madman
Super Moderator
ABSTRACT
Postmenopausal hyperandrogenism is a state of relative or absolute androgen excess originating from the adrenal glands and/or ovaries clinically manifested by the presence of terminal hair in androgen-dependent areas of the body, and other manifestations of hyperandrogenism such as acne and alopecia or the development of virilization. In such circumstances, physicians must exclude the possibility of rare but serious androgen-producing tumors of the adrenal glands or ovaries. Worsening of undiagnosed hyperandrogenic disorders such as polycystic ovary syndrome, congenital adrenal hyperplasia, ovarian hyperthecosis, Cushing syndrome, and iatrogenic hyperandrogenism should be considered for differential diagnosis. Elevated serum testosterone not only causes virilizing effects but also will lead to hypercholesterolemia, insulin resistance, hypertension, and cardiac disease. An ovarian androgen-secreting tumor, which is diagnosed in 1–3 of 1000 patients presenting with hirsutism, comprises less than 0.5% of all ovarian tumors. Adrenal tumors, including non-malignant adenomas and malignant carcinomas, are less common than ovarian tumors but cause postmenopausal virilization. Measurement of serum testosterone, sex hormone-binding globulin, dehydroepiandrosterone sulfate, androstenedione, and inhibin B is necessary for postmenopausal women with complaints and signs of hyperandrogenism. Some tests to discard Cushing syndrome should also be done. After an etiological source of androgen, hypersecretion has been suspected, we recommend performing magnetic resonance imaging of the adrenal glands or ovaries. Medical management with gonadotropin-releasing hormone agonist/analogs or antagonists have been reported for women who are either unfit for surgery or in whom the source of elevated testosterone is unidentified.
Introduction
After menopause, estrogen levels are reduced rapidly; however, androgen secretion declines gradually and is maintained until later stages of life [1]. Luteinizing hormone (LH) stimulation is the reason for androgen secretion in premenopausal and postmenopausal women [1]. A decrease in sex hormone-binding globulin (SHBG) together with a sharp decrease in estrogen levels causes an increase in free androgens [2].
High androgen levels adversely alter the lipid profile with a decrease in high-density lipoprotein, an increase in low-density lipoprotein and an increase in triglyceride levels [3]. The levels of advanced glycation end products and testosterone have been reported to be associated in postmenopausal women [4]. Moreover, high testosterone to estradiol ratio was correlated with impaired insulin resistance and high blood pressure. Additionally, high testosterone levels in women were reported to link with increased risk of breast cancer and cardiac disease. Postmenopausal women with hyperandrogenemia had more evidence of coronary artery disease, as well as more metabolic syndrome, diabetes, and obesity [5].
Because of these significant adverse effects on the health of postmenopausal women, a thorough evaluation and treatment are required in postmenopausal women who present with hyperandrogenism. However, the identification of that source often poses a clinical challenge [6]. Possible endogenous sources of elevated androgen levels include ovarian hyperthecosis (OH) (i.e. hyperplasia of androgenic ovarian tissue) [7–9], ovarian tumors [10–12], and adrenal tumors [13]. Cushing syndrome is also a rare condition producing hyperandrogenism but is not associated with virilization.
The diagnosis of a cause of androgen excess in postmenopausal women may not always be straightforward. A combination of clinical judgment accompanied with appropriate laboratory tests and imaging techniques should be used [1].
Even though normal androgen cut-off levels are not set for the menopausal period, it is widely presumed that the levels are below those of premenopausal women [14,15]. Meanwhile, patients with non-tumorous hyperandrogenism have higher androgen levels when compared with postmenopausal women who are non-hyperandrogenic [16]. For women with testosterone levels >100–140 ng/dl, tumorous hyperandrogenism should be suspected.
*Signs and symptoms
*Hyperandrogenism of non-tumorous origin
*Hyperandrogenism of tumorous origin
*Differential diagnosis between ovarian hyperthecosis and virilizing ovarian tumor
*Diagnostic evaluation of postmenopausal hyperandrogenism
*Laboratory tests
*Radiologic evaluation
*Treatment
*Sequelae of hyperandrogenism
Conclusion
Measurement of testosterone, SHBG, DHEAS, androstenedione, and inhibin B is necessary for postmenopausal women with complaints and signs of hyperandrogenism. Some tests to discard Cushing syndrome should also be done. After an etiological source of androgen, hypersecretion has been suspected, we recommend performing an MRI of the adrenal glands or ovaries, according to the clinical suspicion.
Surgery remains the main curative treatment, particularly for adrenal androgen-secreting tumors, and may be substantiated with adjuvant therapy [1]. GnRH agonists can be used in patients with ovarian hyperandrogenism with no obvious tumors at imaging and/or who are unfit for surgery [58].
Postmenopausal hyperandrogenism is a state of relative or absolute androgen excess originating from the adrenal glands and/or ovaries clinically manifested by the presence of terminal hair in androgen-dependent areas of the body, and other manifestations of hyperandrogenism such as acne and alopecia or the development of virilization. In such circumstances, physicians must exclude the possibility of rare but serious androgen-producing tumors of the adrenal glands or ovaries. Worsening of undiagnosed hyperandrogenic disorders such as polycystic ovary syndrome, congenital adrenal hyperplasia, ovarian hyperthecosis, Cushing syndrome, and iatrogenic hyperandrogenism should be considered for differential diagnosis. Elevated serum testosterone not only causes virilizing effects but also will lead to hypercholesterolemia, insulin resistance, hypertension, and cardiac disease. An ovarian androgen-secreting tumor, which is diagnosed in 1–3 of 1000 patients presenting with hirsutism, comprises less than 0.5% of all ovarian tumors. Adrenal tumors, including non-malignant adenomas and malignant carcinomas, are less common than ovarian tumors but cause postmenopausal virilization. Measurement of serum testosterone, sex hormone-binding globulin, dehydroepiandrosterone sulfate, androstenedione, and inhibin B is necessary for postmenopausal women with complaints and signs of hyperandrogenism. Some tests to discard Cushing syndrome should also be done. After an etiological source of androgen, hypersecretion has been suspected, we recommend performing magnetic resonance imaging of the adrenal glands or ovaries. Medical management with gonadotropin-releasing hormone agonist/analogs or antagonists have been reported for women who are either unfit for surgery or in whom the source of elevated testosterone is unidentified.
Introduction
After menopause, estrogen levels are reduced rapidly; however, androgen secretion declines gradually and is maintained until later stages of life [1]. Luteinizing hormone (LH) stimulation is the reason for androgen secretion in premenopausal and postmenopausal women [1]. A decrease in sex hormone-binding globulin (SHBG) together with a sharp decrease in estrogen levels causes an increase in free androgens [2].
High androgen levels adversely alter the lipid profile with a decrease in high-density lipoprotein, an increase in low-density lipoprotein and an increase in triglyceride levels [3]. The levels of advanced glycation end products and testosterone have been reported to be associated in postmenopausal women [4]. Moreover, high testosterone to estradiol ratio was correlated with impaired insulin resistance and high blood pressure. Additionally, high testosterone levels in women were reported to link with increased risk of breast cancer and cardiac disease. Postmenopausal women with hyperandrogenemia had more evidence of coronary artery disease, as well as more metabolic syndrome, diabetes, and obesity [5].
Because of these significant adverse effects on the health of postmenopausal women, a thorough evaluation and treatment are required in postmenopausal women who present with hyperandrogenism. However, the identification of that source often poses a clinical challenge [6]. Possible endogenous sources of elevated androgen levels include ovarian hyperthecosis (OH) (i.e. hyperplasia of androgenic ovarian tissue) [7–9], ovarian tumors [10–12], and adrenal tumors [13]. Cushing syndrome is also a rare condition producing hyperandrogenism but is not associated with virilization.
The diagnosis of a cause of androgen excess in postmenopausal women may not always be straightforward. A combination of clinical judgment accompanied with appropriate laboratory tests and imaging techniques should be used [1].
Even though normal androgen cut-off levels are not set for the menopausal period, it is widely presumed that the levels are below those of premenopausal women [14,15]. Meanwhile, patients with non-tumorous hyperandrogenism have higher androgen levels when compared with postmenopausal women who are non-hyperandrogenic [16]. For women with testosterone levels >100–140 ng/dl, tumorous hyperandrogenism should be suspected.
*Signs and symptoms
*Hyperandrogenism of non-tumorous origin
*Hyperandrogenism of tumorous origin
*Differential diagnosis between ovarian hyperthecosis and virilizing ovarian tumor
*Diagnostic evaluation of postmenopausal hyperandrogenism
*Laboratory tests
*Radiologic evaluation
*Treatment
*Sequelae of hyperandrogenism
Conclusion
Measurement of testosterone, SHBG, DHEAS, androstenedione, and inhibin B is necessary for postmenopausal women with complaints and signs of hyperandrogenism. Some tests to discard Cushing syndrome should also be done. After an etiological source of androgen, hypersecretion has been suspected, we recommend performing an MRI of the adrenal glands or ovaries, according to the clinical suspicion.
Surgery remains the main curative treatment, particularly for adrenal androgen-secreting tumors, and may be substantiated with adjuvant therapy [1]. GnRH agonists can be used in patients with ovarian hyperandrogenism with no obvious tumors at imaging and/or who are unfit for surgery [58].
