Endometrial Hyperplasia : Classification
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The 1994 WHO classification divided endometrial hyperplasia (EH) into simple hyperplasia, complex hyperplasia, simple atypical hyperplasia and complex atypical hyperplasia. This was based on glandular architectural complexity and cytologic atypia (loss of nuclear polarity, nuclear enlargement and rounding, and prominent nucleoli). It is no longer recommended due to lack of reproducibility.
The revised 2014 WHO Classification divides EH into two categories based on cytologic atypia. The entity endometrioid intraepithelial neoplasia (EIN) - which is a histologic manifestation of accumulation of certain mutations (PTEN, PAX2, KRAS, & microsatellite instability) has been included into the revised WHO terminology resulting in a two-tiered classification: nonatypical EH and atypical EH/EIN.
Nonatypical EH (benign hyperplasia) represents a spectrum of benign reactive histologic changes due to unopposed estrogen effects. It usually regresses spontaneously and progresses to adenocarcinoma in <2% of cases. Atypical EH/EIN is a clonal premalignant process with underlying molecular alterations that progresses to adenocarcinoma in 25-30% of cases if left untreated.
The revised 2014 WHO Classification divides EH into two categories based on cytologic atypia. The entity endometrioid intraepithelial neoplasia (EIN) - which is a histologic manifestation of accumulation of certain mutations (PTEN, PAX2, KRAS, & microsatellite instability) has been included into the revised WHO terminology resulting in a two-tiered classification: nonatypical EH and atypical EH/EIN.
Nonatypical EH (benign hyperplasia) represents a spectrum of benign reactive histologic changes due to unopposed estrogen effects. It usually regresses spontaneously and progresses to adenocarcinoma in <2% of cases. Atypical EH/EIN is a clonal premalignant process with underlying molecular alterations that progresses to adenocarcinoma in 25-30% of cases if left untreated.