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AIM: To characterize specific clinical features of systemic lupus erythematosus (SLE) in male patients. MATERIAL AND METHODS: A total of 146 male patients with verified SLE diagnosis were examined in the Research Institute of Rheumatology. RESULTS: Literature and original data on SLE clinical characteristics in men were analysed. Diagnostic search and variants of SLE in male patients are described. CONCLUSION: To upgrade knowledge on SLE clinical characteristics, further prospective trials should be made.

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AIM: To evaluate clinical significance of heart rate variability (HRV) in patients with systemic lupus erythematosus (SLE). MATERIAL AND METHODS: HRV was investigated by means of time-domain analysis of 24 hour ambulatory ECG of 122 SLE patients under 55 years of age and 32 age-matched healthy controls. In addition to clinical manifestations and activity of SLE, we assessed the presence of basic conventional cardiovascular risk factors (hypertension, smoking, body mass index, dyslipidemia), performed common carotid duplex scanning with measurement of intima-medial thickness (IMT). Inflammatory markers (ESR, CRP, IL-6) were assessed in all the patients. RESULTS: Significantly lower HRV and the trend to tachycardia were detected in SLE patients when compared to the control group. There was a significant positive correlation between HRV and a cumulative dose of cyclophosphamide, a high density lipoprotein cholesterol level, a negative correlation between HRV and cumulative dose of azathioprine, standard risk factors (hypertension, smoking, body mass index, triglyceride level), markers of inflammation (ESR, CRP, IL-6) and IMT. CONCLUSION: Measurement of HRV in combination with routine cardiovascular risk factors and level of inflammatory markers can be used for identification of subjects at risk for faster progression of atherosclerosis in SLE patients.

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AIM: To study association between concentration of soluble receptors of TNF-alpha (sTNFa-R1) and atherosclerotic vascular affection in systemic lupus erythematosus (SLE) in men. MATERIAL AND METHODS: The examination covered 75 patients (mean age 34.76 +/- 11.8 years), duration of the disease 126 +/- 110 months. Standard cardiovascular risk factors were analysed. SLE activity was estimated by SLEDAI and ECLAM scales, SLICC/ACR index was calculated. Atherosclerotic vascular affection was studied with ultrasonic scanning of the carotid arteries. sTNFa-RI concentration in blood serum was determined with enzyme immunoassay technique in 73 SLE patients and 20 healthy donors. RESULTS: By sTNFa-R1 concentration, the patients were divided into two groups. Group 1 consisted of patients with sTNFa-R1 < or = 2.87 ng/ml, group 2 > 2.87 ng/ml. Higher concentrations of the receptors were associated with higher mean values of the damage index and proteinuria occurrence, with older age and higher body mass, with signs of vascular atherosclerotic affection (atherosclerotic plaques and intima-media thickness > 0.9 mm. CONCLUSION: Concentration of sTNFa-R1 can be considered as a laboratory marker of atherosclerotic vascular lesions.

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AIM: To investigate a clinical role of soluble (s) CD40 ligand in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). MATERIAL AND METHODS: A serum concentration of sCD40 ligand was measured with enzyme immunoassay (Bender Medsystems, Austria) in 21 patients with primary antiphospholipid syndrome (PAPS), in 25 patients with secondary APS (SAPS) associated with SLE, in 92 SLE patients and in 16 healthy donors. RESULTS: A sCD40 ligand concentration in sera of SAPS and SLE patients was significantly higher than in donors. Significant differences by the ligand level between the above patients were not seen. In PAPS sCD40 ligand concentration was normal. Elevated serum concentration of the ligand was observed in 9.5% patients with PAPS, 54.0%--with SAPS, 73.9%--with SLE. This rise in SLE and SAPS was not related with the disease activity or renal damage. Hyperexpression of the ligand in APS was associated neither with thromboses nor with a high concentration of IgG/IgM antibodies to cardiolipin. A direct correlation occurred between sCD40 ligand level and platelet count. In SLE and SAPS elevation of the ligand level correlated with increased thickness of carotid artery intima-media complex, hypercholesterinemia and diastolic dysfunction of left ventricular myocardium. CONCLUSION: Hyperexpression of sCD40L in SLE and SAPS is associated with developing cardiovascular diseases and atherosclerosis.

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The aim of the study was to determine the prevalence of various clinical and subclinical manifestations of atherosclerosis (AS) in men with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APLS), as well as to evaluate correlations between vascular atherosclerotic lesions, risk factors, and the levels of C-reactive protein (CRP) and cardiolipin antibodies (CLA). The subjects of the study were 62 patients (mean age 35.7 +/- 11.6 years, disease duration 129 +/- 102 months). Conventional and disease-related risk factors were analyzed. Carotic ultrasonography (CU) was performed in order to reveal vascular atherosclerotic lesions. Serum CRP levels were measured by the high-sensitive immunonephelometric technique. IgG and IgM CLA were studied by solid-phase immunoenzyme assay. CU found carotic arterial involvement in 58% of the patients; clinical manifestations of AS were revealed in 42% of the patients. The patients were divided into two groups: group I included 19 patients with APLS signs, group II consisted of 43 patients without APLS symptoms. The disease duration and lesion index were higher in group I. The study revealed a significant correlation between CRP level and intima-media complex (IMC) thickness in patients suffering from SLE with or without APLS (p < 0.05). Patients with AS displayed higher levels of IgG CLA, although the difference was insignificant. The study demonstrates that men suffering from SLE with or without APLS have a high risk of AS. An increase in CRP level is associated with an increase in IMC thickness.

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AIM: To elicit prevalence of clinical and subclinical manifestations of atherosclerosis in men with systemic lupus erythematosus (SLE), to assess correlation between vascular atherosclerosis, risk factors and concentration of C-reactive protein (CRP). MATERIAL AND METHODS: Analysis of conventional and disease-related factors of risk, ultrasonic scanning of the carotid arteries, high-performance enzyme immunoassay for CRP were made in 37 patients (mean age 36.9 +/- 10.7 years, duration of the disease 130.2 +/- 108.2 months). RESULTS: Clinical symptoms of atherosclerosis were seen in 35% patients. By thickness of the intimamedia complex (IMC), the patients were divided into 2 groups. Group 1 consisted of 21 patients with vascular atherosclerosis (IMC > 0.9 mm), group 2--of 16 patients with IMC < 0.9 mm. Mean age, age of the disease onset, body mass index were greater in group 1. A mean CRP concentration in patients with athrosclerosis was significantly higher than in the group without vascular atherosclerosis (p = 0.004). CONCLUSION: SLE men comprise a group of high atherosclerosis risk. An elevated CRP level is associated with thicker IMC.

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The study was undertaken to examine the clinical value of serum levels of soluble receptors of tumor necrosis factor-alpha with a molecular mass of 55 kDa (rTNF-alpha-55R) in patients with systemic lupus erythematosus (SLE). The serum level of rTNF-alpha-55R was measured by enzyme immunoassay (a "Quantikine" set, R&D System, USA) in 73 patients with SLE and 22 donors. In the patients, the mean level of rTNF-alpha-55R was significantly higher than that in donors. Higher serum levels of rTNF-alpha-55R were noted in 43.8% of the patients with SLE. There was a correlation between the level of rTNF-alpha-55R and the progression of SLE (p < 0.05), the exacerbation (p < 0.05), and the clinical manifestations of the disease (cardiac valvular apparatus damage, active lupus nephritis). rTNF-alpha-55R are a marker of the progression and exacerbation of SLE and reflects that there is a prognostically poor factor, i.e. the involvement of the kidneys in a pathological process.

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AIM: To elucidate clinical implications of nitrates (NO3) concentration as an indicator of nitric oxide (NO) level in blood serum of patients with systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (PAPS). MATERIAL AND METHODS: Blood serum concentration of NO3 was measured by high-performance liquid chromatography in a total of 41 patients with SLE (n = 17), PAPS (n = 14) and secondary APS (n = 9). Sera from 10 healthy subjects (donors) served as control. NO3 concentration > 40 mcmol/l was stated high. SLE activity was assessed by V. A. Nasonova's scale and SLEDAI index (SLEDAI > 9 indicated SLE exacerbation). Patients with PAPS were divided into two groups depending on clinical symptoms: 7 patients with significant thrombosis or history of more than two thrombotic complications (group 1); 7 patients with the history of two or less thromboses (group 2). RESULTS: The mean serum nitrate concentration in the SLE group was 43.59 mcmol/l (range 17.06-113.22). The nitrate level of the sAPS + SLE group was 49.81 +/- 27.54 and did not significantly differ from APS (33.67 +/- 14.70). By univariate standard analyses, serum nitrate concentration was significantly higher in patients with high disease activity (57.31 +/- 25.12 vs. 25.62 +/- 6.96, Mann-Whitney test, p < 0.01). The Spearman correlation coefficient of nitrate level with SLEDAI was 0.8 (p < 0.001). CONCLUSION: A nitrate level is increased in patients with active SLE and in APS patients with severe thrombotic complication.

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AIM: To assess prevalence of cardiac valvular lesions in patients with primary (P) antiphospholipid syndrome (APLS) and systemic lupus erythematosus (SLE) with and without secondary APLS. MATERIAL AND METHODS: Patients with PAPLS (n=56, 15 men and 41 women), SLE and APLS (n=88, 23 men, 65 women) and SLE without APLS (n=51, 19 men, 32 women) were followed up for 9 years. Serological markers of APLS were anticardiolipin antibodies and lupus anticoagulant. RESULTS: Prevalence of various heart defects was the highest in PAPLS (43%) compared with SLE with APLS (c2=5.6, p=0.001) and SLE without APLS (c2=9.3, p=0.0002). In secondary APLS prevalence of valvular involvement was 27% what was substantially more than in SLE without APLS (4%) (c2=7.2, p=0.0007). Changes of mitral valve cusps and mitral regurgitation were found in 33, 41 and 50% of patients with SLE, SLE with APLS and PAPLS, respectively. Pronounced mitral regurgitation and valve defects were significantly more frequent in patients with any APLS compared with those with SLE without APLS. Thickening of aortic cusps was significantly more frequent in patients with PAPLS compared with patients with SLE (with and without APLS). Changes of tricuspid valve were significantly more frequent in patients with any APLS. Progression of valvular pathology was observed in 2 patients with SLE and APLS after 4 and 5 years of follow up. During 9 years thrombotic complications developed in 8 patients with APLS and valvular lesions (6 strokes, 2 retinal thromboses). CONCLUSION: An association exists between presence of APLS and various cardiac valvular lesions. Lesions of aortic valve are associated with PAPLS: Development of valvular pathology in patients with SLE and PAPLS during follow up dictates the necessity to monitor echocardiographical parameters and titers of anticardiolipin antibodies.

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AIM: To evaluate clinical implications of measurements of the level of soluble cell molecules of adhesion (sCMA) in systemic lupus erythematosus (SLE) with antiphospholipid syndrome (APS) and primary APS (PAPS). MATERIAL AND METHODS: Serum levels of sP-selectine, sE-selectine, sVCAM-1 were determined with enzyme immunoassay (R&D, USA) in 23 SLE with APS, 15 SLE patients free of APS and 19 patients with PAPS. RESULTS: Mean levels of sE-selectine and sVCAM-1 in SLE patients with APS, PAPS and SLE was higher than in donors. Elevated mean levels of sP-selectine were observed only in SLE patients free of APS. These patients also showed a correlation between sVCAM-1 level and the disease activity (p < 0.01). CONCLUSION: The development of immunopathological process in APS is associated with increased concentration of sCMA.

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AIM: To examine the level of tumor necrosis factor-alpha (TNFa) in the sera from patients with systemic lupus erythematosus (SLE) and its clinical and pathogenic role. MATERIAL AND METHODS: TNFa was measured with ELISA (Immunogenetics N.V., Belgium) in the sera from 147 SLE patients (70 men and 77 women). The results were compared with those of 20 healthy subjects. RESULTS: TNFa elevated concentrations were found in 49% examinees with SLE. Concentration of TNFa, SLE activity and development of antiphospholipid syndrome correlated. CONCLUSION: The findings indicate that TNFa is involved in pathogenesis of SLE. Quantitation of TNFa may serve a useful tool for monitoring SLE activity.

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The review covers current issues of pharmacotherapy of systemic lupus erythematosus (SLE) with a focus on a novel immunodepressant mofetil microphenolate (MM) which is not inferior in efficiency to a conventional anti-SLE drug cyclophosphamide which has a worse tolerance.

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AIM: To study beta2-GP-I-dependent binding of phospholipid antibodies (PAb) to phospholipids and this process participation in pathogenesis of antiphospholipid syndrome (APS). MATERIALS AND METHODS: IgG-fractions and sera from 20 patients with APS. Cofactor activity of beta2-GP-I isolated from serum of healthy donors was examined with modified immunoassay. RESULTS: Contrary to donor IgG, binding of IgG fractions isolated from sera of APS patients with cardiolipin grows dose-dependently in the presence of beta2-GP-I. Cofactor activity of beta2-GP-I is confirmed in the study of sera of APS patients. Sera containing beta2-GP-I-dependent antibodies to cardiolipin (aCL), unlike aCL-negative sera, react with solid-phase immobilized beta2-GP-I. CONCLUSION: It is confirmed that beta2-GP-I participates in interaction of PAb with cardiolipin. Pathogenetic implication of beta2-GP-I-dependent PAb for onset of APS is discussed.

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Antiphospholipid syndrome (APLS) is defined as a symptom complex characterized by arterial and venous thromboses, obstetric abnormalities, thrombocytopenia and hyperproduction of antiphospholipid antibodies. APLS may be primary and secondary developing in the presence of autoimmune disorders, SLE in particular. At examination of 28 patients with primary and secondary APLS 14 patients proved hypertensive. Renal pathology was absent. Arterial hypertension appeared often in combination with microthrombi of the skin and affections of peripheral vessels. Arterial hypertension as a cardiological sign of APLS occurs more frequently than other symptoms.

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