Personalized and Precision Medicine Journal

Abstract Rheumatic inflammatory diseases, besides affecting joints and other bodily systems, are linked to heightened mortality and morbidity. Cardiovascular reasons are among the most prevalent mortality factors in individuals with these disorders, attributable to the disease's etiology and pathophysiology, chronic inflammation, and the pharmacological treatments employed. Although rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, and gout exhibit distinct pathophysiology and symptoms, persistent inflammation remains their shared pathophysiological characteristic. Metabolic syndrome has recently been linked to several of these disorders. The investigation of metabolic syndrome in inflammatory rheumatic diseases is significant for multiple reasons, including its correlation with cardiovascular disease onset, the emergence of a pre-inflammatory condition, treatment selection, and associated monitoring. This review article initially explores the significance of metabolic syndrome in rheumatic diseases, followed by a detailed analysis of each condition individually. This study concludes, through a review of previous studies, that abdominal obesity in rheumatoid arthritis and lupus patients, abdominal obesity and hypertension in psoriatic arthritis patients, and hypertriglyceridemia and hypertension in gout are significant elements of metabolic syndrome warranting increased focus.

Abstract The synovial joints are most affected by the systemic autoimmune inflammatory condition known as rheumatoid arthritis (RA). A unique and underappreciated link exists between rheumatoid vasculitis (RV), an extra-articular symptom of RA, and Inflammatory Aortic Disease (aortitis). In this article, we describe the case of a 64-year-old lady who had RA-associated aortitis and conducted a literature search on the condition. Patients with RA-associated aortitis received an average oral steroid dosage of 40.2 mg/day of prednisolone (PSL). Due to the patient's RV-related symptoms, including epidermal ulceration, a significant rheumatoid factor titer, and a modest PSL dosage significantly alleviated the clinical features, it was assumed that RV also caused our patient's aortitis. Early identification and the start of therapy are crucial since RA-associated aortitis may be lethal if left untreated.

Abstract In the twenty-first century, there still needs more clarity on rheumatoid arthritis (RA). Rheumatoid arthritis is a widespread but heterogeneous illness with a broad range in its history, clinical symptoms, and response to therapy. It is now known that prevention of joint destruction, functional impairment, and a poor disease prognosis depends on early, correct diagnosis and starting therapy with disease-modifying drugs (DMARDs), among which methotrexate (MTX) remains the gold standard in the treatment of RA. Early rheumatoid arthritis diagnosis is crucial since it enables a speedier start to primary therapy. Pharmacogenetic and pharmacogenomic research, which aid in identifying a patient’s genetic profile, may bring personalized treatment closer to reality. Identifying disease-specific genes while the organism’s resistance to them is still intact should be made feasible by further study into RA.

Abstract Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown etiology that results in progressive joint destruction and ultimately to disability. Currently effective biologic therapies, exist for approximately  40% of patients, but disease activity remains inadequately controlled in others. Therefore, it is crucial  to identify specific markers that predict therapeutic response in various patients, prior to the initiation of therapy.  DNA methylation , as a epigenetic factor, is increasingly being explored as a potential theranostic biomarker. It has been suggested that DNA methylation might contribute to RA development, nonetheless , with conflicting results. Epigenetic modules have provided a possible interface through which genetic and environmental risk factors  contribute to the susceptibility and pathogenesis of RA. Hence,  epigenetic regulators may provide promising drug targets to develop novel therapeutic drugs for tailored treatment of RA patients. Here we review the current knowledge regarding the role of DNA methylation in RA and indicate its potential therapeutic implications.