The World Health Organization classification system for endometrial hyperplasia relies on changes to glandular architecture and nuclear changes within the endometrium [1]. Diffuse glands with normal gland-to-stroma ratio denote simple hyperplasia while irregular glands with increased gland-to-stroma ratio are designated complex hyperplasia. The presence of nuclear atypia gives rise to simple hyperplasia with atypia and complex hyperplasia with atypia, respectively. Since simple hyperplasia with atypia is rare, for all practical purposes, atypical hyperplasia refers mostly to atypical complex hyperplasia [2].

Besides compartmentalizing the spectrum of endometrial hyperplasias, the WHO classification also confers a tendency for malignant transformation. A classic study found that the risk of endometrial cancer was significantly greater when nuclear atypia was present [3]. In the study cohort, the authors reported the risk of endometrial cancer at 1% for simple hyperplasia, 3% for complex hyperplasia, 8% for simple hyperplasia with atypia and 23% for complex hyperplasia with atypia. More recent data for patients found to have atypical complex hyperplasia undergoing hysterectomy within 12 weeks found that the risk of concurrent endometrial cancer was 42.6% [4]. In summary, the malignant potential for complex hyperplasia with atypia approaches 50% and is reported to be from 23% to 43% in the literature.

Briefly, the stimulatory effects of unopposed estrogen are thought to promote hyperplasia and subsequent carcinoma [5]. Thus, the risks for endometrial hyperplasia are very similar to those of endometrial cancer. Chronic unopposed estrogen replacement, anovulation, marked obesity, and estrogen-secreting tumors containing granulosa and theca cells are some of the causes of an excess estrogenic state.