Endometrial hyperplasia overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Swathi Venkatesan, M.B.B.S.[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 estrogen stimulation may be either from an endogenous or exogenous source.[2][1] Endometrial hyperplasia may be broadly classified based on histology into simple and complex types. Endometrial hyperplasia may also be classified based on the presence or absence of cellular atypia (hyperplasia with cellular atypia and hyperplasia without cellular atypia).[3][4][5] Endometrial hyperplasia must be differentiated from conditions that have similar ultrasound appearances such as normal thickening during the secretory phase, sessile endometrial polyp, submucosal uterine fibroids, endometrial cancer, adherent intrauterine blood clot,and pregnancy.[4][6][7] Women of all age groups may develop endometrial hyperplasia.[8] However, endometrial hyperplasia is more common in postmenopausal women. The majority of cases of endometrial hyperplasia, except complex atypical hyperplasia resolve spontaneously with time.[9] If left untreated, 30% of patients with atypical hyperplasia may progress to develop endometrial carcinoma.[10] Malignant transformation into endometrial cancer is the most common complication of endometrial hyperpasia.[11] Prognosis is generally good with treatment. Pelvic ultrasound on days 5 to 10 of menstrual cycle reduce the variability in endometrial thickness and may be helpful in the diagnosis of endometrial hyperplasia. On pelvic ultrasound, endometrial hyperplasia is characterized by a homogeneous increase in the endometrial thickness in the majority of patients. However, endometrial hyperplasia may also cause asymmetric or focal thickening with surface irregularity which should raise a suspicion for malignancy.[12] Progesterone therapy is the preferred drug for the treatment of benign hyperplasia. The management of endometrial hyperplasia depends upon the desire for future childbearing.[13] Total hysterectomy is curative for atypical endometrial hyperplasia or endometrial intraepithelial neoplasia.[14]
Classification
Endometrial hyperplasia may be broadly classified based on histology into simple and complex types. Endometrial hyperplasia may also be classified based on the presence or absence of cellular atypia (hyperplasia with cellular atypia and hyperplasia without cellular atypia).[3][4][5]
Pathophysiology
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]
Causes
Endometrial hyperplasia is caused by high levels of estrogens, combined with insufficient levels of the progesterone-like hormones which ordinarily counteract estrogen's proliferative effects on this tissue.[12]
Differentiating Endometrial Hyperplasia from other Diseases
Endometrial hyperplasia must be differentiated from conditions that have similar ultrasound appearances such as normal thickening during the secretory phase, sessile endometrial polyp, submucosal uterine fibroids, endometrial cancer, adherent intrauterine blood clot, and pregnancy.[4][6][7]
Epidemiology and Demographics
Women of all age groups may develop endometrial hyperplasia.[8] However, endometrial hyperplasia is more common in postmenopausal women.
Risk Factors
Common risk factors in the development of endometrial hyperplasia include age>35 years, white race, nulliparity, late menopause, early menarche, tamoxifen therapy, obesity, Lynch syndrome, history of diabetes, gallbladder disease, or thyroid disease, and family history of ovarian, colon, or uterine cancers.[15]
Screening
Routine screening for endometrial hyperplasia or endometrial carcinoma is not recommended.
Natural History, Complications and Prognosis
The majority of cases of endometrial hyperplasia, except complex atypical hyperplasia resolve spontaneously with time.[9] If left untreated, 30% of patients with atypical hyperplasia may progress to develop endometrial carcinoma.[10] Malignant transformation into endometrial cancer is the most common complication of endometrial hyperpasia.[11] Prognosis is generally good with treatment.
Diagnosis
History and Symptoms
A positive history of irregular menstrual cycles (PCOD) may be present.[12] A detailed drug history may be helpful in the assessment of possible risk factors for endometrial hyperplasia. A history of inappropriate hormone replacement therapy in post menopausal women and history of tamoxifen use in breast cancer patients may be present.[13][16][17]
Physical Examination
Patients with endometrial hyperplasia usually appear well. Physical examination of patients with endometrial hyperplasia is usually not remarkable for any physical findings.
Laboratory Findings
Routine laboratory tests are usually normal among patients with endometrial hyperplasia. Some patients with endometrial hyperplasia may have abnormal complete blood count, which is usually suggestive of anemia from prolonged vaginal bleeding.[18]
CT
There are no CT findings associated with endometrial hyperplasia.
MRI
There are no MRI findings associated with endometrial hyperplasia.
Ultrasound
Pelvic ultrasound on days 5 to 10 of menstrual cycle reduce the variability in endometrial thickness and may be helpful in the diagnosis of endometrial hyperplasia. On pelvic ultrasound, endometrial hyperplasia is characterized by a homogeneous increase in the endometrial thickness in the majority of patients. However, endometrial hyperplasia may also cause asymmetric or focal thickening with surface irregularity which should raise a suspicion for malignancy.[12]
Other Imaging Findings
There are no other imaging findings associated with endometrial hyperplasia.
Other Diagnostic Studies
Hysteroscopy may be helpful in the direct visualization of precancerous lesions.[14] Diagnosis of endometrial hyperplasia is usually performed through curettage of the uterine cavity to obtain endometrial tissue for histopathologic analysis.[18]
Treatment
Medical Therapy
Progesterone therapy is the preferred drug for the treatment of benign hyperplasia. The management of endometrial hyperplasia depends upon the desire for future childbearing.[13]
Surgery
Total hysterectomy is curative for atypical endometrial hyperplasia or endometrial intraepithelial neoplasia.[14]
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 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.
- ↑ 3.0 3.1 Scully RE. Histological typing of female genital tract tumours. Springer; 1994.
- ↑ 4.0 4.1 4.2 4.3 Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 3, 2016.
- ↑ 5.0 5.1 Jorizzo JR, Chen MY, Martin D, Dyer RB, Weber TM (2002). "Spectrum of endometrial hyperplasia and its mimics on saline hysterosonography". AJR Am J Roentgenol. 179 (2): 385–9. doi:10.2214/ajr.179.2.1790385. PMID 12130438.
- ↑ 6.0 6.1 Hulka CA, Hall DA, McCarthy K, Simeone JF (1994). "Endometrial polyps, hyperplasia, and carcinoma in postmenopausal women: differentiation with endovaginal sonography". Radiology. 191 (3): 755–8. doi:10.1148/radiology.191.3.8184058. PMID 8184058.
- ↑ 7.0 7.1 Abnormally thickened endometrium: differential diagnosis. Radiopedia. http://radiopaedia.org/articles/abnormally-thickened-endometrium-differential-diagnosis Accessed on March 3, 2016.
- ↑ 8.0 8.1 Endometrial Hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 9, 2016
- ↑ 9.0 9.1 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.
- ↑ 10.0 10.1 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.
- ↑ 11.0 11.1 Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 16, 2016
- ↑ 12.0 12.1 12.2 12.3 Endometrial hyperplasia. Radiopedia. http://radiopaedia.org/articles/endometrial-hyperplasia-1 Accessed on March 10, 2016.
- ↑ 13.0 13.1 13.2 Emons G, Beckmann MW, Schmidt D, Mallmann P, Uterus commission of the Gynecological Oncology Working Group (AGO) (2015). "New WHO Classification of Endometrial Hyperplasias". Geburtshilfe Frauenheilkd. 75 (2): 135–136. doi:10.1055/s-0034-1396256. PMC 4361167. PMID 25797956.
- ↑ 14.0 14.1 14.2 Trimble CL, Method M, Leitao M, Lu K, Ioffe O, Hampton M; et al. (2012). "Management of endometrial precancers". Obstet Gynecol. 120 (5): 1160–75. doi:http://10.1097/AOG.0b013e31826bb121 Check
|doi=value (help). PMC 3800154. PMID 23090535. - ↑ Endometrial Hyperplasia. The American Congress of Obstetricians and Gynecologists. http://www.acog.org/Patients/FAQs/Endometrial-Hyperplasia. Accessedon March 3, 2016.
- ↑ Reed SD, Newton KM, Clinton WL, Epplein M, Garcia R, Allison K; et al. (2009). "Incidence of endometrial hyperplasia". Am J Obstet Gynecol. 200 (6): 678.e1–6. doi:10.1016/j.ajog.2009.02.032. PMC 2692753. PMID 19393600.
- ↑ Tamoxifen associated endometrial changes. Radiopedia. http://radiopaedia.org/articles/tamoxifen-associated-endometrial-changes Accessed on March 10, 2016
- ↑ 18.0 18.1 Bobrowska K, Pietrzak B, Jabiry-Zieniewicz Z, Cyganek A, Kaminski P, Wielgos M; et al. (2007). "Operative treatment of endometrial hyperplasia in kidney graft recipients: report of seven cases". Transplant Proc. 39 (9): 2756–8. doi:10.1016/j.transproceed.2007.09.023. PMID 18021979.