Stephan Iglseder
7 Papers
19 Citations
Stephan Iglseder is an academic researcher. The author has contributed to research in topics: Tafamidis & Medicine. The author has an hindex of 6, co-authored 6 publications.
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Papers
High efficacy of rituximab for myasthenia gravis: a comprehensive nationwide study in Austria.
Raffi Topakian,Fritz Zimprich,Stephan Iglseder,Norbert Embacher,Michael Guger,Karl Stieglbauer,Dieter Langenscheidt,Jakob Rath,Stefan Quasthoff,Philipp Simschitz,Julia Wanschitz,David Windisch,Petra Müller,Dierk Oel,Günther Schustereder,Stefan Einsiedler,Christian Eggers,Wolfgang Löscher +17 more
TL;DR: In this retrospective study on RTX for MG, the largest to date, RTX appeared safe, efficacious and fast acting, and Benefit from RTX was greatest in MuSK ab + MG.
73
Hereditary transthyretin-related amyloidosis
Josef Finsterer,Stephan Iglseder,Julia Wanschitz,Raffi Topakian,Wolfgang Löscher,Wolfgang Grisold +5 more
TL;DR: Hereditary transthyretin(TTR)‐related amyloidosis is an endemic/non‐endemic, autosomal‐dominant, early‐ and late‐onset, rare, progressive disorder, predominantly manifesting as length‐dependent, small fiber dominant, axonal polyneuropathy and frequently associated with cardiac disorders and other multisystem diseases.
48
Iatrogenic lesions of peripheral nerves
Wolfgang Löscher,Julia Wanschitz,Stephan Iglseder,A. Vass,S. Grinzinger,P. Pöschl,Wolfgang Grisold,M. Ninkovic,Gregor Antoniadis,Maria Teresa Pedro,Ralph König,Stefan Quasthoff,W. Oder,Josef Finsterer +13 more
TL;DR: Management and outcome of INLs can be further improved if the multiprofessional interplay is optimized and adapted to the needs of the patient, the healthcare system, and those responsible for sustaining medical infrastructure.
11
Causally treatable, hereditary neuropathies in Fabry's disease, transthyretin-related familial amyloidosis, and Pompe's disease.
Josef Finsterer,Julia Wanschitz,Stefan Quasthoff,Stephan Iglseder,Wolfgang Löscher,Wolfgang Grisold +5 more
TL;DR: This review summarizes and discusses recent findings and future perspectives concerning etiology, pathophysiology, clinical presentation, diagnosis, treatment, and outcome of neuropathy in FD, TTR‐FA, and PD.
10
Polyglucosan body myopathy caused by defective ubiquitin ligase RBCK1
Johanna Nilsson,Benedikt Schoser,Pascal Laforêt,Ognian Kalev,Christopher Lindberg,Norma B. Romero,Marcela Dávila López,Hasan O. Akman,Karim Wahbi,Stephan Iglseder,Christian Eggers,Andrew G. Engel,Salvatore DiMauro,Anders Oldfors +13 more
TL;DR: It is concluded that RBCK1 deficiency is a frequent cause of polyglucosan storage myopathy associated with progressive muscle weakness and cardiomyopathy.