AB1190 EVALUATION OF THE CORRELATION OF PARK-7 EXPRESSION WITH CLINICAL PARAMETERS IN PATIENTS WITH SYSTEMIC SCLEROSIS
Authors: E. Ozturk, D. Bulut Gökten, R. Mercan
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Systemic sclerosis is an autoimmune connective tissue disease, characterised by unexplained vasculopathy and fibrosis, which contribute to increased morbidity and mortality. PARK-7 is located in the cytoplasm,regulates antioxidant, anti-apoptotic and anti-inflammatory pathways. This is achieved by reducing the production of reactive oxygen species.Studies in SSc have shown that measuring plasma superoxide dismutase activity can be a valuable parameter in assessing the progression of fibrosis and the presence of Raynaud's phenomenon. Oxidative stress resulting from increased production of reactive oxygen species is thought to be associated with fibrosis and vascular damage.[1] <h3>Objectives:</h3> In this study, we investigated the role of PARK-7 in counteracting oxidative stress through multiple pathways, which is thought to contribute to fibrosis and vascular damage in individuals with SSc. The observation that PARK-7 enhances eNOS expression suggests its potential as a therapeutic target for PAH, a condition that significantly increases morbidity and mortality in SSc patients. The aim of our study was to investigate the correlation between PARK-7 levels and both laboratory and clinical aspects of systemic sclerosis patients and treatment approaches. <h3>Methods:</h3> Our study included 50 patients over 18 years of age who had been diagnosed with SSc according to the EULAR criteria. In addition, 30 healthy individuals with no systemic diseases, malignancies or autoimmune diseases were included in the control group. Venous blood samples were taken from participating patients after an average fasting period of 12 hours. The blood samples were then centrifuged.After routine biochemical analyses, the remaining serum samples were separated. The serum samples obtained were stored at -80 °C. Before analysis, the serum samples were thawed at room temperature and then homogenised. PARK-7 levels were measured using PARK7 ELISA kit. <h3>Results:</h3> PARK-7 levels were compared between the patient and control groups, PARK-7 levels were 21.26±15.83 in the patient group and 16.11±11.83 in the control group. Notably, no significant difference in PARK-7 levels was observed between the patient and control groups (p=0.220).PARK-7 levels were 21.35 ± 18.36 in the limited form, 23.18 ± 13.83 in the diffuse form, and 15.20 ± 6.18 in the overlap group. Statistical analysis showed no significant differences in PARK-7 levels when these groups were compared with the control group. When examining the relationship between patient treatments and PARK-7 levels, statistically significant differences were observed with the use of MMF, corticosteroids and PPI (p-values of 0.037, 0.057 and 0.056) No significant correlations were found when evaluating the presence of high frequency positive antibodies in SSc and PARK-7 levels (ANA p=0.211, anti TP-1 p=0.780, ACA p=0.171). The PARK-7 level was 25.69±18.10 in the group with active disease compared to 16.00±10.91 in the inactive group, which was a statistically significant difference (p=0.019). No significant correlations were found between increased pulmonary arterial pressure (PAP), HRCT findings, other systemic involvement and PARK-7 levels. <h3>Conclusion:</h3> A study involving the measurement of PARK-7 levels in early or newly diagnosed patients, followed by randomised and prospective follow-up of their clinical outcomes both with and without treatment, could significantly contribute to a comprehensive understanding of the role of PARK-7 in the pathogenesis and its potential applicability in treatment. It is important to emphasise that this study represents the first investigation of PARK-7 in SSc patients. Modulation of PARK-7 may hold promise for halting or mitigating disease progression in SSc, a disease characterised by complex mechanisms, including oxidative stress, implicated in its etiopathogenesis. <h3>REFERENCES:</h3> [1] Amico D, Spadoni T, Rovinelli M, Serafini M. et al. Intracellular free radical production by peripheral blood T lymphocytes from patients with systemic sclerosis: <i>Arthritis Research &amp; Therapy</i>. 2015;17:1-12. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>