Cushing Disease Masquerading as Polycystic Ovary Syndrome: A Diagnostic Pitfall in Severe Hyperandrogenism
https://doi.org/10.15605/jafes.041.S1
- Author:
Jean Mun Cheah
1
;
Fei Bing Yong
1
;
K.J. Lingeswary
1
;
Jen Hoong Oon
1
;
Sharifah Noor Adrilla binti Long Mohd Noor Affendi
1
;
Gayathri Devi A/P Krishnan
1
;
Shazatul Reza binti Mohd Redzuan
1
;
Subashini Rajoo Rajoo
1
Author Information
1. Endocrine Unit, Department of Medicine, Hospital Kuala Lumpur
- Publication Type:Journal Article
- MeSH:
Female;
Hyperandrogenism;
Pituitary ACTH Hypersecretion;
Polycystic Ovary Syndrome
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):97-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Polycystic ovary syndrome (PCOS) is the most common
cause of hyperandrogenism in women of reproductive
age. However, several endocrine disorders, particularly
Cushing disease (CD), can closely mimic the clinical, biochemical, and radiological features of PCOS. This overlap
may lead to misdiagnosis and delayed recognition of
hypercortisolism, with significant metabolic and reproductive consequences.
Case:We report a 24-year-old female with young-onset diabetes
mellitus who was referred for endocrine co-management
during admission for recurrent mons pubis and labial
abscesses with poorly controlled glycemia. She had a 5-year
history of progressive hirsutism, oligomenorrhoea, scalp
hair loss, significant weight gain, and insulin resistance,
and had previously been labelled as having PCOS during
adolescence, with subsequent default of follow-up. On
examination, she was obese (body mass index 33 kg/
m²) with plethoric facies, acanthosis nigricans, proximal
myopathy, and hirsutism (Ferriman–Gallwey score 10),
without overt virilization or acromegalic features.
Biochemical evaluation demonstrated severe hyperandrogenism with markedly elevated total testosterone
(7.05 nmol/L), suppressed gonadotropins, and adrenocorticotropic hormone (ACTH)-dependent hypercortisolism. Cortisol failed to suppress on low-dose dexamethasone testing, and 24-hour urinary free cortisol
was markedly elevated (>4,900 nmol/24 h). Pelvic ultrasonography and computed tomography imaging showed
polycystic ovarian morphology without evidence of an
ovarian mass. Pituitary magnetic resonance imaging
revealed a small right-sided pituitary microadenoma
measuring 2.6 × 3.7 mm. Inferior petrosal sinus sampling
demonstrated a central-to-peripheral ACTH gradient with
adequate prolactin ratios, confirming pituitary CD.
Conclusion:This case highlights how Cushing disease can closely
mimic PCOS, including polycystic ovarian morphology
and hyperandrogenism. Progressive symptoms, severe
biochemical androgen excess, and marked insulin
resistance should prompt evaluation for secondary causes
of hyperandrogenism, particularly hypercortisolism, to
avoid delayed diagnosis and prolonged morbidity.
- Full text:2026080416102702812EP_A139.pdf
