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Endometriosis is a chronic gynecological disorder that has been widely viewed as a disease of the premenopausal years. Estrogen dependence is considered central to the development and progression of this disease which normally regresses during the menopause, yet has been thought to affect 2–4% of postmenopausal women. In a review of postmenopausal endometriosis, Bendon and Becker [1] have proposed mechanisms for postmenopausal disease which are compatible with our current understanding of this disease. The authors have suggested that it could persist from the premenopausal period into a woman’s postmenopausal years, due to the progressive nature of premenopausal disease or it could arise [i]de novo[/i] in the absence of menstruation. 


The authors have presented new evidence which suggests that [i]locally produced estrogen[/i] plays a significant role in the pathophysiology of endometriosis. It is possible that endometriosis is a self-perpetuating condition, with the lesions themselves driving local estrogen production. Local PGE[-]2[/-] production further enhances local estradiol production which occurs due to high levels of aromatase and StAR (steroidogenic acute regulatory protein) expression and enzyme activity expressed in stromal cells from endometriotic lesions. Estrogen produced within lesions further promotes disease proliferation and progression through autocrine and paracrine effects, resulting in further inflammation and further PGE[-]2[/-] production, enhancing estrogen synthesis. This theory can explain those cases of postmenopausal endometriosis where a source of excessive circulating estrogen cannot be identified. In such a situation, aromatase inhibitors have been found to be useful in treating postmenopausal disease.  


Postmenopausal endometriosis is morphologically similar to premenopausal disease, based on similar distributions of estrogen and progesterone receptors irrespective of age. Thus, endometriotic lesions might have the potential to reactivate when given the appropriate hormonal stimulus. The authors have suggested that excessive obesity, use of phytoestrogens and hormone therapy (HT) can aggravate existing premenopausal disease and also enhance its malignant potential.


  • Duru Shah
    Director Gynaecworld, The Center for Womens Health and Fertility, Mumbai, India


  1. Bendon CL, Becker CM. Potential mechanisms of postmenopausal endometriosis. Maturitas 2012;72:214-19.
  2. Rattanachaiyanont M, Tanmahasamut P, Angsuwatthana S, et al. Hormonal replacement therapy in surgical menopause with underlying endometriosis. J Med Assoc Thai 2003;86:702-7.
  3. Cotroneo MS, Lamartiniere CA. Pharmacologic, but not dietary, genistein supports endometriosis in a rat model. Toxicol Sci 2001;61:68-75.
  4. Fedele L, Bianchi S, Raffaelli R, Zanconato G. Comparison of transdermal estradiol and tibolone for the treatment of oophorectomized women with deep residual endometriosis. Maturitas 1999;32:189-93.
  5. Cumiskey J, Whyte P, Kelehan P, Gibbons D. A detailed morphologic and immunohistochemical comparison of pre and postmenopausal endometriosis. J Clin Pathol 2008;61:455-9.
  6. Brinton LA, Gridley G, Persson I, et al. Cancer risk after a hospital discharge diagnosis of endometriosis. Am J Obstet Gynecol 1997;176:572-9.
  7. Zanetta GM, Webb MJ, Li H, Keeney GL. Hyperestrogenism: a relevant risk factor for the development of cancer from endometriosis. Gynecol Oncol 2000;79:18-22.
  8. Takayama K, Zeitoun K, Gunby RT, et al. Treatment of severe postmenopausal endometriosis with an aromatase inhibitor. Fertil Steril 1998;69:709-13.
  9. Polyzos NP, Fatemi HM, Zavos A, et al. Aromatase inhibitors in post-menopausal endometriosis. Reprod Biol Endocrinol 2011:9:90.
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