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Practice Guideline
. 2025 Oct;103(4):540-566.
doi: 10.1111/cen.15265. Epub 2025 May 13.

Society for Endocrinology Clinical Practice Guideline for the Evaluation of Androgen Excess in Women

Affiliations
Practice Guideline

Society for Endocrinology Clinical Practice Guideline for the Evaluation of Androgen Excess in Women

Yasir S Elhassan et al. Clin Endocrinol (Oxf). 2025 Oct.

Abstract

Context: Androgen excess is common in women and refers to clinical or biochemical evidence of elevated androgenic steroids such as testosterone. It is associated with underlying polycystic ovary syndrome in the majority of cases. However severe androgen excess is less common and may indicate the presence of underlying adrenal or ovarian neoplasms, genetic disorders or severe insulin resistance syndromes. Currently there are few consensus guidelines to assist clinicians with a standardised management approach to the patient with severe androgen excess.

Design: Clinical practice guideline.

Methods: This guideline has been developed with expertise from colleagues in endocrinology, gynaecology, clinical biochemistry and nursing, and furthermore provides a unique patient perspective to guide clinicians.

Results: The Society for Endocrinology commissioned this new guideline to collate multi-disciplinary guidance for clinical practitioners in the investigation of severe androgen excess. Recommendations have been made in the areas of clinical assessment, biochemical work up, dynamic testing and imaging, informed where possible by the best available evidence.

Conclusion: This guideline will provide guidance for clinicians in their approach to patients with severe androgen excess.

Keywords: adrenal; androgen excess; ovarian; severe insulin resistance; testosterone; virilisation.

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Figures

Figure 1
Figure 1
Adrenal, ovarian and peripheral androgen metabolism. Both classic and 11‐oxygenated androgen pathways are demonstrated. Androgenic precursors are secreted predominantly by the adrenal glands and activated to potent androgens in the ovaries and peripheral tissues. 11KA4, 11‐ketoandrostenedione; 11KT, 11‐ketotestosterone; 11OHA4, 11β‐hydroxyandrostenedione; 11OHT, 11β‐hydroxytestosterone; 17OHPreg, 17‐hydroxypregnelone; A4, androstenedione; AKR1C3, aldoketoreductase type 1C3; CYP17A1, cytochrome P450 17A1; DHEA, dehydroepiandrosterone; DHEAS, dehydroepiandrosterone sulfate; DHT, dihydrotestosterone; HSD11B1, 11β‐hydroxysteroid dehydrogenase type 1; HSD11B2, 11β‐hydroxysteroid dehydrogenase type 2; HSD3B2, 3‐beta‐hydroxysteroid dehydrogenase type 2; SRD5A1/2, 5α‐reductase type 1/2; STS, steroid sulfatase; SULT2A1, sulfotransferase family 2A member 1; T, testosterone.
Figure 2
Figure 2
Classification of primary ovarian tumours (VOTs): Primary ovarian tumours can be grouped according to the WHO classification [62] into epithelial and non‐epithelial. Androgen‐secreting tumours typically arise from sex‐cord and stromal cells of the ovary.
Figure 3
Figure 3
Clinical algorithm for the investigation of androgen excess in women. The diagnostic approach should be divided into routine or urgent pathways based on the presence or absence a number of central clinical and biochemical factors. Baseline biochemical work up: FSH, LH, oestradiol, 17‐hydroxyprogesterone (17OHP), testosterone (T), dehydroepiandrosterone sulphate (DHEAS), androstenedione (A4), sex hormone‐binding globulin (SHBG) and prolactin (PRL). FSH, follicle‐stimulating hormone; LH, luteinising hormone; OGTT, oral glucose tolerance test; ONDST, overnight dexamethasone suppression test; PCOS, polycystic ovary syndrome; PET, positron emission tomography; UFC urinary free cortisol.

References

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