MON-146 - Rare Etiology of Infertility: Severe Hyperandrogenism with Virilization Revealing Suspected Androgen-Secreting Ovarian Tumor

Background:
Severe hyperandrogenism with virilization is a clinical flag for androgen-secreting neoplasms and represents a time-sensitive diagnosis. Although infertility is commonly attributed to functional disorders, rare endocrine causes may be overlooked leading to delayed definitive treatment.

Case:
Our case is of a middle-aged woman with systemic lupus erythematosus, rheumatic heart disease, and polysubstance use disorder who presented with secondary amenorrhea and dyspareunia. She reported no ongoing hormonal therapy aside from a remote single medroxyprogesterone dose. Importantly, she had never conceived despite prolonged unprotected intercourse and expressed a strong desire for fertility.
On exam, she had virilization with clitoromegaly, male-pattern facial hair, and a deepened voice. This prompted further endocrine evaluation. Total testosterone was markedly elevated at 418.2 ng/dL (repeat fasting 391.8 ng/dL), well above levels seen in functional hyperandrogenism. Other laboratory values of DHEA-S (31 µg/dL), 17-hydroxyprogesterone (196 ng/dL), LH (19.9 IU/L), FSH (21 IU/L), and estradiol (36.8 pg/mL) were within our facility’s normal ranges.
The discordance between markedly elevated testosterone and normal adrenal markers strongly suggested an ovarian source. MRI of the abdomen and pelvis further validated this suspicion with identification a 1.6 cm solid lesion in the left ovary without any adrenal abnormalities. Given the biochemical severity despite a small lesion size, an androgen-secreting ovarian tumor was considered highly likely. The patient was referred for gynecologic evaluation and possible surgical planning.

Discussion:
While Polycystic Ovary Syndrome accounts for most cases of hyperandrogenism, testosterone levels >200 ng/dL with virilization should prompt evaluation for a tumor. Adrenal etiologies such as Congenital Adrenal Hyperplasia in our patient is unlikely given normal adrenal hormone levels and imaging findings.
This case highlights two clinically important points: (1) small ovarian tumors, including Sertoli-Leydig cell tumor, may produce profound biochemical abnormalities despite minimal imaging findings; and (2) reliance on imaging size alone may delay diagnosis. Instead, biochemical severity and clinical phenotype should drive decision-making.

Conclusion:
This case emphasizes a rare, important cause of infertility and demonstrates that recognizing severe hyperandrogenemia is critical as an endocrine pathology. Early, systematic evaluation of hormone levels and imaging can expedite diagnosis and definitive surgical or medical management. Timely recognition has direct implications for both symptom reversal and potential restoration of fertility, representing a meaningful opportunity for practice improvement.

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