Is there an association between sarcoidosis and atherosclerosis?

Yilmaz Y., Kul S., Kavas M., Erman H., Aciksari G., Ozcan F. B. , ...More

INTERNATIONAL JOURNAL OF CARDIOVASCULAR IMAGING, 2020 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume:
  • Publication Date: 2020
  • Doi Number: 10.1007/s10554-020-02041-x
  • Journal Indexes: Science Citation Index Expanded, Scopus, Agricultural & Environmental Science Database, Biotechnology Research Abstracts, EMBASE
  • Keywords: Carotid intima-media thickness, Copeptin, Flow-mediated dilatation, Sarcoidosis, ENDOTHELIAL DYSFUNCTION, DISEASE, BIOMARKERS, GUIDELINES, MANAGEMENT, THICKNESS, COPEPTIN


Sarcoidosis is a multisystemic chronic inflammatory disease that the specific etiology is not known clearly. The aim of this study is, to investigate the presence of subclinical atherosclerosis and endothelial dysfunction by using carotid intima-media thickness and flow-mediated dilatation measurements, measuring the copeptin values, which is a stress marker, and interpreting the association of copeptin values with these two variables in sarcoidosis patients without conventional risk factors for coronary artery disease. Seventy-four patients (50 f, 24 m) with histopathological diagnosis of sarcoidosis and 60 healthy volunteers (35 f, 25 m) with similar sociodemographic characteristics were included in this study. CIMT, FMD, and serum copeptin levels of all participants were measured. The values of CIMT and Copeptin in sarcoidosis patients were significantly higher (p = 0.001, p < 0.001 respectively), and FMD was significantly lower (p = 0.01) than the control group. In sarcoidosis patients not significant correlation found among CIMT with copeptin (r: 0.16, p = 0.18) and FMD with copeptin (r: 0.01, p = 0.96). With the demonstration of the presence of subclinical atherosclerosis and endothelial dysfunction, we suggest; sarcoidosis patients may be followed more closely in terms of cardiovascular diseases. And new studies are needed to investigate the pathophysiology and the effects of high copeptin levels in sarcoidosis patients.