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10.1210/jc.2016-2986 http://scihub22266oqcxt.onion/10.1210/jc.2016-2986 C5460723!5460723!28388725     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28388725&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Endocrinol+Metab 2017 ; 102 (4): 1182-92 Nephropedia Template TP {{tp|p=28388725|t=2017. Histopathological Classification of Cross-Sectional Image?Negative Hyperaldosteronism |pdf=|usr=}}{{28388725}} gab.com Text Histopathological Classification of Cross-Sectional Image Negative Hyperaldosteronism JO: J Clin Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=28388725 #FOAvip 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. Twit Text FOAVip Histopathological Classification of Cross-Sectional Image Negative Hyperaldosteronism ????J Clin Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=28388725 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28388725 #FOAvip English Wikipedia <ref>{{Cite pmid|28388725}}</ref> 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): 1182-92 PMID28388725show 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. äHistopathological Classification of Cross-Sectional Image?Negative Hyp(epmc).pdf DeepDyve Pubget Overpricing