Castration failure in prostate carcinoma due to a functioning adrenocortical carcinoma

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Abstract

Summary

We report concurrent metastatic prostatic adenocarcinoma (PC) and functioning androgen-secreting adrenocortical carcinoma (ACC) in a 77-year-old man. The failure to achieve adequate biochemical castration via androgen deprivation therapy (ADT) as treatment for PC metastases, together with elevated DHEA-S, androstenedione, and discordant adrenal tracer uptake on FDG-PET and PSMA-PET, suggested the presence of a concurrent functional primary adrenal malignancy. On histopathological analysis, scant foci of PC were present throughout the ACC specimen. Castration was achieved post adrenalectomy with concurrent drop in prostate-specific antigen. We outline the literature regarding failure of testosterone suppression on ADT and salient points regarding diagnostic workup of functioning adrenal malignancies.

Learning points

Failure to achieve castration with androgen deprivation therapy is rare and should prompt careful review to identify the underlying cause.
All adrenal lesions should be evaluated for hormone production, as well as assessed for risk of malignancy (either primary or secondary).
Adrenocortical carcinomas are commonly functional, and can secrete steroid hormones or their precursors (androgens, progestogens, glucocorticoids and mineralocorticoids).
In this case, a co-incident, androgen-producing adrenocortical carcinoma was the cause of failure of testosterone suppression from androgen deprivation therapy as treatment for metastatic prostate cancer. Pathological adrenal androgen production contributed to the progression of prostate cancer.

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Most cited references 10

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There is few data on what constitutes the distribution of metastatic sites in prostate cancer (PCa). The aim of our study was to systematically describe the most common sites of metastases in a contemporary cohort of PCa patients. Patients with metastatic PCa were abstracted from the Nationwide Inpatient Sample (1998-2010). Most common metastatic sites within the entire population were described. Stratification was performed according to the presence of single or multiple (≥ 2 sites) metastases. Additionally, we evaluated the distribution of metastatic sites amongst patients with and without bone metastases. Overall, 74,826 patients with metastatic PCa were identified. The most common metastatic sites were bone (84%), distant lymph nodes (10.6%), liver (10.2%), and thorax (9.1%). Overall, 18.4% of patients had multiple metastatic sites involved. When stratifying patients according to the site of metastases, only 19.4% of men with bone metastases had multiple sites involved. Conversely, among patients with lymph nodes, liver, thorax, brain, digestive system, retroperitoneum, and kidney and adrenal gland metastases the proportion of men with multiple sites involved was 43.4%, 76.0%, 76.7%, 73.0%, 52.2%, 60.9%, and 76.4%, respectively. When focusing exclusively on patients with bone metastases, the most common sites of secondary metastases were liver (39.1%), thorax (35.2%), distant lymph nodes (24.6%), and brain (12.4%). Although the majority of patients with metastatic PCa experience bone location, the proportion of patients with atypical metastases is not negligible. These findings might be helpful when planning diagnostic imaging procedures in patients with advanced PCa. © 2013 Wiley Periodicals, Inc.

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This article reviews the issues and controversies relevant to the treatment of advanced prostate cancer with androgen deprivation therapy. Initially, diethylstilbestrol was used for achieving androgen deprivation, but was replaced by luteinizing hormone-releasing hormone (LHRH). Adverse events associated with LHRH agonists include the flare phenomenon, hot flashes, loss of libido, erectile dysfunction, depression, muscle wasting, anemia, and osteoporosis. Intermittent therapy has been advocated to reduce morbidity of treatment. The addition of an antiandrogen provides maximum androgen blockade. There remains controversy regarding the timing of the addition of an antiandrogen. Secondary hormonal therapies include antiandrogens, adrenal androgen inhibitors, and estrogens.

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Eveline P. C. J. Janssen, H. F. B. M. Sleddens, A Santerse … (1994)

Heterogeneity in human androgen receptor (hAR) expression in prostate cancer is considered to be implicated in tumor progression. hAR expression was therefore studied immunohistochemically in localized and locally progressive, hormone refractory (HR) prostate cancer. Because altered functional activity of the hAR may be due to changes in the structural integrity of the hAR gene, exons 2 to 8 of the hAR gene were assessed for mutations by single-strand conformation polymorphism (SSCP) analysis and exon 1 was analyzed for the size of the CAG repeat. The hormone binding capacity, a prerequisite for ligand-regulated receptor function, was determined by a ligand binding assay. Coexpression of the hAR and prostate-specific antigen (PSA) was studied by a sequential double immunoenzymatic staining to verify whether PSA expression is a parameter of hAR function. Almost all human prostatic carcinomas revealed heterogeneous hAR expression, regardless of tumor differentiation and progression. Putative predominance of hAR-negative tumor areas in HR prostate cancer was not observed. No hAR gene mutations or major changes in the CAG repeat were found in the 18 HR carcinomas or in the 9 control samples. Moreover, all selected hAR-expressing cancers were able to bind the synthetic androgen methyltrienolone (R1881). Immunoenzymatic double staining revealed even PSA expression in hAR-negative tumor areas. PSA immunohistochemistry in human prostatic carcinomas therefore is of no use in determining hAR functional activity. Thus, most prostatic carcinomas, even when progressed to a state of hormone insensitivity, contain a structurally intact hAR gene, heterogeneously expressed with retained androgen binding capacity.

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Author and article information

Journal

Journal ID (nlm-ta): Endocrinol Diabetes Metab Case Rep

Journal ID (iso-abbrev): Endocrinol Diabetes Metab Case Rep

Journal ID (hwp): EDM

Title: Endocrinology, Diabetes & Metabolism Case Reports

Publisher: Bioscientifica Ltd (Bristol )

ISSN (Electronic): 2052-0573

Publication date (Electronic): 28 September 2021

Publication date Collection: 2021

Volume: 2021

Electronic Location Identifier: 21-0036

Affiliations

[1 ]Department of Medical Oncology, Calvary Mater Hospital, Newcastle, New South Wales , Australia

[2 ]School of Medicine and Public Health , University of Newcastle, Newcastle, New South Wales, Australia

[3 ]Department of Nuclear Medicine , John Hunter Hospital, Newcastle, New South Wales, Australia

[4 ]Surgical Services , John Hunter Hospital, Newcastle, New South Wales, Australia

[5 ]University of Newcastle , Newcastle, New South Wales, Australia

[6 ]Department of Endocrinology , John Hunter Hospital, Newcastle, New South Wales, Australia

Author notes

Correspondence should be addressed to C W Rowe Email christopher.rowe@ 123456hnehealth.nsw.gov.au

Author information

Vishal Navani http://orcid.org/0000-0002-6795-009X

Article

Publisher ID: EDM210036

DOI: 10.1530/EDM-21-0036

PMC ID: 8558880

PubMed ID: 34673545

SO-VID: 70e5d537-dd35-4b26-8ec6-c06c39f9e9e9

License:

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License..

History

Date received : 11 August 2021

Date accepted : 28 September 2021

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