A case of insulin edema with inappropriate hyperaldosteronism

dc.contributor.authorKalambokis, G.en
dc.contributor.authorTsatsoulis, A.en
dc.contributor.authorEconomou, G.en
dc.contributor.authorTsianos, E. V.en
dc.date.accessioned2015-11-24T19:40:42Z
dc.date.available2015-11-24T19:40:42Z
dc.identifier.issn0391-4097-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24393
dc.rightsDefault Licence-
dc.subjectAdulten
dc.subjectDiabetes Mellitus/*drug therapyen
dc.subjectEdema/*chemically induceden
dc.subjectHumansen
dc.subjectHyperaldosteronism/*chemically induceden
dc.subjectInsulin/*adverse effects/*therapeutic useen
dc.subjectMaleen
dc.subjectWater-Electrolyte Balanceen
dc.titleA case of insulin edema with inappropriate hyperaldosteronismen
heal.abstractEdema of variable severity is an uncommon complication of insulin treatment. Increased sodium reabsorption, transient proteinuria and hypoalbuminemia are the most frequently reported laboratory disorders at the time of edema formation. This case report describes a 44-yr-old man with a 4-month history of anorexia, polyuria, polydipsia and weight loss of 25 kg who presented with diabetic ketoacidosis. On admission, there were no clinical or laboratory signs of volume depletion. Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. The diagnostic work-up showed the presence of high renin and aldosterone values despite the absence of evident hypovolemia and no evidence of gastrointestinal, cardiovascular, renal, thyroid, hepatic or other endocrine disorder. Complement values were normal; autonomic neuropathy and venoocclusive intraabdominal lesions were excluded and no other drugs except insulin were administered. Initiation of spironolactone was associated with prompt resolution of the edema and gradual correction of the laboratory abnormalities. Our findings show that hyperaldosteronism may occur in patients with insulin edema, even in the absence of volume depletion, contributing to the development of increased sodium reabsorption and of other laboratory disorders.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/15762045-
heal.journalNameJournal of Endocrinological Investigationen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2004-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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