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Pathology Update 2025
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Ovarian hyperthecosis presenting with hyperandrogenism: a case report and review of pathophysiology

Roche Scientific E Poster Display

Roche Scientific E-Poster Display

Discipline Streams

Anatomical Pathology

Abstract Description

David Patton1, Rinky Langan1
1South East Area Laboratory Services, NSW Health Pathology, Wollongong Hospital Campus


Ovarian hyperthecosis is an uncommon, non-neoplastic ovarian disorder primarily affecting postmenopausal women. Three key features are consistently described:

Insulin Resistance and Hyperinsulinemia: Cases of ovarian hyperthecosis occur in the context of insulin resistance and associated hyperinsulinemia. The exact mechanism by which insulin dysregulation contributes to the development of ovarian hyperthecosis remains unclear.

Histopathological Findings: Ovarian hyperthecosis is characterized by the proliferation of ovarian stroma and the formation of clusters of luteinized theca cells. These unique features are essential for the definitive diagnosis of the condition.

Hyperandrogenism: Luteinized theca cells in ovarian hyperthecosis are responsible for the excessive production of androgens, resulting in marked hyperandrogenism. This manifests clinically with symptoms such as hirsutism, acne, and virilisation, and testosterone may be peripherally aromatised to oestrogen, leading to increased risk of breast and endometrial carcinoma.

Beyond these established features, understanding of ovarian hyperthecosis remains limited due to its rarity and the largely biochemical nature of its pathogenesis. This report aims to highlight a presentation of ovarian hyperthecosis and survey the available literature, serving as a reminder to practicing pathologists to consider this unusual condition in their differential diagnosis.

AUTHOR CONTRIBUTIONS
The authors confirm their contributions to the poster as follows.
David Patton: Conception and design, literature review.
David Patton and Rinky Langan: Analysis and drafting of manuscript.
All authors reviewed and approved the final version of the manuscript
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David Patton -

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