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.

Download full-text


Available from: Esther Krug, Aug 31, 2015
  • Source
    • "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]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Mild clinical signs of hyperandrogenism such as hirsutism may appear during the menopausal transition as part of the normal aging process, but the development of frank virilization suggests a specific source of androgen excess. We report a case of a 68-year-old woman with signs of virilization that had started 6 months before. Clinical analyses revealed high levels of serum testosterone for a postmenopausal woman. Pelvic MRI and abdomen CT showed no evidence of ovarian and adrenal tumor. Postmenopausal hyperandrogenism can be the result of numerous etiologies ranging from normal physiologic changes to ovarian or rarely adrenal tumors. Our patient was found to have iatrogenic hyperandrogenism. This condition is rarely reported cause of virilization.
    Case Reports in Endocrinology 12/2014; 2014:987272. DOI:10.1155/2014/987272
  • Source
    • "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. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Genetically modified follitrophin receptor knockout female mice with total FSH-receptor (FSH-R) deletion are sterile and their combined estrogen deficiency-hyperandrogenemic status provides an experimental paradigm to study the effect of hormonal imbalances on ovarian function and metabolic alterations. Elevated LH levels causing hyperandrogenemia perturb normal folliculogenesis. To control diverse pathophysiology associated with hormonal imbalances, we investigated the effects of transplanting a single normal mouse ovary in young mutants. An intact FSH-R signalling system in the graft responded promptly to the up-regulated pituitary gonadotrophins circulating in the host mutant. Resumption of regular estrous cycles validated stimulation of uterine functions. Secretions from the viable functioning grafts partially corrected follicular abnormalities originally present in host ovaries. Stromal hyperplasia responsible for high ovarian LH-receptor and key enzymes in host thecal/interstitial complex and hyperandrogenemia was reduced in host ovaries. Increases in plasma estradiol and reduced LH and free testosterone re-established the negative-feedback system. Reduced android obesity and activation of mammary glands indicated the combined beneficial effects of normalized steroid hormones on target organs. These data provide evidence that ovarian transplantation in mutants corrects estrogen loss and hyperandrogenemia. However, correction of hormonal imbalances is not sufficient to fully restore effects of FSH-R loss in host granulosa cells.
    Molecular Human Reproduction 06/2007; 13(5):287-97. DOI:10.1093/molehr/gam008 · 3.75 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cardiovascular disease is the leading cause of death in women and claims the lives of more than half a million women every year. Hypertension is one of the most prevalent and powerful contributors to atherosclerotic cardiovascular disease. Hypertension affects more men than women until 55 years of age, but after age 55, the percentage of women is higher. Estrogen deficiency has been linked to the rapid increase in cardiovascular disease in women who have undergone natural or surgical menopause. Hormone replacement therapy (HRT) has been shown to decrease the incidence of cardiovascular disease and, in some studies, to reduce blood pressure in postmenopausal women. However, little information is available on the effects of HRT on blood pressure in hypertensive postmenopausal patients. The cardioprotective effects of estrogens are not completely understood but may involve direct effects on blood vessels through modulation of endogenous vasoconstrictors and vasodilators and through reductions in serum lipoprotein and cholesterol levels. Experimental evidence suggests that estrogen increases the biological actions of nitric oxide and decreases the actions of angiotensin. After menopause, loss of the vascular protective effects of estrogens may unmask a population of women particularly prone to hypertension who would be at higher risk for cardiovascular disease.
    Current Hypertension Reports 05/2000; 2(2):202-7. DOI:10.1007/s11906-000-0083-2 · 3.44 Impact Factor
Show more