| Literature DB >> 27514282 |
Ai Tamura1, Koshiro Nishimoto2, Tsugio Seki3, Yoko Matsuzawa1, Jun Saito1, Masao Omura1, Celso E Gomez-Sanchez4, Kohzoh Makita5, Seishi Matsui6, Nobukazu Moriya6, Atsushi Inoue7, Maki Nagata7, Hironobu Sasano8, Yasuhiro Nakamura8, Yuto Yamazaki8, Yasuaki Kabe9, Kuniaki Mukai10, Takeo Kosaka11, Mototsugu Oya11, Sachiko Suematsu1, Tetsuo Nishikawa12.
Abstract
We report a case of non-familial juvenile primary aldosteronism (PA). Super-selective adrenal venous sampling identified less aldosterone production in the right inferior adrenal segment than others. Bilateral adrenalectomy sparing the segment normalized blood pressure and improved PA. Both adrenals had similar histologies, consisting of a normal adrenal cortex and aldosterone synthase-positive hyperplasia/adenoma. An aldosterone-driving KCNJ5 mutation was detected in the lesions, but not in the histologically normal cortex. After taking into account that the two adrenal glands displayed a similar histological profile, as well as the fact that hyperplastic lesions in both glands exhibited a common KCNJ5 mutation, we conclude that the specific mutation may have occurred at an adrenal precursor mesodermal cell, at an early stage of development; its daughter cells were mixed with non-mutant cells and dispersed into both adrenal glands, resulting into a form of the condition known as genetic mosaicism.Entities:
Keywords: Genetic mosaicism; Juvenile; KCNJ5; Primary aldosteronism
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Year: 2016 PMID: 27514282 PMCID: PMC5482904 DOI: 10.1016/j.mce.2016.07.031
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN: 0303-7207 Impact factor: 4.102