Acta Diabetologica

, Volume 55, Issue 3, pp 301–303 | Cite as

Agonistic autoantibodies against adrenergic receptors correlating with antihypertensive therapy in long-standing diabetes type 2

  • Christoph WernerEmail author
  • Nicolle Müller
  • Ulrich Alfons Müller
Letter to the Editor

Dear Prof. Porta (Editor in Chief),

We would like to present the results of a preliminary small study performed in our institution as a research letter.


Many factors for the development of diabetic complications have been intensively investigated, and, to date, the cellular mechanisms of hyperglycemic damage are well understood [1].

Control of blood glucose and HbA1c levels does not always achieve the aim of preventing diabetic complications. In conclusion, there may be more pathogenic factors despite hyperglycemia to account for the development of damage.

Possible pathogenic factors are agonistic autoantibodies (agAAB) directed against alpha1- and beta2-adrenergic, endothelin and angiotensin receptors. They were found in other diseases with substantial vascular impairments like dementia (agAAB in 59%), dilatative cardiomyopathy (agAAB in 70%) and Buerger’s disease (agAAB in 74–82%). Removal of such antibodies via immunoadsorption resulted in significant improved cardiac...



Antibody detection was performed by E.R.D.E-AAB-Diagnostics GmbH, Berlin, Germany. The authors would like to thank Marion Bimmler and Petra Hempel for their cooperation and perfect technical work.

Compliance with ethical standards

Conflict of interest

Based on these results, we initiated a larger study, substantially financed by Fresenius Medical Care. All investigations published in this article were financed by house funds of the authors.

Ethical approval

This article does not contain any studies with human participants performed by any of the authors.


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    Klein-Weigel PF, Bimmler M, Hempel P et al (2014) G-protein coupled receptor auto-antibodies in thromboangiitis obliterans (Buerger’s disease) and their removal by immunoadsorption. VASA Zeitschrift fur Gefasskrankheiten 43(5):347–352. CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Italia S.r.l., part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of Internal Medicine IIIJena University HospitalJenaGermany

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