help button home button Endocrine Society JCEM JCEM Call for Nominations for EIC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Barkan, A.
Right arrow Articles by Blum, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barkan, A.
Right arrow Articles by Blum, I.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*FLUDROCORTISONE
*SODIUM

Journal of Clinical Endocrinology & Metabolism, Vol 51, 144-147, Copyright © 1980 by Endocrine Society


ARTICLES

Primary hyperparathyroidism: possible cause of primary hyperaldosteronism in a 60-year-old woman

A Barkan, R Marilus, G Winkelsberg, D Yeshurun and I Blum

Hypertension and hypokalemia were found in a 60-yr-old woman suffering from primary hyperparathyroidism. Laboratory investigations in this patient disclosed 1) elevated levels of plasma aldosterone (PA) which could not be suppressed by a high sodium diet alone or in combination with fludrocortisone (Florinef); 2) a decline of the elevated PA levels after 4 h of ambulation; and 3) low PRA which was unresponsive to stimulation by a low sodium diet coupled with diuretic-induced volume depletion and 4 h of ambulation. These findings were consistent with the diagnosis of primary hyperaldosteronism. Extirpation of a parathyroid adenoma reduced the patient's serum calcium level to normal, and subsequently, a normalization of her blood pressure, serum electrolytes, PA, and PRA were observed. On the basis of these data is is suggested that in this case hyperaldosteronism may have been caused directly or indirectly by primary hyperparathyroidism.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1980 by The Endocrine Society