В статье изложены современные представления о фенотипах остеоартрита (ОА), принципах немедикаментозного и медикаментозного лечения, предложенных в международных рекомендациях. Представлены основные результаты публикаций, рассматривающих возможности применения компонентов лекарственных растений и нутрицевтиков (босвеллия, куркума, экстракт черного перца, гиалуроновая кислота, коллаген) у пациентов с остеоартритом с учетом их эффективности и безопасности. The article presents current views on the phenotypes of osteoarthritis (OA), principles of non-pharmacological treatment and pharmacological therapy proposed in the international recommendations. We have summarized main results of publications considering the possibility of using medicinal plant components and nutraceuticals (Boswellia, turmeric, black pepper extract, hyaluronic acid, collagen) in patients with osteoarthritis with regard to their effectiveness and safety.
Vitamin D deficiency is an important environmental risk factor that influences the prevalence and severity of several autoimmune diseases, including rheumatoid arthritis (RA). The aim of this study was to determine the incidence of vitamin D insufficiency and deficiency in patients with RA, to establish the relationship between serum vitamin D levels and indicators of disease activity. 156 patients with RA were included in the study, mean age 60.2 ± 13.9 years. Assessment of clinical status was performed, serum concentrations of rheumatoid factor (RF), C-reactive protein (CRP), total vitamin D (25(OH)D), antibodies to cyclic citrullinated peptide (ACCP) were determined. RA disease activity was evaluated using DAS28 (disease activity score), SDAI (Simplified Disease Activity Index) и CDAI (Clinical Disease Activity Index) scores. Average levels of 25(OH)D in the surveyed sample were 25.2 ± 13.2 ng/ml. The results of the study indicate a high prevalence of vitamin D deficiency in patients with RA. Normal indicators of vitamin D, its insufficiency and deficiency were observed in 47 (30.3 %), 45 (28.7 %) and 64 (40.7 %) patients, respectively. Low level of serum 25(OH)D was associated with higher indices of RA activity according to DAS28, SDAI and CDAI, as well as with greater tender joint count. Vitamin D should be prescribed as an adjunctive therapy in patients with active RA due to its potential immunomodulatory effect, as well as for the prevention and treatment of bone metabolism disorders.
A total of 40 patients with systemic lupus erythematosus (SLE), 45 females with rheumatoid arthritis (RA), 22 patients with ischemic heart disease (IHD) as well as 54 women without a history of rheumatic disease (RD) or IHD were examined. The levels of hs-CRP, fibrinogen (FG), IL-6, TNF-α, antibodies to oxidized low-density lipoproteins (aOxLDL), and antiphospholipid antibodies (aPL) were determined. Despite ongoing therapy, there was no achievement of drug remission in patients with SLE and RA, which was confirmed by increased levels of hs-CRP, ESR, FG, IL-6 and TNF-α. Similar qualitative and quantitative autoimmune changes in SLE and RA were established. A similar concentration of antibodies to β2-glycoprotein I confirmed the importance of autoimmune inflammation for the development of subclinical atherosclerosis in RD and aseptic autoimmune inflammation in IHD.
Background Systemic inflammation has been postulated to be an independent cardiovascular risk factor, particularly in patients with autoimmune rheumatic disorders (ARD), such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), and is associated with accelerated atherosclerosis. There is some evidence to suggest that antiphospholipid antibodies (aPL) may also play a role in the development of atherosclerosis. However, it is few data about the relationship between these autoantibodies and inflammatory mediators in the development of atherosclerosis. Objectives To clarify the involvement of inflammatory mediators and aPL in the atherosclerotic process in patients with ARD. Methods The study included 87 female patients with ARD (RA (n=47), mean age 45,0 (33,0; 51,0) years old, disease duration 9,0 (3,0; 14,0) years, disease activity (DAS28=5,37 (4,69; 5,86) points); SLE (n=40), mean age 33,5 (27,5; 44,5) years old, disease duration 8,0 (5,0; 14,5) years, disease activity SLEDAI-2K 7,0 (4,0; 11,5) points). Sixty healthy women (mean age 40,5 (36,0; 47,0) years old) formed the control group. The levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor - α (TNF-α), LA, IgG/IgM antibodies to cardiolipin (aCL), β2-glucoprotein-1(aβ2-GP1), annexin V (aAnV) and prothrombin (aPT)) were determined with ELISA. Intima-media thickness (IMT) of the carotid artery wall and the presence of atherosclerotic plaques were revealed ultrasonographically according to the described ESH/ESC Guidelines. Results The levels of hs-CRP, IL-6, TNF-α were significantly higher in ARD patients than in the control group, which indicates the disease activity. Furthermore, the patients with SLE had a significant correlation between IL-6 and SLEDAI-2K (r=0,471, p=0,002), TNF-α and SLEDAI-2K (r=0,499, p=0,001), whereas the patients with RA had only significant correlation between hs-CRP and DAS28 (r=0,355, p=0,031). The concentration of IgG aCL, IgG and IgM aβ2-GP1, IgM aAnV, IgG aPT, LA were higher in patients with SLE than in the control group, and the levels of IgG and IgM aCL, IgM aβ2-GP1, IgG and IgM aAnV, LA were higher in patients with RA v.s. the control group. We revealed a correlation between IgG aCL, IgG aβ2-GP1, IgG aAnV and TNF-α, IgG aCL and IL-6 in SLE patients, and only one between IgG aAnV and hs-CRP in RA patients. There wasn9t any correlation between aPL and inflammatory mediators in the control group. Univariate analysis has demonstrated an association of IgG aAnV with IMT (r=0,320, p=0,044) in SLE patients and positive association between TNF-α and IMT (r=0,362, p=0,028) in RA patients. Furthermore, we found an association between IL-6 and IgG aPT (r=0,426, p=0,038), TNF-α and IgG aCL (r=0,419, p=0,042) in SLE patients with carotid atherosclerosis. There wasn9t any association between investigated parameters in the control group. Conclusions The association between inflammatory mediators and disease activity has been confirmed in ARD patients. Increased autoimmune activity has been verified both in patients with SLE and RA. It has been determined that IgG aAnV had more significance for IMT in patients with SLE, TNF-α - in RA patients. Our data can suggest that inflammatory mediators and antiphospholipid antibodies are involved in the atherosclerotic process in patients with ARD. Disclosure of Interest None declared
Background There is increasing evidence that oxidatively modified form of low-density lipoprotein cholesterol (LDL) is more important than native LDL in atherogenesis and vascular damage. The accelerated development of atherosclerosis has been recognized in patients with autoimmune rheumatic diseases, such as rheumatoid arthritis and systemic lupus erythematosus. Recent studies reported about the oxidation ratio of LDL that can be more significant in the premature development of coronary artery disease. Objectives To estimate the oxidated forms of LDL and their involvement in atherosclerotic lesions of the vessel wall in female-patients with autoimmune rheumatic diseases (ARD). Methods The study included 77 female-patients with ARD (RA (n=37), mean age 45,0 (33,0; 51,0) years old, disease duration 9,0 (3,0; 14,0) years, disease activity (DAS28=5,37 (4,69; 5,86) points) and SLE (n=40), mean age 33,5 (27,5; 44,5) years old, disease duration 8,0 (5,0; 14,5) years, disease activity SLEDAI-2K 7,0 (4,0; 11,5) points). Twenty-two women with the history of myocardial infarction (MI) (i.e. clinical manifestation of atherosclerosis) formed the control group. The levels of OxLDL, high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor - α (TNF-α) were determined with ELISA according to the instruction of manufacturer. The oxidation ratio of LDL (Ox-LDL/TC, Ox-LDL/HDL-C, Ox-LDL/LDL-C) was calculated. The presence of carotid atherosclerotic alterations (intima-media thickness and the presence of atherosclerotic plaques) was revealed ultrasonographically according to the described ESH/ESC Guidelines for the management of arterial hypertension. Results The levels of OxLDL, hs-CRP, IL-6, TNF-α, Ox-LDL/HDL-C were significantly higher in ARD patients than in the control group, what may indicate the disease activity. The presence of subclinical atherosclerosis was observed in 54,55% patients with ARD. When we compared the values of investigated parameters in patients with subclinical and clinical atherosclerosis, we revealed that only inflammatory markers (hs-CRP, IL-6, TNF-α) were significantly higher in ARD patients with atherosclerosis. However those without atherosclerosis had significantly higher values of OxLDL, hs-CRP, IL-6, Ox-LDL/TC, Ox-LDL/HDL-C, Ox-LDL/LDL-C than the control group. The positive association between hs-CRP, IL-6 and oxidation ratio Ox-LDL/TC was found in patients with subclinical atherosclerosis (p=0,0003 and p=0,007, respectively), between TNF-α and Ox-LDL/LDL-C in patients without atherosclerosis (p=0,002). The negative association between TNF-α and Ox-LDL/TC was found in patients with MI that can explain because of the lower levels of OxLDL in this group of patient considering that statins can inhibit oxidative stress. Conclusions More than half of patients with ARD had subclinical atherosclerosis. We demonstrated the elevated levels of OxLDL and inflammatory markers (hs-CRP, IL-6, TNF-α) in patients with ARD. The presence of OxLDL, especially when used in combination with TC, is better than only OxLDL for estimation of association with inflammation in patients with clinical and subclinical atherosclerosis. Thus we suggest that inflammation can influence to oxidative modification of LDL in patients with RA and SLE and during this process induce endothelial dysfunction and early development of atherosclerosis as its result. Disclosure of Interest None declared
Background It is known that some factors of the fibrinolytic pathway, such as fibrinogen, D-dimer, have been associated with an increased risk of coronary events and stroke. Many publications demonstrated an increase of early development of atherosclerosis in patients with rheumatic diseases. The data have been focused on carotid arterial atherosclerotic alterations, such as intima-media thickness and plaque formation. Objectives The aim of our study was to assess the procoagulation state and its assotiation with inflammation in female patients with rheumatoid arthritis (RA) and early atherosclerosis. Methods The study included 37 female patients with rheumatoid arthritis (ACR, 1987), mean age 45,0 (33,0; 51,0) years old, disease duration 9,0 (3,0; 14,0) years, disease activity (DAS28=5,37 (4,69; 5,86) points. Twenty-eight healthy women of the same age formed the control group. The levels of platelet cells (PLT), activated partial thromboplastin time (APTP), fibrinogen were determined with coagulation analyser, while D-Dimer, LA, IgG/IgM antibodies to cardiolipin (aCL), β2-glycoprotein-1 (aβ2-GP1), high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), were determined with ELISA. The presence of carotid atherosclerotic alterations was revealed ultrasonographically according to standard procedures. Results The patients with RA had significantly higher levels of fibrinogen, D-Dimer, LA, aCL IgG, aβ2-GP1 IgG/IgM, hs-CRP, IL-6 and TNF-α than in the control group (Table 1). The atherosclerotic alterations were found in 48,65% patients with RA, 28,57% in the control group. We reveled positive correlation between PLT and DAS28 (r=0,626, p=0,005), aCL IgM (r=0,513, p=0,029), D-Dimer and hs-CRP (r=0,747, p=0,003), DAS28 (r=0,819, p=0,0006) in RA patients with carotid atherosclerosis, that reflects association between prothrombotic and inflammatory markers. Conclusions We demonstrated the presence of prothrombotic state in patients with RA, who had higher levels of inflammatory markers too. Thus, we suggest that inflammation can influence the prothrombotic state in patients with RA, induce endothelial dysfunction and, as a result, early development of atherosclerosis. Disclosure of Interest None declared
Background According to many studies systemic lupus erythematosus (SLE) is associated with an elevated risk of cardiovascular diseases due to early development of atherosclerosis. Several investigators have found that cytokines, C-reactive protein are increased both in patients with systemic inflammatory disease and with cardiovascular pathology. However the evidences of the autoimmune etiology of atherogenesis are discussed. Objectives The aim of our study was to determine an association of antiphospholipid antibodies (aPL), inflammatory markers and cardiovascular risk factors in patients with systemic lupus erythematosus and atherosclerotic alterations of the vessel wall. Methods The study included 40 female patients with SLE (met the ACR diagnostic criteria 1997), mean age 33,5 (27,5; 44,5) years old, disease duration 8,0 (5,0; 14,5) years, disease activity SLEDAI-2K 7,0 (4,0; 11,5) points. The control group was formed by 28 healthy women of the same age. The levels of LA, IgG/IgM antibodies to cardiolipin (aCL), β2-glycoprotein-1 (aβ2-GP1), high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor - α (TNF-α), were determined with ELISA, according to the instruction of the manufactures. The presence of traditional (age, smoking, arterial hypertension, obesity, hypercholesterolemia) and non-traditional (disease duration, disease activity, the dose of prednisone) risk factors was assessed in patients with SLE. The atherosclerotic alterations of the common carotid artery were revealed ultrasonographically according to standard procedures. Results The asymptomatic atherosclerotic alterations of the vessel wall were found in 60,00% patients with SLE, 28,57% in the control group. The comparative analysis of aPL, inflammatory markers revealed an increase of aCL IgG, aβ2-GP1 IgG, LA, hs-CRP, IL-6, TNF-α levels in SLE patients with atherosclerosis as compared to the control subjects without it (p<0,0001, p=0,0007, p=0,002, p=0,011, p<0,0001, p=0,00007, respectively). The levels of aCL IgG/IgM, aβ2-GP1 IgG/IgM, LA, IL-6, TNF-α in patients with SLE without atherosclerosis were higher than in the control group, but the levels of inflammatory markers and antibodies under study were lower, than in SLE patients with atherosclerosis. An association between aCL IgG and TNF-α in patients with atherosclerosis was revealed during correlation analysis. We did not find any correlations between aPL and inflammatory markers in SLE patients without atherosclerosis. Selection by traditional and non-traditional risk factors in subjects with atherosclerotic alterations revealed positive correlation between aCL IgG and TNF-α in obesity (r=0,610, p=0,021), in arterial hypertension (r=0,509, p=0,044), in nonsmokers (r=0,587, p=0,013), in the disease duration less than 10 years (r=0,626, p=0,039). Conclusions Thus, we revealed an association between disease duration, disease activity, detected by the degree of increased proinflammatory cytokines (TNF-α) and by the presence of cardiovascular risk factors, which confirms polyetiology of atherosclerotic damage of the vessel wall in patients with SLE. Disclosure of Interest None declared
The article deals with the analysis of literature data, which describe the results of experimental and clinical studies of the efficacy and safety of Aceclofenac (Airtal), as a non-selective nonsteroidal antiinflammatory drug. There are presented data about the administration of Aceclofenac in patients with osteoarthritis, rheumatoid arthritis, ankylosing spondylitis and in patients with acute and chronic pain syndromes.
Background: Clinical evidence suggests that oxidatively modified form of low-density lipoprotein cholesterol (LDL) is more important than native LDL in atherogenesis and vascular damage. The accelerated development of atherosclerosis has been recognized in patients with autoimmune diseases. An autoimmune component of atherogenesis is actually discussed.
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
Summary. Osteoarthritis is currently being mined to a problem that is related to its enormous prevalence, as well as a large number of elderly patients and persons with obesity. Inflammation plays an important role in the implementation of pathogenetic processes in osteoarthritis, so the use of anti-inflammatory drugs is warranted. The article is a literature review of rational choice of anti-inflammatory therapy of osteoarthritis and specifically relates to the using of the aceclofenac. The modern views of efficiency and safety of aceclofenac in osteoarthritis are presented. The chondroprotective properties of aceclofenac are substantiated. Keywords: osteoarthritis, chondroprotection, aceclofenac. О стеоартроз (остеоартрит, ОА) – гетерогенная группа забо-леваний различной этиологии, в основе которых лежит хроническое заболевание суставов с поражением всех компонентов (хряща, субхон-дральной кости, синовиальной обо-лочки, связочного аппарата, капсулы сустава, мышц). Термин ОА введен в клиническую практику вследствие накопления данных, подтверждаю-щих роль воспаления в формирова-нии заболевания. На сегодняшний день ОА являет-ся доминирующей проблемой в рев-матологии, что связано с его огром-ной распространенностью (болеют около 20% населения), а также с большим количеством пожилых па-циентов (после 75 лет клинические признаки ОА выявляются у каждого второго жителя, а рентгенологиче-ские – у 80% населения) и лиц с по-вышенной массой тела. По данным эпидемиологического исследова-ния, в России ОА с преимуществен-