The Open Conference Proceedings Journal

(Biological Sciences, Chemical Sciences, Physical Sciences, Medicine, Engineering & Technology)


ISSN: 2210-2892 ― Volume 10, 2020

Inhibiting C-Reactive Protein Synthesis by Cardiac Glycosides in Humans

Jan Torzewski*, Matthias Graf, Katharina Weber, Myron Zaczkiewicz, Manuela Leier, Matthias Froehlich, Oliver Zimmermann
Cardiovascular Center Oberallgäu-Kempten, Robert Weixler Str. 50, 87439 Kempten, Germany


The role of C-reactive protein (CRP) in cardiovascular disease has been controversially discussed for almost two decades. Specific CRP inhibition, followed by use of CRP inhibitors in controlled clinical trials may be the only way to prove or disprove a causative role for CRP in cardiovascular disease. Endogenous and plant-derived inhibitors of the Na(+)/K(+)-ATPase, i.e. the cardiac glycosides ouabain, digoxin and digitoxin, potently inhibit CRP synthesis in human hepatoma cells and primary human hepatocytes in vitro.

In the herein described single-center C-reactive protein-Digoxin Observational Study (C-DOS), 60 patients with decompensated heart failure, NYHA III-IV and severely reduced Left Ventricular Ejection Fraction (LVEF<40%), and elevated CRP plasma levels will be treated by either digoxin+conventional heart failure therapy (30 patients) or by conventional heart failure therapy alone (30 patients). Plasma CRP levels in both groups will be assessed for 21 days. Plasma CRP levels (day21-day0) will be compared by regression analysis in order to find out whether digoxin significantly lowers CRP plasma levels in humans.

The trial will not answer the question whether CRP is causative in cardiovascular disease but, by following a step by step approach, investigates for the first time whether cardiac glycosides lower CRP plasma levels in humans. The study hereby serves as a pilot study for subsequent phase III trials. Importantly, it is the first trial ever that systematically uses a direct CRP synthesis inhibitor in vivo in humans.

Keywords: C-reactive protein, C-reactive protein synthesis, cardiovascular disease, cardiac failure, clinical study, drug development.

Article Information

Identifiers and Pagination:

Year: 2016
Volume: 7
First Page: 7
Last Page: 11
Publisher Id: TOPROCJ-7-1-7
DOI: 10.2174/2210289201607010007

Article History:

Received Date: 8/9/2015
Revision Received Date: 28/11/2015
Acceptance Date: 12/1/2016
Electronic publication date: 14/3/2016
Collection year: 2016

© Torzewski et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (, which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Cardiovascular Center Oberallgäu-Kempten, Robert Weixler-Straße 50, 87439 Kempten, Germany; Tel/Fax: ++49-8323-910-8950, ++49-8323-910-395; Email:

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