Postmenopausal hyperthecosis: Functional dysregulation of androgenesis in climacteric ovary

Magee-Womens Hospital, Pittsburgh, Pennsylvania, United States
Obstetrics and Gynecology (Impact Factor: 5.18). 06/2002; 99(5 Pt 2):893-7. DOI: 10.1016/S0029-7844(01)01588-5
Source: PubMed


Hyperandrogenism of ovarian origin is rare in postmenopausal women. However, there is evidence that the ovaries of postmenopausal women are active endocrine glands, secreting mainly androgens.
A postmenopausal woman sought treatment for progressive hirsutism. Endocrine evaluation revealed androgen excess. Transvaginal ultrasound revealed enlarged ovaries. Hysterectomy and bilateral oophorectomy were recommended. However, surgery had to be withheld for 6 months while the patient recovered from an acute myocardial infarction. In the interim, the patient's hyperandrogenemia was successfully treated with monthly injections of the gonadotropin-releasing hormone agonist (GnRH), leuprolide acetate.
This report illustrates the potential for postmenopausal ovaries to become active androgen-secreting endocrine organs. It also demonstrates the efficacy of pharmacologic intervention for postmenopausal ovarian hyperthecosis when the patient is a poor surgical candidate.

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Available from: Esther Krug, Aug 31, 2015
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    • "Although the exact aetiology is unclear, some authors claım that hyperthecosis ın postmenopausel women originate from elevated gonodotrophin productions. Patients with hyperthecosis typically have normal serum dehydroepiandrosterone sulfate (DHEA sulfate) concentrations [22] [23]. Ultrasonography in women with hyperthecosis usually shows a bilateral increase in ovarian stroma and the ovaries appear more solid [24]. "
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    • "In the menopausal ovary, follicles undergo atresia, with sparing of androgen-producing theca –interstitial cell components (Shifren and Schiff, 2000). Post-menopausal ovaries are smaller and consist primarily of stromal cells, which retain receptors for LH (Foth and Romer, 2001), that could respond to its rise in circulation secreting testosterone but produce little estrogen (Longcope, 2001; Krug and Berga, 2002). Advancing age coupled with estrogen loss and hyperandrogenemia could lead to insulin resistance, increasing the risks of type II diabetes, hyperlipidemia and cardiovascular disease. "
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