Abstract Disclosure: C. Musurakis: None. J.L. Gilden: None. Background: Isolated DHEA-S levels and worsening hirsutism often prompt the clinician to investigate more serious causes for the elevation, such as an adrenal mass. Clinical Case: A 29-year-old female G0P0 with Norwegian and English heritage and familial hypertriglyceridemia, was referred for elevated DHEA-S levels, and difficulty conceiving for past three years. She had hirsutism of face, chest, and abdomen, worsening over the last two years. Acne had also progressively worsened to cystic type. Menarche was at age 12, and menses were regular. She had never used contraception. Medications: docosahexanoic acid, eicosapentanoic acid, topical azelaic acid, benzoyl peroxide, clindamycin, pantoprazole, prenatal vitamins, and cholecalciferol. There was a family history of acne, but not for hirsutism or menstrual irregularities. Vitals: BP 137/73, HR 81, Ht 165.10 cm, Wt 86.18 Kg, BMI 31.68. Ferriman-Gallwey score was 10 with normal genitalia. Labs (luteal phase): DHEA-S 756 mcg/dL with repeat of 596 mcg/dl(n=35-430), total testosterone 25 ng/dL(n=2-45), free testosterone 4.3 pg/mL(n=0.1-6.4), prolactin 6.6 ng/mL(n=2.2-30.3), LH 5.1 mIU/mL(n=0.6-16.6), FSH 4.7 mIU/mL(n=1.7-12.9), 17-OH progesterone 74 ng/dL(n=139-431), androstenedione 163 ng/dL(n=73-184), estradiol 59.79 pg/mL(n=55.8-214.2), AMH 1.38 ng/mL(n=0.69-13.39), midnight salivary cortisol <0.03 and 0.05 mcg/dL(n<5), IGF-1 258 ng/mL(n=63-373), ACTH 31 pg/mL(n=0-47), AM cortisol 12.58 ug/dL(n=5.3-22.5), TSH 1.27 uIU/mL(n=0.358-3.74), Free T4 0.88 ng/dL (n=0.76-1.46), peroxidase antibodies 49.8 U/m (n=0-60), thyroglobulin antibodies <15(n=0-60), HbA1c 5.5% (n<=5.6%), 25-OH vitamin D 42.7 ng/mL(n=30-100) and negative pregnancy urine test. US pelvis: small follicles in ovaries and normal size. MRI abdomen w/wo contrast: normal bilateral adrenal glands. Cosyntropin stimulation test: baseline cortisol 15.03 ug/dL,17-OH progesterone 168 ng/dL. 30 mins: Cortisol 30.39ug/dL(n>18),17-OH progesterone 130ng/dL(n<200). 60 mins: cortisol 38.95ug/dL(n>18), 17-OH progesterone 153ng/dL(n<200). Non-Classical Congenital Adrenal Hyperplasia was excluded. Polycystic Ovary Syndrome (PCOS) was diagnosed based on clinical and biochemical hyperandrogenism, lack of adrenal mass, and clinical signs of anovulation. Conclusion: As reported by Carmina et al, few patients with PCOS exhibit isolated increase of serum DHEA-S. It is important to recognize that non-classic forms of PCOS (normal ovaries or normal ovulatory cycles) can present with a higher prevalence of adrenal hyperandrogenism than the common classical forms of PCOS. Reference: Carmina E, Longo RA. Increased Prevalence of Elevated DHEAS in PCOS Women with Non-Classic (B or C) Phenotypes: A Retrospective Analysis in Patients Aged 20 to 29 Years. Cells. 2022 Oct 17;11(20):3255. doi: 10.3390/cells11203255. PMID: 36291122; PMCID: PMC9601254. Presentation: Friday, June 16, 2023
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