[
Journal
Nature medicine
ISSN: 1546-170X
Titre abrégé: Nat Med
Pays: United States
ID NLM: 9502015
Informations de publication
Date de publication:
01 2023
01 2023
Historique:
received:
16
12
2021
accepted:
31
10
2022
pubmed:
17
1
2023
medline:
27
1
2023
entrez:
16
1
2023
Statut:
ppublish
Résumé
Primary aldosteronism (PA) due to a unilateral aldosterone-producing adenoma is a common cause of hypertension. This can be cured, or greatly improved, by adrenal surgery. However, the invasive nature of the standard pre-surgical investigation contributes to fewer than 1% of patients with PA being offered the chance of a cure. The primary objective of our prospective study of 143 patients with PA ( NCT02945904 ) was to compare the accuracy of a non-invasive test, [
Identifiants
pubmed: 36646800
doi: 10.1038/s41591-022-02114-5
pii: 10.1038/s41591-022-02114-5
pmc: PMC9873572
doi:
Substances chimiques
metomidate
Z18ZYL8Y51
Banques de données
ClinicalTrials.gov
['NCT02945904']
Types de publication
Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
190-202Subventions
Organisme : Medical Research Council
ID : MR/S006869/1
Pays : United Kingdom
Organisme : Department of Health
ID : 14/145/09
Pays : United Kingdom
Organisme : Department of Health
ID : IS-BRC-1215-20022
Pays : United Kingdom
Organisme : Department of Health
ID : BRC-1215-20009
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/P01710X/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_UP_1605/15
Pays : United Kingdom
Organisme : Department of Health
ID : IS-BRC-1215-20014
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/19/50/34566
Pays : United Kingdom
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2022. The Author(s).
Références
Rossi, G. P. et al. A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive patients. J. Am. Coll. Cardiol. 48, 2293–2300 (2006).
doi: 10.1016/j.jacc.2006.07.059
Monticone, S. et al. Prevalence and clinical manifestations of primary aldosteronism encountered in primary care practice. J. Am. Coll. Cardiol. 69, 1811–1820 (2017).
doi: 10.1016/j.jacc.2017.01.052
Käyser, S. C. et al. Study heterogeneity and estimation of prevalence of primary aldosteronism: a systematic review and meta-regression analysis. J. Clin. Endocrinol. Metab. 101, 2826–2835 (2016).
doi: 10.1210/jc.2016-1472
Libianto, R. et al. Detecting primary aldosteronism in Australian primary care: a prospective study. Med. J. Aust. 216, 408–412 (2022).
doi: 10.5694/mja2.51438
Monticone, S. et al. Cardiovascular events and target organ damage in primary aldosteronism compared with essential hypertension: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 6, 41–50 (2018).
doi: 10.1016/S2213-8587(17)30319-4
Hundemer, G. L., Curhan, G. C., Yozamp, N., Wang, M. & Vaidya, A. Cardiometabolic outcomes and mortality in medically treated primary aldosteronism: a retrospective cohort study. Lancet Diabetes Endocrinol. 6, 51–59 (2018).
doi: 10.1016/S2213-8587(17)30367-4
Hundemer, G. L., Curhan, G. C., Yozamp, N., Wang, M. & Vaidya, A. Renal outcomes in medically and surgically treated primary aldosteronism. Hypertension 72, 658–666 (2018).
doi: 10.1161/HYPERTENSIONAHA.118.11568
Hundemer, G. L., Curhan, G. C., Yozamp, N., Wang, M. & Vaidya, A. Incidence of atrial fibrillation and mineralocorticoid receptor activity in patients with medically and surgically treated primary aldosteronism. JAMA Cardiol. 3, 768–774 (2018).
doi: 10.1001/jamacardio.2018.2003
Brown, J. M. et al. The unrecognized prevalence of primary aldosteronism: a cross-sectional study. Ann. Intern. Med. 173, 10–20 (2020).
doi: 10.7326/M20-0065
Gomez-Sanchez, C. E., Kuppusamy, M., Reincke, M. & Williams, T. A. Disordered CYP11B2 expression in primary aldosteronism. Horm. Metab. Res. 49, 957–962 (2017).
doi: 10.1055/s-0043-122238
Funder, J. W. et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an endocrine society clinical practice guideline. J. Clin. Endocrinol. Metab. 101, 1889–1916 (2016).
doi: 10.1210/jc.2015-4061
Funder, J. W. Primary aldosteronism as a public health issue. Lancet Diabetes Endocrinol. 4, 972–973 (2016).
doi: 10.1016/S2213-8587(16)30272-8
Burton, T. J. et al. Evaluation of the sensitivity and specificity of
doi: 10.1210/jc.2011-1537
Williams, T. A. et al. Outcomes after adrenalectomy for unilateral primary aldosteronism: an international consensus on outcome measures and analysis of remission rates in an international cohort. Lancet Diabetes Endocrinol. 5, 689–699 (2017).
doi: 10.1016/S2213-8587(17)30135-3
Rossi, G. P. et al. An expert consensus statement on use of adrenal vein sampling for the subtyping of primary aldosteronism. Hypertension 63, 151–160 (2014).
doi: 10.1161/HYPERTENSIONAHA.113.02097
Gill, J. S., Zezulka, A. V., Beevers, D. G. & Davies, P. Relation between initial blood pressure and its fall with treatment. Lancet 1, 567–569 (1985).
doi: 10.1016/S0140-6736(85)91219-X
Backman, S. et al. RNA sequencing provides novel insights into the transcriptome of aldosterone producing adenomas. Sci. Rep. 9, 6269 (2019).
doi: 10.1038/s41598-019-41525-2
Azizan, E. A. et al. Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nat. Genet. 45, 1055–1060 (2013).
doi: 10.1038/ng.2716
Fernandes-Rosa, F. L. et al. A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism. Nat. Genet. 50, 355–361 (2018).
doi: 10.1038/s41588-018-0053-8
Scholl, U. I. et al. CLCN2 chloride channel mutations in familial hyperaldosteronism type II. Nat. Genet. 50, 349–354 (2018).
doi: 10.1038/s41588-018-0048-5
Nanba, K. et al. Genetic characteristics of aldosterone-producing adenomas in Blacks. Hypertension 73, 885–892 (2019).
doi: 10.1161/HYPERTENSIONAHA.118.12070
Azizan, E. A. et al. Microarray, qPCR, and KCNJ5 sequencing of aldosterone-producing adenomas reveal differences in genotype and phenotype between zona glomerulosa- and zona fasciculata-like tumors. J. Clin. Endocrinol. Metab. 97, E819–E829 (2012).
doi: 10.1210/jc.2011-2965
Monticone, S. et al. Immunohistochemical, genetic and clinical characterization of sporadic aldosterone-producing adenomas. Mol. Cell. Endocrinol. 411, 146–154 (2015).
doi: 10.1016/j.mce.2015.04.022
Akerstrom, T. et al. Novel somatic mutations and distinct molecular signature in aldosterone-producing adenomas. Endocr. Relat. Cancer 22, 735–744 (2015).
doi: 10.1530/ERC-15-0321
De Sousa, K. et al. Genetic, cellular, and molecular heterogeneity in adrenals with aldosterone-producing adenoma. Hypertension 75, 1034–1044 (2020).
doi: 10.1161/HYPERTENSIONAHA.119.14177
Kobuke, K. et al. Calneuron 1 increased Ca
doi: 10.1161/HYPERTENSIONAHA.117.10205
Williams, T. A. et al. Teratocarcinoma-derived growth factor-1 is upregulated in aldosterone-producing adenomas and increases aldosterone secretion and inhibits apoptosis in vitro. Hypertension 55, 1468–1475 (2010).
doi: 10.1161/HYPERTENSIONAHA.110.150318
Boulkroun, S. et al. Prevalence, clinical, and molecular correlates of KCNJ5 mutations in primary aldosteronism. Hypertension 59, 592–598 (2012).
doi: 10.1161/HYPERTENSIONAHA.111.186478
Ye, P., Mariniello, B., Mantero, F., Shibata, H. & Rainey, W. E. G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism. J. Endocrinol. 195, 39–48 (2007).
doi: 10.1677/JOE-07-0037
Nishimoto, K. et al. Aldosterone-stimulating somatic gene mutations are common in normal adrenal glands. Proc. Natl Acad. Sci. USA 112, E4591–E4599 (2015).
doi: 10.1073/pnas.1505529112
Teo, A. E. et al. Physiological and pathological roles in human adrenal of the glomeruli-defining matrix protein NPNT (nephronectin). Hypertension 69, 1207–1216 (2017).
doi: 10.1161/HYPERTENSIONAHA.117.09156
Tezuka, Y. et al. 18-Oxocortisol synthesis in aldosterone-producing adrenocortical adenoma and significance of KCNJ5 mutation status. Hypertension 73, 1283–1290 (2019).
doi: 10.1161/HYPERTENSIONAHA.118.12064
Williams, T. A. et al. Genotype-specific steroid profiles associated with aldosterone-producing adenomas. Hypertension 67, 139–145 (2016).
doi: 10.1161/HYPERTENSIONAHA.115.06186
Eisenhofer, G. et al. Mass spectrometry-based adrenal and peripheral venous steroid profiling for subtyping primary aldosteronism. Clin. Chem. 62, 514–524 (2016).
doi: 10.1373/clinchem.2015.251199
Guo, Z. et al. Biochemical, histopathological, and genetic characterization of posture-responsive and unresponsive APAs. J. Clin. Endocrinol. Metab. 105, e3224–e3235 (2020).
doi: 10.1210/clinem/dgaa367
Bergström, M. et al. PET with [
doi: 10.1016/S1095-0397(99)00099-0
Bergstrom, M. et al. PET imaging of adrenal cortical tumors with the 11β-hydroxylase tracer
Abe, T. et al. A novel CYP11B2-specific imaging agent for detection of unilateral subtypes of primary aldosteronism. J. Clin. Endocrinol. Metab. 101, 1008–1015 (2016).
doi: 10.1210/jc.2015-3431
Soinio, M. et al. Functional imaging with
doi: 10.1530/EJE-20-0532
Silins, I. et al. Para-chloro-2-[
doi: 10.7150/ijms.51206
Zarnegar, R. et al. The aldosteronoma resolution score: predicting complete resolution of hypertension after adrenalectomy for aldosteronoma. Ann. Surg. 247, 511–518 (2008).
doi: 10.1097/SLA.0b013e318165c075
Utsumi, T. et al. Development of a novel nomogram to predict hypertension cure after laparoscopic adrenalectomy in patients with primary aldosteronism. World J. Surg. 38, 2640–2644 (2014).
doi: 10.1007/s00268-014-2612-1
Burrello, J. et al. The primary aldosteronism surgical outcome score for the prediction of clinical outcomes after adrenalectomy for unilateral primary aldosteronism. Ann. Surg. 272, 1125–1132 (2020).
doi: 10.1097/SLA.0000000000003200
Kitamoto, T. et al. Comparison of cardiovascular complications in patients with and without KCNJ5 gene mutations harboring aldosterone-producing adenomas. J. Atheroscler. Thromb. 22, 191–200 (2015).
doi: 10.5551/jat.24455
Mulatero, P. et al. 18-hydroxycorticosterone, 18-hydroxycortisol, and 18-oxocortisol in the diagnosis of primary aldosteronism and its subtypes. J. Clin. Endocrinol. Metab. 97, 881–889 (2012).
doi: 10.1210/jc.2011-2384
Meyer, L. S. et al. Single-center prospective cohort study on the histopathology, genotype, and postsurgical outcomes of patients with primary aldosteronism. Hypertension 78, 738–746 (2021).
doi: 10.1161/HYPERTENSIONAHA.121.17348
Nishimoto, K. et al. Adrenocortical zonation in humans under normal and pathological conditions. J. Clin. Endocrinol. Metab. 95, 2296–2305 (2010).
doi: 10.1210/jc.2009-2010
Omata, K. et al. Aldosterone-producing cell clusters frequently harbor somatic mutations and accumulate with age in normal adrenals. J. Endocr. Soc. 1, 787–799 (2017).
doi: 10.1210/js.2017-00134
Omata, K. et al. Cellular and genetic causes of idiopathic hyperaldosteronism. Hypertension 72, 874–880 (2018).
doi: 10.1161/HYPERTENSIONAHA.118.11086
Hacini, I. et al. Somatic mutations in adrenals from patients with primary aldosteronism not cured after adrenalectomy suggest common pathogenic mechanisms between unilateral and bilateral disease. Eur. J. Endocrinol. 185, 405–412 (2021).
doi: 10.1530/EJE-21-0338
Zhou, J. et al. Somatic mutations of GNA11 and GNAQ in CTNNB1-mutant aldosterone-producing adenomas presenting in puberty, pregnancy or menopause. Nat. Genet. 53, 1360–1372 (2021).
doi: 10.1038/s41588-021-00906-y
Gros, R., Ding, Q., Liu, B., Chorazyczewski, J. & Feldman, R. D. Aldosterone mediates its rapid effects in vascular endothelial cells through GPER activation. Am. J. Physiol. Cell Physiol. 304, C532–C540 (2013).
doi: 10.1152/ajpcell.00203.2012
Funder, J. W. GPR30, mineralocorticoid receptors, and the rapid vascular effects of aldosterone. Hypertension 57, 370–372 (2011).
doi: 10.1161/HYPERTENSIONAHA.110.165076
Dickerson, J. E., Hingorani, A. D., Ashby, M. J., Palmer, C. R. & Brown, M. J. Optimisation of antihypertensive treatment by crossover rotation of four major classes. Lancet 353, 2008–2013 (1999).
doi: 10.1016/S0140-6736(98)07614-4
Williams, B. et al. Spironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment for drug-resistant hypertension (PATHWAY-2): a randomised, double-blind, crossover trial. Lancet 386, 2059–2068 (2015).
doi: 10.1016/S0140-6736(15)00257-3
Azizan, E. A. et al. Somatic mutations affecting the selectivity filter of KCNJ5 are frequent in 2 large unselected collections of adrenal aldosteronomas. Hypertension 59, 587–591 (2012).
doi: 10.1161/HYPERTENSIONAHA.111.186239
Wu, V.-C. et al. Subtypes of histopathologically classical aldosterone-producing adenomas yield various transcriptomic signaling and outcomes. Hypertension 78, 1791–1800 (2021).
doi: 10.1161/HYPERTENSIONAHA.121.18006
Deinum, J., Groenewoud, H., van der Wilt, G. J., Lenzini, L. & Rossi, G. P. Adrenal venous sampling: cosyntropin stimulation or not? Eur. J. Endocrinol. 181, D15–D26 (2019).
doi: 10.1530/EJE-18-0844
Kline, G. A., Leung, A. A., Sam, D., Chin, A. & So, B. Repeat adrenal vein sampling in aldosteronism: reproducibility and interpretation of persistently discordant results. J. Clin. Endocrinol. Metab. 106, e1170–e1178 (2021).
doi: 10.1210/clinem/dgaa930
Yatabe, M. et al. Cosyntropin stimulation in adrenal vein sampling improves the judgment of successful adrenal vein catheterization and outcome prediction for primary aldosteronism. Hypertens. Res. 43, 1105–1112 (2020).
doi: 10.1038/s41440-020-0445-x
Newcombe, R. G. Interval estimation for the difference between independent proportions: comparison of eleven methods. Stat. Med. 17, 873–890 (1998).
doi: 10.1002/(SICI)1097-0258(19980430)17:8<873::AID-SIM779>3.0.CO;2-I
UK Government. List of ethnic groups. GOV.UK https://www.ethnicity-facts-figures.service.gov.uk/style-guide/ethnic-groups (2022).
Young, W. F. & Stanson, A. W. What are the keys to successful adrenal venous sampling (AVS) in patients with primary aldosteronism? Clin. Endocrinol. 70, 14–17 (2009).
doi: 10.1111/j.1365-2265.2008.03450.x
Strajina, V. et al. Primary aldosteronism: making sense of partial data sets from failed adrenal venous sampling—suppression of adrenal aldosterone production can be used in clinical decision making. Surgery 163, 801–806 (2018).
doi: 10.1016/j.surg.2017.10.012
Committee for Proprietary Medicinal Products. Points to Consider on Switching Between Superiority and Non-Inferiority (The European Agency for the Evaluation of Medicinal Products, 2000).
Fuss, C. T. et al. Radiation exposure of adrenal vein sampling: a German multicenter study. Eur. J. Endocrinol. 179, 261–267 (2018).
doi: 10.1530/EJE-18-0328
Haase, M. et al. Outcome of adrenal vein sampling performed during concurrent mineralocorticoid receptor antagonist therapy. J. Clin. Endocrinol. Metab. 99, 4397–4402 (2014).
doi: 10.1210/jc.2014-2788
Hinchliffe, E., Carter, S., Owen, L. J. & Keevil, B. G. Quantitation of aldosterone in human plasma by ultra high performance liquid chromatography tandem mass spectrometry. J. Chromatogr. B Anal. Technol. Biomed. Life Sci. 913–914, 19–23 (2013).
doi: 10.1016/j.jchromb.2012.11.013
Williams, T. A. et al. International histopathology consensus for unilateral primary aldosteronism. J. Clin. Endocrinol. Metab. 106, 42–54 (2021).
doi: 10.1210/clinem/dgaa484
Livak, K. J. & Schmittgen, T. D. Analysis of relative gene expression data using real-time quantitative PCR and the [Formula: see text] method. Methods 25, 402–408 (2001).
Bancos, I. et al. Urine steroid metabolomics for the differential diagnosis of adrenal incidentalomas in the EURINE-ACT study: a prospective test validation study. Lancet Diabetes Endocrinol. 8, 773–781 (2020).
doi: 10.1016/S2213-8587(20)30218-7
Sagmeister, M. S. et al. Glucocorticoid activation by 11β-hydroxysteroid dehydrogenase enzymes in relation to inflammation and glycaemic control in chronic kidney disease: a cross-sectional study. Clin. Endocrinol. 90, 241–249 (2019).
doi: 10.1111/cen.13889