognosis.
    • Oestrogen-induced adenocarcinomas are also endometrioid, arising from an atrophic or a rather weakly proliferating endometrium.
      • Frequently of higher histological grade
      • Less favourable prognosis.
    • Finally, endometrial carcinomas of the non-endometrioid cell type, mainly serous papillary and clear cell carcinomas, are non-oestrogen induced and non-hyperplasia associated.
      • Adverse aggressive histological features
      • Extremely poor prognosis.[5]


Complications

  • Malignant transformation is the most common complication of endometrial hyperpasia.[3]
  • Complications of untreated or poorly controlled endometrial hyperplasia can be serious.
  • To minimize risk of serious complications follow the treatment plan provided by health care professional designed specifically for patient.
  • Complications of endometrial hyperplasia include:
    • Absenteeism from work or school
    • Anemia
    • Cancer of the uterus
    • Inability to participate normally in activities
    • Infertility
    • Menorrhagia

Prognosis

  • Prognosis is generally good with treatment for endometrial hyperplasias without atypia.
  • Chronic anovulation, obesity, polycystic ovarian syndrome, metabolic syndrome, insulin resistance, and type 2 diabetes mellitus must be appreciated as risk factors for endometrial pathology.
  • Initiating pre-emptive strategies is highly important. This includes; risk reduction with lifestyle modification, weight loss, and glycemic control can improve regression and overall health.
  • Fertility outcomes for these patients are promising, especially with assisted reproductive technology.[6]

References

  1. ↑ 1.0 1.1 Terakawa N, Kigawa J, Taketani Y, Yoshikawa H, Yajima A, Noda K; et al. (1997). "The behavior of endometrial hyperplasia: a prospective study. Endometrial Hyperplasia Study Group". J Obstet Gynaecol Res. 23 (3): 223–30. PMID 9255033.
  2. ↑ Lacey JV, Chia VM (2009). "Endometrial hyperplasia and the risk of progression to carcinoma". Maturitas. 63 (1): 39–44. doi:10.1016/j.maturitas.2009.02.005. PMID 19285814.
  3. ↑ 3.0 3.1 Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 16, 2016
  4. ↑ Widra, E.A.; Dunton, C.J.; McHugh, M.; Palazzo, J.P. (1995). "Endometrial hyperplasia and the risk of carcinoma". International Journal of Gynecological Cancer. 5 (3): 233–235. doi:10.1046/j.1525-1438.1995.05030233.x. ISSN 1048-891X.
  5. ↑ Rakha E, Wong SC, Soomro I, Chaudry Z, Sharma A, Deen S, Chan S, Abu J, Nunns D, Williamson K, McGregor A, Hammond R, Brown L (November 2012). "Clinical outcome of atypical endometrial hyperplasia diagnosed on an endometrial biopsy: institutional experience and review of literature". Am. J. Surg. Pathol. 36 (11): 1683–90. doi:10.1097/PAS.0b013e31825dd4ff. PMID 23073327.
  6. ↑ Gressel, Gregory M.; Parkash, Vinita; Pal, Lubna (2015). "Management options and fertility-preserving therapy for premenopausal endometrial hyperplasia and early-stage endometrial cancer". International Journal of Gynecology & Obstetrics. 131 (3): 234–239. doi:10.1016/j.ijgo.2015.06.031. ISSN 0020-7292.

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