Endothelial dysfunction in patients with systemic sclerosis

Postepy Dermatol Alergol. 2020 Aug;37(4):495-502. doi: 10.5114/ada.2019.83501. Epub 2020 Sep 2.

Abstract

Introduction: Patients with systemic sclerosis experience endothelial dysfunction and damage even in the absence of clinical manifestations.

Aim: To evaluate various methods for assessing the endothelial function for their applicability to clinical practice.

Material and methods: Forty-two patients (7 men and 35 women) with systemic sclerosis and 36 controls (11 men and 25 women) matched for age, sex, body mass index, smoking habit, and comorbidities were enrolled in the study. We assessed each participant for typical risk factors for cardiovascular diseases and measured serum levels of vascular cell adhesion molecule-1 (VCAM-1) and thrombomodulin together with flow-mediated dilatation (FMD) of the brachial artery and intima-media thickness (IMT) of the common carotid artery using ultrasonography.

Results: Patients with systemic sclerosis did not differ from controls in serum levels of VCAM-1 and thrombomodulin, however, the statistical analysis with adjustment for potential confounders revealed increased levels of thrombomodulin in the patients (p = 0.03). They also had a 45% lower relative increase of FMD (FMD%), and 13% higher IMT (p < 0.01, both, also after adjustment for potential confounders). In a simple regression model, lower FMD% was determined by age (β = -0.57, 95% confidence interval (CI): -0.72 to -0.43) and C-reactive protein levels (β = -0.38, 95% CI: -0.55 to -0.22). Thicker IMT was related to age (β = 0.64, 95% CI: 0.52-0.67), glomerular filtration rate (β = -0.34, 95% CI: -0.5 to -0.18), and blood thrombomodulin levels (β = 0.45, 95% CI: 0.13-0.76).

Conclusions: Patients with systemic sclerosis present with endothelial dysfunction which may be detected using ultrasonographic methods. The exact mechanism of observed abnormalities is unknown, but it is possibly related to the chronic inflammation and ischemia-reperfusion injury.

Keywords: atherosclerosis; endothelium; flow-mediated dilatation; intima-media thickness; scleroderma.