Endometrial hyperplasia is pretty much what it says on the label, excessive proliferation of endometrial glands relative to stroma, more so than just proliferative endometrium.
This is usually driven by unopposed estrogen.
The high estrogen encourages the endometrium to proliferate more than it usually would, but without enough progesterone around to keep the growth in check.
And with unchecked proliferation, the risk of cell damage increases.
So that all sounds bad, but where do we see unopposed estrogen, Maddy?
Well, like we mentioned last episode, causes of unopposed estrogen include obesity, anovulatory cycles like we see with PMOS, taking estrogen like estrogen-only menopausal hormone therapy, taking tamoxifen or hormone-producing granulosa cell tumors.
So watch out for an adenexal mass and increased endometrial thickness concurrently on ultrasound.
Other risk factors we discussed previously include genetic syndromes like Lynch or Bracca.
Also, diabetes is another important risk factor for two reasons.
The high glucose levels can promote tumour growth and excessive insulin reduces sex hormone binding globulin, resulting in even more unopposed estrogen.
But looking back at hyperplasia, Chloe, tell us about how we classify this condition.
So the Contemporary World Health Organization classification of endometrial hyperplasia splits it into two, with or without atypia.
It used to be called simple and complex, but those terms are not used anymore.
So hyperplasia without atypia has closely packed glands and variation in gland size, often with increased volume of endometrial tissues, but without the similar cytological features of background endometrium.
The risk of progression to cancer is
less than 5%.
Conversely, with atypical hyperplasia, There is atypical cell appearance with features like hyperchromasia, nuclear enlargement or prominent nucleoli.
This is also sometimes called endometrioid intraepithelial neoplasia and is associated with a much higher risk of progression to endometrioid adenocarcinoma with a concurrent cancer identified in 25 to 40% of cases.
So this
is where tissue is the issue.
Endometrial hyperplasia is pretty much what it says on the label, excessive proliferation of endometrial glands relative to stroma, more so than just proliferative endometrium.
This is usually driven by unopposed estrogen.
The high estrogen encourages the endometrium to proliferate more than it usually would, but without enough progesterone around to keep the growth in check.
And with unchecked proliferation, the risk of cell damage increases.
So that all sounds bad, but where do we see unopposed estrogen, Maddy?
Well, like we mentioned last episode, causes of unopposed estrogen include obesity, anovulatory cycles like we see with PMOS, taking estrogen like estrogen-only menopausal hormone therapy, taking tamoxifen or hormone-producing granulosa cell tumors.
So watch out for an adenexal mass and increased endometrial thickness concurrently on ultrasound.
Other risk factors we discussed previously include genetic syndromes like Lynch or Bracca.
Also, diabetes is another important risk factor for two reasons.
The high glucose levels can promote tumour growth and excessive insulin reduces sex hormone binding globulin, resulting in even more unopposed estrogen.
But looking back at hyperplasia, Chloe, tell us about how we classify this condition.
So the Contemporary World Health Organization classification of endometrial hyperplasia splits it into two, with or without atypia.
It used to be called simple and complex, but those terms are not used anymore.
So hyperplasia without atypia has closely packed glands and variation in gland size, often with increased volume of endometrial tissues, but without the similar cytological features of background endometrium.
The risk of progression to cancer is
less than 5%.
Conversely, with atypical hyperplasia, There is atypical cell appearance with features like hyperchromasia, nuclear enlargement or prominent nucleoli.
This is also sometimes called endometrioid intraepithelial neoplasia and is associated with a much higher risk of progression to endometrioid adenocarcinoma with a concurrent cancer identified in 25 to 40% of cases.
So this
is where tissue is the issue.
The rest of this transcript — segmented and speaker-labeled, so you land on the exact moment something was said
Search every transcript — by keyword, by phrase, or by meaning, across every show Radar indexes
Trends — what is surging across podcasts, measured against its own baseline
Alerts — when a name you follow appears in a newly indexed episode
No account is needed to search Radar.