Comorbidity is an important medical and social problem due to its increasing prevalence and increased risk of adverse outcomes. Rheumatoid arthritis (RA) is a disease that is often combined with pathology of internal organs, mostly with cardiovascular diseases. The increased risk of comorbidity in RA is associated not only with immune inflammation, but also with adverse effects of antirheumatic therapy. As clinical practice has shown, glucocorticoids (GC), used in immune-inflammatory rheumatic diseases, are the leading drugs that can impact on the frequency of cardiovascular diseases, the digestive system, and metabolic disorders. The effect of GC on the course of RA, on comorbidity, and on the frequency of adverse outcomes has been discussed in this article. Presented results of our own studies demonstrate a high level of comorbidity in patients with advanced and late RA, relatively high frequency of long-term GC therapy. It was found that comorbid patients significantly less often achieve treatment goals and are more often on systemic GC therapy. The obtained results confirm the relationship between long-term therapy with systemic GC and comorbidity, as well as an insufficient response to rational therapy in patients with RA.

Background/Purpose. Upadacitinib (UPA) is an oral Janus kinase inhibitor, which has selectivity of JAK1 over JAK2, JAK3, and tyrosine kinase 2. UPA demonstrated efficacy for the treatment of RA, with acceptable safety profiles. We analyzed efficacy and tolerability of UPA in small Russian cohort of patients with rheumatoid arthritis.

Materials and methods. Patients (n=24) with high RA activity (DAS 28 5.1±1.1, SDAI 27,5±11,2, CDAI 24,5±9,7) and an inadequate response of synthetic DMARDs (mainly methotrexate, 71 %) and biologics (mainly TNF-α blockers, 24 %) were included in the study. The majority of patients were middle-aged (46,8±15,4), RF (88 %) and ACPA (84 %) positive, with moderate functional impairment – 1.6 (1.25–2). UPA were administered per os, 15 mg daily. The evaluation of the effectiveness of the therapy was carried out according to the EULAR/ACR 2011 criteria and using SDAI, CDAI.

Results. UPA led to a significant (p<0.05) decrease activity of RA. Initially, more than half of the patients have high activity of the RA by SDAI (52 %; n=12), and moderate disease activity by CDAI (52 %; n=12), DAS 28 (58 %; n=14). After 6 months of therapy, the percentage of patients achieving low disease activity by CDAI was 42,9 % (n=6), after 12 months was 75 % (n=6), respectively. After 12 month of therapy DAS 28 was 2,2 (1,2–3,3), SDAI was 7,6 (3–10,9), CDAI was 7,5 (3–10,5). Clinical improvement according to EULAR criteria after 3 months of treatment was registered in 86,7 %, after 6 months was 76,9 %, after 9 months 92,3 % and after 12 months was 87,5 %. More than half of patients (53,3 %) achieved a good response after 3 months of therapy, 70 % – after 6 months and 87,5 % – after 12 months. Adverse events (AE) were registered in 14 % patients, the most frequent AE were upper respiratory tract infections. One case of Herpes Zoster infection was registered.

Conclusion. UPA has shown significant improvement clinical status in patients who had an inadequate response to previous therapy. UPA was well tolerated. AE were registered in a small number of patients.

There are suggestions that Hyperuricemia (HU) can often accompany calcium pyrophosphate deposition (CPPD) disease and affect the clinical manifestations of it.

The aim was to determine the frequency of HU and its clinical significance in patients with CPPD.

Materials and Methods. The study included 213 patients with an established diagnosis of CPPD. The serum uric acid (sUA) level was determined in all patients, after which the patients were divided into 2 groups depending on the presence of sUA level (sUA level of ≥360 mmol/l was taken as HU): patients with CPPD and HU (n=75) and with CPPD and without HU (n=138). A comparative characteristic of the groups was carried out according to the clinical manifestations of the disease, comorbidity, therapy taken, and laboratory blood parameters.

Results. The groups did not differ in age. HU was detected in 75 out of 213 patients (35.2 %). The average sUA level in the group with CPPD and HU was 444.6±77.7 mmol/l, in the group with CPPD without HU – 273.2±53.0 mmol/l. In patients with CPPD and HU, chronic kidney disease was more frequently detected (18.7 % vs 8.7 %) and increased parathyroid hormone level (39.0 [29.8; 61.0] pmol/l vs 29.8 [18.4; 41.5] pmol/l). Hypertension, chronic heart failure (CHF), diabetes mellitus (DM) (for all p<0.05), and obesity (p<0,01) were also more frequently detected with CPPD and HU. Among the patients with CPPD and HU there were more people with chronic arthritis (60.0 % vs 45.0 %), and their ankle joints were more often involved (24.0 % vs 13.0 %). The median serum c-reactive protein level was also higher (3.8 [1.7; 6.7] mg/l vs. 2.1 [0.8; 5.9] mg/l).

Conclusion. The high frequency of HU in CPPD (35.2 %) and their combination with each other determines the high probability of comorbidity and metabolic disorders (obesity, hypertension, CHF, DM), and also creates conditions for the development of chronic inflammation.

Objective. To study the frequency of low bone mineral density (BMD) and BMD-related factors in patients with systemic sclerosis (SSc).

Material and Methods. 210 patients with SSc (median age 52,0 [41,3; 62,1] years) were included: 165 (78,6 %) women and 45 (21,4 %) men. BMD was measured by DXA. In postmenopausal women and men ≥ 50 years OP was diagnosed with T-score at any region < –2.5 SD, in fertile women and men under 50 years of age low BMD was detected with – Z-score <-2.0 SD. To identify the factors associated with low BMD, a logistic regression analysis was performed.

Results. Low BMD was detected in 63 (30,0 %) persons. Multivariate analysis showed association between low BMD and age (OR 1,03; [95 % CI 1,01; 1,07]; р<0,05), body mass index (BMI) ≤24 kg/m² (OR 3,81; [95 % CI 1,76; 8,07]; p < 0.001), acroosteolysis (AO) of distal phalanges (OR 4,56; [95 % CI 1,29; 16,17]; р<0,05), duration of glucocorticoids (GСs) taking (OR1,07; [95% CI 1,01; 1,14]; р<0,05) and anti-topoisomerase I positivity (OR 2,07; [95% CI 1,06; 4,16]; р<0,05).

Conclusion. Low BMD was detected in 63 (30,0 %) persons. Age, BMI ≤24 kg/m², AO of distal phalanges, duration of GСs taking and antitopoisomerase I positivity increased the risk of OP/low BMD in patients with SSc.

Objective. To present an analysis of the updated national clinical guidelines «Gonarthrosis (GA) 2024» with an emphasis on non-drug treatment methods.

Results. The following have a high level of persuasiveness of recommendations and reliability of evidence for the effectiveness of non-drug therapy for GA: modification of sports/physical loads and unloading of the affected joint, application of methods of therapeutic physical training, aerobic exercises, weight correction, methods of knee joint orthosis, physiotherapeutic effects and manual therapy. New in the recommendations was the reliability of the effectiveness of shock wave therapy and the lack of such in acupuncture in the treatment of GA.

Conclusions. Currently, the effectiveness of non-drug treatments for GA has a high evidence base combination with drug therapy. An important advantage of non-drug treatments for GA is their ability to reduce the need for analgesics, which can cause dangerous complications in patients with GA and comorbid conditions.

A feature of post-covid syndrome (PCS) as a nosological unit is a wide range of clinical manifestations, which significantly complicates its diagnosis and makes diagnosis possible only after excluding other potential causes. The article discusses symptoms that occur both in PCS and in rheumatic diseases. The authors emphasize the similarities and differences in clinical manifestations in both cases, as well as the methods of diagnosis and monitoring that are found in the literature. The need for a thorough examination of patients with newly occurring symptoms for the timely detection of rheumatic disease is emphasized.

Calprotectin is a heterodimer formed by two proteins, S100A8 and S100A9, which are mainly produced by activated monocytes and neutrophils. The role of calprotectin in the pathogenesis, diagnosis and monitoring of rheumatic diseases has attracted a high attention in the last years. According to modern data, circulating serum calprotectin can be considered as a marker of the inflammatory process due to neutrophil activity. An association between its high level and some severe manifestations of autoimmune diseases, such as glomerulonephritis and pulmonary fibrosis, has been found. Also, of interest is its potential role as a target for drug therapy, an indicator of prognosis of therapeutic response to treatment. This article reviews the key biological functions of calprotectin that may be involved in the pathogenesis of rheumatologic diseases, presenting its potential use as a biomarker of these pathologies.

Cogan’s syndrome is a systemic vasculitis belonging to the group of variable vasculitis. It is characterized by damage to the eyes (interstitial keratitis) and the audiovisual system (sensorineural hearing loss, vestibular disorders), less often by the development of systemic manifestations (aortitis, neurological disorders). Systemic damage involving the eyes and audiovestibular apparatus requires differential diagnosis of a wide range of diseases, including Wegener's granulomatosis. The review provides detailed information on the etiopathogenesis, clinical picture, diagnosis, principles of therapy, and prognosis of this rare disease. The complexity of the diagnosis and treatment of Cogan’s syndrome highlights the need for an interdisciplinary approach to the management of such patients.

Systemic sclerosis (SS) is a disease with diverse clinical manifestations, with common damage of the gastrointestinal tract (GIT). The traditional description of GIT disorders includes the development of strictures of the lower third of the esophagus due to its scarring with recurrent ulcerative lesions, gastric bleeding due to telangiectasis of the gastric mucosa or ulcerative defects due to ischemia and drug therapy. The development of GIT bleeding is a life-threatening complication of SS. The causes of gastrointestinal bleeding in this category of patients may be both abnormalities of the gastrointestinal mucosa associated with the manifestations of the disease, as well as the effect of basic drug therapy, as well as the presence and treatment of concomitant diseases. In this aspect, early diagnosis of mucosal changes from the digestive tract is a key point in choosing methods for patients monitoring to determine the best tactics of drug therapy, taking into account the benefit/risk ratio while achieving symptom control with improved prognosis. Doctors treating patients with SS should pay attention to the increased risk of gastrointestinal bleeding, especially among patients with comorbid vascular pathology (diabetes mellitus, hypertension, atrial fibrillation), requiring additional use of vasodilators, anticoagulants. Consideration should be given to the endoscopic monitoring of GIT complications among patients with SS, especially those with additional risk factors for damage to the upper GIT, which will useful an appropriate assessment of the risk of bleeding and may ensure timely preventive measures.