The year 2026 marks the 130th anniversary of the birth of the eminent American rheumatologist Philip Showalter Hench, who in 1950 (along with biochemists Edward Kendall and Tadeusz Reichstein) was awarded the Nobel Prize in Physiology or Medicine “for their discoveries relating to the hormones of the adrenal cortex, their structure and biological effects”. The article summarizes data concerning the history of the study and contribution of P. Hench to the development of glucocorticoids, and examines the prospects of glucocorticoid therapy in immune-mediated rheumatic diseases.

Antiphospholipid syndrome (APS) is defined as “an autoimmune thromboinflammatory disease characterized by an increased risk of thrombosis localized in the venous and arterial vascular beds, thrombotic damage to microvessels, placental insufficiency, cytopenia, skin and heart valves lesions, nephropathy, pulmonary hemorrhages, etc.”. Long with clinical symptoms, the cardinal hallmark of APS is antibodies to phospholipids and phospholipid-binding proteins and including lupus anticoagulant, antibodies to cardiolipin, and antibodies to β2-glycoprotein I, highlighting the leading autoimmune mechanism of this pathogenesis. APS is considered an important problem in modern medicine, located at the intersection of rheumatology and hematology. A distinctive feature of APS is heterogeneity, which manifests itself both at the clinical (phenotypes, course variants) and pathogenetic levels (molecular endotypes). Particular attention is drawn to the potentially lethal form of APS, manifested by the fulminant development of multiorgan thrombosis, which was first identified by Ronald A. Asherson in 1992 as the “catastrophic” form of APS (CAPS). Currently, approaches to personalized therapy of APS using artificial intelligence and, on this basis, the implementation of the concept of “treat-to-target” aimed at achieving remission, which in APS should be considered as the absence of recurrent thrombosis, are being actively discussed. The implementation of this strategy in autoimmune rheumatic diseases has largely become possible thanks to the development and introduction of a wide range of biologics, which are monoclonal antibodies or hybrid molecules that selectively modulate key mechanisms of immunopathogenesis. The clinical forms of CAPS and the pathogenetic mechanisms of APS are considered, and on this basis, new possibilities for the treatment of CAPS using anti-B-cell therapy, complement inhibitors (eculizumab), prospects for the prevention of thrombosis associated with comorbid cardiometabolic pathology.

A group of leading rheumatologists from the Commonwealth of Independent States (CIS) countries has prepared clinical guidelines for the diagnosis, treatment, and monitoring of systemic lupus erythematosus. These clinical guidelines are based on the recommendations of the national rheumatology associations of the CIS countries, the international guidelines of the European Alliance of Associations for Rheumatology, and the American College of Rheumatology. These guidelines are intended for a wide range of specialists in the CIS countries, including rheumatologists and general practitioners.

Calcium pyrophosphate deposition disease (CPPD) is a disease associated with inflammation at the sites of deposition of calcium pyrophosphate crystals, is at the same time one of the most widespread and least well-studied rheumatic diseases. Among the most pressing issues is the possibility of CPPD influencing the risk of cardiovascular diseases (CVDs) and mortality. The suspected causes contributing to the development of CVDs include microcrystalline inflammation and pathological vascular calcification, due to the common mechanisms of articular and vascular calcification. These assumptions are supported by data from several cross-sectional studies that have shown an independent direct association of CPPD with CVDs outcomes, but without the influence of CPPD on cardiovascular mortality. It is possible that the lack of association of CPPD with cardiovascular mortality with a high frequency of cardiovascular events at the same time is explained by the intake of colchicine, as well as the physiological anti-infective effects of interleukin 1. It is important to further search for mechanisms linking CPPD with CVDs and therapy aimed at preventing CVDs in this disease.

The aim of this single‑center study was to investigate the relationship between hyperuricemia (HU) and biochemical and immunological parameters in patients with knee osteoarthritis (KOA).

Materials and methods. The study included 255 patients aged 40–75 years with a confirmed diagnosis of KOA, Kellgren – Lawrence radiological stages I–III, who provided informed consent. The mean age of the patients was 53.0±10.5 years, body mass index (BMI) was 28.8±6.7 kg/m² , and the median disease duration was 2 [0.8; 7] years. The following assessments were performed: questionnaire survey, laboratory testing, standard radiography, knee ultrasound, magnetic resonance imaging (MRI) of the target joint, and dual-energy X‑ray absorptiometry of the axial skeleton.

Results. HU was detected in 16.9 % of cases. These patients exhibited significantly higher values (p < 0.05 in all cases) for: pain on the visual analogue scale, total WOMAC (Western Ontario and McMaster Universities Osteoarthritis Index) score, including all its components, and general health status, as well as worse scores on the KOOS (Knee injury and Osteoarthritis Outcome Score), compared with participants without HU. Furthermore, elevated uric acid levels were significantly associated with higher incidence of synovitis, neuropathic pain component, advanced radiological stages, and more severe joint structural damage on MRI (WORMS (WholeOrgan Magnetic Resonance Imaging Score)). However, after adjusting for BMI and waist circumference (WC), these differences lost statistical significance. At the same time, patients with HU showed higher bone mineral density values in the proximal femur and a higher prevalence of coronary artery disease. Additionally, associations were found with higher levels of triglycerides, creatinine, alkaline phosphatase, and lower levels of high-density lipoprotein (p < 0.05 in all cases). No associations were found with pro- and anti-inflammatory cytokines (interleukin (IL) 1β, IL-6, IL-10, IL-34), metalloproteinase (MMP) 3, MMP-9, markers of cartilage and bone tissue degradation (CTX-I, CTX-II, COMP), or C‑reactive protein.

Conclusion. The relationship between HU and KOA severity is most likely indirect and is determined by excess body weight and visceral obesity (as indicated by WC). The lack of associations between HU and CRP levels, pro‑inflammatory cytokines, and cartilage degradation markers suggests that uric acid does not have a direct effect on these parameters in patients with KOA.

The aim – to evaluate the cytokine profile of patients with systemic lupus erythematosus (SLE) depending on the presence of increased expression of interferon (IFN) stimulated genes.

Materials and methods. The analysis included 140 patients (123 (88%) women and 17 (12%) men) with a confirmed diagnosis of SLE. Disease duration was 3.0 [0.3; 12.0] years, SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) score was 6.5 [4.0; 10.5] points, SDI (Systemic Lupus International Collaborating Clinics/ American College of Rheumatology Damage Index) – 0 [0; 2] points. IFN status was assessed by the expression of IFN-stimulated genes (MX1, RSAD2, EPSTI1) using real-time polymerase chain reaction. A study of 48 serum cytokines was performed using a multiplex immunoassay based on xMAP suspension microarray technology (BioPlex® 200 Pro Human Cytokine Screening Panel, 48-Plex, Bio-Rad Laboratories, USA) according to the manufacturer’s instructions. The control group consisted of 13 healthy donors matched for gender and age.

Results. Expression of IFN-stimulated genes and the IFN score were significantly higher in patients with SLE compared to healthy donors (p < 0.05). The IFN signature was present in 103 (81.7%) patients and absent in 23 (18.3%) patients. Patients with the IFN signature had higher levels of proinflammatory cytokines (tumor necrosis factor α (TNF-α), interleukin (IL) 18, TRAIL (TNF-related apoptosis-inducing ligand)), chemokines (IP-10 (interferon gamma-induced protein 10)), growth factors (macrophage colony-stimulating factor (M-CSF), anti-inflammatory cytokines (IL-1 receptor antagonist (IL-1Ra)), and lower levels of hepatocyte growth factor.

Conclusion. The immunological phenotype with the IFN signature is characterized by higher levels of proinflammatory cytokines (TNF-α, IL-18, TRAIL), chemokines (IP-10), growth factors (M-CSF), and anti-inflammatory cytokines (IL-1Ra), which suggests higher inflammatory activity in this group of patients.

The aim – to determine the clinical significance of hyperproduction of antibodies to ribosomal protein P (a-Rib-P) in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS).

Material and methods. The study included 68 patients with reliable diagnoses of SLE and APS (SLE – 25, SLE+APS – 19, primary APS (PAPS) – 24). Young (35,1±10,2 years) women prevailed (72,1%). All patients were examined according to the standards recommended by the Association of Rheumatologists of Russia, and also examined by a psychiatrist. a-Rib-P was determined in all patients and 20 healthy donors, matched by gender and age, by enzyme immunoassay in blood serum.

Results. The concentration of a-Rib-P in patients was significantly higher than in healthy donors (0.004 [0.003; 0.015] vs 0.002 [0.002; 0.003] U/ml, respectively; p=0.002). Elevated a-Rib-P values were detected in 6 (13.6%) out of 44 patients with SLE, but were not detected in PAPS and in healthy donors. In patients with current neurological disorders (stroke/epilepsy/hyperkinesis), the concentration of a-Rib-P is statistically significantly higher than in their absence (0.004 [0.003; 0.021] vs 0.002 [0.002; 0.003] U/ml, respectively; p=0.001). The concentration of a-Rib-P is significantly higher in patients with SLE and elevated values of antibodies to double stranded DNA/anti-Smith antibodies (a-Sm), compared with those with normal values of these autoantibodies (0.005 [0.004; 0.106] vs 0.004 [0.002; 1.35], respectively; p=0.007 and 2.41 [0.058; 10.3] vs 0.005 [0.002; 0.012] U/ml, respectively; p=0.001). Patients with an increased a-Rib-P value had a significantly higher chance of skin (odds ratio (OR) – 17.0; p<0.001) lesions and a statistically insignificant – mucous lesions (OR=9.0), central nervous system lesion (OR=1.32), polyarthritis (OR=3.75), hematological imparements (OR=3.75), high SLE activity according to the SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) (OR=4.33), bipolar affective disorder (OR=4.25), major depressive disorder (OR=1.4), elevated concentrations of a-Sm (OR=5.0), anti-cardiolipin/anti-β2 glycoprotein 1 antibodies (OR=2.61), anti-phosphatidylserine/prothrombin antibodies (OR=2.33) and anti-N-methyl-D-aspartate receptor antibodies (OR=2.2), as well as a high risk of thrombosis according to GAPSS (Global AntiphosPholipid Syndrome Score) (OR=3.77).

Conclusion. a-Rib-P are highly specific for patients with SLE and aren’t typical for patients with PAPS. They are associated with various clinical and laboratory manifestations of high SLE activity, primarily skin-mucosal, neurological, and immunological.

The aim of the study – to clarify the relationship between serum levels of galectins-1, -3, and -9 and type I interferon gene signature (IFNGS) and to compare its potential as biomarkers of “positive” interferon status in patients with systemic lupus erythematosus (SLE).

Material and methods. The cross-sectional study included 60 women and 11 men with a diagnosis of SLE established according to the SLICC (Systemic Lupus International Collaborating Clinics) 2012 criteria. The patients’ age was 33 [25; 43] years, and the median duration of the disease was 30 [2; 132] months. 19 (26.8 %) patients had high and very high SLE activity (SLEDAI-2K (Systemic Lupus Erythematosus Disease Activity Index 2000) >10), and 24 (33.8%) had moderate activity (SLEDAI-2K=5–10). Glucocorticoids were received by 58 (81.7%), hydroxychloroquine – by 57 (80.3%), immunosuppressants – by 28 (39.4%) patients. The control group included 20 people without immunoinflammatory rheumatic diseases. IFNGS were evaluated by the expression of interferoninduced genes (MX1, RSAD2, EPSTI1) using real-time polymerase chain reaction. If the average indicated genes expression in the patient exceeded that in the control group, IFNGS was considered “positive”, if not – “negative”. Galectin-1, -3 and -9 levels were determined in the blood serum of SLE patients by the enzyme-linked immunosorbent assay (reagents by Cloud-Clone Corp., China).

Results. “Positive” IFNGS was detected in 53 (74.6%) of 71 patients with SLE. The galectin-1 and galectin-3 concentrations were comparable in patients with “positive” and “negative” IFNGS, while the level of galectin-9 was higher in patients with gene overexpression (0.009 [0.002; 0.69] vs 0.002 [0.001; 0.003] pg/ml, respectively; p=0.02). A weak correlation was found between serum galectin-9 levels and EPSTI1 gene expression (r=0.26; p=0.03). In the ROC analysis of using galectin-9 levels as a marker of “positive” IFNGS, the area under the curve was 0.682 (95% confidence interval: 0.537–0.827; p=0.021), and the cutoff point was 0.0025 pg/ml (sensitivity 71.7%, specificity 72.2%).

Conclusion. In SLE patients, serum concentrations of galectin-9, but not galectin-1 and galectin-3, were associated with overexpression of type I interferon-induced genes, namely, EPSTI1. ROC-analysis demonstrated the average quality of the model in the case of using galectin-9 as the only serological biomarker of “positive” IFNGS in SLE. Further research is needed to clarify the diagnostic value of the combination of galectin-9 with other proteins whose synthesis depends on type I interferon.

Background. Despite the integration of imaging methods such as ultrasound and magnetic resonance imaging for the detection of enthesitis, clinical assessment remains the foundation of diagnosis in both everyday practice and clinical studies. However, the frequency of detecting enthesitis in patients with psoriatic arthritis (PsA) varies considerably, which may be primarily due to differences in assessment methods.

The aim – to evaluate the frequency of enthesitis in patients with psoriatic arthritis using modern assessment scales and to investigate the association between enthesitis measures and disease characteristics.

Materials and methods. This cross-sectional study included 116 patients with PsA diagnosed according to the CASPAR (ClASsification for Psoriatic ARthritis) criteria. Enthesitis was assessed using the Leeds Enthesitis Index (LEI), the Maastricht Ankylosing Spondylitis Enthesitis Score (MASES), the Spondyloarthritis Research Consortium of Canada Enthesitis Index (SPARCC), and a combination of these indices.

Results. A total of 96 (82.8%) patients had at least one tender enthesis. Among these, 47 (49%) patients had tenderness at 1–3 entheses (1 enthesis – 19.8%; 2 entheses – 18.8%; 3 entheses – 10.4%), while the remaining patients had tenderness at 4 or more entheses. The median values of the indices were as follows: LEI – 1.0 [0.0; 2.25], SPARCC – 3.0 [1.0; 5.25], MASES – 1.0 [0.0; 2.0]. The frequency of enthesitis (at least one tender enthesis) according to each index was: LEI – 60 (62.5%) patients, MASES – 61 (63.5%) patients, SPARCC – 84 (87.5%) patients. In 9 (9.4%) patients, MASES identified one or more enthesitis sites, whereas no tender entheses were detected by SPARCC or LEI. A moderate positive correlation was found between body mass index (BMI) and the SPARCC index (ρ=0.32; p=0.001). Patients with normal BMI had lower values for the number of tender entheses (3 [1; 5] vs. 4 [2; 10]; p=0.043), the SPARCC index (2 [1; 3] vs. 3 [1; 6]; p=0.025), and the combined SPARCC + MASES index (4 [1; 11] vs. 6.5 [5; 11]; p=0.034).

Conclusion. Enthesitis is present in a significant proportion of patients with PsA (82.1%). To improve the detection rate of enthesitis in patients with PsA, the combined use of the SPARCC and MASES indices is preferable.

The aim of the study was to develop a method for predicting the achievement of a patient acceptable symptoms state (PASS) in patients with psoriatic arthritis (PsA).

Material and methods. The study included 52 patients (28 female and 24 male) diagnosed with PsA according to the CASPAR (ClASsification criteria for Psoriatic ARthritis) criteria (2006). The mean age of the patients was 46±11.8 years, the median (Me) duration of psoriasis (PsO) was 132 [96; 183] months, PsA – 90 [72; 99] months, DAPSA (Disease Activity in Psoriatic Arthritis) – 18 [5.5; 37]. All patients at an early stage of PsA (duration up to 2 years) were monitored and treated according to the principles of the “treat-to-target” (T2T) strategy. By 24 months of observation, patients completed monitoring according to T2T and continued therapy in accordance with current clinical guidelines. After 7 years, all patients underwent a standard rheumatological examination, including assessment of PsA activity by DAPSA. Health-related quality of life (HRQoL) was evaluated using the PsAID-12 (Psoriatic Arthritis Impact of Disease) questionnaire. PsAID-12≤4 corresponded to achieving the PASS. To determine the predictors of achieving PASS, Spearman correlation analysis, univariate logistic regression, and subsequent multivariate stepwise logistic regression analysis were performed.

Results. By 7 years of observation, remission and low disease activity (LDA) by DAPSA were observed in the majority of patients – 31 (60%), swollen joint count (SJC) ≤3 in 38 (73%), C-reactive protein (CRP) ≤5 mg/L in 31 (60% and the number of patients achieving PASS was 38 (73%). Analysis showed that 32 out of 52 (61.5%) patients achieved remission within the first year of treatment and observation at the early stage of PsA.

Based on the results of the final analysis, a discriminant function was obtained, which included the following indicators associated with achieving PASS: age≤60 years (p=0.099), SJC≤3 (p=0.075), CRP≤5 mg/L (p=0.023), and achievement of DAPSA remission within the first year of treatment (p=0.324). A predictive expression for assessing the probability of achieving PASS was obtained: 1.824 × Age≤60 years (0 – no, 1 – yes) + 1.585 × SJC≤3 (0 – no, 1 – yes) + 2.062 × CRP ≤5 mg/L (0 – no, 1 – yes) + 0.783 × Achievement of DAPSA remission within the first year of treatment (0 – no, 1 – yes) – 2.775. According to the model, the probability of achieving PASS for each patient is calculated using the expression: . With calculated p<0.5, low probability of achieving PASS is determined, with values ≥0.5 – high probability. The prognostic model demonstrated high diagnostic accuracy: sensitivity 89.5%, specificity 64.3%, accuracy – 82.7%.

Conclusions. The developed method for predicting the achievement of a patient acceptable symptoms state for PsA patients, incorporating a set of indicators such as patient age, SJC, CRP level, and patient history data (achievement of remission within the first year of treatment), enables assessment of treatment prospects for PsA patients. Depending on the results obtained, the method allows for adjustment of the patient’s therapy.

The aim – to study of the relationship between the prevalence and severity of fibromyalgia (FM) symptoms in patients with psoriatic arthritis (PsA) and the characteristics of the clinical course and type of therapy for PsA

Subjects and methods. The study is based on an analysis of data from 97 patients with PsA, who were prescribed adalimumab (25 patients) and netakimab (34 patients) after the initial evaluation. The remaining patients (38 patients) continued taking methotrexate. In addition to a general clinical and laboratory examination, all patients underwent ultrasonography of painful and/or swollen joints, tendons, and ligaments using linear transducers with a frequency of 12–18 MHz, supplemented by power Doppler imaging with a pulse frequency of 6.6 MHz.

Results and discussion. In the observed patients with PsA, the diagnosis of FM was established in 24 (24.7%) patients. In patients with concomitant FM, the frequency of active enthesitis was increased (70.8% compared to 28.8% in patients without FM; p<0.05). A decrease in the percentage of patients with a diagnosis of FM was found over 6 months of using of biologic agents: from 29.4% to 11.7% among patients taking netakimab, and from 24 to 16% among patients taking adalimumab. In PsA patients with concomitant FM, a decrease in the values of the pain prevalence index and the FM symptom severity scale was noted.

Conclusion. A relationship has been established between concomitant FM and enthesitis in patients with PsA. The use of an interleukin 17 inhibitor in the treatment of patients with PsA is characterized by a reduction in the frequency and severity of clinical manifestations of concomitant FM.