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INTRODUCTIONEndometrial hyperplasia is characterized by a proliferation of endometrial glands

that may progress to or coexist with endometrial carcinoma [1]. Endometrial hyperplasia virtually

always results from chronic estrogen stimulation unopposed by the counterbalancing effects of

progesterone.

The classification, clinical manifestations, diagnosis, and evaluation of endometrial hyperplasia arereviewed here. Related topics can be found separately:

Management of endometrial hyperplasia (See"Management of endometrial hyperplasia".)

Other etiologies of abnormal uterine bleeding (See"Approach to abnormal uterine bleeding in

nonpregnant reproductive-age women"and"Postmenopausal uterine bleeding".)

Endometrial cancer (See"Endometrial carcinoma: Epidemiology and risk factors".)

HISTOLOGY AND CLASSIFICATIONEndometrial hyperplasia is a characterized by a proliferation

of endometrial glands resulting in a greater gland-to-stroma ratio than observed in normal

endometrium [1]. The proliferating glands vary in size and shape and cells may have cytologic atypia.

Endometrial hyperplasia may be non-neoplastic (most simple and some complex hyperplasias) or

neoplastic (some complex and all complex atypical hyperplasias). Neoplastic hyperplasia is a non-

obligate precursor to the most common form of endometrial carcinoma, endometrioid histology. This

pattern of precursor and carcinoma is similar to intraepithelial neoplasms in other body sites (eg,

cervical intraepithelial neoplasia, adenoma in the colon, or ductal carcinoma in situ of the breast).

Unfortunately, the terminology for endometrial hyperplasia does not make the relationship to

malignant potential clear.

World Health Organization classificationThe World Health Organization (WHO) classification of

endometrial hyperplasia is the most widely used system [2].

In general, the WHO system correlates well with the risk of progression to endometrial carcinoma(see'Risk of carcinoma'below). However, a major limitation of this system is interobserver variability

across pathologists reviewing the same slides [3-6]. The finding of nuclear atypia, which is the most

important indicator of malignant potential, has the lowest level of interobserver agreement

(see'Nuclear atypia'below). As an example, two studies of 100 or more endometrial biopsy slides

found concordance across pathologists for a report of nuclear atypia was only 38 to 47 percent [3,4].

CategoriesThe WHO classification of endometria hyperplasia is based upon two features:

The glandular/stromal architectural pattern of the endometrium, which is described as either

simple or complex

The presence or absence of nuclear atypia

This results in four possible categories of endometrial hyperplasia:

Simple hyperplasia without atypia

Complex hyperplasia without atypia

Simple atypical hyperplasia

Complex atypical hyperplasia

Simple atypical hyperplasia is rare, and many reports use the term atypical hyperplasia to refer to all

women with either simple or complex atypical hyperplasia.
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small overall number of events and the fact that most of these women had some intervention between

initial endometrial sampling and hysterectomy. Endometrial carcinoma at hysterectomy was more

than 10-fold higher in women with atypical hyperplasia than in women with no atypia (23 versus 1.6

percent). The incidence of cancer for each histologic category was:

Simple hyperplasia without atypia1 of 93 patients (1 percent)

Complex hyperplasia without atypia1 of 29 patients (3 percent)

Simple atypical hyperplasia1 of 13 patients (8 percent)

Complex atypical hyperplasia10 of 35 patients (29 percent)

Similar findings reported in a case control study found that the cumulative risk of endometrial

carcinoma at 19 years after diagnosis of endometrial hyperplasia was higher for women with atypia

compared with those without atypia (28 versus 5 percent) [10].

The time course from a diagnosis of endometrial hyperplasia to carcinoma is not well established. The

case control study cited above reported that the average time to diagnosis of cancer was six years in

women with all types of endometrial hyperplasia [10].

Many women with atypical endometrial hyperplasia have coexistent endometrial carcinoma. A

literature review noted the frequency of concurrent carcinoma among patients with atypical

endometrial hyperplasia ranged from 17 to 52 percent across studies [8]. Thus, women with a finding

of atypical endometrial hyperplasia on endometrial biopsy require further evaluation. (See'Positive

endometrial sampling'below.)

Endometrial intraepithelial neoplasia systemThe endometrial intraepithelial neoplasia

classification system was proposed by an international group of gynecologic pathologists in 2000 [11].

This system has not gained widespread acceptance, but is used in some institutions. The system

defines two classes of endometrial changes that are relevant to clinical management:

Endometrial hyperplasia (EH)Changes typically observed with anovulation or other etiology

of prolonged exposure to estrogen. The morphology of EH varies from proliferative

endometrium with a few cysts (persistent proliferative endometrium) to bulkier endometria

with many dilated and contorted glands that in other systems have been designated as cystic

glandular hyperplasia, mild hyperplasia, or simple hyperplasia.

Endometrial intraepithelial neoplasia (EIN)Endometrial precancers. Epithelial crowding in

precancers displaces stroma to a point at which stromal volume is less than approximately

half of total tissue volume (stroma + epithelium + gland lumen). Stromal volume can be

measured using computerized morphometric analysis and assigned a D-score [12,13]. Using

this method, specimens are classified as benign (D>1), indeterminate (0


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premenopausal women. Occasionally, women with no abnormal uterine bleeding present with

abnormal findings on cervical cytology.

The clinical presentation for endometrial hyperplasia is the same as for endometrial carcinoma. This is

discussed in detail separately. (See"Endometrial carcinoma: Clinical features and diagnosis", section

on 'Clinical presentation'.)

EVALUATION OF WOMEN WITH SUSPECTED ENDOMETRIAL NEOPLASIAWomen with a

clinical presentation suspicious for endometrial hyperplasia are evaluated initially with physical

examination. Pelvic sonography may also be performed to exclude another etiology of abnormal

uterine bleeding or to assess endometrial thickness in postmenopausal women. This evaluation is the

same as for women with suspected endometrial carcinoma and is discussed in detail separately.

(See"Endometrial carcinoma: Clinical features and diagnosis", section on 'Evaluation of women with

suspected endometrial neoplasia'.)

DIAGNOSISEndometrial hyperplasia is a histologic diagnosis made based upon the results of

evaluation of an endometrial biopsy, curettage sample, or hysterectomy specimen.

Diagnostic methods are the same as for endometrial carcinoma and are discussed in detail

separately. (See"Endometrial carcinoma: Clinical features and diagnosis".)

DIFFERENTIAL DIAGNOSISThe differential diagnosis of endometrial hyperplasia includes other

conditions that present with abnormal uterine bleeding. Women with presumed uterine bleeding

should be evaluated to confirm that the source of the blood is the uterus, and not another part of the

genital tract or the anus or rectum. The etiologies of uterine bleeding and other sources of genital tract

bleeding are discussed separately. (See"Differential diagnosis of genital tract bleeding in women".)

In addition, for women who present with abnormal finding on cervical cytology, the differential

diagnosis includes benign endometrium and cervical neoplasia. (See"Cervical and vaginal cytology:

Interpretation of results", section on 'Benign-appearing endometrial cells in a woman 40

years'and"Cervical cytology: Evaluation of atypical and malignant glandular cells", section on 'Risk of

premalignant or malignant disease'.)

FURTHER EVALUATION AFTER ENDOMETRIAL SAMPLING

Negative endometrial sampling

Office endometrial biopsy with insufficient endometrial cellsWomen with an endometrial

biopsy result that has insufficient endometrial cells should have sampling repeated with an office

biopsy or dilation and curettage (D&C). If two office endometrial biopsies have been unsuccessful, a

D&C should be performed. Cervical stenosis, a common cause of an unsuccessful biopsy, can be

managed with preprocedure cervical preparation or dilation. (See"Endometrial sampling procedures",

section on 'Cervical preparation and dilation'.)

Persistent or recurrent bleedingIf bleeding persists or recurs after endometrial sampling with

benign findings, further evaluation is required. In our practice, we reevaluate such cases after three to

six months.

Abnormal uterine bleeding symptoms may be due to an etiology other than endometrial neoplasia.

Transvaginal ultrasound, sonohysterography, or diagnostic hysteroscopy should be performed to

exclude structural lesions (leiomyomas, endometrial polyp). Any structural lesions that are found

should be treated, as appropriate. (See"Evaluation of the endometrium for malignant or premalignant

disease"and"Hysteroscopic myomectomy"and"Endometrial polyps", section on 'Choosing amanagement approach'.)
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In addition to evaluation for structural lesions, it is essential to repeat endometrial sampling to exclude

endometrial hyperplasia or carcinoma. Reported rates of endometrial neoplasia in women evaluated

for persistent or recurrent postmenopausal bleeding vary widely, from 4 to 21 percent [18,19].

Positive endometrial samplingWomen with endometrial hyperplasia should be treated, as

appropriate. (See"Management of endometrial hyperplasia".)

Office endometrial biopsyFor women with atypical endometrial hyperplasia on an office

endometrial biopsy, if a hysterectomy is not planned, we suggest further evaluation with dilation and

curettage to exclude a coexistent endometrial carcinoma [20,21]. Coexistent endometrial carcinoma is

present in 17 to 52 percent of women with complex hyperplasia at time of hysterectomy, as noted

above [8]. Women with endometrial carcinoma should be treated, as appropriate. (See"Overview of

endometrial carcinoma".)

If the uterine curettage results are less severe or negative, the patient should be managed based

upon the results of the office endometrial biopsy.

Postmenopausal women with no known estrogen sourceDevelopment of endometrialhyperplasia with or without atypia in a woman who should be estrogen-deficient requires an

explanation. In the absence of other sources of estrogen (eg, estrogen therapy, obesity), such women

require evaluation for an estrogen-producing tumor. This is discussed in detail separately.

(See"Endometrial carcinoma: Clinical features and diagnosis", section on 'Postmenopausal women

not on hormone therapy'.)

SUMMARY AND RECOMMENDATIONS

Endometrial hyperplasia is characterized by a proliferation of endometrial glands that may

progress to or coexist with endometrial carcinoma. (See'Introduction'above.)

The most commonly used classification system for endometrial hyperplasia is the WorldHealth Organization system, which has four categories: simple without nuclear atypia,

complex without atypia, simple atypical hyperplasia, and complex atypical hyperplasia.

(See'Histology and classification'above.)

The endometrial intraepithelial neoplasia system is another classification system.

(See'Endometrial intraepithelial neoplasia system'above.)

The presence of nuclear atypia is the most important indicator of the risk of endometrial

carcinoma in women with endometrial hyperplasia. The risk of progression from atypical

hyperplasia to carcinoma is approximately 23 to 29 percent. In addition, 17 to 52 percent of

women with atypical hyperplasia are found to have coexistent endometrial carcinoma when a

hysterectomy is performed. (See'Risk of carcinoma'above.)

Endometrial hyperplasia almost always results from excess estrogen exposure. This may be

caused by obesity, anovulation, estrogen therapy without a progestin, or estrogen producing

ovarian tumors (rare). (See'Risk factors'above.)

Endometrial hyperplasia typically presents with abnormal uterine bleeding and is most

common in women who are postmenopausal and with increasing age in premenopausal

women. Occasionally, women with no abnormal uterine bleeding present with abnormal

findings on cervical cytology. (See'Clinical presentation'above.)

Endometrial hyperplasia is a histologic diagnosis made with sampling of the endometrium.

Either an office endometrial biopsy or dilation and curettage may be performed.

(See'Diagnosis'above.)
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For women with atypical endometrial hyperplasia on an office endometrial biopsy, if a

hysterectomy is not planned, we suggest further evaluation with dilation and curettage to

exclude a coexistent endometrial carcinoma. (See'Office endometrial biopsy'above.)

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2. Scully RE, Bonfiglio TA, Kurman, et al. Uterine corpus. In: Histological Typing of Female Genital TractTumours, 2nd ed., Springer-Verlag, New York 1994. p.13.

3. Zaino RJ, Kauderer J, Trimble CL, et al. Reproducibility of the diagnosis of atypical endometrialhyperplasia: a Gynecologic Oncology Group study. Cancer 2006; 106:804.

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2009; 200:678.e1.18.Twu NF, Chen SS. Five-year follow-up of patients with recurrent postmenopausal bleeding. Zhonghua

Yi Xue Za Zhi (Taipei) 2000; 63:628.19.Ronghe R, Gaudoin M. Women with recurrent postmenopausal bleeding should be re-investigated but

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