Hyperthyreose und akute Tonsillitis bei einer 23-jährigen Patientin

Beyer, Georg; Küster, Inga; Budde, Christoph; Wilhelm, Ethel A.; Hoene, Andreas; Evert, Katja; Stracke, Sylvia; Friesecke, Sigrun; Mayerle, Julia; Steveling, Antje

doi:10.1007/s00108-016-0044-8

Cited by 2 publications

(1 citation statement)

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“…In a small clinical trial, treatment of Graves’ disease with rituximab, a B-cell depleting monoclonal antibody specifically reduced the production of TSH-receptor antibodies [ 24 ]. In a case of thyreotoxic crisis, TPE is also used to remove agAABs against TSH-receptor and albumin-bound thyroid hormones [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Immunoadsorption for Treatment of Patients with Suspected Alzheimer Dementia and Agonistic Autoantibodies against Alpha1a-Adrenoceptor—Rationale and Design of the IMAD Pilot Study

Stracke

Lange

Bornmann

et al. 2020

JCM

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Background: agonistic autoantibodies (agAABs) against G protein-coupled receptors (GPCR) have been linked to cardiovascular disease. In dementia patients, GPCR-agAABs against the α1- and ß2-adrenoceptors (α1AR- and ß2AR) were found at a prevalence of 50%. Elimination of agAABs by immunoadsorption (IA) was successfully applied in cardiovascular disease. The IMAD trial (Efficacy of immunoadsorption for treatment of persons with Alzheimer dementia and agonistic autoantibodies against alpha1A-adrenoceptor) investigates whether the removal of α1AR-AABs by a 5-day IA procedure has a positive effect (improvement or non-deterioration) on changes of hemodynamic, cognitive, vascular and metabolic parameters in patients with suspected Alzheimer’s clinical syndrome within a one-year follow-up period. Methods: the IMAD trial is designed as an exploratory monocentric interventional trial corresponding to a proof-of-concept phase-IIa study. If cognition capacity of eligible patients scores 19–26 in the Mini Mental State Examination (MMSE), patients are tested for the presence of agAABs by an enzyme-linked immunosorbent assay (ELISA)-based method, followed by a bioassay-based confirmation test, further screening and treatment with IA and intravenous immunoglobulin G (IgG) replacement. We aim to include 15 patients with IA/IgG and to complete follow-up data from at least 12 patients. The primary outcome parameter of the study is uncorrected mean cerebral perfusion measured in mL/min/100 gr of brain tissue determined by magnetic resonance imaging with arterial spin labeling after 12 months. Conclusion: IMAD is an important pilot study that will analyze whether the removal of α1AR-agAABs by immunoadsorption in α1AR-agAAB-positive patients with suspected Alzheimer’s clinical syndrome may slow the progression of dementia and/or may improve vascular functional parameters.

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Section: Introductionmentioning

confidence: 99%