Background Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease which is characterized by the early development of atherosclerosis. Several possible reasons for accelerated atherosclerosis in SLE have been suggested. An elevated homocysteine level that can result from genetic mutations in methylenetetrahydrofolate reductase (MTHFR) is associated with an increased risk for developing atherosclerosis due to the damaged endothelium wall. According to numerous studies, the patients with hyperhomocysteinemia and coronary artery disease may have approximately twice as high the risk of cardiovascular events as compared with those who have normal level.
Objectives The aim of our study was to determine the presence of hyperomocysteine, methylenetetrahydrofolate reductase mutation in patients with SLE and with or without atherosclerotic carotid artery alterations.
Methods We examined 40 female patients with SLE, mean age 34,0 (lower quartile 28,5; upper quartile 45,0) years old, disease duration 8,0 (5,0;14,5) years, and SLEDAI – 2K activity 6,5 (4,0;10,0) points. We assessed the presence of traditional risk factors (smoking, obesity, physical inactivity, arterial hypertension, high cholesterol levels, low levels of high-density lipoproteins, elevated levels of low-density lipoproteins). The levels of homocysteine were determined with ELISA (Axis-Shild, UK) according to the instruction of manufacturer. Gene mutation was identified using the PCR and immunofluorescence methods with reagent «Pronto TromboRisk Kit» (Israel). The extracranial carotid arteries were examined ultrasonographically in 3 points of 1 cm long, located approximately below the carotid-artery bifurcation. The intima-media thickness (IMT) of common carotid artery of more than 0,9 mm and/or the presence of atherosclerotic plaques confirm atherosclerotic alterations.
Results Atherosclerotic alterations were revealed in 24 patients. IMT of CCA measured at the point of maximum value was 1.15 (1.0, 1.25) mm. Ten patients had atherosclerotic plaques. This group of patients was significantly older (p (M-U)<0,001) and had longer disease duration (p (M-U)=0,021) in comparison to patients without atherosclerotic changes. The SLEDAI – 2K activity was not significantly different between the groups. Frequency of occurrence of traditional risk factors (smoking, obesity, physical inactivity, high cholesterol levels, low levels of high-density lipoproteins, elevated levels of low-density lipoproteins) was not statistically different (p (χ2)>0,05). Arterial hypertension was more typical for patients with SLE and atherosclerotic lesions (χ2=11,38, p=0,0007) than without them. Hyperhomocysteinemia was identified in 14 (58,33%) patients with atherosclerotic alterations and in 4 (25,00%) patients without them and was considered to be statistically more significant in the first group. MTHFR mutation was revealed in 4 (16,67%) patients with atherosclerotic alterations and in 3 (18,75%) patients without them.
Conclusions These data allow considering the presence of hyperhomocysteinemia as an additional risk factor for atherosclerosis in patients with SLE, caused both by a genetic factor and the peculiarities of the disease and the administered treatment.
Disclosure of Interest None Declared