Sabina Oreska1, Hana Storkanova1, Maja Spiritovic2, Barbora Hermankova2, Michal Vrablík3, Karel Pavelka4, Jiří Vencovský5, Ladislav Šenolt5, Radim Becvar1 and Michal Tomcik1, 1Institute of Rheumatology, Department of Rheumatology, 1st Faculty of Medicine, Charles University, Prague, Czech Republic, Prague, Czech Republic, 2Institute of Rheumatology, Department of Physiotherapy, Faculty of Physical Education and Sport, Charles University, Prague, Czech Republic, Prague, Czech Republic, 33rd Department of Internal Medicine, General University Hospital and 1st Faculty of Medicine, Charles University, Prague, Czech Republic, Prague, Czech Republic, 4Institute of Rheumatology, Department of Rheumatology, 1st Faculty of Medicine, Charles University, Prague, Czech Republic, Praha, Czech Republic, 5Institute of Rheumatology and Department of Rheumatology, First Faculty of Medicine, Charles University, Prague, Czech Republic
Background/Purpose: Systemic sclerosis (SSc) is characterized by skin and organ involvement and chronic disease course. Systemic inflammation, involvement of the gastrointestinal tract, and glucocorticoid treatment can have a negative impact on intermediate metabolic pathways, especially on lipid metabolism. The aim of this study was to assess the differences in the lipid profile of SSc patients and healthy controls (HC) and the association with disease-specific features.
Methods: 100 patients with SSc (85 females; mean age 55.5; disease duration 4.0 years; lcSSc 59 / dcSSc 41) and 100 age-/sex-matched HC (85 females, mean age 55.3) without rheumatic diseases were included. Patients with SSc fulfilled the 2013 ACR/EULAR criteria. Levels of selected parameters of lipid metabolism were measured in sera drawn after 8 hours of fasting by routine analytic methods. In SSc patients, disease activity was evaluated by the ESSG composite index, skin involvement by the modified Rodnan skin score (mRSS), and organ involvement and current treatment were recorded.
Results: We observed differences in disease activity and skin involvement between dcSSc and lcSSc, whereas comorbidities, internal organ involvement, and treatment were statistically comparable. Levels of triglycerides (TG) tended to be higher, especially in the dcSSc group. However, total cholesterol (TC), LDL-C, and also HDL-C demonstrated a trend towards a decrease compared to HC (p< 0.10). Although levels of Apo-B (a part of non-HDL-C, a negative cardiovascular predictive marker) were comparable, levels of Apo-A (a part of HDL) were significantly decreased in the whole SSc group and both SSc subtypes compared to age-/sex-matched HC (p< 0.05). There was a trend towards a higher (unfavorable) atherogenic index in dcSSc compared to the corresponding age-/sex-matched HC (p< 0.10). Patients with dcSSc had significantly lower HDL-C levels (p=0.006) and a trend to lower apo-A (p=0.079) but significantly increased lipoprotein A and atherogenic index of plasma compared to the lcSSc group (p< 0.05). Levels of TC, LDL-C, apo-B, and nonHDL positively correlated with disease duration, the current dose of glucocorticoids (p< 0.05), and LDL-C levels correlated borderline negatively with CRP (p=0.061). Higher levels of HDL-C and apo-A were associated with higher age, lower disease activity (ESSG composite index and CRP) (p< 0.05), and borderline with less severe skin involvement (p=0.067 for HDL-C; p=0.046 for Apo-A). Moreover, Apo-A positively correlated with the current dose of glucocorticoids and higher DLCO, and the atherogenic index was increased (worse) in higher disease activity and lower age (p< 0.05 for all).
Conclusion: We have observed significant alterations in serum lipid parameters in our SSc patients compared to age-/sex-matched healthy individuals. Differences were also found between lcSSc and dcSSc; more unfavorable alterations were detected in dcSSc. These alterations were associated with disease duration and activity, skin and lung involvement, and the current dose of corticosteroids.
Acknowledgment: Supported by AZV NV18-01-00161A, MHCR-00023728, and SVV-260523.
Disclosures: S. Oreska, None; H. Storkanova, None; M. Spiritovic, None; B. Hermankova, None; M. Vrablík, None; K. Pavelka, MSD, Pfizer, Roche, Eli Lilly, Medac, UCB, SOBI, Biogen, Sandoz, Viatris; J. Vencovský, Abbvie, Biogen, Boehringer, Eli Lilly, Gilead, Kezar, Merck, Novartis, Octapharma, Pfizer, Takeda, UCB, Werfen, Argenx; L. Šenolt, None; R. Becvar, None; M. Tomcik, None.
