Figure 14.

Progesterone resistance: HSD17B2 deficiency in endometriotic epithelium. HSD17B2 is specifically expressed in eutopic endometrial epithelial cells during the secretory phase. This expression coincides with progesterone secretion by the corpus luteum. HSD17B2 converts the biologically potent estrogen, estradiol (E2), to estrogenically weak estrone (E1). In endometriotic tissue, however, this epithelial HSD17B2 is severely deficient, giving rise to E2 excess. These findings are suggestive that progesterone stimulates HSD17B2 in eutopic endometrium and that its deficiency in endometriosis is a consequence of progesterone resistance. [Reproduced from Zeitoun K, Takayama K, Sasano H, Suzuki T, Moghrabi N, Andersson S, Johns A, Meng L, Putman M, Carr B, Bulun SE. Deficient 17β-hydroxysteroid dehydrogenase type 2 expression in endometriosis: failure to metabolize 17β-estradiol. J Clin Endocrinol Metab. 1998;83(12):4474–4480.]