Endometrial Hyperplasia - ClinicalKey

24/10/23, 10:13 Endometrial Hyperplasia - ClinicalKey
CLINICAL OVERVIEW
Endometrial Hyperplasia
Elsevier Point of Care (ver detalles)
Actualizado July 21, 2022. Copyright Elsevier BV. All rights reserved.
Synopsis
Urgent Action
Patients presenting with acute abnormal uterine bleeding are at risk of hemodynamically significant blood loss.
Promptly assess for hypovolemia and hemodynamic instability; resuscitate with fluids and blood products as
indicated
Key Points
Endometrial hyperplasia is defined as precancerous proliferation of the endometrium resulting in increased volume of
endometrial tissue. It is classified as either hyperplasia without atypia or atypical hyperplasia/endometrioid intraepithelial
neoplasia
Excess or unopposed estrogen exposure from a variety of causes (eg, early menarche, late menopause, polycystic ovarian
syndrome, exogenous estrogen therapy, obesity) is the typical cause of endometrial hyperplasia
Abnormal uterine bleeding is the most common manifestation of endometrial hyperplasia
Diagnosis is suspected based on abnormal uterine bleeding, specific risk factors, and physical examination. Transvaginal
ultrasonogram showing a thickened endometrial stripe increases suspicion, but diagnosis must be confirmed by endometrial
biopsy 1
Hormonal treatment with progestins is the general recommended treatment of endometrial hyperplasia without atypia
Total hysterectomy is the current standard of care for atypical hyperplasia and endometrioid intraepithelial neoplasia,
providing definitive assessment of a possible concurrent carcinoma, and effectively treating premalignant lesions
Female patients with endometrial hyperplasia are at increased risk for both concurrent and subsequent endometrial cancer
Atypical hyperplasia and endometrioid intraepithelial neoplasia are characterized as direct precancerous lesions and carry a
higher risk of progression to carcinoma 2
Pitfalls
Obtain a pregnancy test in all patients of reproductive age
https://www-clinicalkey-es.sibulgem.unilibre.edu.co/#!/content/clinical_overview/67-s2.0-d3b08cb3-e083-43d8-a63c-59edad0f283c 1/13
Terminology
Clinical Clarification
Endometrial hyperplasia is a proliferation of the endometrium resulting in increased volume of endometrial tissue, 2 3
defined histologically as an increase in the gland to stroma ratio greater than 1:1 4
It is a precursor lesion to endometrial cancer
Classification
Revised (2015) WHO classification of endometrial hyperplasia is based on histologic presence of atypia or intraepithelial
neoplasia 3 4
Hyperplasia without atypia
Includes the following previous WHO-defined classifications:
Simple endometrial hyperplasia without atypia
Complex endometrial hyperplasia without atypia
Risk of progression to endometrial carcinoma is 1% 5
Atypical hyperplasia and endometrioid intraepithelial neoplasia
Includes the following previous WHO-defined classifications:
Simple endometrial hyperplasia with atypia

Complex endometrial hyperplasia with atypia
Endometrial intraepithelial neoplasia
Atypia is characterized by presence of enlarged epithelial cells with an increased nuclear to cytoplasmic ratio
25% to 59% of patients in this category are found to have coexistent invasive endometrial carcinoma 6
Diagnosis
Clinical Presentation
History
Many patients are asymptomatic
Most common presenting symptom is abnormal uterine bleeding, which includes: 1
Bleeding during menstrual period that is heavier or lasts longer than usual
Intermenstrual bleeding
Any bleeding after menopause
History usually reflects prolonged or increased estrogenic stimulation of the endometrium
Menstrual history may include early menarche, late menopause, or irregular menses
Pregnancy history may include nulliparity or difficulty becoming pregnant owing to anovulation
Medication history may include use of unopposed estrogen or tamoxifen
Current or recent medical history may include:
Polycystic ovary syndrome
History of obesity
Estrogen-secreting tumors such as granulosa cell tumors
Diabetes
Patient may seek medical attention for potential endometrial hyperplasia when Papanicolaou test results show presence of
endometrial cells or atypical endometrial cells 7
With or without abnormal vaginal bleeding
Atypical endometrial cells shown on Papanicolaou test are associated with a 1% risk for endometrial hyperplasia and a 3%
risk for endometrial carcinoma 7
Physical examination
In patients with acute abnormal uterine bleeding 1
Physical examination should initially focus on signs of acute blood loss (signs of hypovolemia and anemia) and
identification of the source of bleeding
In patients with acute and nonacute abnormal uterine bleeding 1
Evaluate with pelvic examination (including a speculum examination and a bimanual examination) to determine whether
bleeding is uterine or from other areas of the genital tract
Identify any trauma to the vagina or cervix that could cause vaginal bleeding
Determine amount and intensity of bleeding
Identify any uterine enlargement or irregularity, which can be associated with a structural cause of acute abnormal
uterine bleeding (eg, leiomyoma)
No physical diagnostic signs are specific for endometrial hyperplasia; this condition can be diagnosed only by biopsy
evaluation
Causes and Risk Factors
Causes
Endometrial hyperplasia typically occurs when unopposed estrogen (ie, in the absence of progesterone) stimulates abnormal
proliferation of endometrial glands 5
Risk factors and/or associations
Age
Incidence of endometrial hyperplasia without atypia peaks in early postmenopausal years; highest incidence is in females
aged 50 to 54 years 8
Incidence of atypical hyperplasia or endometrioid intraepithelial neoplasia is highest in females aged 60 to 64 years 8
Endometrial hyperplasia is rare in females younger than 30 years 8
Genetics
PTEN tumor suppressor gene is mutated in more than 20% of patients with endometrial hyperplasia 9
Hereditary nonpolyposis colorectal cancer increases risk 5
Autosomal dominant genetic condition associated with increased risk of several cancers
Female patients with hereditary nonpolyposis colorectal cancer have a 40% to 60% lifetime risk of developing endometrial
carcinoma (relative risk, 20) compared with noncarriers of mismatch repair gene mutations
Other risk factors/associations

Conditions characterized by unopposed estrogen increase the risk of endometrial hyperplasia, such as: 4 5
Polycystic ovary syndrome with oligomenorrhea
Endometrial hyperplasia occurs in 20% of these patients 5
Unopposed estrogen use
Relative risk for atypical hyperplasia or endometrioid intraepithelial neoplasia: 12 5
Tamoxifen use
Relative risk for endometrial hyperplasia: 5 5
Obesity or increased BMI
Relative risk for atypical hyperplasia or endometrioid intraepithelial neoplasia: 4 5
In females with BMI higher than 40 kg/m², relative risk for atypical hyperplasia or endometrioid intraepithelial
neoplasia increases to 13 5
Infertility
Relative risk for endometrial hyperplasia: 3.6 5
Nulliparity
Relative risk for endometrial hyperplasia: 2.8 5
Diabetes
Relative risk for endometrial cancer: 2 (for which endometrial hyperplasia is a precursor) 5
Early menarche
Late-onset menopause
Chronic anovulation
Estrogen-secreting tumors such as granulosa cell tumors
Diagnostic Procedures
Primary diagnostic tools

Abnormal uterine bleeding is suggestive of diagnosis in a patient with risk factors 1
Transvaginal ultrasonography is the first line imaging test to direct strategy for tissue sampling; additional imaging may
be helpful in some circumstances 5 10
Guidelines do not specify indications for transvaginal ultrasonography in younger patients with abnormal uterine
bleeding who do not have risk factors for endometrial hyperplasia or carcinoma
Endometrial biopsy is the definitive diagnostic test 5
May obtain tissue by nonfocal endometrial biopsy performed in the office or by an alternative method (eg, via
hysteroscopic guidance or dilation and curettage)
Obtain in all patients aged 45 years and older
Obtain in younger patients with any of the following: 1
Risk factors for endometrial hyperplasia
Failed medical management

Persistent abnormal uterine bleeding
Guideline recommendations differ regarding use of endometrial biopsy in younger patients without risk factors for
endometrial hyperplasia who present with abnormal uterine bleeding 1 11
Perform a pregnancy test on all premenopausal patients before endometrial biopsy
Evaluate for anemia all patients with heavy, acute vaginal bleeding 1
Additional laboratory (eg, coagulation tests) or imaging studies may help identify other causes of abnormal uterine
bleeding
Laboratory
Imaging
Procedures
Differential Diagnosis
Most common 14
Endometrial polyp
Typically benign mass resulting from overproliferation of endometrial cells
Polyps are a common cause of abnormal bleeding in premenopausal and postmenopausal female patients
Diagnosed by biopsy
Biopsy specimen may show admixture of normal cyclical endometrium and fragments that are morphologically
different
Stroma of polyp is generally more fibrous than in the surrounding endometrium
Glandular tissue within a polyp often shows proliferative activity, even when that in the surrounding endometrium does
not
Other morphologic features commonly found in polyps include collections of thick‐walled stromal blood vessels,
glandular architectural abnormality, and epithelial metaplasia
Submucosal uterine fibroids (Related: Fibroids (Uterine Myomas))
Benign tumors developing from the smooth muscle cells of the uterine myometrium
Female patients with uterine fibroids are at risk of eventually developing endometrial hyperplasia
Abnormal bleeding accompanied by blood clots is a key symptom, whereas endometrial hyperplasia usually presents as
abnormal bleeding without clots
Ultrasonography can detect the presence of uterine fibroids
von Willebrand disease 1
Inherited hemorrhagic disorder leading to impaired primary hemostasis
Abnormal uterine bleeding is a common symptom
Up to 13% of females with heavy menstrual bleeding have some variant of von Willebrand disease, and up to 20% of
females may have an underlying coagulation disorder 1
Differentiating symptoms include the presence of epistaxis, gum bleeding, easy bruising, and prolonged bleeding after
trauma in patients with von Willebrand disease, although these are variable in individual patients
Diagnosis is based on abnormal laboratory test results, including:
Reduced levels of von Willebrand factor antigen

Reduced or abnormal function of von Willebrand factor antigen (including reduced platelet, collagen, or factor VIII
binding)
Reduced factor VIII levels
Treatment
Goals
Reduce or eliminate abnormal uterine bleeding (initial goal in all patients)
For a patient with newly diagnosed atypical hyperplasia or endometrioid intraepithelial neoplasia, exclude a concurrent
adenocarcinoma and provide appropriate treatment based on the patient's age, desire for future fertility, surgical risk, and
presence or absence of acute uterine bleeding 15
Disposition
Admission criteria
Patients with vaginal bleeding may require hospitalization in the following scenarios:
If bleeding results in signs and symptoms of hemodynamic instability
If patient presents with symptomatic anemia requiring transfusion
If patient has heavy vaginal bleeding and is unable to tolerate oral drug therapy, inpatient IV treatment or surgical
management may be required to stop heavy bleeding
Recommendations for specialist referral

Refer patients presenting with symptomatic endometrial hyperplasia to an obstetrician or gynecologist for medical and
surgical treatment planning
Treatment Options
Patient- and pathology-specific factors determine the treatment of endometrial hyperplasia 4
Patient-specific factors:
Age
Desire for future fertility
Surgical risk
Clinical acuity or hemodynamic stability
Pathology-specific factors:
Presence versus absence of cytologic atypia
Presence of endometrioid intraepithelial neoplasia
Guidelines differ in their recommendation for definitive diagnosis of endometrial hyperplasia (ie, by endometrial biopsy)
before empiric treatment in younger patients without risk factors for endometrial hyperplasia who present with abnormal
uterine bleeding 1 11
For patients with acute abnormal uterine bleeding, treat emergently with 1 of the following alternatives to reduce or stop acute
bleeding: 1
IV estrogen
Stops abnormal uterine bleeding in 72% of patients within 8 hours of administration 16
Combined oral contraceptives
Stop abnormal vaginal bleeding in 88% of females within 3 days 17
Oral medroxyprogesterone acetate
Stops abnormal vaginal bleeding in 76% of females within 3 days 17
Tranexamic acid
Guideline-recommended to treat acute abnormal vaginal bleeding, but there is no clinical trial evidence for its
effectiveness 1
For patients with endometrial hyperplasia without atypia, treat with: 2 5
Combined oral contraceptives
Decrease risk of endometrial carcinoma by approximately 50%; this protective effect seems to persist for decades after
treatment cessation 5
Progestins
Progestins alone are used to treat endometrial hyperplasia in female patients who are not candidates for combined oral
contraceptives owing to medical contraindications or adverse effects. These include: 3 5
Medroxyprogesterone acetate
Regression of hyperplasia (without or with atypia) has been observed in 80% to 90% of patients receiving oral
medroxyprogesterone 3
Megestrol acetate
Levonorgestrel-releasing intrauterine system
Hysterectomy 5
Indicated for patients with endometrial hyperplasia without atypia if medical management of bleeding or hyperplasia has
failed
For patients with atypical hyperplasia or endometrioid intraepithelial neoplasia, treat with: 3
Total hysterectomy 3 15
Current standard of care
Provides definitive assessment for a possible concurrent carcinoma
Effectively treats premalignant lesions
Curative for all patients diagnosed with atypical hyperplasia or endometrioid intraepithelial neoplasia
Surgical treatment with less than total hysterectomy is not recommended
Uterine morcellation is contraindicated
Supracervical hysterectomy is unacceptable for treatment of atypical hyperplasia and endometrioid intraepithelial
neoplasia
Medical therapy with progestins may be an alternative to hysterectomy in some patients 3
May be considered for:
Premenopausal female patients
Preserves fertility if this is desired, but hysterectomy is first line treatment in those who are surgical candidates
Hysterectomy is still indicated after childbearing is completed
Most elderly patients with medical comorbidities
Regression of hyperplasia (without and with atypia) has been observed in 80% to 90% of patients treated with oral
medroxyprogesterone or progesterone vaginal cream 3
However, if endometrial intraepithelial neoplasia is present, there is a higher incidence of failure of medical management
and subsequent development of cancer
Patients presenting with acute abnormal uterine bleeding are at risk of hemodynamically significant blood loss
Promptly assess for hypovolemia and hemodynamic instability; resuscitate with fluids and blood products as indicated
Drug therapy
For uterine bleeding
Estrogens
Conjugated Estrogens Solution for injection; Adult and Adolescent females: 25 mg IV every 4 to 6 hours for 24 hours.
The IV route is preferred for a more rapid response; inject IV slowly to reduce flushing. The use of conjugated estrogens
parenterally does not preclude the use of other appropriate measures. 1
Estrogen-progestin combined contraceptives
Ethinyl Estradiol 35 mcg, Norethindrone 1 mg Oral tablet; Adult and Adolescent females: 1 tablet PO 3 times daily for 7
days. 17
Progestogens
Medroxyprogesterone Acetate Oral tablet; Adult and Adolescent females: 20 mg PO 3 times daily for 7 days. 17
Tranexamic acid 1
Tranexamic Acid Oral tablet; Adults: 1,300 mg PO 3 times daily for 5 days during monthly menstruation.
For endometrial hyperplasia
Estrogen-progestin combined contraceptives
Ethinyl Estradiol 35 mcg, Norethindrone 1 mg Oral tablet; Adult and Adolescent females: 1 tablet PO daily for 12 to 14
days per month. 5
Progestogens
Medroxyprogesterone
Medroxyprogesterone Acetate Oral tablet; Adult and Adolescent females: 5 to 10 mg PO once daily for 12 days every
month. 5
Megestrol
Megestrol Acetate Oral tablet; Adult females: 40 to 320 mg/day PO, given in divided doses. 5
Depot medroxyprogesterone
Medroxyprogesterone Acetate Suspension for injection; Adult and Adolescent females: 150 mg (using 150 mg/mL
depot injection suspension) IM every 3 months. 5
Micronized vaginal progesterone
Progesterone Vaginal gel; Adult females: Administer 4% (45 mg) or 8% (90 mg) gel PV once daily for 14 days per
month. 5
Levonorgestrel intrauterine device 18 19
Levonorgestrel Vaginal insert; Adult and Adolescent females: Insert 1 intrauterine device into the uterus as per
instructions. Intrauterine device delivers 20 mcg/day. Provides efficacy for up to 5 years, then remove and replace. 5
Nondrug and supportive care
Procedures
Hysterectomy 3 5
General explanation
Surgical removal of the uterus
Total hysterectomy is recommended, with or without bilateral salpingo-oophorectomy
Indication 3 5
If endometrial biopsy shows presence of atypical hyperplasia or endometrioid intraepithelial neoplasia, a total hysterectomy
is indicated because there is a 29% to 52% chance that the condition will progress to endometrial cancer if untreated 2
When clinically appropriate, total hysterectomy for endometrial intraepithelial neoplasia provides definitive assessment of a
possible concurrent carcinoma and effectively treats premalignant lesions
Lymphadenectomy may be indicated at time of hysterectomy in patients found with endometrial carcinoma on frozen
section; however, it may be appropriate to review final pathologic assessment of the uterus to better select patients who would
benefit from later comprehensive surgical staging
Comprehensive surgical staging with pelvic and para-aortic lymph node dissection at the time of hysterectomy for
endometrial intraepithelial neoplasia would result in overtreatment and increased surgical risk for the vast majority of
patients
Contraindications
Major medical comorbidities 3
Complications
Urinary tract injuries 20
Abdominal wall infections
Vaginal hysterectomy has a lower rate of complications than laparoscopic hysterectomy 20
When vaginal hysterectomy is not possible, laparoscopic hysterectomy has advantages (when compared with open
abdominal hysterectomy) including:
Faster return to normal activity
Shorter hospital stay

Fewer wound infections
Interpretation of results
If hysterectomy is performed for atypical hyperplasia or endometrioid intraepithelial neoplasia, an intraoperative assessment
of the uterine specimen for occult carcinoma is recommended 21
Correlation between frozen section and final pathology for histology is 97.5% 21
Monitoring
For endometrial hyperplasia without atypia: 11
Perform endometrial biopsy at least every 6 months, although schedules should be individualized and responsive to
changes in patient's clinical condition
Obtain at least 2 consecutive negative biopsies (spaced 6 months apart) before discharge from follow-up
For endometrial hyperplasia with atypia or endometrioid intraepithelial neoplasia: 3
Guidelines differ in recommendations for surveillance in these patients
One guideline recommends that endometrial surveillance during or after medical management of hyperplasia with
atypia or endometrioid intraepithelial neoplasia should include serial endometrial sampling every 3 to 6 months 3
Another guideline recommends endometrial surveillance every 3 months until 2 consecutive negative biopsies are
obtained 11
In asymptomatic patients with a uterus and evidence of histologic disease regression based on a minimum of 2
consecutive negative biopsies, long-term follow-up with endometrial biopsy every 6 to 12 months is recommended
until hysterectomy is performed
Complications and Prognosis
Complications
Continued irregular, possibly heavy bleeding associated with endometrial hyperplasia can eventually lead to anemia
Prognosis
About 80% of cases of simple hyperplasia resolve naturally, with no treatment; complex hyperplasia has a higher risk of
progression to endometrial cancer, but it also regresses in most cases 2
Untreated, progression to endometrial cancer occurs in 1% to 3% of cases of endometrial hyperplasia without atypia 2
Untreated, 8% to 52% of cases of atypical hyperplasia or endometrioid intraepithelial neoplasia can be expected to progress
to endometrial cancer 2
Screening and Prevention
Prevention
Weight loss in obese female individuals may lower the risk of endometrial hyperplasia, as overproduction of estrogen by fat
cells contributes to a higher risk for hyperplasia and endometrial cancer in these patients 2 22
Hormonal therapy may be used to prevent endometrial hyperplasia in some high-risk patients 23
Levonorgestrel-releasing intrauterine system reduces risk of endometrial hyperplasia in female patients with breast cancer
who are taking adjuvant tamoxifen; however, there is no clear evidence that this prevents endometrial cancer in these
patients
Referencias
1. American College of Obstetricians and Gynecologists: ACOG committee opinion no. 557: management of acute abnormal uterine bleeding
in nonpregnant reproductive-aged women. Obstet Gynecol. 121(4):891-6, 2013
Ver en el Artículo (https://www-clinicalkey-es.sibulgem.unilibre.edu.co/#!/content/clinical_overview/67-s2.0-d3b08cb3-e083-43d8-a63c-59edad0f283c#inline-
reference-1) | Referencia cruzada (https://pubmed.ncbi.nlm.nih.gov/23635706)
2. Chandra V et al: Therapeutic options for management of endometrial hyperplasia. J Gynecol Oncol. 27(1):e8, 2016
3. Committee on Gynecologic Practice, Society of Gynecologic Oncology: The American College of Obstetricians and Gynecologists committee
opinion no. 631. Endometrial intraepithelial neoplasia. Obstet Gynecol. 125(5):1272-8, 2015
4. Hannemann MM et al: Endometrial hyperplasia: a clinician's review. Obstet Gynaecol Reprod Med. 20(4):116-20, 2010
reference-4) | Referencia cruzada (http://dx.doi.org.sibulgem.unilibre.edu.co/10.1016/j.ogrm.2010.01.002)
5. Armstrong AJ et al: Diagnosis and management of endometrial hyperplasia. J Minim Invasive Gynecol. 19(5):562-71, 2012
6. Emons G et al: New WHO classification of endometrial hyperplasias. Geburtshilfe Frauenheilkd. 75(2):135-6, 2015
7. Schnatz PF et al: Clinical significance of atypical glandular cells on cervical cytology. Obstet Gynecol. 107(3):701-8, 2006
8. Reed SD et al: Incidence of endometrial hyperplasia. Am J Obstet Gynecol. 200(6):678.e1-6, 2009

9. Ellenson LH et al: The female genital tract. In: Kumar V et al, eds: Robbins and Cotran Pathologic Basis of Disease. 10th ed. Elsevier;
2021:985-1036
reference-9) | Referencia cruzada (https://www-clinicalkey-com.sibulgem.unilibre.edu.co/#!/content/book/3-s2.0-B9780323531139000224)
10. Committee on Practice Bulletins--Gynecology: Practice bulletin no. 128: diagnosis of abnormal uterine bleeding in reproductive-aged
women. Obstet Gynecol. 120(1):197-206, 2012
11. Royal College of Obstetricians and Gynaecologists: Management of Endometrial Hyperplasia. Green-top Guideline No. 67. RCOG/BSGE
Joint Guideline. Royal College of Obstetricians and Gynaecologists website. Published February 26, 2016. Accessed July 14, 2022.
https://www.rcog.org.uk/globalassets/documents/guidelines/green-top-guidelines/gtg_67_endometrial_hyperplasia.pdf
reference-11) | Referencia cruzada (https://www.rcog.org.uk/globalassets/documents/guidelines/green-top-
guidelines/gtg_67_endometrial_hyperplasia.pdf )
12. Committee on Adolescent Health Care et al: Committee opinion no. 580: von Willebrand disease in women. Obstet Gynecol. 122(6):1368-73,
2013
13. American College of Radiology: ACR Appropriateness Criteria: Abnormal Uterine Bleeding. ACR website. Revised 2020. Accessed July 14,
2022. https://acsearch.acr.org/docs/69458/Narrative/
reference-13) | Referencia cruzada (https://acsearch.acr.org/docs/69458/Narrative/)
14. McCluggage WG: My approach to the interpretation of endometrial biopsies and curettings. J Clin Pathol. 59(8):801-12, 2006
15. Trimble CL et al: Management of endometrial precancers. Obstet Gynecol. 120(5):1160-75, 2012
16. DeVore GR et al: Use of intravenous premarin in the treatment of dysfunctional uterine bleeding: a double-blind randomized control study.
Obstet Gynecol. 59:285, 1982
17. Munro MG et al: Oral medroxyprogesterone acetate and combination oral contraceptives for acute uterine bleeding: a randomized
controlled trial. Obstet Gynecol. 108(4):924-9, 2006
18. Luo L et al: Levonorgestrel-releasing intrauterine system for atypical endometrial hyperplasia. Cochrane Database Syst Rev. 6:CD009458,
2013
19. Leone Roberti Maggiore U et al: Efficacy and fertility outcomes of levonorgestrel-releasing intra-uterine system treatment for patients with
atypical complex hyperplasia or endometrial cancer: a retrospective study. J Gynecol Oncol. 30(4):e57, 2019
20. American College of Obstetricians and Gynecologists: Committee opinion no. 701: choosing the route of hysterectomy for benign disease.
Obstet Gynecol. 129(6):e155-9, 2017
21. Stephan JM et al: Intra-operative frozen section results reliably predict final pathology in endometrial cancer. Gynecol Oncol. 133(3):499-505,
2014
22. Wise MR et al: Obesity and endometrial hyperplasia and cancer in premenopausal women: a systematic review. Am J Obstet Gynecol.
214(6):689.e1-17, 2016
23. Dominick S et al: Levonorgestrel intrauterine system for endometrial protection in women with breast cancer on adjuvant tamoxifen.
Cochrane Database Syst Rev. 12:CD007245, 2015
(https://play.google.com/store/apps/details?id=com.elsevier.cs.ck&hl=es) (https://itunes.apple.com/es/app/clinicalkey/id1041998175) (https://www.facebook.com/ClinicalKey)

(https://www.linkedin.com/company/3969981) (https://www.twitter.com/ClinicalKey)
(https://www.elsevier.com/)
Contáctenos (https://es-service-elsevier-com.sibulgem.unilibre.edu.co/app/contact/supporthub/clinicalkey/)
Centro de Recursos (https://www-elsevier-com.sibulgem.unilibre.edu.co/es-es/solutions/clinicalkey/resource-center?campid=CK_Es_LinkInFooter&dgcid=campid=CK_ES_LinkInFooter)
Acuerdo de Usuario Registrado (http://www.elsevier.com.sibulgem.unilibre.edu.co/legal/elsevier-registered-user-agreement)
Ayuda (https://es-service-elsevier-com.sibulgem.unilibre.edu.co/app/home/supporthub/clinicalkey/)
Términos y condiciones (https://www.elsevier.com/legal/elsevier-website-terms-and-conditions) Política de privacidad (http://www.elsevier.com/legal/privacy-policy)
Accesibilidad (https://www.elsevier.com/about/accessibility)
We use cookies to help provide and enhance our service and tailor content. By continuing you agree to the Preferencias de cookies .
Copyright © 2023 Elsevier Inc., its licensors, and contributors. All rights are reserved, including those for text and data mining, AI training, and similar technologies.
(https://www.relx.com/)

Endometrial Hyperplasia - ClinicalKey

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Endometrial Hyperplasia - ClinicalKey

Uploaded by

Copyright:

Available Formats

24/10/23, 10:13 Endometrial Hyperplasia - ClinicalKey

Abnormal uterine bleeding is the most common manifestation of endometrial hyperplasia

It is a precursor lesion to endometrial cancer

Hyperplasia without atypia

Includes the following previous WHO-defined classifications:

Simple endometrial hyperplasia without atypia

Complex endometrial hyperplasia without atypia

Risk of progression to endometrial carcinoma is 1% 5

Atypical hyperplasia and endometrioid intraepithelial neoplasia

Includes the following previous WHO-defined classifications:

Simple endometrial hyperplasia with atypia

Endometrial intraepithelial neoplasia

Most common presenting symptom is abnormal uterine bleeding, which includes: 1

Any bleeding after menopause

History usually reflects prolonged or increased estrogenic stimulation of the endometrium

Medication history may include use of unopposed estrogen or tamoxifen

Current or recent medical history may include:

Polycystic ovary syndrome

Estrogen-secreting tumors such as granulosa cell tumors

With or without abnormal vaginal bleeding

In patients with acute and nonacute abnormal uterine bleeding 1

Determine amount and intensity of bleeding

Causes and Risk Factors

Risk factors and/or associations

Other risk factors/associations

Polycystic ovary syndrome with oligomenorrhea

Endometrial hyperplasia occurs in 20% of these patients 5

Unopposed estrogen use

Relative risk for atypical hyperplasia or endometrioid intraepithelial neoplasia: 12 5

Relative risk for endometrial hyperplasia: 5 5

Obesity or increased BMI

Relative risk for atypical hyperplasia or endometrioid intraepithelial neoplasia: 4 5

Relative risk for endometrial hyperplasia: 3.6 5

Relative risk for endometrial hyperplasia: 2.8 5

Estrogen-secreting tumors such as granulosa cell tumors

Primary diagnostic tools

Endometrial biopsy is the definitive diagnostic test 5

Obtain in all patients aged 45 years and older

Obtain in younger patients with any of the following: 1

Risk factors for endometrial hyperplasia

Failed medical management

Perform a pregnancy test on all premenopausal patients before endometrial biopsy

Typically benign mass resulting from overproliferation of endometrial cells

Stroma of polyp is generally more fibrous than in the surrounding endometrium

Submucosal uterine fibroids (Related: Fibroids (Uterine Myomas))

Ultrasonography can detect the presence of uterine fibroids

von Willebrand disease 1

Inherited hemorrhagic disorder leading to impaired primary hemostasis

Abnormal uterine bleeding is a common symptom

Diagnosis is based on abnormal laboratory test results, including:

Reduced levels of von Willebrand factor antigen

Reduced factor VIII levels

If bleeding results in signs and symptoms of hemodynamic instability

If patient presents with symptomatic anemia requiring transfusion

Recommendations for specialist referral

Desire for future fertility

Clinical acuity or hemodynamic stability

Presence versus absence of cytologic atypia

Presence of endometrioid intraepithelial neoplasia

Stops abnormal uterine bleeding in 72% of patients within 8 hours of administration 16

Combined oral contraceptives

Stop abnormal vaginal bleeding in 88% of females within 3 days 17

Oral medroxyprogesterone acetate

Stops abnormal vaginal bleeding in 76% of females within 3 days 17