Identification of Virilizing Adrenal Tumors in Hirsute Women

Derksen, J.J.L.; Nagesser, S.K.; Meinders, A. E.; Haak, Harm R.; Velde, C. J. H. van de

doi:10.1056/nejm199410133311502

Cited by 155 publications

(83 citation statements)

References 22 publications

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“…1). However, there is a wide variation in testosterone cut-offs employed between the different studies mainly due to the relative paucity of data in postmenopausal women (12,16,17,18).…”

Section: Causes Of Hyperandrogenism After Menopausementioning

confidence: 99%

“…When the underlying cause is CAH or NCAH basal or stimulated 17-OHP levels usually suffice to make the diagnosis (38). Very high serum testosterone (O150-200 ng/dl) and/or DHEAS (O6000 ng/ml) levels are more in favor of an androgensecreting tumor of ovarian and adrenal origin respectively, whereas testosterone appears to be the most consistently raised androgen (17,74). Although similarly high testosterone levels may also be found in women with OH, distinguishing between these two entities may not always be possible, whereas other than testosterone raised androgen levels are more in favour of a tumor.…”

Section: Diagnosis and Differential Diagnosismentioning

confidence: 99%

“…Androgen-secreting neoplasms are usually associated with absolute hyperandrogenism (testosterone levels O100-140 ng/dl); this relatively broad range of testosterone cut-offs reflects the wide variation of testosterone levels in the different studies and the lack of meticulous registration of such patients (7,8,12,17,18). The androgen-secreting neoplasms usually have distinct clinical features and have traditionally been associated with a rapid onset of signs and symptoms resulting in various degrees of virilization (7,8).…”

Section: Tumorous Hyperandrogenismmentioning

confidence: 99%

“…However, these cut-offs have been obtained from series that have included both pre-and postmenopausal hyperandrogenic women and their predictive value varies considerably (18). In order to improve the diagnostic accuracy of raised serum androgens, the testosterone response to dexamethasone administration has been used based on the rationale that elevated testosterone levels due to adrenal or ovarian tumors are not responsive to dexamethasone administration (17,18). However, lack of suppression of testosterone levels may similarly occur in nontumorous cases, as a O40% testosterone reduction following a formal low dose dexamethasone suppression test was found in only 88% of them (18).…”

Section: Diagnosis and Differential Diagnosismentioning

confidence: 99%

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MANAGEMENT OF ENDOCRINE DISEASE: Hyperandrogenism after menopause

Markopoulos

Kassi

Alexandraki

et al. 2015

European Journal of Endocrinology

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Postmenopausal hyperandrogenism is a state of relative or absolute androgen excess originating from either the adrenals and/or the ovaries, clinically manifested as the appearance and/or increase in terminal hair growth or the development of symptoms/signs of virilization. In either settings, physicians need to evaluate such patients and exclude the presence of the relatively rare but potentially life-threatening underlying tumorous causes, particularly adrenal androgen-secreting tumors. It has been suggested that the rapidity of onset along with severity of symptom and the degree of androgen excess followed by relevant imaging studies may suffice to identify the source of excessive androgen secretion. However, up to date, there is no consensus regarding specific clinical and hormonal indices and/or imaging modalities required for diagnostic certainty. This is particularly relevant as the aging population is increasing and more cases of postmenopausal women with clinical/biochemical evidence of hyperandrogenism may become apparent. Furthermore, the long-term sequels of nontumorous hyperandrogenism in postmenopausal women in respect to cardiovascular morbidity and mortality still remain unsettled. This review delineates the etiology and pathophysiology of relative and absolute androgen excess in postmenopausal women. Also, it attempts to unravel distinctive clinical features along with specific hormonal cut-off levels and/or appropriate imaging modalities for the facilitation of the differential diagnosis and the identification of potential long-term sequels.

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“…1). However, there is a wide variation in testosterone cut-offs employed between the different studies mainly due to the relative paucity of data in postmenopausal women (12,16,17,18).…”

Section: Causes Of Hyperandrogenism After Menopausementioning

confidence: 99%

Section: Diagnosis and Differential Diagnosismentioning

confidence: 99%

Section: Tumorous Hyperandrogenismmentioning

confidence: 99%

Section: Diagnosis and Differential Diagnosismentioning

confidence: 99%

See 2 more Smart Citations

MANAGEMENT OF ENDOCRINE DISEASE: Hyperandrogenism after menopause

Markopoulos

Kassi

Alexandraki

et al. 2015

European Journal of Endocrinology

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“…ACTH suppression is required to have only autonomous adrenal function picked up on scanning. In addition, measurement of androgens in serum after 5 days of adrenal suppression will distinguish between androgens maintained by suppressible ACTH stimulation as in the case of CAH and androgens secreted autonomously by tumours of adrenal glands or ovaries (29). Prolonged, 5-day adrenal suppression is necessary to allow time for the normal slow clearance of adrenal androgens, particularly DHEAS.…”

Section: Screening For Adrenal Tumourmentioning

confidence: 99%

Investigation of patients with atypical or severe hyperandrogenaemia including androgen-secreting ovarian teratoma

Dennedy

Smith²,

O’Shea³

et al. 2010

European Journal of Endocrinology

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Approximately 7% of women of reproductive age manifest polycystic ovary syndrome (PCOS) and !0.5% have other causes of hyperandrogenism including congenital adrenal hyperplasia (CAH), androgen-secreting tumour of an ovary or an adrenal gland, Cushing's syndrome or hyperthecosis. The presence of features atypical of PCOS should prompt more extensive evaluation than that usually undertaken. Features atypical of PCOS include the onset of symptoms outside the decade of 15-25 years, rapid progression of symptoms, the development of virilization and a serum testosterone concentration in excess of twice the upper limit of the reference range. Ethnic background, family history and specific clinical findings, e.g. Cushingoid appearance, may inform a focused investigation. Otherwise, patients should have measurement of 17-hydroxyprogesterone (17-OHP) under basal conditions ideally in the early morning, and if abnormal, they should have measurement of 17-OHP one hour after the administration of synthetic ACTH, 250 mg i.v., to screen for CAH, which is present in w2% of hyperandrogenic patients. The overnight cortisol suppression test employing 1 mg dexamethasone at midnight is a sensitive test for Cushing's syndrome. Coronal tomographic (CT) scanning of the adrenals and transvaginal ultrasonography of the ovaries are the investigations of choice when screening for tumours in these organs. Less frequently required is catheterization and sampling from both adrenal and ovarian veins, which is a technically demanding procedure with potential complications which may provide definitive diagnostic information not available from other investigations. Illustrative case reports highlight some complexities in the investigation of hyperandrogenic patients presenting with features atypical of PCOS and include only the ninth case report of an androgen-secreting ovarian teratoma.

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