Literature DB >> 9247760

Primary aldosteronism: a new understanding.

R D Gordon1.   

Abstract

Primary aldosteronism (PAL) may always have a genetic basis. This leads to either abnormally regulated, increased biosynthesis (Familial Hyperaldosteronism Type I, FHI) or to unrestrained hyperplasia and neoplasia, usually benign. The distinction between diffuse hyperplasia, nodular hyperplasia and adenoma may be relatively unimportant in functional and etiological terms. The genetic basis must be understood before diagnosis of disease (FHI) or of predisposition (all other PAL) can be made at birth and appropriate surveillance commenced. The natural history of PAL other than FHI is for progressive increase in severity, with both adrenals eventually involved. Long-term follow-up of PAL is therefore mandatory, and postoperative assessment of residual non-suppressible aldosterone production by fludrocortisone suppression testing useful in defining biochemical cure or improvement, and the need for specific medical treatment.

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Year:  1997        PMID: 9247760     DOI: 10.3109/10641969709083191

Source DB:  PubMed          Journal:  Clin Exp Hypertens        ISSN: 1064-1963            Impact factor:   1.749


  1 in total

1.  Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2.

Authors:  Y Kotelevtsev; R W Brown; S Fleming; C Kenyon; C R Edwards; J R Seckl; J J Mullins
Journal:  J Clin Invest       Date:  1999-03       Impact factor: 14.808

  1 in total

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