SAT-478 - Extreme DHEA-S Elevation Without Adrenal Tumor in a Young Woman With Minimal Clinical Hyperandrogenism

Introduction:
Dehydroepiandrosterone sulfate (DHEA-S) is the primary circulating adrenal androgen. Levels >700 μg/dL typically raise concern for adrenal neoplasm; however, elevations may also occur in polycystic ovary syndrome (PCOS) and functional adrenal disorders. Markedly elevated DHEA-S without corresponding clinical or imaging findings presents a diagnostic challenge.
Clinical

Case:
A 22-year-old woman was referred for markedly elevated DHEA-S identified during evaluation of weight gain. BMI was 30.2 kg/m². She reported normal pubertal development with menarche at age 11–12 years and previously regular menses. A progestin intrauterine device was placed at age 19–20 for heavy menstrual bleeding.
Physical examination was unremarkable, without clinical signs of hyperandrogenism or virilization.
Laboratory evaluation showed DHEA-S >1000 μg/dL (repeat 906 μg/dL), elevated total testosterone initially (105 ng/dL) with normalization on repeat (34 ng/dL), mildly elevated free testosterone, and low sex hormone–binding globulin. Androstenedione, ACTH, and cortisol were within normal limits. Early-morning follicular phase 17-hydroxyprogesterone was 83 ng/dL, effectively excluding non-classic congenital adrenal hyperplasia; cosyntropin stimulation testing was not performed. A 1 mg dexamethasone suppression test demonstrated appropriate cortisol suppression ( < 1 μg/dL).
Abdominal CT and MRI showed normal adrenal glands with no masses, nodules, or enlargement. Brain MRI was unremarkable. Transvaginal ultrasound demonstrated polycystic ovarian morphology with normal ovarian volumes.
Given the degree of DHEA-S elevation, adrenal neoplasm was initially considered; however, lack of virilization and repeatedly negative imaging argued against this diagnosis. Although PCOS may be associated with adrenal androgen excess, reported elevations are typically modest and accompanied by concordant increases in other androgens. The disproportionate and isolated elevation of DHEA-S in this case suggests functional adrenal hyperandrogenism.

Conclusions:
Marked elevation of DHEA-S does not invariably indicate adrenal neoplasm. This case illustrates an uncommon presentation of extreme isolated adrenal androgen excess in a young woman without radiographic adrenal pathology or significant clinical hyperandrogenism. The biochemical pattern does not fully conform to classical PCOS-related adrenal hyperandrogenism or tumor-associated androgen excess, suggesting a possible overlap between functional adrenal dysregulation and atypical PCOS spectrum physiology.
This case underscores the importance of comprehensive endocrine evaluation and cautious interpretation of isolated DHEA-S elevations. Further studies are needed to better characterize functional adrenal hyperandrogenism and its relationship to PCOS phenotypes and metabolic status.

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