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Endothelial dysfunction in patients with systemic sclerosis
Renata Pacholczak-Madej1,2, Piotr Kuszmiersz3, Stanisława Bazan-Socha3
1Department of Anatomy, Jagiellonian University, Medical College, Krakow, Poland.
Postepy Dermatologii I Alergologii
|September 30, 2020
Summary
Systemic sclerosis patients show endothelial dysfunction, detectable by ultrasonography, with higher thrombomodulin and intima-media thickness, and lower flow-mediated dilation. These findings suggest chronic inflammation may play a role.
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Vascular Biology
Background:
- Systemic sclerosis (SSc) is characterized by endothelial dysfunction and damage, even before clinical symptoms appear.
- Early detection of endothelial dysfunction is crucial for managing SSc patients and preventing cardiovascular complications.
Purpose of the Study:
- To assess the clinical applicability of various methods for evaluating endothelial function in SSc patients.
- To compare endothelial function markers between SSc patients and healthy controls.
Main Methods:
- Ultrasonography was used to measure flow-mediated dilation (FMD) of the brachial artery and intima-media thickness (IMT) of the common carotid artery.
- Serum levels of vascular cell adhesion molecule-1 (VCAM-1) and thrombomodulin were measured.
- Participants included 42 SSc patients and 36 matched controls, assessed for cardiovascular risk factors.
Main Results:
- SSc patients exhibited significantly lower FMD% (45% reduction) and higher IMT (13% increase) compared to controls, even after adjusting for confounders.
- While serum VCAM-1 and thrombomodulin levels did not differ initially, adjusted analysis revealed higher thrombomodulin in SSc patients (p=0.03).
- Lower FMD% correlated with age and C-reactive protein; thicker IMT correlated with age, glomerular filtration rate, and thrombomodulin levels.
Conclusions:
- Ultrasonographic methods effectively detect endothelial dysfunction in systemic sclerosis patients.
- The observed abnormalities may stem from chronic inflammation and ischemia-reperfusion injury, highlighting the need for further mechanistic studies.
