New diagnostic methods for primary aldosteronism with specific antibodies

Cristina Volpe; Anders Hoog; Tadashi Ogishima; Kuniaki Mukai; Beril Hamberger; Marja Thoren

doi:10.1530/endoabs.32.P14

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Endocrine Abstracts (2013) 32 P14 | DOI: 10.1530/endoabs.32.P14

ECE2013 Poster Presentations Adrenal cortex (64 abstracts)

New diagnostic methods for primary aldosteronism with specific antibodies

Cristina Volpe ^1, , Anders Höög ^3, , Tadashi Ogishima ⁵ , Kuniaki Mukai ⁶ , Beril Hamberger ^1, & Marja Thorén ^1,

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¹Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; ²Division of Endocrinology, Department of Internal Medicine, Södersjukhuset, Stockholm, Sweden; ³Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden; ⁴Department of Clinical Pathology and Cytology, Karolinska University Hospital, Solna, Stockholm, Sweden; ⁵Department of Chemistry, Faculty of Sciences, Kyushu University, Fukuoka, Japan; ⁶Department of Biochemistry, School of Medicine, Keio University, Tokyo, Japan; ⁷Department of Breast and Endocrine Surgery, Karolinska University Hospital, Solna, Stockholm, Sweden; ⁸Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Solna, Stockholm, Sweden.

Background: Among patients diagnosed with primary aldosteronism (PA) due to an aldosterone producing adenoma (APA), about 10% fail to normalize aldosterone hypersecretion after unilateral adrenalectomy, and may instead have bilateral aldosterone producing hyperplasia. With routine histopathology it may be difficult to distinguish between APA and hyperplasia. We have recently reported the use of specific antibodies to identify the source of aldosterone excess in the removed adrenal (Journal of Clinical Patholology, in press). The clinical utility of the procedure has now been evaluated in an extended patient material.

Material and Methods: Between 1986 and 2010, 121 patients underwent adrenalectomy for PA. The cure rate was 88% and median follow-up 4 years. Immunohistochemistry with specific antibodies against the steroidogenic enzymes for aldosterone (CYP11B2) and cortisol (CYP11B1) synthesis was performed in addition to routine histopathology in, until now, a subset of 40 adrenals from both cured and uncured patients.

Results: With immunohistochemistry, the cured patients had typically positive staining for aldosterone synthesis in the adenoma, but not in cortical nodules. Interestingly, in two patients where routine histopathology suggested hyperplasia, it was possible to diagnose an APA as only one nodule showed immunoreactivity for aldosterone. Rarely, cured patients showed nodular hyperplasia, staining positively for aldosterone, which may represent unilateral or bilateral disease. Uncured patients showed nodular hyperplasia with positive staining for aldosterone synthesis. Three assumed APAs stained negatively for aldosterone production but positively for cortisol synthesis.

Discussion: Immunohistochemistry can help to localize aldosterone hypersecretion. This is important for the postoperative follow up as APAs are usually cured, while patients with hyperplasia need long term follow-up due to risk of recurrence.

Conclusion: Immunostaining with antibodies against CYP11B2 and CYP11B1 provides important information about the origin of aldosterone hypersecretion. If our results are confirmed, routine use of immunohistochemistry should be recommended.