THE IMPACT OF HOMOCYSTEINE IN LUPUS ERYTHEMATOSUS: A LINK OF INFLAMMATION, SKIN AND CARDIOVASCULAR RISK

Lupus erythematosus (LE) is a complex autoimmune disease with diverse clinical manifestations, ranging from systemic involvement to cutaneous lesions. Cutaneous lupus erythematosus (CLE) is the second most common manifestation of LE, resulting in disfiguring scaring, hair loss and significant burden for the patients’ quality of life. Elevated homocysteine (Hcy) levels, or hyperhomocysteinemia (HHcy), are observed in both SLE and CLE. Hcy contributes to endothelial dysfunction, thrombosis risk, and immune activation through pro-inflammatory cytokine release, oxidative stress, and vascular damage. Additionally, it disrupts T-cell function and epigenetic regulation, further exacerbating autoimmune responses. Several factors can cause HHcy, including genetics (such as MTHFR mutations), kidney problems, metabolic disorders, certain medications, and deficiencies in B vitamins (B6, B9, B12). Since B vitamins help regulate Hcy, a poor diet or an inability to properly absorb nutrients may contribute to higher Hcy levels in lupus patients. Additionally, HHcy is a recognized risk factor for cardiovascular disease (CVD), a major cause of morbidity in lupus patients. Increased Hcy levels contribute to arterial stiffness, endothelial injury, and thrombotic complications, elevating the risk of atherosclerosis, stroke, and myocardial infarction. Hcy may act as a biomarker for disease severity and vascular risk in CLE. Interventions such as B-vitamin supplementation and lifestyle changes could offer therapeutic benefits. However, further research is needed to clarify its role in CLE pathogenesis and its potential for clinical management.