Anita Liliana Susanti, Anita Liliana
Clinical Pathology Department, Faculty Of Medicine, General Achmad Yani University, Jl. Terusan Jenderal Sudirman, Cimahi

Published : 12 Documents Claim Missing Document
Claim Missing Document
Check
Articles

Found 12 Documents
Search

Pathophysiology of Atherosclerosis Formation in Autoimmune Diseases: Rheumatoid Arthritis, Systemic Lupus Erythematosus, Primary Sjögren’s Syndrome, and Antiphospholipid Syndrome Pranaja, Dwi Aryasatya; Anita Liliana Susanti; Andri A. Rusman
Health & Medical Sciences Vol. 3 No. 1 (2025): November
Publisher : Indonesian Journal Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.47134/phms.v3i1.556

Abstract

This study aimed to systematically examine the autoimmune mechanisms contributing to atherosclerosis development in patients with Rheumatoid Arthritis, Systemic Lupus Erythematosus, Sjögren’s syndrome, and Antiphospholipid Syndrome. The focus was on identifying immunological pathways, inflammatory mediators, and vascular changes that accelerate atherosclerosis in these autoimmune conditions. A systematic scoping review was conducted following established scoping review guidelines. Peer-reviewed studies on immune-mediated processes, endothelial dysfunction, lipid changes, or cardiovascular outcomes in autoimmune diseases were sourced from PubMed, Scopus, and Web of Science, screened via electronic searches and predefined inclusion criteria. Data extraction focused on immune cell involvement, cytokine profiles, mechanisms of vascular injury, and indicators of atherosclerotic progression.The results demonstrated that chronic systemic inflammation is a central mechanism driving accelerated atherosclerosis in autoimmune diseases. Activated immune cells, particularly monocytes, macrophages, and T lymphocytes, were consistently reported to infiltrate the vascular endothelium, promoting endothelial dysfunction and intimal thickening. Pro-inflammatory cytokines such as tumor necrosis factor-alpha and interferon-gamma were frequently associated with increased expression of adhesion molecules, oxidative stress, and foam cell formation. Altered lipid metabolism, including increased levels of oxidized low-density lipoprotein, further contributed to plaque development. In Antiphospholipid Syndrome, autoantibody-mediated endothelial injury and thrombogenic processes were prominent, while immune complex deposition and complement activation were key contributors in Systemic Lupus Erythematosus. Overall, the findings indicate that immune dysregulation and persistent inflammation substantially increase cardiovascular risk in patients with autoimmune diseases, underscoring the need for targeted anti-inflammatory and immunomodulatory strategies to reduce atherosclerotic burden
Differences in Glutathione Peroxidase (GPx) Levels Before and After Pulmonary Tuberculosis Treatment Putri, Ersty Marthalia; Anita Liliana Susanti; Deasy Wirasiti
Health & Medical Sciences Vol. 3 No. 1 (2025): November
Publisher : Indonesian Journal Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.47134/phms.v3i1.557

Abstract

This study aimed to review changes in glutathione peroxidase or GPx levels or activity before and after pulmonary tuberculosis treatment. A systematic scoping review was conducted on articles published between 2016 and 2025 retrieved from Google Scholar, ScienceDirect, and PubMed. Article selection followed PRISMA guidelines and applied eligibility criteria based on the PICO framework. Six studies met the inclusion criteria and were included in the analysis. All reviewed studies reported changes in GPx levels or activity after tuberculosis treatment, with most showing an increase in GPx activity following anti-tuberculosis therapy. Several studies also reported that adjunct antioxidant interventions, such as N-acetylcysteine, contributed to enhanced glutathione system function and increased GPx activity compared to standard therapy alone. The observed increase in GPx activity was associated with reduced oxidative stress and improved redox balance during treatment. These findings indicate that GPx has potential as a biomarker for monitoring treatment response in pulmonary tuberculosis. However, variations in study design, sample size, and measurement methods were identified across the included studies. Further well-designed clinical studies with standardized GPx assessment protocols are needed to confirm its clinical utility and to clarify the role of antioxidant supplementation in supporting tuberculosis treatment outcomes.