Diagnosis and management of androgen excess presenting after menopause
Postmenopausal hyperandrogenism is a rare yet clinically relevant condition. It can result from a wide variety of sources and etiologies, from benign functional disorders to life-threatening androgen-secreting tumors. Polycystic ovary syndrome is the most frequent cause of hyperandrogenism in postmenopausal patients. Ovarian or adrenal tumors are rare but must be promptly recognized because any delay in diagnosis is associated with a significant risk of mortality. Sudden onset and rapid progression of symptoms or virilizing features are clinical red flags that must lead to the use of imaging to rule out malignancy. Hormonal assessment using accurate assays, in combination with targeted imaging, dynamic testing in selected cases, and a structured diagnostic algorithm will help to establish the etiology of androgen excess in less severe cases. Surgery is the cornerstone of treatment in most cases of severe hyperandrogenism. Gonadotropin-releasing hormone analogs or low-dose glucocorticoids may be helpful for the control of symptoms in gonadal or adrenal functional hyperandrogenism, respectively. Antiandrogens are also helpful in patients with mild functional hyperandrogenism who are concerned about dermocosmetic symptoms. In cases of endocrinopathies or iatrogenic causes, treatment of the underlying cause and avoidance of the drug responsible are needed. This review summarizes the varied etiology of postmenopausal androgen excess, and emphasizes the importance of an accurate diagnostic workup and tailored management.
Authors
- Héctor F. Escobar-Morreale
- Andrés E. Ortiz-Flores
- Manuel Luque-Ramírez
Institutions
- Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas (ES)
- Hospital Universitario Ramón y Cajal (ES)
Publication Details
- Journal
- Maturitas
- Published
- 2026-07-02
- DOI
- https://doi.org/10.1016/j.maturitas.2026.109037
- Primary Topic
- Ovarian function and disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00