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N-terminal prohormone brain natriuretic peptide: a biomarker for detecting cardiovascular risks in patients with rheumatoid arthritis or osteoarthritis?
  1. Thomas Häupl1,
  2. Gerd R Burmester1,
  3. Evangelos Giannitsis2,
  4. Thorsten Rohrlach3,
  5. Eberhard Spanuth4,
  6. Hans Parsch5,
  7. Kay Brune6
  1. 1Department of Rheumatology and Clinical Immunology, Charité, University-Hospital, Berlin, Germany
  2. 2Department of Cardiology, Ruprecht-Karls-University, Heidelberg, Germany
  3. 3Oligene GmbH, Berlin, Germany
  4. 4Roche Diagnostics GmbH, Mannheim, Germany
  5. 5Central Laboratory of the Clinical Center of the Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany
  6. 6Institute of Experimental and Clinical Pharmacology and Toxicology, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany
  1. Correspondence to:
    Professor K Brune
    Department of Experimental and Clinical Pharmacology and Toxicology, FAU Erlangen-Nuremberg, Fahrstr 17, 91054 Erlangen, Germany;kay.brune{at}pharmakologie.uni-erlangen.de

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Rheumatoid arthritis (RA) is associated with an increased risk for cardiovascular (CV) events including cardiac insufficiency, acute myocardial infarction and stroke.1 It is assumed that the release of proinflammatory cytokines and acute-phase proteins furthers the progression of atherosclerosis.2,3 This process seems to be further accelerated and aggravated by the administration of cyclooxygenase (Cox) inhibitors (coxibs and non-steroidal anti-inflammatory drugs (NSAIDs)). Therefore, without defining how this could be done, the Food and Drug Administration and European Agency for the Evaluation of Medicinal Products have recommended CV-risk stratification and individualised risk assessment in patients with RA before using coxibs or NSAIDs.

The B type natriuretic peptide (BNP) is a hormone synthesised by cardiomyocytes in response to increased wall tension. The plasma level of its stable, inactive breakdown product, N-terminal prohormone BNP (NT-proBNP), has been identified as a universal predictor of CV risks4 even in patients with clinically inapparent impaired CV function. Patients with RA are known to be burdened with an increased incidence of CV impairment.1 There is preliminary evidence that the serum levels of NT-proBNP in these patients reflect this burden.5

Recently, we observed that the use of NSAIDs and …

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