Youichi Ohno1, Masakatsu Sone1, Nobuya Inagaki1, Yoshiyu Takeda2, Isao Kurihara3, Mika Tsuiki4, Takamasa Ichijo5, Norio Wada6, Takuyuki Katabami7, Yoshihiro Ogawa8, Shintaro Okamura9, Tomikazu Fukuoka10, Tatsuya Kai11, Shoichiro Izawa12, Yuichiro Yoshikawa13, Shigeatsu Hashimoto14, Masanobu Yamada15, Yoshiro Chiba16, Mitsuhide Naruse17,18. 1. Department of Diabetes, Endocrinology and Nutrition, Kyoto University, Kyoto, Japan. 2. Department of Internal Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan. 3. Department of Endocrinology, Metabolism and Nephrology, School of Medicine Keio University, Tokyo, Japan. 4. Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan. 5. Department of Diabetes and Endocrinology, Saiseikai Yokohamashi Tobu Hospital, Yokohama, Japan. 6. Department of Diabetes and Endocrinology, Sapporo City General Hospital, Sapporo, Japan. 7. Division of Metabolism and Endocrinology, Department of Internal Medicine, St. Marianna University School of Medicine Yokohama City Seibu Hospital, Yokohama, Japan. 8. Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. 9. Department of Endocrinology, Tenri Hospital, Tenri, Nara, Japan. 10. Department of Internal Medicine, Matsuyama Red Cross Hospital, Matsuyama, Japan. 11. Department of Cardiology, Saiseikai Tondabayashi Hospital, Tondabayashi, Japan. 12. Division of Cardiovascular Medicine, Endocrinology and Metabolism, Department of Molecular Medicine and Therapeutics, Tottori University Faculty of Medicine, Yonago, Japan. 13. Department of Endocrinology and Diabetes Mellitus, Misato Kenwa Hospital, Misato, Japan. 14. Division of Nephrology, Hypertension, Endocrinology, and Diabetology/Metabolism, Fukushima Medical University Hospital, Fukushima, Japan. 15. Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Japan. 16. Endovascular Treatment Group, Mito Saiseikai General Hospital, Mito, Japan. 17. Clinical Research Institute of Endocrinology and Metabolism, Kyoto Medical Center, National Hospital Organization, Kyoto, Japan. 18. Endocrinology Center, Ijinkai Takeda General Hospital, Kyoto, Japan.
Abstract
CONTEXT: Adrenal tumors (ATs), even those diagnosed as nonfunctioning, may cause metabolic disorders. Some primary aldosteronism (PA) patients with ATs are diagnosed with bilateral PA based on adrenal venous sampling (AVS), and their ATs are apparently nonfunctioning. OBJECTIVE: To clarify the influence of apparently nonfunctioning ATs, we compared hormone levels and clinical complications between bilateral PA cases with and without ATs. DESIGN, SETTING, AND PARTICIPANTS: After retrospectively assessing 2814 patients with PA in the multicenter Japan PA study, bilateral PA cases on AVS were divided into cases with and without ATs by computed tomography findings. Importantly, patients with cortisol levels >1.8 µg/dL after the 1-mg dexamethasone suppression test (DST) were excluded. Clinical characteristics and biochemical data were compared between them. The correlation between AT size and hormone levels was also analyzed. MAIN OUTCOME MEASURES: Analyzed were 196 bilateral PA patients with ATs and 331 those without ATs. Although basal cortisol and aldosterone levels were similar between them, cortisol levels after the 1-mg DST and the prevalences of diabetes mellitus and proteinuria were significantly higher and ACTH levels and plasma renin activity were significantly lower in cases with ATs than in those without. After adjusting for patients' backgrounds, cortisol levels after the 1-mg DST and plasma renin activity remained significantly different between them. Moreover, cortisol levels after the 1-mg DST and ACTH levels correlated with AT size. CONCLUSIONS: Apparently nonfunctioning ATs in bilateral PA cases may cause latent autonomous cortisol secretion, inducing diabetes and proteinuria.
CONTEXT: Adrenal tumors (ATs), even those diagnosed as nonfunctioning, may cause metabolic disorders. Some primary aldosteronism (PA) patients with ATs are diagnosed with bilateral PA based on adrenal venous sampling (AVS), and their ATs are apparently nonfunctioning. OBJECTIVE: To clarify the influence of apparently nonfunctioning ATs, we compared hormone levels and clinical complications between bilateral PA cases with and without ATs. DESIGN, SETTING, AND PARTICIPANTS: After retrospectively assessing 2814 patients with PA in the multicenter Japan PA study, bilateral PA cases on AVS were divided into cases with and without ATs by computed tomography findings. Importantly, patients with cortisol levels >1.8 µg/dL after the 1-mg dexamethasone suppression test (DST) were excluded. Clinical characteristics and biochemical data were compared between them. The correlation between AT size and hormone levels was also analyzed. MAIN OUTCOME MEASURES: Analyzed were 196 bilateral PA patients with ATs and 331 those without ATs. Although basal cortisol and aldosterone levels were similar between them, cortisol levels after the 1-mg DST and the prevalences of diabetes mellitus and proteinuria were significantly higher and ACTH levels and plasma renin activity were significantly lower in cases with ATs than in those without. After adjusting for patients' backgrounds, cortisol levels after the 1-mg DST and plasma renin activity remained significantly different between them. Moreover, cortisol levels after the 1-mg DST and ACTH levels correlated with AT size. CONCLUSIONS: Apparently nonfunctioning ATs in bilateral PA cases may cause latent autonomous cortisol secretion, inducing diabetes and proteinuria.
Authors: Gregory A Kline; Alexander Ah-Chi Leung; Davis Sam; Alex Chin; Benny So Journal: J Clin Endocrinol Metab Date: 2021-03-08 Impact factor: 5.958