Abstract

Introduction/ObjectiveIn our study, we investigated the role of Parkinsonism-associated protein 7 (PARK-7), known as DJ-1, which is involved in several pathways that counteract oxidative stress. This stress is thought to contribute to the development of fibrosis and vascular damage in patients with systemic sclerosis (SSc). Our study aims to investigate the correlation between PARK-7 levels, laboratory and clinical findings related to SSc and treatment regimens. Materials and methodsIn our study, we included fifty patients aged 18 years and older diagnosed with SSc and thirty healthy individuals without any systemic, malignant, or autoimmune diseases as a control group. We collected demographic data, clinical manifestations, laboratory and radiological findings, pulmonary function test (PFT), and echocardiography reports, information on comorbidities and prescribed medications from medical records, hospital database analysis, and direct patient interviews. Disease activity was quantified and documented using activity scoring systems developed by the European Scleroderma Study Group (EScSG) and the United Kingdom's (UK) Functional Activity Scoring. PARK-7 levels in venous blood samples from participating patients were quantified by Enzyme-Linked Immunosorbent Assay (ELISA). ResultsThe PARK-7 level was 21.26±15.83 in the patient group and 16.11±11.83 in the control group. There was no significant difference in PARK-7 levels between the patient and control groups (p=.22). In terms of disease subtypes, PARK-7 levels were 21.35±18.36 in the limited form, 23.18±13.83 in the diffuse form. No statistically significant differences were observed between PARK-7 levels, the control group, and the different disease forms (p>.05). In patients classified as having active disease according to the EScSG scoring system, the PARK-7 level was 25.69±18.10 compared to 16.00±10.91 in the inactive group. No significant correlation was found between the presence of high-resolution computed tomography (HRCT) findings, other systemic involvement, and PARK-7 levels. ConclusionsOver the past decade, numerous reports have highlighted the therapeutic potential of PARK-7 and its related molecules for the treatment of various diseases. Whether PARK-7 can be effectively used in the treatment of SSc remains unclear due to the cross-sectional design of our study. We believe that a study measuring PARK-7 levels in patients newly diagnosed or in the early stages of SSc, followed by randomised and prospective follow-up of clinical outcomes with and without treatment, could significantly improve our understanding of the role of PARK-7 in the pathogenesis of SSc and its potential applicability in the treatment of SSc patients.

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