Epstein–Barr virus is a highly prevalent human herpesvirus type 4, infecting more than 90% of the world’s population. Its role in the development of rheumatic diseases is actively being investigated. This article presents an analysis of key  aspects of this association based on current research.

Objective: to study the structure of use of biologic disease-modifying antirheumatic drugs (bDMARDs) and selective immunosuppressants (SIs) in immune-mediated inflammatory rheumatic diseases (IMIRDs) in the Russian Federation (RF), as well as an analysis of the key barriers to ensuring access to bDMARDs and SIs.
Material and methods. Analysis of the results of monitoring statistical data on the use of bDMARDs and SIs in IMIRDs for 2023–2024, provided by chief external rheumatology specialists of the constituent entities of the RF.
Results and discussion. It was found that in 78 regions of the RF, bDMARD and SI therapy across all funding channels covered 47.02 thousand patients with IMIRDs (33.1 patients per 100 thousand population). The frequency of use of these drugs differs in the structure of both international nonproprietary names (INN) and nosologies, as well as in regional prescribing specifics and funding channels. In the constituent entities of the RF, the maximum and minimum values of the indicator “Provision of bDMARDs and SIs per 100 thousand population, patients” differed 15-fold. Provision of bDMARDs and SIs per 100 thousand population above the nationwide level was identified in 34 regions, whereas in 44 regions it was below. Substantial regional differences in approaches to drug provision (DP) were noted: in 37 regions of the RF, financing from budget funds predominated (average level of funding via this channel was 91%). The compulsory medical insurance (CMI) system was actively used only in 12 constituent entities, whereas in 29 mixed financing of DP prevailed.
Conclusion. A positive trend is observed toward an increase in the number of patients with IMIRDs receiving bDMARDs and SIs. However, substantial regional differences in approaches to DP were demonstrated, which creates barriers to the rational use of innovative therapy. Management decisions aimed at increasing access to bDMARDs and SIs in the treatment of IMIRDs are needed.

Objective: to perform a comparative analysis of the imaging characteristics of axial psoriatic arthritis (axPsA) and other variants (ov) of axial spondyloarthritis (axSpA) at the early stage (ESt) and the advanced stage (ASt) of the disease.
Material and methods. A total of 222 patients were examined: 108 with ov-axSpA (Group 1) and 114 with axPsA (Group 2). Group 1 included patients meeting the criteria for axSpA or ankylosing spondylitis; Group 2 included patients with psoriatic arthritis meeting the CASPAR criteria and having axial involvement. Axial involvement was confirmed by the presence of radiographically definite sacroiliitis (SI; bilateral grade II or unilateral grade III), or active SI detected by magnetic resonance imaging, or by the presence of 1 syndesmophyte in the cervical spine (C-spine) and/or lumbar spine (L-spine). Syndesmophytes were assessed as symmetric and asymmetric, bridging and non-bridging, thin (disc-like) and bulky (non-disc-like), solitary and multiple. The severity of radiographic changes in the spine was assessed using the modified mSASSS score. Each group of patients was divided into two subgroups: those with inflammatory back pain (IBP)/chronic back pain (CBP) duration 24 months (ESt) and those with IBP/CBP duration >24 months (ASt).
Results and discussion. ESt was observed in 25 and ASt in 83 patients with ov-axSpA. In ASt, syndesmophytes were more common than in Est both in the C-spine (p=0.007) and in the L-spine (p=0.035); in ASt thin disc-like syndesmophytes were also more frequent (p=0.021) and more structural changes in the spine overall were noted (p=0.001), and higher mSASSS scores were observed (p=0.001). No significant differences in sacroiliac joint (SIJ) changes were found depending on disease stage. In axPsA, ESt was identified in 37 and ASt in 77 patients. In patients with axPsA, no differences were found between ESt and ASt in the frequency of spine and SIJ changes (for any parameter).
Conclusion. It can be assumed that the differences between the groups in the progression of structural changes in the spine are associated with different mechanisms of new bone formation in axPsA and ov-axSpA.

An altered distribution of peripheral B cells is a marker of B cell hyperactivation in Sjögren’s disease (SjD).
Objective: to determine the relationship between the levels of various peripheral blood B lymphocyte subpopulations and the clinical and laboratory manifestations of SjD.
Material and methods. The study included 103 patients with SjD (main group) and 31 healthy donors (control group). The diagnosis of SjD was established based on the 2016 ACR/EULAR criteria; all patients underwent a complete clinical and laboratory examination. B lymphocyte subpopulations were analyzed by flow cytometry. The following were assessed: CD19+ B cells, CD19+CD27+ memory B cells, memory B cells with an unswitched immunoglobulin phenotype (“unswitched”, CD19+IgD+CD27+), memory B cells with a switched immunoglobulin phenotype (“switched”, CD19+IgD-CD27+), naive B cells (CD19+IgD+CD27-), double-negative memory B cells (CD19+IgD-CD27-), transitional B cells (CD19+IgD+CD10+CD38+), plasmablasts (CD19+CD38+++IgD-CD27+), and plasma cells (CD19+CD38+). Statistical analysis was performed using GraphPad Prism 8.
Results and discussion. Compared with healthy donors, patients with SjD showed a decrease in the number of CD19+ B cells (p=0.0089) and CD27+ memory cells (p=0.018), and an increase in the number of plasmablasts (p<0.0001). Correlation analysis demonstrated an association of IgG levels with increased plasmablast counts (r=0.76, p=0.0038) and plasma cell counts (r=0.81, p=0.0001), as well as an inverse correlation with the number of memory B cells (r=-0.72, p=0.006). Patients with elevated IgG concentrations (>16 mg/L) had a higher number of naïve B cells (p=0.0047) and a lower number of “switched” memory cells (p=0.009). Glucocorticoid therapy was associated with a decrease in the number of naive B cells (p=0.0066) and plasmablasts (p=0.0296), but an increase in the number of “switched” memory cells (p=0.0002). In patients with systemic manifestations (vasculitis, interstitial lung disease), an increase in the number of double-negative memory B cells was detected (p=0.028).
Conclusion. The obtained data highlight the altered distribution of B-lymphocytes in SjD and their potential for patient stratification and selection of optimal therapy.

Objective: to assess the association between an ability to work (AW) and disease activity in patients with psoriatic arthritis (PsA) combined with spinal involvement.
Material and methods. The study included 114 patients with PsA (50.8% men and 49.2% women) who met the 2006 CASPAR criteria (ClASsification criteria for Psoriatic ARthritis) and had spinal involvement confirmed by imaging of axial structures (syndesmophytes and/or radiographically definite sacroiliitis (SI) and/or active SI on magnetic resonance imaging). The mean age of the patients was 46.1±11.6 years; PsA duration was 48.6±41.5 months, psoriasis duration – 197.9±159.7 months, and chronic back pain duration – 67.5±63 months. All patients underwent a standard rheumatologic assessment, including tender and swollen joint counts (TJC/68 and SJC/66, respectively), physician/patient global assessment of health (PhGA/PtGA), and assessment of pain intensity using a visual analog scale; night back pain (NBP) using a numeric rating scale; blood CRP level; and the activity indices BASDAI (Bath Ankylosing Spondylitis Disease Activity Index), DAPSA (Disease Activity in Psoriatic Arthritis), and ASDAS (Ankylosing Spondylitis Disease Activity Score). AW was assessed using the WPAI-SHP (Work Productivity and Activity Impairment; Specific Heath Problem) questionnaire on the scales of absenteeism, presenteeism, overall work productivity loss (OWPL), and activity impairment (AI). Additionally, the proportion of patients (%) with an overall reduction in AW across all scales >50% (ORAW50) was evaluated.
Results and discussion. Absenteeism, presenteeism, OWPL, and AI were identified in 44.6%, 49.7%, 55.6%, and 43.1% of patients, respectively. ORAW50 was observed in 57.8% (66 of 114) of patients. A significant positive correlation was found between impaired AW across all WPAI scales (p<0.05) and female sex and PsA activity: SJC66 >5, DAPSA ≥14, ASDAS ≥2.1, and BASDAI ≥4. Factors contributing to ORAW50 were identified: presence of ≥1 enthesitis (odds ratio (OR) 1.72; 95% confidence interval (CI) 0.745–3.714), DAPSA ≥14 (OR 1.814; 95% CI 0.486–6.158), ASDAS ≥2.1 (OR 1.296; 95% CI 0.6877–2.444), for all cases p<0.05. In patients with high ASDAS activity, impairment was noted on all WPAI scales except OWPL. DAPSA activity affected absenteeism (p=0.04) and AI (p=0.01). High BASDAI activity statistically significantly worsened all WPAI outcomes. Separately, factors associated with impaired AW and high ASDAS activity were identified: inflammatory back pain (IBP; OR 5.285; 95% CI 0.373–6.836), enthesitis by the LEI index ≥1 (OR 2.268; 95% CI 0.479–10.733), and SJC >5 (OR 1.037; 95% CI 0.243–4.418). Impaired AW with high DAPSA activity was associated with significant factors such as SJC >5 (OR 1.145; 95% CI 0.27–4.85), TJC >5 (OR 1.789; 95% CI 0.405–7.905), presence of enthesitis by LEI ≥1 (OR 2.683; 95% CI 0.633–11.377), and CRP >5 mg/L (OR 1.007; 95% CI 0.978–1.036). Impaired AW and high BASDAI activity were associated with TJC >5 (OR 1.489; 95% CI 0.322–6.895), presence of enthesitis by LEI ≥1 (OR 2.33; 95% CI 0.524–10.363), IBP (OR 20.11; 95% CI 11.128–36.45), and NBP (OR 1.435; 95% CI 0.344–5.984).
Conclusion. In half of patients with PsA and spinal involvement, predominantly women, reduced AW was found on the absenteeism, presenteeism, OWPL, and AI scales, which was associated with high activity of spondylitis and peripheral arthritis. The use of biologic disease-modifying agents makes it possible to reduce PsA activity and improve patients’ AW, which may have major socio-economic significance.

Interleukin (IL)-6 is a key mediator in the pathogenesis of rheumatoid arthritis (RA). Olokizumab (OKZ, Artlegia®, R-Pharm) is a direct IL-6 inhibitor whose efficacy has been demonstrated in randomized controlled trials, post-marketing studies, and real-world practice. However, different dosing regimens of OKZ and their impact on its usage frequency, as well as on doses of glucocorticoids (GCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), have been insufficiently studied.
Objective: to evaluate the efficacy and safety of OKZ in routine clinical practice, with emphasis on the use of different dosing regimens and concomitant use of GCs and NSAIDs in patients with RA.
Material and methods. In a multicenter retrospective observational program included patients in whom OKZ therapy was initiated in real-world clinical practice from 01.12.2023 to 30.11.2024 with subsequent 12-month follow-up. A total of 1240 adult patients with active RA meeting the 2010 ACR/EULAR criteria were enrolled. Of these, 80.5% were women; median age was 55 years; median RA duration was 87 months; 86.5% of patients were rheumatoid factor positive, 82.7% were positive for anti-cyclic citrullinated peptide antibodies; a high comorbidity burden was noted. Patients with incomplete DAS28-CRP/CDAI data or follow-up <3 months were excluded from the efficacy analysis. Assessments were performed at baseline and at 3, 6, and 12 months.
Results and discussion. At baseline, 89.4% of patients had high/moderate RA activity according to DAS28-CRP. OKZ was prescribed once every 4 weeks in 89.8% of cases; in patients with higher laboratory activity, once every 2 weeks in 10.2% (p<0.01). A marked positive response with achievement of remission/low disease activity according to DAS28-CRP by month 12 was observed in 78.4% of cases. The proportion of patients receiving GCs decreased from 51.3% to 15.7%; median daily GCs dose decreased from 7.5 to 5.0 mg (p<0.05); the proportion of patients continuously using NSAIDs decreased from 32.8% to 1.9%. Adverse events (AEs) were reported in 9.0% of patients (OKZ was discontinued in 4.5%); no new AEs were identified.
Conclusion. In the vast majority of cases, OKZ is used at a dose of 64 mg once every 4 weeks, providing achievement of therapeutic targets in real-world clinical practice in most patients (by month 12 – in 78.4%). In our observation trial the proportion of patients who require every 2 week administration was insignificant and included no more than 3% over 12 months of therapy. Therapy is accompanied by a significant reduction in the need for GCs and NSAIDs.

The likelihood of occurrence and progression of cardiovascular diseases (CVD) and the risk of death from them is increased in patients with rheumatoid arthritis (RA) in the presence of risk factors compared with the general population.
Objective: comparative study of the characteristics of RA pharmacotherapy in patients with and without CVD.
Material and methods. The analysis included 1074 RA patients who were divided into three groups. Group A included patients with CVD (n=551, 48.7%), Group B included those without CVD (n=523, 51.3%), and Group C included patients from Group B comparable in age and RA duration to patients from Group A (n=241, 22.4%). Based on medical records, a patient “medication chart” was compiled; the presence of adverse reactions and concomitant diseases was assessed. The CIRS index was used to determine the profile and severity of comorbid conditions.
Results and discussion. Patients in Group A compared with those in Group B were older (57.8±11.2 years; p<0.0001), included more men (odds ratio, OR 1.7; 95% confidence interval, CI 1.2–2.4; p=0.001), and had a longer RA duration (median 11 [5; 19] years; p=0.0003). The CIRS multimorbidity index in Group A was higher than in Group C (p<0.0001), while the severity index was comparable. The structure and duration of prior foundational therapy did not differ between the groups; at the time of analysis, patients in Group A significantly more often did not receive conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) compared with patients in Group B (OR 1.4; 95% CI 1–1.8; p=0.04), but no significant differences were found between Groups A and C for this parameter (p>0.05). The frequency and duration of glucocorticoid (GC) use in Groups A and C also did not differ significantly. There were no differences between the groups in the frequency of use of biologic DMARDs (bDMARDs) and targeted csDMARDs; however, in patients with CVD, initiation of such therapy occurred at an older age than in Groups B (p<0.0001) and C (p=0.002). The duration of interleukin-6 inhibitor (IL-6i) use in Group A was shorter than in Groups B (p=0.0007) and C (p=0.004). A history of tumor necrosis factor á inhibitor inefficacy in Group A was less common than in Group C (OR 0.3; 95% CI 0.1–0.8; p=0.005).
Conclusion. Therapy with the main groups of antirheumatic drugs was carried out predominantly in accordance with existing recommendations. Undesirable trends were also identified: frequent use of leflunomide, later initiation of bDMARD therapy, and an unjustifiably shorter duration of IL-6i use in patients with CVD. No reliable data on the association of GC and nonsteroidal anti-inflammatory drugs with CVD were obtained in our study.

In the last decade, an interest has increased in autoinflammatory diseases (AIDs) associated with a mutation in a specific gene, while the pathogenetic significance of the identified genetic variants continues to be clarified.
Objective: to study the frequency and spectrum of genetic variants identified by molecular genetic testing (MGT) and the clinical features in patients with suspected monogenic AIDs (mAIDs).
Material and methods. MGT of target genes was performed in 115 patients with suspected mAIDs (median age 10 [5; 14] years; male-to-female ratio 1:1.1) using massively parallel sequencing (in 89% of cases, a 65-gene panel was used).
Results and discussion. The patients were divided into two groups. Group 1 included 44 (38%) patients with identified genetic variants, and Group 2 included 71 patients with genetically negative MGT results. Thirty-six monogenic variants were identified (11 in the MEFV gene, 5 in NOD2, 4 in NLRP3, 3 in TNFRSF1A, 2 each in MVK, RAG1, NLRP1, ADA2, and 1 each in IFIH1, NLRP12, UNC13D, RIPK1, IL36RN), as well as 8 digenic/oligogenic combinations (2 in MEFV/TNFRSF1A; 1 each in MEFV/MVK/TNFAIP3, MEFV/NOD2/PSTPIP1, NOD2/MEFV, IL36RN/STX11, MEFV/NLRP12, SH2D1A/TNFAIP3). In both groups, the most common were: fever (in 89% and 88% of cases), skin involvement (59% and 47%), arthralgia (61% and 45%), arthritis (36% and 25%), gastrointestinal symptoms (34% and 37%), and lymphadenopathy (28% and 35%), hyperproduction of autoantibodies was detected in 15% and 27% of cases, respectively. Differences between the groups for these parameters were not statistically significant. Chest pain was observed significantly more often in Group 1 than in Group 2 (14% vs 1%, respectively; p=0.008).
Conclusion. MGT identified mutations in 38% of patients with suspected mAIDs. Genetic variants from the group of major monogenic AIDs (FMF, TRAPS, CAPS, HIDS/MKD) were most common. When clinical and laboratory data were compared between the groups with positive and negative MGT results, no substantial differences were found. Patients with negative MGT results who meet AIDs criteria require extended evaluation, including whole-exome/whole-genome sequencing.

Fibrodysplasia ossificans progressiva (FOP) is an ultra-rare monogenic disease manifested by an uncontrolled process of generalized heterotopic ossification. The first and only drug that has demonstrated in clinical trials the ability to slow the growth of new ossifications is palovarotene (PVT), a selective agonist of the gamma subtype of the retinoic acid receptor (RARã), which has been approved for the treatment of FOP in certain age groups in several countries. Published real-world data on its use are limited.
Objective: to analyze the experience of using PVT in FOP in real-world Russian clinical practice, with an emphasis on detailed patients’ characteristics description and assessment of treatment efficacy and safety.
Material and methods. Nineteen patients with severe FOP (mean age 12.4 years; 14 patients younger than 14 years) who met the selection criteria were chosen for PVT therapy. Progression of the total volume of heterotopic ossifications (HO) was assessed using low-dose whole-body computed tomography (LDCT). The number of flare-ups before and during therapy was analyzed. Functional status was assessed using the CAJIS and CHAQ scales. Adverse events (AEs) occurring during treatment were recorded.
Results and discussion. All 19 patients with FOP had the classic disease phenotype with a pathogenic variant of the ACVR1 gene. Of these, 15 are currently receiving PVT in the ongoing regimen in combination with the Janus kinase inhibitor tofacitinib (TOFA); in 8 of these patients, treatment duration exceeds 1 year (median 18 months). Another 4 patients are awaiting access to the drug. According to serial LDCT examinations with a 12-month interval, no substantial increase in the total HO volume was detected. No deterioration in functional status was observed during therapy. No serious AEs were recorded. In 14 of 15 patients, mucocutaneous AEs (dryness, pruritus, retinoid dermatitis) of varying severity were observed.
Conclusion. Preliminary analysis of PVT use in patients with FOP showed no significant progression of HO and, at the same time, a favorable safety profile. Complementarity of the pathogenetic effects of PVT and TOFA may become a new therapeutic strategy for FOP.

Nervous system (NS) involvement in systemic lupus erythematosus (SLE) comprises a heterogeneous spectrum of neurological and psychiatric syndromes and represents one of the most severe disease manifestations, associated with a high risk of mortality.
Objective: to identify clinical characteristics and prognostic factors associated with neuropsychiatric manifestations of SLE (npSLE) in patients of the Kyrgyz population.
Material and methods. The study included 800 patients with a confirmed diagnosis of SLE who were followed at the clinic of the National Center of Cardiology and Therapy named after Academician Mirsaid Mirrakhimov from January 2012 to December 2024. Diagnosis of npSLE was performed according to the modified ACR 2001 classification criteria. Neurophysiological evaluation included electroencephalography, echoencephalography, and electroneuromyography. Structural neuroimaging of the brain was performed using magnetic resonance imaging and/or computed tomography.
Results and discussion. The prevalence of npSLE in the Kyrgyz cohort was 41%. Patients with npSLE were characterized by a higher frequency of acute disease course (41.2%; p=0.006), very high disease activity (p=0.0001), and irreversible organ damage (damage index >0 identified in 27.4% of cases; p<0.001). Severe depression (18.5%), polyneuropathy (7.5%), and psychosis (6.6%) were the most common npSLE manifestations. Independent predictors of npSLE development included high SLE activity, acute disease course, active lupus nephritis, respiratory system involvement, severe pulmonary arterial hypertension, fever, serositis, high damage index values, and C4 hypocomplementemia.
Conclusion. npSLE were identified in 41% of patients in the Kyrgyz cohort and represented the one of the first manifestations of the disease in 40% of cases, which may complicate the diagnosis of SLE. Severe depression (18.5%), polyneuropathy (7.5%), and psychosis (6.6%) were the most frequent npSLE variants. Independent predictors of npSLE included high disease activity, acute SLE course, active lupus nephritis, respiratory involvement, severe pulmonary arterial hypertension, fever, serositis, high damage index, and C4 hypocomplementemia.

Previously, we demonstrated that the development of rheumatoid arthritis (RA) is accompanied not only by inflammation but also by disturbances in central metabolic processes, which are reflected in altered expression of genes involved in energy metabolism. Given the insufficient efficacy of current therapies and the occurrence of adverse events in some cases, the use of nutrients, such as taurine, may be reasonable.
Objective: to evaluate the effect of taurine on the expression of genes responsible for the main pathways of energy metabolism, as well as inflammatory and regenerative activity, during in vitro culture of blood cells and articular cartilage explants obtained from patients with late-stage RA.
Material and methods. Blood samples and articular cartilage explants were obtained from 20 patients with RA (3 men and 17 women; mean age 62.2±10.9 years; mean disease duration 18.2 years) prior to knee joint arthroplasty. Blood cells and cartilage explants were cultured in the presence of 50 μM taurine. Gene expression in cartilage explants was assessed using reverse transcription and real-time polymerase chain reaction.
Results and discussion. Cultivation of blood cells from patients with RA in the presence of 50 μM taurine resulted in a significant increase in the expression of genes encoding pyruvate kinase (PKM2), succinate dehydrogenase (SDHB), uncoupling protein 2 (UCP2), ATP synthase (ATP5B), and unc-51-like kinase 1 (ULK1). In cartilage explants, taurine also activated the expression of SDHB and UCP2 genes and, to a lesser extent, ULK1 (p=0.07). Moreover, cultivation of the studied tissues in the presence of taurine was associated with a marked decrease in the expression of tumor necrosis factor alpha (TNF-á). Culturing articular cartilage explants with taurine significantly increased the expression of the collagen type II gene (COL2A1).
Conclusion. Taurine exerts a beneficial effect on energy metabolism by increasing the expression of genes responsible for oxidative phosphorylation and autophagy in blood cells and articular cartilage explants, while reducing the expression of the inflammatory marker – TNF-á. However, unlike chondrocytes, taurine also enhanced glycolytic activity and increased ATP synthase expression in blood cells. Enhancement of the regenerative potential of chondrocytes in cartilage explants from patients with RA in the presence of taurine is evidenced by increased expression of the collagen type II gene.

Baricitinib (BARI) is widely used in rheumatoid arthritis (RA); however, real-world data on its place in therapy and efficacy in patients with difficult-to-treat (D2T) RA are limited.
Objective: to assess the clinical and demographic characteristics of patients with RA, including those in the D2T RA subgroup, the outcomes of BARI use in routine practice across different lines of therapy (LT) and switching strategies, as well as its steroid-sparing effect.
Material and methods. A retrospective analysis was performed of patients included in the Moscow registry of immune-mediated inflammatory/autoimmune diseases who were followed up from 19.08.2021 to 26.12.2024 and were prescribed BARI. Data from three visits (V1–V3) with a 6-month interval were analyzed. Study endpoints were changes in DAS28-ESR/CRP, CDAI/SDAI, tender joint count (TJC) and swollen joint count (SJC), patient and physician global assessment of disease activity; the proportion of patients in remission and with low disease activity; the number of patients receiving glucocorticoids (GCs) and methotrexate (MTX), as well as GCs and MTX doses. Current therapy at the time of the study and prior therapy were analyzed; a separate analysis was performed for the D2T RA subgroup.
Results and discussion. The study included 188 patients (82% women); mean age was 56.0±12.1 years; median RA duration was 11 (7–18) years. The mean follow-up duration was 12.6 (2.3–29.7) months. The intervals between visits averaged 6.5 months. The D2T RA subgroup included 17 (9%) patients. BARI was prescribed as 1st LT in 62.2% of patients, as 2nd LT in 14.9%, and as 3rd LT in 22.9%; 62.2% of patients had not previously received biologic DMARDs (bDMARDs) or targeted synthetic DMARDs (tsDMARDs), whereas 37.8% were switched to BARI from bDMARDs or tsDMARDs. By V3, with BARI used as 1st LT, the median DAS28-ESR decreased from 3.4 to 3.1 (-8.8%; p<0.05); as 2^nd LT, from 3.3 to 2.9 (-12.1%); and as 3rd LT, from 4.1 to 2.9 (-29.3%); the median DAS28-CRP decreased by 6.9%, 6.9%, and 24.1%, respectively. The greatest reduction in activity indices was observed after switching from interleukin-6 inhibitors (IL-6i): the median DAS28-ESR decreased from 4.02 to 2.99 (-25.6%; p=0.0174) and CDAI from 14.47 to 10.88 (-24.8%). The smallest decrease in indices was recorded after prior therapy with Janus kinase inhibitors (JAKi). In such patients, DAS28-ESR decreased on average by 3.0%, while CDAI increased by 9.1%. In the D2T RA group, a significant reduction in SJC (-74.1%) and TJC (-59.6%) was noted (p<0.05), with a clinically noticeable but statistically non-significant decrease in DAS28-ESR (-18.3%), DAS28-CRP (-23.8%), CDAI (-34.6%), and SDAI (-39.4%). By V3, in 52.1% of patients (p<0.05) it was possible to reduce the GCs dose (21.7%) or discontinue GCs completely (30.4%); the MTX dose and the proportion of patients receiving it also decreased.
Conclusion. In real-world practice, BARI therapy provided a reduction in RA activity across different LT and demonstrated a steroid-sparing effect. Even in patients with D2T RA, a clinically meaningful decrease in arthritis activity was observed. The most favorable switching outcomes were noted in patients previously treated with IL-6i, whereas in patients who had used JAKi, the effect of BARI was limited, which is associated with a change in the mechanism of action when another drug is prescribed. These findings require confirmation in prospective studies.

Therapeutic and preventive nutrition is not only a means of providing patients with essential nutrients to meet the metabolic demands of the body, but also an important non-pharmacological method for correcting multiple pathogenetic mechanisms of disease, enhancing the effects of pharmacotherapy, and normalizing adaptive-compensatory and regulatory components of sanogenesis. Based on contemporary literature data and own data, the authors analyze the therapeutic effects of dietary components on key mechanisms involved in the development of rheumatic diseases (RDs). Algorithms for individualizing therapeutic nutrition programs for patients with major RDs are presented. Principles of modern clinical dietetics that may be of interest to practicing physicians are also discussed.

Autoinflammatory diseases (AIDs) represent a heterogeneous group of conditions pathogenetically associated with dysregulation of the innate immune system and clinically characterized by recurrent episodes of sterile inflammation in the affected organs in the absence of infection, allergy, and high titers of circulating autoantibodies or autoreactive T cells. The spectrum of genetically determined AIDs is quite diverse and continues to expand. Cutaneous manifestations are among the key components of AIDs and often serve as an important clue to diagnosis. This applies both to the classical, most extensively studied monogenic AIDs (mAIDs) and to more rare and less familiar forms of AIDs.
Part 1 of the article presented the characteristics of skin manifestations in classical mAIDs (Familial Mediterranean Fever, FMF; Cryopyrin-Associated Periodic Syndromes, CAPS; Tumor Necrosis Factor Receptor-Associated Periodic Syndrome, TRAPS; Hyper-IgD Syndrome / Mevalonate Kinase Deficiency, HIDS/MKD). Part 2 focuses on patterns of skin involvement in more rare mAIDs, whose pathogenesis is based not only on interleukin-1 activation but also on alternative disease mechanisms, including activation of interferon signaling pathways (interferonopathies) and neutrophilic dermatoses. Diagnostic assessment is greatly facilitated not only by knowledge and correct interpretation of specific cutaneous manifestations in AIDs but also by consideration of characteristic histological markers identified through pathology examination of the skin. Close collaboration between rheumatologists and dermatologists enables timely diagnosis and initiation of targeted therapy.

This literature review presents current data on alterations in body composition (BC) in musculoskeletal diseases. Isolated phenotypes – such as obesity, sarcopenia, osteopenia/osteoporosis – and their combinations are considered as possible consequences and modulators of disease pathogenesis. The predominant phenotypes and their prevalence are described: in rheumatoid arthritis the most commonly identified phenotypes are sarcopenia, sarcopenic obesity, isolated obesity, and osteoporosis; in psoriatic arthritis – excess body weight or obesity and sarcopenic obesity prevail; in ankylosing spondylitis – bone mineral density, `osteoporosis, and sarcopenia are most frequent; in osteoarthritis – obesity, sarcopenic obesity, and sarcopenia predominate. The role of proinflammatory mediators and predictors of BC alterations are discussed. The necessity of assessing BC, including in patients with a normal body mass index, is emphasized, and potential approaches to correction of these alterations are also considered.

 This review presents current data on the safety of Janus kinase inhibitors (JAKi) in patients with immune-mediated rheumatic diseases. Special attention is given to the risks of infections, cardiovascular complications, and malignancies. 

Tendon and ligament involvement is a common rheumatic pathology and one of the most frequent causes of chronic musculoskeletal pain, accompanied by significant functional impairment and reduced quality of life. These disorders may be localized and regarded as an independent nosological entity (rotator cuff impingement syndrome, lateral epicondylitis, patellar tendonitis, etc.) or represent a manifestation of a systemic immune-mediated inflammatory rheumatic disease (most typically in spondyloarthritis). The pathogenesis of tendino-, ligamento-, and enthesopathy is determined by local destruction of collagen fibers, a short-term inflammatory reaction, and degenerative changes (fibrosis, neoangiogenesis, axonal sprouting, heterotopic ossification) that substantially worsen biomechanics and increase the risk of recurrent injury. Pain chronicity in this disorders is associated with sensitization of nociceptors caused by hyperproduction of neurotrophic factors. Risk factors for tendino- and ligamentopathy include trauma, type 2 diabetes mellitus, cardiovascular pathology, and smoking. Treatment of tendon and ligament disorders is complex and includes pharmacological and non-pharmacological approaches. The former includes nonsteroidal antiinflammatory drugs, local injection therapy with glucocorticoids, hyaluronic acid, and platelet-rich plasma. In some cases, muscle relaxants, antidepressants, anticonvulsants, slow-acting symptomatic agents, and botulinum toxin preparations are used. A new direction in the comprehensive therapy of tendino- and ligamentopathies is the use of specialized dietary supplements with analgesic, anti-inflammatory, and reparative effects.

Lupus nephritis (LN) is one of the most common and clinically significant manifestations of systemic lupus erythematosus (SLE) and is associated with a high risk of disability. Delayed diagnosis of SLE in the Russian Federation and insufficient efficacy of standard treatment regimens necessitate the search for and implementation of new therapeutic approaches to improve patient outcomes. During the Expert Council meeting, current Russian and international clinical guidelines, data on the effectiveness of standard therapy, and the results of the international randomized phase III REGENCY clinical trial evaluating the efficacy and safety of obinutuzumab in patients with active LN were reviewed. The Expert Council resolution emphasizes that LN therapy requires a multidisciplinary approach. At the same time, the use of biologics, particularly obinutuzumab, opens new opportunities for achieving sustained remission, reducing glucocorticoid doses, and improving long-term prognosis in patients with highly active LN, including those with inadequate response to standard therapy.