Myocardial fibrosis is considered a key pathological process in the development of cardiovascular diseases. In epicardial obesity (EO), the main cause of fibrosis development is lipotoxic myocardial damage. It is important to detect myocardial fibrosis at an early stage, using non-invasive diagnostic methods. According to the results of echocardiography (ECG), 110 men with general obesity were divided into the following two groups: Group I with epicardial fat thickness (tEAT) ≥ 7 mm (n = 70) and Group II with tEAT < 7 mm (n = 40) without diastolic dysfunction. The levels of metabolic factors, pro-inflammatory cytokines, adipokines, and free fatty acids (FFA), profibrotic markers were determined in both groups. In Group I, the level of interleukin (IL)-6, C-reactive protein, and tumor necrosis factor (TNF)-α increased and that of leptin and adiponectin decreased compared with those in Group II. There was an increase in the level of all studied profibrotic factors in Group I. The level of TNF-α and IL-6 showed a positive correlation with the level of leptin and FFA and a negative correlation with the level of adiponectin. We also observed a relationship between the level of collagen, transforming growth factor (TGF)-β, and metalloproteinase (MMP)-3 and EO. Our results showed that confirmed EO correlates with not only disadipocytosis and increased levels of pro-inflammatory cytokines, but also increased levels of profibrotic factors. This suggests that the studied markers of fibrosis may be used to determine preclinical cardiac fibrosis with lipotoxic myocardial damage in patients with EO.

Extensive use of magnetic resonance imaging (MRI) in clinical practice revolutionized our understanding of the pathogenesis of axis spondyloarthritis (aSpA) and treatment approaches. The use of MRI to diagnose non-radiographic aSpA is well established. At the same time, the possibility of its use for follow-up and treatment assessment is actively discussed.Objective: To present comparative analysis of clinical and laboratory data, reflecting the activity of the disease, and analysis of MRI results in patients with ankylosing spondylitis (AS) receiving biological disease modifying anti-rheumatic drugs therapy (bDMARDs).Patients and methods. The study included 39 patients with AS, mainly men (74.3%), 24 patients (61.5%) had late and 15 (38.5%) – advanced stage of the disease. The average age was 41.0 [34.0; 48.0] years. All patients were administered bDNARDs; inhibitors of the tumor necrosis factor α or inhibitors of interleukin 17 were drug of choice. The median of treatment duration was 1.5 [1.0; 4,5] year. All patients had sacroiliac (SI) and spinal MRI. The activity of the disease was estimated using BASDAI and ASDAS-CRP/ESR indexes, functional disorders – using the BASFI questionnaire. Results and discussion. There was no significant difference in disease activity between patients with osteitis in the SI/spine or without it: BASDAI – 4.7 [2.7; 5,5] and 4.2 [2.9; 8,1], respectively (p=0.533); ASDAS-ESR – 2.6 [2.2; 3,0] and 2.6 [2.2; 3,2], respectively (p=0.725); ASDAS-CRP – 2.5 [2.1; 3,4] and 3.1 [2.8; 3.9], respectively (p=0.172). There was no significant difference in the number of osteitis foci between group of patients who have achieved the therapeutic target (ASDAS < 2.1) and those who have not (ASDAS ≥2.1) – 1.0 [0.0; 3.5] and 1.0 [1.0; 4.0], respectively, (p=0.376), and no difference in amount of inflammatory changes – 1.0 [0.2; 1.7] and 0.1 [0.0; 1,1] cm3, respectively (p=0.124). Conclusion. The data suggests a limited MRI informative value as a method for managing the efficacy of bDMARDs treatment in patients with the advanced / late stage of the AS.

Blockade of interleukin-6 (IL-6) is one of the most promising areas in the treatment of a number of immunoinflammatory diseases. Tocilizumab (TCZ), the first registered anti-IL-6 receptor monoclonal antibody, has been used effectively by rheumatologists since 2010. During this period, the spectrum of adverse reactions (ARs) of TCZ has been clearly defined. However, the multifaceted biological effects of IL-6 determine the probability of unexpected ARs. The article describes a clinical case of drug-induced encephalopathy with cognitive dysfunction during TCZ therapy.

Background. Maintaining of a favourable response of tumour necrosis factor inhibitors is one of the most challenging to rheumatologist. Only limited data have been published addressing this field. The aim of our study was investigate efficacy of etanercept (ETN) and evaluate maintaining response after ETN discontinuation in patients who have achieved remission or low disease activity (REM/LDA) of rheumatoid arthritis (RA). Methods. Patients with high disease activity (n = 29) received ETN 50 mg injection and methotrexate 10-20 mg once weekly were included in analysis. Frequency of REM/LDA scoring by DAS 28-joint counts and C-reactive protein level (DAS28-CRP), changes from baseline in DAS28-CRP, Health Assessment Questionnaire (HAQ), global assessment of disease activity by patient and provider (PtGA and PrGA) were evaluated. We assessed persistent of achieved REM/LDA after the ETN discontinued. Results. We saw fast decreasing of active flare already after first month: HAQ (1.4 ± 0.6 vs 2.0 ± 0.6, p = 0.048), PtGA (49.5 ± 17.9 vs 75.6 ± 14.9, p = 0.016) and PrGA (46.6 ± 14.7 vs 77.0 ± 12.3, p = 0.014). DAS28-CRP changes from baseline become significant after second month (3.9 ± 1.1 vs 6.2 ± 0.6, р = 0.005). After 6 months 82.6% patients had DAS28-CRP < 3.2 and 41.4% patients had HAQ < 0.5. Maintenance of REM/LDA lasted 3 month after ETN discontinuation. Conclusion. ETN+MTX is very effective combination in treat to target strategy of RA treatment. In patients who have achieved REM/LDA maintained stable condition during three months after ETN withdrawn. It might be consider in a number of patients in case of accidental or necessary treatment interruption.

The aim of current study was to compare profiles of T cell subsets in the patients with ankylosing spondylitis (AS) who received different modes of genetically engineered biological therapy (GEBT). The research involved 58 patients aged 20 to 58 years diagnosed with AS and treated with anti-TNFα and antiIL-17 drugs, as well as those receiving common anti-inflammatory therapy. The AS diagnostics was based on the modified New York criteria. Disease activity was assessed by means of nomenclature approved by the Assessment of Spondyloarthritis International Society and Outcome Measures in Rheumatology. 45 healthy people aged 18 to 57 were included into the control group. Peripheral blood T cell subsets were analysed by multicolor flow cytometry. It was found that the T lymphocyte subpopulation profiles in AS patients showed significant differences depending on the therapy type. First, T lymphocyte counts were decreased in AS patients receiving traditional anti-inflammatory therapy, whereas relative numbers of T cells with high levels of effector potential and cytokine secretion were increased. Negative correlations between the levels of effector memory and pre-effector cytotoxic T cells and other laboratory and clinical indexes of inflammatory activity in AS may reflect lower efficiency of traditional therapy. Next, the levels of main T cell subsets in AS patients during antiIL-17 therapy fully corresponded to the control values. However, based on numerous correlations between immunological and clinical laboratory parameters, it was concluded that anti-IL-17 therapy had an inhibitory effect on the joint inflammation activity, while the state of T cell subsets was mainly dependent on standard anti-inflammatory therapy. The most pronounced changes in T cell subsets were found in AS patients during anti-TNFα therapy was associated with decreased effector potential of Th cells and cytotoxic T lymphocytes. At the same time, the lowest frequency of extraskeletal manifestations was found in AS patients treated with anti-TNFα drugs. Finally, the higher efficiency of GEBT, compared with conventional methods of therapy, is determined by the effects upon immune targets of AS pathogenesis which manifested, e.g., by changes in the T lymphocyte subpopulation profile. Moreover, usage of anti-TNFα versus anti-IL-17 inhibitors was associated with greater effect upon phenotypic profile of T cells.