#1706859 Localizing The Source of Androgens

Document Type

Article

Publication Date

5-8-2024

Publication Title

Endocrine Practice

Abstract

Introduction: There are multiple etiologies of excess testosterone in a female of childbearing age. Over 95% cases are due to PCOS but this is a diagnosis of exclusion after other pathologies like Cushing’s, nonclassical congenital adrenal hyperplasia, ovarian and adrenal tumors have been ruled out.

Case(s) Description: We present a case of a 22-year-old female evaluated for hyperandrogenic symptoms including hirsutism across all areas of body, secondary amenorrhea for 2 years, balding in a male pattern and deepening of her voice. Physical exam revealed frontal balding, absence of clitoromegaly and excessive hair on chin and upper lip. Initial evaluation showed elevated total testosterone of 235 ng/dL and a free testosterone of 7.99 ng/dL. Repeat testing showed similar results. Other testing revealed normal DHEA-S, estradiol, 17 hydroxyprogesterone, 24-hour urine cortisol and adequate suppression with 1 mg dexamethasone suppression testing. Ultrasound of the ovaries revealed multi follicular ovaries. An initial diagnosis of PCOS was made. Given her elevated testosterone level above 150, we proceeded to rule out an adrenal or ovarian source of excess androgens. 2-day dexamethasone androgen suppression test showed adequate suppression of DHEA-S and cortisol but no suppression of total and free testosterone, which pointed towards an ovarian source. Further evaluation included MRI of the pelvis which did not reveal any pelvic masses and tumor markers including beta hCG, CA125 and alpha-fetoprotein were all normal. This was deemed as a case of PCOS with excessively elevated testosterone with hyperandrogenic symptoms. Once other pathologies were ruled out, she was treated along PCOS guidelines.

Discussion: Testosterone above 150 ng/dl is normally not seen in PCOS, and guidelines recommend ruling out other sources of hyperandrogenism. Initial lab testing includes total and free testosterone, 17-hydroxyprogesterone, TSH, prolactin and DHEA-S. Elevated 17-hydroxyprogresterone points towards nonclassical CAH. If labs show normal 17-OH progesterone, the next step involves a 2-day dexamethasone-androgen suppression test which helps differentiate adrenal from ovarian sources depending on cortisol, testosterone and DHEA-S levels post suppression. If the testosterone level fails to be suppressed but DHEA-S and cortisol respond, the source of testosterone is primarily the ovaries. Lack of suppression of androgens and cortisol points to adrenal hyperfunction, like Cushing’s. If the high level of testosterone is suppressed more than 40% and DHEAS is suppressed more than 60% after administration of dexamethasone, the source of the increased androgen is most likely the adrenal glands. Although not outlined in the guidelines, ruling out an ovarian tumor with a transvaginal ultrasound or MRI pelvis with or without tumor markers of ovarian origin can be undertaken if suspicion is high. Other testing like GnRH analogues for androgen suppression or ovarian vein sampling can be undertaken on a case-by-case basis but not always needed. Treatment depends on underlying etiology.

Volume

30

Issue

5 Supplement

First Page

S129

Last Page

S130

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