Non-neoplastic/hyperplastic primary aldosteronism – Its histopathology and genotype

Yuto Yamazaki; Kei Omata; Yuta Tezuka; Xin Gao; Hiroko Ogata; Jacopo Pieroni; Yoshikiyo Ono; Ryo Morimoto; Yasuhiro Nakamura; Celso E. Gomez-Sanchez; Fumitoshi Satoh; Hironobu Sasano

doi:10.1016/j.coemr.2019.08.006

Non-neoplastic/hyperplastic primary aldosteronism – Its histopathology and genotype

Yuto Yamazaki, Kei Omata, Yuta Tezuka, Xin Gao, Hiroko Ogata, Jacopo Pieroni, Yoshikiyo Ono, Ryo Morimoto, Yasuhiro Nakamura, Celso E. Gomez-Sanchez, Fumitoshi Satoh, Hironobu Sasano

Research output: Contribution to journal › Review article › peer-review

3 Citations (Scopus)

Abstract

Recent development of genetic analysis has revealed the molecular characteristics of aldosterone-producing adrenocortical lesions, including gene mutations of KCNJ5, ATP1A1, ATP2B3, CACNA1D, CACNA1H, CTNNB1, and CLCN2. In addition, CYP11B2-based immunohistochemical analysis has made it possible to classify non-neoplastic lesions of primary aldosteronism (PA) into two distinct histological subtypes based on the localization of aldosterone-producing cells: multiple adrenocortical micronodules (MN) and diffuse hyperplasia of zona glomerulosa (DH). Among MNs, CACNA1D somatic mutation was most frequently detected in 60–80% of micronodules. The number and size of those CYP11B2-positive cell clusters/micronodules could therefore contribute to the pathogenesis or development of hyperaldosteronism. In addition, this newly developed histology- and genetics-based classification of non-neoplastic PA lesions have enabled the precise identification of the responsible lesions of aldosterone excess and enormous improvement of postoperative clinical management of patients with adrenocortical disorders.

Original language	English
Pages (from-to)	122-131
Number of pages	10
Journal	Current Opinion in Endocrine and Metabolic Research
Volume	8
DOIs	https://doi.org/10.1016/j.coemr.2019.08.006
Publication status	Published - 2019 Oct

Keywords

CYP11B2
Hyperplasia
Immunohistochemistry
KCNJ5
Next-generation sequencing (NGS)
Primary aldosteronism

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.coemr.2019.08.006

Cite this

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title = "Non-neoplastic/hyperplastic primary aldosteronism – Its histopathology and genotype",

abstract = "Recent development of genetic analysis has revealed the molecular characteristics of aldosterone-producing adrenocortical lesions, including gene mutations of KCNJ5, ATP1A1, ATP2B3, CACNA1D, CACNA1H, CTNNB1, and CLCN2. In addition, CYP11B2-based immunohistochemical analysis has made it possible to classify non-neoplastic lesions of primary aldosteronism (PA) into two distinct histological subtypes based on the localization of aldosterone-producing cells: multiple adrenocortical micronodules (MN) and diffuse hyperplasia of zona glomerulosa (DH). Among MNs, CACNA1D somatic mutation was most frequently detected in 60–80% of micronodules. The number and size of those CYP11B2-positive cell clusters/micronodules could therefore contribute to the pathogenesis or development of hyperaldosteronism. In addition, this newly developed histology- and genetics-based classification of non-neoplastic PA lesions have enabled the precise identification of the responsible lesions of aldosterone excess and enormous improvement of postoperative clinical management of patients with adrenocortical disorders.",

keywords = "CYP11B2, Hyperplasia, Immunohistochemistry, KCNJ5, Next-generation sequencing (NGS), Primary aldosteronism",

author = "Yuto Yamazaki and Kei Omata and Yuta Tezuka and Xin Gao and Hiroko Ogata and Jacopo Pieroni and Yoshikiyo Ono and Ryo Morimoto and Yasuhiro Nakamura and Gomez-Sanchez, {Celso E.} and Fumitoshi Satoh and Hironobu Sasano",

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year = "2019",

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doi = "10.1016/j.coemr.2019.08.006",

language = "English",

volume = "8",

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journal = "Current Opinion in Endocrine and Metabolic Research",

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TY - JOUR

T1 - Non-neoplastic/hyperplastic primary aldosteronism – Its histopathology and genotype

AU - Yamazaki, Yuto

AU - Omata, Kei

AU - Tezuka, Yuta

AU - Gao, Xin

AU - Ogata, Hiroko

AU - Pieroni, Jacopo

AU - Ono, Yoshikiyo

AU - Morimoto, Ryo

AU - Nakamura, Yasuhiro

AU - Gomez-Sanchez, Celso E.

AU - Satoh, Fumitoshi

AU - Sasano, Hironobu

PY - 2019/10

Y1 - 2019/10

N2 - Recent development of genetic analysis has revealed the molecular characteristics of aldosterone-producing adrenocortical lesions, including gene mutations of KCNJ5, ATP1A1, ATP2B3, CACNA1D, CACNA1H, CTNNB1, and CLCN2. In addition, CYP11B2-based immunohistochemical analysis has made it possible to classify non-neoplastic lesions of primary aldosteronism (PA) into two distinct histological subtypes based on the localization of aldosterone-producing cells: multiple adrenocortical micronodules (MN) and diffuse hyperplasia of zona glomerulosa (DH). Among MNs, CACNA1D somatic mutation was most frequently detected in 60–80% of micronodules. The number and size of those CYP11B2-positive cell clusters/micronodules could therefore contribute to the pathogenesis or development of hyperaldosteronism. In addition, this newly developed histology- and genetics-based classification of non-neoplastic PA lesions have enabled the precise identification of the responsible lesions of aldosterone excess and enormous improvement of postoperative clinical management of patients with adrenocortical disorders.

AB - Recent development of genetic analysis has revealed the molecular characteristics of aldosterone-producing adrenocortical lesions, including gene mutations of KCNJ5, ATP1A1, ATP2B3, CACNA1D, CACNA1H, CTNNB1, and CLCN2. In addition, CYP11B2-based immunohistochemical analysis has made it possible to classify non-neoplastic lesions of primary aldosteronism (PA) into two distinct histological subtypes based on the localization of aldosterone-producing cells: multiple adrenocortical micronodules (MN) and diffuse hyperplasia of zona glomerulosa (DH). Among MNs, CACNA1D somatic mutation was most frequently detected in 60–80% of micronodules. The number and size of those CYP11B2-positive cell clusters/micronodules could therefore contribute to the pathogenesis or development of hyperaldosteronism. In addition, this newly developed histology- and genetics-based classification of non-neoplastic PA lesions have enabled the precise identification of the responsible lesions of aldosterone excess and enormous improvement of postoperative clinical management of patients with adrenocortical disorders.

KW - CYP11B2

KW - Hyperplasia

KW - Immunohistochemistry

KW - KCNJ5

KW - Next-generation sequencing (NGS)

KW - Primary aldosteronism

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EP - 131

JO - Current Opinion in Endocrine and Metabolic Research

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ER -

Non-neoplastic/hyperplastic primary aldosteronism – Its histopathology and genotype

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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