Current recommendations for RA treatment determine the need to reduce the dose and duration of glucocorticoid

(GC) use. This is due to the wide spectrum and high frequency (up to 100%) of serious adverse events (AE) during GC treatment. However, in real practice GCs in RA are used very often (in Russia, Western Europe and the USA they are used in about 50% of patients), and often in long-term courses. This is explained by the fact that the combination of disease-modifying antirheumatic drugs (DMARDs), including biologics (bDMARDs) and Janus kinase inhibitors (JAK), with GCs allows to achieve faster improvement of patients’ condition and therefore is very “convenient” for many patients and physicians.

However, it is very difficult to ensure dose reduction and (especially!) complete discontinuation of GC administration afterwards. Clinical and observational studies show that 30–40% of patients manage to discontinue the use of GCs during treatment with bDMARDs and JAK. In addition, discontinuation of GCs may significantly increase the risk of RA flare, even with complex pathogenetic therapy.

Nevertheless, prolonged use of GCs, including low doses (less than 7.5 mg/day of prednisolone) should be considered as an indicator of the severity of the disease course and inadequacy of the current therapy. Therefore, we should strive for personalization of RA therapy, selection of DMARDs based on the assessment of the disease phenotype and predictors of response to treatment with different drugs, achieving the main goal of therapy – remission/low disease activity and achievement of acceptable quality of life, without the use of GCs.

The article presents an updated version of the definitions of spinal lesions that are observed in patients with axial spondyloarthritis on MRI. It was developed by a special working group ASAS. The aim of the work is to unify the definitions and concepts used in the description of spinal MRI in patients with chronic back pain to improve the diagnosis of axial spondyloarthritis.

Giant cell arteritis (GCA) and polymyalgia rheumatica (RPM) are immune-mediated rheumatic disease (IMRDs), which typically develop in people over 50 years of age. Currently, GCA and PMR are considered within a single complex autoimmune-autoinflammatory pathology, defined as “GCA-PMR spectrum disease”. This was reflected in the development of general recommendations for pharmacotherapy within the framework of the “treat-to-tar get” strategy, although specific approaches to the treatment of patients with GCA and RPM differ depending on the clinical and pathogenetic characteristics of each nosological form. Glucocorticoids (GCs) are central to the treatment of GCA and RPM. Attention is drawn to the paradoxical discrepancy between the high effectiveness of GCs in the short term and the increasing severity of pathology associated with persistent inflammatory activity and the accumulation of organ damage induced by GCs in the long term, which indicates the need to improve therapy, primarily in the direction of optimizing the use of GCs. New opportunities for pharmacotherapy of GCA and RPM (as well as other IMRDs) are associated with the use of biologic agents that block the activity of cytokines involved in the immunopathogenesis of diseases, and in recent years, JAK (Janus kinase) inhibitors. Among pharmacological “targets,” special attention is drawn to interleukin (IL) 6, a pleiotropic cytokine involved in the development of inflammation, immune response, immunometabolism, cancerogenesis, vascular wall remodeling, etc. Currently, several biologic agents have been developed that are specific to both IL-6 receptor and IL-6: humanized monoclonal antibodies (mAbs) to the IL-6 receptor (tocilizumab), and human mAbs to IL-6 receptor (sarilumab and levilimab (BIOCAD)), humanized mAbs to IL-6 olokizumab (R-PHARM), etc. The article summarizes data regarding the effectiveness and safety of tocilizumab in GCA and RPM, recommendations for the use of IL-6 inhibitors in these diseases and discusses the prospects for further research.

Pericarditis is one of the most common forms of inflammatory diseases of the cardiovascular system, diseases that are observed in cardiology, immunology and rheumatology. Anti-inflammatory therapy is the mainstay of treatment for pericarditis. Low recommendations for the diagnosis and treatment of pericarditis for about 10 years, and in 2025, guide their next update. Professor Massimo Imasio, who is a member of the Working Group on Diagnosis and Various Diseases of the Pericardium of the European Society of Cardiology (ESC, European Society of Cardiology) and the Association of Cardiothoracic Surgery (EACTS, European Association of Cardiothoracic Surgery) 2015 and Chairman of the 2025 ESC Working Guidelines on Myocarditis and Pericarditis, gave an interview regarding the most pressing issues in the diagnosis and treatment of pericarditis.

Osteoporosis (OP) is a disease characterized by a decrease in bone strength, leading to an increased risk of fractures. Bone fragility in children may be due to genetic disorders, chronic underlying conditions or taking medications that negatively affect bone metabolism. The article considers the modern classification of OP in children, approaches to its diagnosis, the role of dual-energy X-ray absorptiometry for diagnosis.

The main goal of OP prevention and treatment is to achieve a higher peak of bone mass, improve bone microarchitectonics, and, as in adults, reduce the risk of fractures, prevent skeletal deformities, improve mobility, independence and quality of life. Recommendations for lifestyle changes are presented, including adequate calcium intake and vitamin D, taking antiresorptive drugs, as well as prospective management of children with OP.

The second part of the review presents current data on the treatment strategy for lupus nephritis, considering the morphological class of kidney damage, course and activity. Approaches to monitoring and evaluating the effectiveness of treatment, the problems of achieving a complete and partial renal response are described. The characteristic of classical and innovative methods of therapy is given.

The treatment of systemic lupus erythematosus with juvenile onset (jSLE) remains a difficult task, taking into account the more aggressive course of the disease, requiring the appointment of various therapy regimens, including mainly a combination of high doses of glucocorticoids (GC) with immunosuppressive drugs, which on the one hand improves control by the course of the disease, but on the other hand leads to an increase in serious adverse effects from therapy. Modern therapy capabilities have improved significantly with the advent of the belimumab – first and alone registered biologics for children with SLE.

The aim of the study – based on an open single-center retrospective study, to analyze the efficacy and safety of belimumab in children with SLE.

Material and methods. The study included all patients with jSLE who were observed in the pediatric department of V.A. Na sonova Research Institute of Rheumatology and received at least 1 infusion of belimumab. Diagnosis of SLE based on 2012 SLICC (Systemic Lupus Erythematosus International Collaborating Clinics) criteria. The efficacy of therapy was evaluated among patients who received belimumab for 6 months or more, and safety in all who received at least 1 infusion.

Results. The study included 31 patients, 24 girls/7 boys. The median (Me) age at onset of the disease was 12.6 [10.18; 13.5] years, the Me duration of the disease at the time of initiation of belimumab therapy was 2.15 [0.9; 4.4] years. The Me activity on the SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) at the time of diagnosis verification was 12 [9; 17.5], at the time of start of belimumab – 8 [6; 12], 35.5% patients had severe activity, 51.6% – moderate, 12.9% – mild activity. The dose of GC per os at start of belimumab was 15 [10; 21.25] mg/day, 32.26% of patients received a high dose of GC, 54.84% – moderate dose, 12.9% – low dose. 9 patients had SDI (Systemic Lupus International Collaborating Clinics Damage Index) ≥1, Me – 1 [1; 2]. After 6 months of therapy, the Me of disease activity according to SLEDAI was 4 [2; 6], the dose of GC per os was reduced to 10 [8.25; 17.5] mg/day. In 15 patients, a decrease in antiDNA was recorded (57.7% of those who initially had elevated values of antiDNA), in 9 the level of complement was normalized (50% of those who initially had hypocomplementemia). After 12 months of therapy, the Me of SLEDAI was 4 [2; 4] (p=0.034), the dose of GC per os was 5 [5; 8.125] mg/day (p=0.012). 5 patients completed therapy within 12 months or more: 1 patient – remission, 4 patients – secondary inefficiency. Belimumab treatment was well tolerated, with the exception of three cases of serious adverse reactions (9.7%): prolonged diarrheal syndrome (after the 1st infusion), Lyell’s syndrome (after the 2nd infusion), infusion reaction (during the 2^nd infusion). During the therapy of belimumab, no new damage were recorded; in 2 patients there was a decrease in the SDI.

Conclusion. Belimumab therapy in patients with jSLE demonstrated high efficacy with a decrease in the activity of the disease according to SLEDAI, normalization of antiDNA and complement, the possibility of a significant reduction the dose of GC, the absence of progression of the SDI with a good safety profile in the vast majority of patients.

The aim – to evaluate subpopulations of B lymphocytes and features of interferon (IFN) status in patients with systemic lupus erythematosus (SLE), to clarify the relationship of immunological parameters with clinical manifestations of the disease

Material and methods. 139 patients (123 (88%) women and 16 (12%) men) with a definite diagnosis of SLE were included in the analysis. The disease duration was 3.0 [0.3; 12.0] years, SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) – 7 [4; 11] points, SDI (Systemic Lupus International Collaborating Clinics Damage Index) – 0 [0; 1] points. Immunophenotyping of peripheral blood lymphocytes, including determination of B cells, the general population of memory B cells, non-switched and switched memory B cells, naive, transient B cells, and plasmablasts was carried out using multicolor flow cytometry. IFN status was assessed by the expression of IFN-stimulated genes (MX1, RSAD2, EPSTI1) using real-time polymerase chain reaction

Results. Two immunological “patterns” were identified – the prevailing immunological mechanism of the pathogenesis of the disease – SLE – with predominant activation of type I IFN and with predominant activation of the B cell component of the immune system. The immunological phenotype with activation of type I IFN was associated with high immunological activity, predominant skin damage, leukopenia, and the phenotype with predominant activation of the B cell link was associated with damage to the kidneys and nervous system.

Conclusion. The results of the work suggest a wide variety of immune mechanisms underlying the pathogenesis of SLE. It is possible to identify a number of leading molecular “patterns” of the pathogenesis of the disease, which must be taken into account to select an effective “targeted” drug.

The aim of the study was to determine the clinical and diagnostic value of interleukin (IL) 17A, IL-17F and IL-23 in rheumatoid arthritis (RA) patients in the advanced stage of the disease.

Materials and methods. We examined 154 patients with a reliable diagnosis of RA according to ACR/EULAR (American College of Rheumatology/European Alliance of Associations for Rheumatology) criteria (2010), predominantly (73.4%) female, middle-aged (56.0 (50.0; 64.0) years), disease duration of 9.4 (3.0; 13.0) years, radiologic stages II (34.4%) and III (37.0%), and moderate to high activity (DAS28-ESR – 5.40 (4.65; 6.00). 83.8% of patients were seropositive for IgM rheumatoid factor (IgM RF) and 68.8% had antibodies to cyclic citrullinated peptide (ACCP). 144 (93.5%) patients were taking DMARDs (methotrexate, leflunamide, sulfasalazine) as well as nonsteroidal antiinflammatory drugs (NSAIDs) and glucocorticoids (GCs) up to 10 mg/day in terms of prednisolone.

The serum levels of IL-17A, IL-17F and IL-23 were investigated using multiplex xMAR technology. The upper limit of norm (M+3σ) in 20 sera of healthy donors was 1.78 pg/mL for IL-17A, 9.5 pg/mL for IL-17F and 91.55 pg/mL for IL-23.

Results. IL-17A (1.16 (0.50; 2.39) pg/mL) and IL-17F (5.02 (1.00; 138.80) pg/mL) concentrations in RA patients were not significantly different from controls (0.78 (0.00; 1.65) and 4.02 (1.46; 7.31) pg/mL; p>0.05). In contrast, IL-23 levels were significantly higher in patients than in donors (21.36 (2.50; 4626.22) and 14.63 (0.00; 91.55) pg/mL; p<0.05).

High values of IL-17F (71 patients – 46.1%) and IL-23 (66 patients – 42.9%) were significantly more frequently detected than IL-17A (46 patients – 29.9%; p=0.003 and p=0.02, respectively). Hyperproduction of IL-17A and IL-17F was simultaneously observed in 37 (24.0%) patients, and 32 (20.8%) patients had an increase in IL-17A, IL-17F and IL-23. Correlations between IL-17A and IL-17F concentration (r=0.44; p<0.05), IL-17A and IL-23 (r=0.40; p<0.05), IL-17F and IL-23 (r=0.94; p<0.05) were found.

No statistically significant differences were observed between the concentration of IL-17A, IL-17F, IL-23 and the frequency of their elevation in RA patients positive or negative for IgM RF, as well as ACCP.

When IL-17A level was elevated, CDAI (Clinical Disease Activity Index) and SDAI (Simplified Disease Activity Index) indices and IgM RF concentration were significantly higher than in the comparison group (p<0.05). In patients with IL-17F hyperproduction predominance of ESR and C-reactive protein values was revealed in comparison with normal values of this index (p<0,05). At the same time, IL-17A concentration correlated with SDAI (r=0,17; p<0,05), IgM RF values (r=0,19; p<0,05) and ACCP (r=0,19; p<0,05). When IL-23 values were high, the HR was significantly lower 28 (p<0.05), and the groups did not differ in other measures of disease activity, IgM RF and ACCP. No differences in clinical and laboratory indicators of RA activity were found between patients with simultaneous elevation of one, two or three cytokines and groups of patients with their normal concentrations.

In RA patients in the advanced stage of the disease, IL-17F hyperproduction prevails over the frequency of IL-17A elevation. The concentration of IL-23 in serum is significantly higher in patients with RA compared to the control group, and its high values are found in 42.7% of patients. The combined hyperproduction of IL-17A and IL-17F; IL-17A, IL-17F and IL-23 does not increase the proinflammatory potential of each individual cytokine.

Thrombotic antiphospholipid syndrome (APS) is a condition affecting young people in whom a thromboembolic event occurs in the presence of circulating antiphospholipid antibodies (aPL).

The aim of this study was the evaluation of the incidence of recurrent thrombosis and its risk factors in antiphospholipid syndrome.

Material and methods. The retrospective study included 98 patients with aPL who were followed up at the institute from 2014 to 2023, of whom 66 (67%) were women and 32 (33%) were men. Of the 98 patients with aPL, 48 (49%) had a diagnosis of systemic lupus erythematosus (SLE). Antiphospholipid antibodies (aPL), including antibodies to cardiolipin (IgG/IgM aCL), antibodies to ß2-glycoprotein 1 (IgG/IgM aß2GP1), antibodies to ß2-glycoprotein IgG against domain 1 (IgG aß2GP1-D1), antibodies to phosphatidylserine/prothrombin complex (IgG/ IgM aPS/PT) and other thrombotic risk factors. aPL was assessed by enzyme-linked immunosorbent assay (ELISA) and chemoluminescence assay (CHLA).

Results. Thrombosis recurrence was reported in 62 (63%) of 98 patients, and 36 (35%) did not. The main cause of recurrent thrombosis was treatment with direct oral anticoagulants (DOACs). 24 (38.7%) of 62 patients with recurrent thrombosis were treated with DOACs, the duration of which ranged from 6 to 24 months. The next most common cause of recurrent thrombosis was the lack of continuous anticoagulant therapy in 20 (32.5%) of the patients. In 17 (27.4%) of the patients, the recurrence occurred while they were still taking warfarin. In 10 (41.7%) of the 24 patients, the recurrent thrombosis was arterial in origin. This was associated with recurrent cerebral circulation problems. The level of positivity did not matter, but all had triple IgG aPL positivity. 5 had lupus anticoagulant (LA) at the onset of the disease before anticoagulant use. IgG aPS/PT was most important in association with recurring thrombosis in the ELISA: 45 (72.6%) of 62 patients with recurring thrombosis were positive for IgG aPS/PT, compared with 19 (52.8%) of 36 patients without recurring thrombosis. The detection of all aPL was more frequent in CHMA than in ELISA. However, the definition of aPL in ELISA is recommended according to the latest classification criteria. Triple IgG positivity for aCL of IgG aß2GP1, IgG aß2GP1-D1 and CHMA remained a risk factor for recurrent thrombosis and increased the risk of recurrence more than threefold. Obesity was a risk factor for recurrent thrombosis, with a 5-fold increased risk of recurrent thrombosis in obese compared to non-obese patients (p=0.01).

Conclusions. Recurrent thrombosis in APS is largely associated with IgG aCL, IgG aß2GP1, IgG aß2GP1-D1, IgG aPS/PT. Triple IgG aPL positivity in any combination significantly increased recurrent thrombosis risk.

The presence of any type of aPL IgG in both ELISA and CHLA influenced the recurrence rate of thrombosis in APS.

Obesity was a significant risk factor for recurrent thrombosis.

Introduction. Syndesmophyte, which is the hallmark of ankylosing spondylitis (AS), is a vertically oriented ossification located outside the fibrous ring of the intervertebral disc. In recent decades, the most widespread theory is that after inflammation in the area of attachment of the fibrous ring to the vertebral body, fatty degeneration occurs with reparative processes, as a result of which the growth of new bone – syndesmophyte – begins. It is believed that the likelihood of developing syndesmophyte is two to three times higher in the angles of those vertebrae in which active inflammation or fatty changes were detected on magnetic resonance tomography (MRI) in the previous 2 years, the latter having a stronger association with subsequent pathological bone formation. However, this relationship is ambiguous according to different studies.

The aim – comparison of the exact localization of magnetic resonance tomography and computed tomography (CT) signs of lesions on the vertebral endplates, characteristic of axial spondyloarthritis, in patients with ankylosing spondylitis.

Material and methods. The cross-sectional study included 10 patients with AS who met the inclusion criteria.

All patients underwent a standard examination for AS, as well as MRI and CT examination of the lumbar spine.

A special technique for joint assessment of changes detected during MRI and CT examination has been developed.

For the primary analysis, changes found on the upper endplates of 5 lumbar vertebrae were taken.

Results. On the upper endplates of 5 lumbar vertebrae, a CT examination revealed 35 syndesmophytes (from 1 to 7 syndesmophytes in 1 patient), and MRI revealed 9 foci of acute inflammation and 24 of chronic inflammation (fatty degeneration). When jointly analyzing the MRI foci of detectable inflammation and syndesmophytes transferred to the vertebral diagram, it turned out that in the majority of cases (68%), the latter were not associated with sites of active and/or chronic inflammation. Correlation analysis showed a certain direct relationship only between the number of syndesmophytes and foci of chronic inflammation (r=0.68).

Discussion. Preliminary data show that the proposed method for comparing MRI and CT lesions in AS allows us to jointly study the localization of MRI and CT spinal injuries in patients with AS using multidirectional sections. The first results of our one-time study showed that in most cases the localization of developing syndesmophytes does not coincide with the foci of inflammation detected by MRI (both acute and chronic).

The aim of the study – to identify the factors associated with the development of chronic post-traumatic pain (CPTP) in patients with knee joint (KJ) injury.

Materials and methods. The study group consisted of 136 patients (51.5% women, age 38.7±12.4 years) who suffered a KJ injury with damage to the anterior cruciate ligament and/or menisci. The inclusion criterion was the presence of pain in KJ ≥4 on a numerical rating scale (NRS 0–10) for at least 1 month after injury. Surgical intervention (plastic surgery of the anterior cruciate ligament, meniscus suture, meniscus resection, combined operations) was performed immediately after injury in 48.5% of patients. The incidence of CPTP was assessed (persistence of pain during movement ≥4 on NRS after 3 and 6 months of follow-up) and factors related to the development of CPTP. All patients were recommended to use orthoses of KJ, physical therapy and taking nonsteroidal anti-inflammatory drugs in the “on-demand” mode. Results. CPTP was detected after 3 months in 33.1%, and after 6 months in 32.4% of patients. Surgical treatment did not affect the development of CPTP: odds ratio (OR) – 1.241, 95% confidence interval (95% CI): 0.775–1.986 (p=0.474). The risk of CPTP after 6 months was statistically significantly higher in women, persons with a high body mass index (≥30 kg/m²), initially severe pain (≥7 on NRS), in the presence of initial signs of depression and anxiety (HADS (Hospital Anxiety and Depression Scale) ≥8) and highly probable central sensitization (CSI (Central Sensitization Inventory) ≥40): OR=2,152, 95% CI: 1,383–3,348 (p=0,002); OR=1,243, 95% CI: 1,054–1,465 (p=0,05); OR=3,567, 95% CI: 1,717–5,708 (p=0,001); OR=2,330, 95% CI: 1,070–5,726 (p=0.0044); OR=2,446, 95% CI: 1,220–4,905 (p=0,016); OR=2,584, 95% CI: 1,101–8,133 (p=0.043), respectively.

Glucocorticoids are the basis for the treatment of giant cell arteritis (GCA) and polymyalgia rheumatica (PMR), however, their long-term use is associated with a number of well-known side effects. Despite the fact that a significant number of patients with these diseases require long-term treatment, approaches to long-term therapy remain insufficiently developed. The role of traditional anti-inflammatory drugs remains uncertain due to insufficient efficacy and inconclusive evidence base. A possible solution of this problem is the use of biological agents, in particular, affecting the interleukin (IL-6) axis. This series of clinical observations presents the experience of using the IL-6 inhibitor olokizumab in the treatment of GCA and PMR. The data obtained are consistent with the positive international experience of using drugs of this group and demonstrate both efficiency of disease activity control and a pronounced steroid-sparring effect. Olokizumab is a promising drug for the treatment of GCA and PMR.

Anti-Ku antibodies are a special type of myositis-associated antibodies that are characteristic of patients with the overlap syndrome of systemic scleroderma and immune-inflammatory myopathy, as well as occurring in other autoimmune diseases. Patients with these antibodies have their own clinical and laboratory features of the disease and can be identified as a separate anti-Ku syndrome.

For the first time in the domestic literature, descriptions of two clinical cases of the development of a cross syndrome associated with anti-Ku antibodies are presented. The features of the course of the disease and the response to various options for immunosuppressive therapy were analyzed.