Serum 18-hydroxycortisol in primary aldosteronism, hypertension, and normotensives

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dc.contributor.authorMosso, L
dc.contributor.authorGomez Sanchez, CE
dc.contributor.authorFoecking, MF
dc.contributor.authorFardella, C
dc.date.accessioned2024-01-10T13:17:34Z
dc.date.available2024-01-10T13:17:34Z
dc.date.issued2001
dc.description.abstractThis study reports the determination of plasma 18-hydroxycortisol (18-OHF) using a new and easy enzyme-linked immunosorbent assay (ELISA) method in primary aldosteronism and compares the values found in essential hypertensives and normotensive controls. In primary aldosteronism, we evaluated usefulness of plasma 18-OHF determination and the dexamethasone suppression test in the diagnosis of glucocorticoid-remediable aldosteronism using the genetic test as the gold standard. We studied 31 primary aldosteronism patients, 101 essential hypertensives, and 102 healthy normotensive controls. The plasma 18-OHF was measured using a biotin-avidin enzyme-linked assay by a new and purified polyclonal antibody. The 18-OHF value in primary aldosteronism was 6.3 +/- 8.05 nmol/L; this value is significantly higher than the value found in essential hypertensives and normotensive controls (2.81 +/- 1.42 and 2.70 +/- 1.41 nmol/L, respectively; P <0.0005). In primary aldosteronism, 4 of 31 patients had 18-OHF levels that were 10 times higher than the normal upper limit (2.983 nmol/L). The dexamethasone suppression test in primary aldosteronism patients was positive (serum aldosterone <4 ng/dL) in 13 of 31 cases. A chimeric CYP11B1/CYP11B2 gene was demonstrated in 4 primary aldosteronism patients, corresponding to the same cases that had higher level of 18-OHF. In conclusion, plasma 18-OHF determination by this ELISA method is reliable for detecting glucocorticoid-remediable aldosteronism, and it does so better than the dexamethasone suppression test.
dc.description.funderNHLBI NIH HHS
dc.description.funderNATIONAL HEART, LUNG, AND BLOOD INSTITUTE
dc.fechaingreso.objetodigital2024-05-16
dc.format.extent4 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1161/01.HYP.38.3.688
dc.identifier.issn0194-911X
dc.identifier.pubmedidMEDLINE:11566957
dc.identifier.urihttps://doi.org/10.1161/01.HYP.38.3.688
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/78673
dc.identifier.wosidWOS:000171308400032
dc.information.autorucMedicina;Fardella C;S/I;66235
dc.information.autorucMedicina;Mosso L;S/I;88201
dc.issue.numero3
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final691
dc.pagina.inicio688
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.revistaHYPERTENSION
dc.rightsacceso restringido
dc.subject18-hydroxycortisol
dc.subjecthypertension, mineralocorticoid
dc.subjectglucocorticoids
dc.subjectaldosterone
dc.subjectGLUCOCORTICOID-REMEDIABLE ALDOSTERONISM
dc.subjectSUPPRESSIBLE HYPERALDOSTERONISM
dc.subjectCHIMERIC GENE
dc.subject18-OXOCORTISOL
dc.subjectDIAGNOSIS
dc.subjectDEXAMETHASONE
dc.subjectPHENOTYPE
dc.subjectEXCRETION
dc.subjectSTEROIDS
dc.subjectBINDING
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleSerum 18-hydroxycortisol in primary aldosteronism, hypertension, and normotensives
dc.typeartículo
dc.volumen38
sipa.codpersvinculados66235
sipa.codpersvinculados88201
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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