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Endocrine Abstracts (2014) 35 P50 | DOI: 10.1530/endoabs.35.P50

ECE2014 Poster Presentations Adrenal cortex (56 abstracts)

The pathophysiology of aldosterone-producing adenomas associated with their tumor size: the smaller, the higher expression of CYP11B2

Yoshikiyo Ono 1, , Yasuhiro Nakamura 2 , Takashi Maekawa 2 , Saulo J A Felizola 2 , Ryo Morimoto 1 , Yoshitsugu Iwakura 1 , Masataka Kudo 1 , Kazumasa Seiji 3 , Kei Takase 3 , Celso E Gomez-Sanchez 4 , Sadayoshi Ito 1 , Hironobu Sasano 2 & Fumitoshi Satoh 1

1Division of Nephrology, Endocrinology and Vascular Medicine, Tohoku University Hospital, Sendai, Japan; 2Department of Pathology, Tohoku University Hospital, Sendai, Japan; 3Department of Diagnostic Radiology, Tohoku University Hospital, Sendai, Japan; 4Division of Endocrinology, G.V. Montgomery VA Medical Center, and the University of Mississippi Medical Center, Jackson, Mississippi, USA.

The pathophysiology of aldosterone-producing adenomas (APA), especially those manifesting clinically overt hyperaldosteronism despite their small size, remains unknown. Therefore, we examined the correlation between tumor size and the status of intratumoral steroidogenic enzymes involved in aldosterone biosynthesis using immunohistochemistry. Forty patients with surgically proven APAs following adrenal venous sampling were retrospectively studied. The tumor area at the maximum diameter of the sections was precisely measured by Image J software. The status of steroidogenic enzymes was immunohistochemically analyzed according to the H-score system, based on both the number of immunopositive cells and relative immunointensity. Adrenal masses were not detected by computed tomography (CT) in 20 patients. Maximum tumor area obtained in the specimens was significantly correlated with preoperative plasma aldosterone concentration, urinary aldosterone excretion, the H-score of CYP11B1, and was inversely correlated with the H-score of CYP11B2. These results demonstrated that small adenomas could produce sufficient aldosterone to cause clinically overt primary aldosteronism because of the significantly higher CYP11B2 expression per tumor area.

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