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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Clin+Endocrinol+Metab
2017 ; 102
(4
): 1182-1192
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Histopathological Classification of Cross-Sectional Image-Negative
Hyperaldosteronism
#MMPMID28388725
Yamazaki Y
; Nakamura Y
; Omata K
; Ise K
; Tezuka Y
; Ono Y
; Morimoto R
; Nozawa Y
; Gomez-Sanchez CE
; Tomlins SA
; Rainey WE
; Ito S
; Satoh F
; Sasano H
J Clin Endocrinol Metab
2017[Apr]; 102
(4
): 1182-1192
PMID28388725
show ga
CONTEXT: Approximately half of patients with primary aldosteronism (PA) have
clinically evident disease according to clinical (hypertension) and/or laboratory
(aldosterone and renin levels) findings but do not have nodules detectable in
routine cross-sectional imaging. However, the detailed histopathologic,
steroidogenic, and pathobiological features of cross-sectional image-negative PA
are controversial. OBJECTIVE: To examine histopathology, steroidogenic enzyme
expression, and aldosterone-driver gene somatic mutation status in
cross-sectional image-negative hyperaldosteronism. METHODS: Twenty-five
cross-sectional image-negative cases were retrospectively reviewed. In situ
adrenal aldosterone production capacity was determined using immunohistochemistry
(IHC) of steroidogenic enzymes. Aldosterone-driver gene somatic mutation status
(ATP1A1, ATP2B3, CACNA1D, and KCNJ5) was determined in the CYP11B2 immunopositive
areas [n = 35; micronodule, n = 32; zona glomerulosa (ZG), n = 3] using
next-generation sequencing after macrodissection. RESULTS: Cases were classified
as multiple adrenocortical micronodules (MN; n = 13) or diffuse hyperplasia (DH)
of ZG (n = 12) based upon histopathological evaluation and CYP11B2 IHC.
Aldosterone-driver gene somatic mutations were detected in 21 of 26 (81%) of
CYP11B2-positive cortical micronodules in MN; 17 (65%) mutations were in CACNA1D,
2 (8%) in KCNJ5, and 1 each (4% each) in ATP1A1 and ATP2B. One of 6 (17%) of
nodules in DH harbored somatic aldosterone-driver gene mutations (CACNA1D);
however, no mutations were detected in CYP11B2-positive nonnodular DH areas.
CONCLUSION: Morphologic evaluation and CYP11B2 IHC enabled the classification of
cross-sectional image-negative hyperaldosteronism into MN and DH. Somatic
mutations driving aldosterone overproduction are common in micronodules of MN,
suggesting a histological entity possibly related to aldosterone-producing cell
cluster development.
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