Searchable abstracts of presentations at key conferences in endocrinology

ea0029p1726 | Thyroid (non-cancer) | ICEECE2012

Spontaneous splenic rupture following plasmapheresis in a patient with refractory amiodarone-induced thyrotoxicosis

Streuli R. , Pfisterer D. , Fischli S. , Burget L. , Metzger J. , Kauper M. , Henzen C.

Introduction: Amiodarone-induced thyrotoxicosis (AIT) is a well-known complication of amiodarone therapy. Type 1 AIT is caused by excessive iodine-induced thyroid hormone synthesis in abnormal thyroid glands and treated with thionamides; type 2 AIT is a drug induced destructive thyroiditis that responds to glucocorticoids. Mixed forms of AIT need a combined treatment of thionamides and glucocorticoids. In refractory cases of AIT plasmapheresis before total thyroidectomy is an ...

ea0007p47 | Diabetes, metabolism and cardiovascular | BES2004

A novel non-steroidal inhibitor of 11beta-hydroxysteroid dehydrogenase type 1 improves features of metabolic syndrome in murine disease models

Thieringer R , Balkovec J , Chen H , Frazier E , Le Grand C , Li Z , Metzger J , Mundt S , Nunes C , Strowski M , Olson S , Robertson N , Strack A , Schaeffer J , Wright S , Zhang B , Hermanowski-Votska A

Chronic exposure to elevated circulating glucocorticoids can lead to metabolic changes, which resemble those observed in Metabolic Syndrome. Features of the Metabolic Syndrome can be reversed by lowering systemic glucocorticoid levels or by treatment with a glucocorticoid receptor antagonist. At the intracellular level, exposure to glucocorticoids is regulated by two distinct 11beta-hydroxysteroid dehydrogenases, 11beta-HSD type 1 and type 2. 11beta-HSD1 predominantly acts as ...