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Updated: May 8, 2026

Murine Prostate Micro-dissection and Surgical Castration
Published on: May 11, 2016
Inadequate testosterone suppression after medical and subsequent surgical castration in a patient with prostate
Oskar Ragnarsson1, Gudmundur Johannsson, Kjell Geterud
1Department of Endocrinology, Diabetes and Metabolism, Sahlgrenska University Hospital, Gothenburg, Sweden. oskar.ragnarsson@medic.gu.se
Abstract:
Androgen deprivation is a cornerstone in prostate cancer management. We present a 69-year-old man, with a poorly differentiated prostate cancer with skeletal and lymph node metastases. After medical and subsequent surgical castration serum testosterone concentrations remained inappropriately high (4.9 and 4.5 nmol/L; castration range < 0.5). For cancer staging a CT was performed which showed bilateral adrenal enlargement. Endocrine workup revealed elevated levels of adrenal androgens and adrenal precursors. Mutation analysis confirmed a non-classical 21-hydroxylase deficiency, that is, a mild form of congenital adrenal hyperplasia (CAH). To suppress adrenocorticotrophic hormone and the excess adrenal androgen secretion, treatment with hydrocortisone and prednisolone was started with success. Inadequate testosterone suppression after castration due to previously undiagnosed CAH has not previously been reported. Considering the estimated prevalence of 1% in selected populations, non-classical CAH should be considered when testosterone is not adequately suppressed after castration in men with prostate cancer.
Insights
A previously undiagnosed mild form of congenital adrenal hyperplasia (CAH) can cause high testosterone levels after castration in prostate cancer patients. This endocrine disorder should be considered in such cases.
Area of Science:
- Endocrinology
- Oncology
Background:
- Androgen deprivation therapy is a standard treatment for prostate cancer.
- Maintaining low testosterone levels is crucial for effective management.
Observation:
- A 69-year-old man with metastatic prostate cancer had persistently high testosterone levels post-castration.
- Imaging revealed adrenal enlargement, and endocrine tests showed elevated adrenal androgens.
Findings:
- Mutation analysis identified a non-classical 21-hydroxylase deficiency, a mild form of congenital adrenal hyperplasia (CAH).
- This previously unreported cause of inadequate testosterone suppression was successfully managed with hydrocortisone and prednisolone.
Implications:
- Undiagnosed non-classical CAH may affect treatment efficacy in prostate cancer patients.
- Consider screening for CAH in men with prostate cancer experiencing suboptimal testosterone suppression after castration.
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