Immunoinflammatory Diseases Research Articles

Are seronegative patients with rheumatoid arthritis and clinically suspect arthralgia properly represented in randomized clinical trials?

Rheumatoid arthritis (RA) is a chronic immuno-inflammatory disease whose outcomes can vary greatly from one patient to another. One of the main prognostic factors is the presence of serum autoantibodies, such as rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACPA). Indeed, when seropositive, patients with RA are at higher risk of radiographic progression, disability, and increased mortality. Moreover, while the introduction of the 2010 American College of Rheumatology/European Alliance of Associations for Rheumatology (ACR/EULAR) classification criteria has allowed for an earlier diagnosis, studies on large early arthritis cohorts have also shown that these criteria are less capable of identifying seronegative patients, who are therefore at a higher risk of being diagnosed and treated late. In light of these, the major randomized controlled trials have mostly enrolled patients with autoantibody-positive disease. However, in recent years, it became evident that the two serotypes of RA differ significantly from many points of view. Alongside this, a greater understanding of the disease pathogenesis, particularly the presence of antibodies in patients' serum even before the onset of arthritis, has generated significant interest in exploring whether the disease could be prevented by treating patients in the pre-arthritis phases. Once again, emerging trials predominantly enroll subjects positive for RA autoantibodies, potentially overlooking seronegative individuals with arthralgia-at-risk.

Use of rituximab in the of immunoinflammatory rheumatic diseases combined with Graves' disease (autoimmune polyglandular syndrome in adults): case report and literature review

Rituximab (RTM) is a chimeric (murine and human) monoclonal antibody against B-lymphocytes (CD20). RTM is widely used in hematology for lymphoproliferative diseases and in rheumatology for rheumatoid arthritis, Sjögren's disease, some types of vasculitis and systemic connective tissue diseases. The administration of RTM is associated with a depletion of B-cells mediated by the regulation of apoptosis and cytotoxic effects via complement-dependent and antibody-dependent mechanisms. Considering the pathogenesis of autoimmune damage in Graves' disease (GD), an autoimmune thyroid disease associated with thyrotoxicosis, the use of RTM could be effective in this pathology. We present three patients with a combination of diffuse toxic goiter and rheumatic pathology treated with RTM; different outcomes of GD were observed.

A novel variant BCL11B mutation in a pediatric patient with difficult‐to‐treat eosinophilic esophagitis

AbstractEosinophilic esophagitis (EoE) is an immunoinflammatory disease of the esophagus attributable to a complex interaction between genetic and environmental factors. While several genetic risk variants have been linked with EoE, we report a novel association between B‐cell lymphoma/leukemia 11B genetic mutation in a child with dysmorphic facies, developmental delays, atopic comorbidities, and difficult‐to‐treat EoE. After a prolonged course of EoE and multiple esophagogastroduodenoscopies with biopsies, this patient achieved clinical and histologic remission on a combination of swallowed topical steroids and high‐dose proton pump inhibitor (PPI) therapy. However, her EoE relapsed when we attempted to wean her off PPI, and it was finally controlled after adding PPI back to her regimen. This report underscores the importance of genetic testing in patients with unusual clinical features and difficult‐to‐treat EoE. Relevant to real‐world clinical practice, this case also raises the question of the treatment goals in children with EoE and underlying genetic mutation(s).

Immunomodulatory Effects and Regulatory Mechanisms of (R)-6-HITC, an Isothiocyanate from Wasabi (Eutrema japonicum), in an Ex Vivo Mouse Model of LPS-Induced Inflammation.

The present study aimed to investigate the effects of (R)-(-)-1-isothiocyanato-6-(methylsulfinyl)-hexane [(R)-6-HITC], the major isothiocyanate present in wasabi, in an ex vivo model of inflammation using lipopolysaccharide-stimulated murine peritoneal macrophages. (R)-6-HITC improved the immune response and mitigated oxidative stress, which involved suppression of reactive oxygen species, nitric oxide, and pro-inflammatory cytokines (IL-1β, IL-6, IL-17, IL-18, and TNF-α) production and downregulation of pro-inflammatory enzymes such as inducible nitric oxide synthase, COX-2, and mPGES-1. In addition, (R)-6-HITC was able to activate the Nrf2/HO-1 axis while simultaneously inhibiting key signaling pathways, including JAK2/STAT3, mitogen-activated protein kinases, and canonical and noncanonical inflammasome pathways, orchestrating its potent immunomodulatory effects. Collectively, these findings demonstrate the potential of (R)-6-HITC as a promising nutraceutical for the management of immuno-inflammatory diseases and justify the need for further in vivo validation studies.

Prevalence of co-morbidities among periodontitis and non-periodontitis Indian patients.

Periodontitis being an immuno-inflammatory disease can act as an aggravating factor for various systemic diseases. Therefore, it is of interest to document the prevalence of comorbidities among periodontitis and non-periodontitis Indian patients. 680 patients were enrolled, categorized into non-periodontitis group (Group A) and periodontitis group (Group B). Each group was again sub-grouped into comorbidities and non-co-morbidities. Periodontitis patients were found to have significantly more co-morbidities than non-periodontitis patients. Osteoporosis and obesity showed statistically higher levels in periodontitis patients. Hypertension, diabetes mellitus, cardiovascular diseases, and COVID-19 infection showed higher prevalence in periodontitis group, though the difference was statistically non-significant.

Pro-inflammatory activation of monocytes in patients with immunoinflammatory rheumatic diseases

Pro-inflammatory activation of monocytes in patients with immunoinflammatory rheumatic diseases

Proinflammatory Activation of Monocytes in Patients with Immunoinflammatory Rheumatic Diseases.

. The objective of this study was to evaluate the proinflammatory activation of circulating monocytes in patients with IRDs. . The study involved 149 participants (53 patients with rheumatoid arthritis (RA), 45patients with systemic lupus erythematosus (SLE), 34 patients with systemic scleroderma (SSc), and 17participants without IRDs) 30 to 65 years old. Basal and lipopolysaccharide (LPS)-stimulated secretion of monocytes was studied in a primary culture of monocytes obtained from blood by immunomagnetic separation. Quantitative assessment of the cytokines tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), as well as the chemokine monocyte chemoattractant protein-1 (MCP-1) was carried out in the culture fluid by ELISA. Proinflammatory activation of monocytes was calculated as the ratio of LPS-stimulated and basal secretions. . It was shown that the basal secretion of all studied cytokines was significantly increased in all groups of patients with IRDs, except for the secretion of IL-1β in the SLE group, compared to the control. LPS-stimulated secretion of TNF-α was increased and MCP-1 was decreased in patients with IRDs compared to the control group; LPS-stimulated IL-1β secretion only in the SSc group significantly differed from the control group. In the RA group, monocyte activation was reduced for all cytokines compared to the control; in the SLE group, for TNF-α and MCP-1; in the SSc group, for MCP-1. . The decrease in proinflammatory activation of monocytes in patients with IRDs is due to a high level of basal secretion of cytokines, which can lead to disruption of the adequate immune response in these diseases and is an important link in the pathogenesis of chronic inflammation.

Anemia of chronic diseases in the early stages of chronic kidney disease as a risk factor for cardiovascular complications in patients with glomerulonephritis

To determine biomarkers of anemia of chronic disease (ACD) in patients with glomerulonephritis (GN) in the early stages of CKD, to assess their role as risk factors for cardiovascular complications (CVС). Seventy nine patients with GN were studied, among them: 40 with primary сhronic GN (CGN), 39 with secondary forms:19 - GN with ANCA-associated systemic vasculitis, 20 - GN with systemic lupus erythematosus (SLE) at early (all I-II) CKD stages. In all patients, the level of serum C-reactive protein (CRP), hepcidin, interferon γ, and the circulating form of protein Klotho (s-Klotho) were determined. When a relative iron deficiency was detected [transferrin iron saturation coefficient (TSAT) <20%], patients were administered parenterally iron [III] sucrose hydroxide complex (Venofer). The frequency of anemia among patients with systemic diseases is 3.2 times higher than among patients with primary CGN. Patients with anemia (group I; n=43) had higher rates of daily proteinuria (p<0.001), systolic blood pressure (p<0.05), serum levels of interferon γ (p<0.001) and hepcidin (p<0.001) and lower values of eGFR (p<0.05) than patients without anemia (group II; n=36). A strong inverse correlation was noted between the level of hepcidin and the content of iron in serum (r=-0.856; p<0.001), between the level of hemoglobin and the level of interferon γ (r=-0.447; p<0.05), hepcidin (r=-0.459; p<0.05) and CRP (r=-0.453; p<0.05). A significant inverse correlation was found between the level of hemoglobin and CVC risk factors - the value of systolic blood pressure (r=-0.512; p<0.05) and the mass index of the left ventricular myocardium (r=-0.619; p<0.01). At the same time, the contribution of 2 from 6 analyzed factors, hepcidin and eGFR, to the development of ACD was 92.5%, of which 86.6% accounted for hepcidin. A strong direct correlation was also found between a decrease in hemoglobin level and a decrease in the level of s-Klotho protein (r=0.645; p<0.001), a decrease in the level of s-Klotho and an increase in the level of serum hepcidin (r=-0.541; p<0.05). The leading value of anemia (beta -0,29; p=0,04) and depression of the s-Klotho level (beta -0,44; p=0,02) as independent cardiovascular risk factors in this group of patients was confirmed by multivariate analysis. In patients with identified deficiency of iron (n=40), after 3-4 weeks of intravenous administration of venofer, the target level of hemoglobin (Нb>120 g/l) and transferrin saturation with iron (TSAT>20%) were achieved. Among the biomarkers of ACD in patients with immunoinflammatory diseases of the kidneys (primary and secondary СGN), the increase in the serum level of hepcidin is greatest importance. The concomitant to anemia decrease in s-Klotho is a leading risk factor for CVС in CKD. Early correction of ACD with iron supplements makes it possible to achieve target levels of Hb and TSAT and have subsequently a positive effect on the production of s-Klotho and the severity of left ventricular hypertrophia.

Clinical cases of vasculitis associated with antineutrophil cytoplasmic antibodies (ANCA vasculitis) induced by COVID-19

COVID-19 is similar to immunoinflammatory rheumatic diseases in clinical manifestations, immune responses and pathogenetic mechanisms. Specific autoantibodies as markers of autoimmune diseases can be detected in patients with coronavirus infection. Most often, after COVID-19, antinuclear antibodies, antibodies to phospholipids, to cardiolipin, to β2-glycoprotein, to cytoplasmic antigens SS-A and SS/B, and cyclic citrulline-containing peptide are detected. In moderate and severe cases of COVID-19 infection with pulmonary-renal syndrome, cytokine storm, antineutrophil cytoplasmic antibodies, antibodies to myeloperoxidase and to proteinase 3 have become more frequent, which can trigger neutrophil NETosis with the formation of extracellular neutrophil traps — networks and induce the development of autoimmune processes and the appearance of de novo immunoinflammatory rheumatic diseases: arthritis , systemic lupus erythematosus, vasculitis associated with antineutrophil cytoplasmic antibodies (ANCA vasculitis). Our study presents 4 clinical cases of patients with ANCA vasculitis with a history of recent coronavirus infection, chronologically verified. The average time after COVID-19 and the onset of ANCA vasculitis was about 3 months; damage to the upper respiratory tract, lower respiratory tract, skin and renal syndromes were observed. The severity of ANCA vasculitis did not depend on the severity of coronavirus infection: a mild course of COVID-19 infection did not exclude a severe course of ANCA vasculitis. It is recommended that all patients during and after coronavirus infection with post-COVID syndrome in the presence of damage to the ENT organs, kidneys, and skin are screened the presence of antineutrophil cytoplasmic antibodies to exclude the onset of ANCA vasculitis.

Clinical Significance of Antibodies to DFS70 in Immunoinflammatory Rheumatic Diseases.

The relevance of the problem of immunoinflammatory rheumatic diseases(IIRD) for modern medicine is determined by their high prevalence in the population, the difficulty of early diagnosis, the rapid development of disability and poor life prognosis. Recent data on the significance of anti-DFS70 have opened up new possibilities for optimizing the step-by-step diagnosis of IIRD. The detection of these antibodies can help in the interpretation of a positive result for antinuclear antibodies (ANA) by indirect immunofluorescence assay on HEp-2 cells (IIFA-HEp-2) in the absence of autoantibodies specific for IIRD. Detection of anti-DFS70 in antinuclear factor (ANF) seropositive patients without clinical and/or serological markers characteristic of a certain disease from the IIRD group can be considered as a potential marker that excludes this group of diseases.

Standing the test of COVID-19: charting the new frontiers of medicine

The COVID-19 pandemic accelerated research and innovation across numerous fields of medicine. It emphasized how disease concepts must reflect dynamic and heterogeneous interrelationships between physical characteristics, genetics, co-morbidities, environmental exposures, and socioeconomic determinants of health throughout life. This article explores how scientists and other stakeholders must collaborate in novel, interdisciplinary ways at these new frontiers of medicine, focusing on communicable diseases, precision/personalized medicine, systems medicine, and data science. The pandemic highlighted the critical protective role of vaccines against current and emerging threats. Radical efficiency gains in vaccine development (through mRNA technologies, public and private investment, and regulatory measures) must be leveraged in the future together with continued innovation in the area of monoclonal antibodies, novel antimicrobials, and multisectoral, international action against communicable diseases. Inter-individual heterogeneity in the pathophysiology of COVID-19 prompted the development of targeted therapeutics. Beyond COVID-19, medicine will become increasingly personalized via advanced omics-based technologies and systems biology—for example targeting the role of the gut microbiome and specific mechanisms underlying immunoinflammatory diseases and genetic conditions. Modeling proved critical to strengthening risk assessment and supporting COVID-19 decision-making. Advanced computational analytics and artificial intelligence (AI) may help integrate epidemic modeling, clinical features, genomics, immune factors, microbiome data, and other anthropometric measures into a “systems medicine” approach. The pandemic also accelerated digital medicine, giving telehealth and digital therapeutics critical roles in health system resilience and patient care. New research methods employed during COVID-19, including decentralized trials, could benefit evidence generation and decision-making more widely. In conclusion, the future of medicine will be shaped by interdisciplinary multistakeholder collaborations that address complex molecular, clinical, and social interrelationships, fostering precision medicine while improving public health. Open science, innovative partnerships, and patient-centricity will be key to success.

Efficacy and Safety of Crisaborole Ointment 2% in Chinese Patients Aged ≥ 2 Years with Mild to Moderate Atopic Dermatitis.

Atopic dermatitis (AD) is a chronic immuno-inflammatory skin disease. Crisaborole ointment, 2%, is a nonsteroidal phosphodiesterase 4 inhibitor approved for the treatment of mild to moderate AD. This post hoc analysis assesses the efficacy and safety of crisaborole in Chinese patients aged ≥ 2years with mild to moderate AD. We evaluated the efficacy and safety of crisaborole in Chinese patients from the vehicle-controlled, phase 3 CrisADe CLEAR study. Patients were randomly assigned 2:1 to receive crisaborole or vehicle twice daily, respectively, for 28days. The primary endpoint was percent change from baseline in Eczema Area and Severity Index (EASI) total score at day 29. Key secondary endpoints were improvement in Investigator's Static Global Assessment (ISGA), ISGA success, and change from baseline in weekly average Peak Pruritus Numerical Rating Scale (PP-NRS) score. Adverse events were documented. Of 391 patients in the overall study, 237 were from China, 157 assigned to crisaborole and 80 assigned to vehicle. A greater reduction in percent change from baseline in EASI total score at day 29 was shown in the crisaborole vs. vehicle group (least squares mean [LSM]: -66.34 [95% (confidence interval) CI -71.55 to -61.12] vs. -50.18 [95% CI -58.02 to -42.34]). Response rates for achievement of ISGA improvement (43.2% [95% CI 35.4-51.1] vs. 33.4% [95% CI 22.5-44.2]) and ISGA success (31.7% [95% CI 24.3-39.0] vs. 21.5% [95% CI 12.1-30.9]) at day 29 were higher in the crisaborole vs. vehicle group. A greater reduction in change from baseline in weekly average PP-NRS score at week 4 was observed in the crisaborole vs. vehicle group (LSM: -1.98 [95% CI -2.34 to -1.62] vs. -1.08 [95% CI -1.63 to -0.53]). No new safety signals were observed. Crisaborole was effective and well tolerated in Chinese patients aged ≥ 2years with mild to moderate AD. ClinicalTrials.gov, NCT04360187.

Methotrexate and immunogenicity of vaccines in patients with rheumatic diseases

Currently, methotrexate (MT) remains one of the immunosuppressive drugs most commonly used in rheumatology. However, its effect on the immunogenicity of vaccines has until recently been studied only to a limited extent, which has led to the lack of clear recommendations for the use of MT during vaccination. Significant progress was made during the COVID-19 pandemic due to the dynamic development of vaccine research, including in patients with immuno-inflammatory rheumatic diseases. The review presents data on the effect of MT on the immunogenicity of vaccines against influenza, pneumococcus, herpes zoster, tetanus/diphtheria/pertussis, yellow fever and COVID-19 (including humoral and cellular responses) in rheumatological patients. The necessity of observing certain time intervals during vaccination in the case of MT use has been demonstrated. The potential mechanisms by which MT influences the immunogenicity of vaccines are presented. The importance of further clinical studies is emphasized in order to assess the effect of MT therapy on the vaccine response and to develop methods for its optimization.

Glucagon-like peptide-1 receptor agonists: Prospects for use in rheumatology

Glucagon-like peptide-1 receptor agonists (ArGLP-1) are effective drugs for the treatment of type 2 diabetes mellitus and obesity. Recent studies in patients with a wide range of immunoinflammatory diseases suggest important pleiotropic mechanisms of action of these drugs, primarily related to the suppression of inflammation. The article presents new data indicating the prospects for the use of ArGLP-1 in immunoinflammatory rheumatic diseases, which dictates the need for clinical studies. GLP-1 receptor agonists are effective drugs for the treatment of type 2 diabetes mellitus and obesity. Recent studies in patients with a wide range of immune-mediated diseases suggest important pleiotropic mechanisms of action of these drugs, primarily related to the suppression of inflammation. The article presents new data indicating the prospects for the use of ArGLP-1 in immune-mediated rheumatic diseases, which dictates the need for clinical studies.

Vaccinoprophylaxis of infections and activity of immuno-inflammatory rheumatic diseases: pro et contra

In modern conditions, patients with immuno-inflammatory rheumatic diseases (IIRD) are at significant risk of influenza, pneumococcal and herpes viral infections, as well as COVID-19, in some cases fatal. The most effective way to prevent infectious diseases and reduce mortality from them is vaccination, which is recommended in the inactive phase of IIRD. However, a number of patients with IIRD have a refractory course of the disease, and achieving remission in them turns out to be a difficult task, and therefore the problem of vaccination of such patients against the background of an active inflammatory process is very relevant. The review analyzes data on the use of vaccine prophylaxis for the above infections in the active phase of IIRD. In the vast majority of cases, vaccination was safe and did not lead to an exacerbation of IIRD or the development of new autoimmune phenomena.

Ulcerative colitis and autoimmune uveitis. Case report

The article provides information on the pathogenesis, classification and frequency of ophthalmic extra-intestinal manifestations in patients with inflammatory bowel diseases (IBD). A clinical observation of a patient with autoimmune uveitis and IBD is described, demonstrating the importance of early diagnosis of immuno-inflammatory diseases in the implementation of multidisciplinary management of patients with IBD and extraintestinal manidestations. The use of genetically engineered biological drugs helps to control the course of IBD, ophthalmic manifestations and prevents the development of complications.

Assessment of the endothelial glycocalyx state in patients with axial spondyloarthritis associated with Crohn’s disease

BACKGROUND: Epithelial barrier dysfunction, including their permeability increment, is supposed to be a pathogenetic link in the development of various immunoinflammatory diseases, including Crohn’s disease and axial spondyloarthritits. Endothelial permeability regulation is provided by both intercellular contacts and endothelial glycocalyx. AIM: To study the microcirculatory state by measuring the endothelial glycocalyx thickness in patients with axial spondyloarthritits associated with Crohn’s disease. To identify an association between the endothelial glycocalyx thinning and the epithelial permeability severity in patients with Crohn’s disease, axial spondyloarthritits and their combination. MATERIALS AND METHODS: 12 patients with axial spondyloarthritits associated with Crohn’s disease (group A), 22 patients with idiopathic axial spondyloarthritits (group B), 24 patients with Crohn’s disease (group C) and 16 healthy individuals (group D) were examined. The endothelial glycocalyx thickness was assessed in the sublingual region using dark-field microscopy. Fecal calprotectin and fecal zonulin was studied. RESULTS: A statistically significant increase in the perfused boundary region high flow was found (p = 0.001), as well as the MicroVascular Health Score (p = 0.004) in group A compared with the control. In Group A, a positive correlation between perfused boundary region high flow and scores Ankylosing Spondylitis Disease Activity Score, Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Metrology Index 10 (p 0.05) was found; perfused boundary region 5–9 mµ correlated positively with the fecal calprotectin (p = 0.007). Perfused boundary region high flow measurement provides 77.1% accuracy for correct classification of axial spondyloarthritits associated with Crohn’s disease and idiopathic axial spondyloarthritits (p = 0.010). In group C, a positive correlation between fecal zonulin and perfused boundary region 5–9 mµ, 10–19 mµ, 5–25 mµ (p 0.05) was also found. CONCLUSIONS: The findings suggest that the patients with axial spondyloarthritits associated with Crohn’s disease have endothelial glycocalyx impairment; the detection of these abnormalities may be useful in assessing the disease integral activity and in the differential diagnosis of axial spondyloarthritits associated with Crohn’s disease and idiopathic axial spondyloarthritits. Further studies of microcirculation will allow better understanding of spondyloarthritis and inflammatory bowel diseases pathogenesis and improve the management of patients with these diseases.

Serologic, Virologic and Pathologic Features of Cats with Naturally Occurring Feline Infectious Peritonitis Enrolled in Antiviral Clinical Trials.

Feline infectious peritonitis (FIP) is a multisystemic, generally lethal immuno-inflammatory disease of domestic cats caused by an infection with a genetic variant of feline coronavirus, referred to as the FIP virus (FIPV). We leveraged data from four different antiviral clinical trials performed at the University of California, Davis. Collectively, a total of 60 client-owned domestic cats, each with a confirmed diagnosis of naturally occurring FIP, were treated with a variety of antiviral compounds. The tested therapies included the antiviral compounds GS-441524, remdesivir, molnupiravir and allogeneic feline mesenchymal stem/stroma cell transfusions. Four client-owned cats with FIP did not meet the inclusion criteria for the trials and were not treated with antiviral therapies; these cats were included in the data set as untreated FIP control cats. ELISA and Western blot assays were performed using feline serum/plasma or ascites effusions obtained from a subset of the FIP cats. Normalized tissue/effusion viral loads were determined in 34 cats by a quantitative RT-PCR of nucleic acids isolated from either effusions or abdominal lymph node tissue. Twenty-one cats were PCR "serotyped" (genotyped) and had the S1/S2 region of the coronaviral spike gene amplified, cloned and sequenced from effusions or abdominal lymph node tissue. In total, 3 untreated control cats and 14 (23.3%) of the 60 antiviral-treated cats died or were euthanized during (13) or after the completion of (1) antiviral treatment. Of these 17 cats, 13 had complete necropsies performed (10 cats treated with antivirals and 3 untreated control cats). We found that anticoronaviral serologic responses were persistent and robust throughout the treatment period, primarily the IgG isotype, and focused on the viral structural Nucleocapsid and Membrane proteins. Coronavirus serologic patterns were similar for the effusions and serum/plasma of cats with FIP and in cats entering remission or that died. Viral RNA was readily detectable in the majority of the cats in either abdominal lymph node tissue or ascites effusions, and all of the viral isolates were determined to be serotype I FIPV. Viral nucleic acids in cats treated with antiviral compounds became undetectable in ascites or abdominal lymph node tissue by 11 days post-treatment using a sensitive quantitative RT-PCR assay. The most common pathologic lesions identified in the necropsied cats were hepatitis, abdominal effusion (ascites), serositis, pancreatitis, lymphadenitis, icterus and perivasculitis. In cats treated with antiviral compounds, gross and histological lesions characteristic of FIP persisted for several weeks, while the viral antigen became progressively less detectable.

The difficult way in diagnostics of neurological manifestations of Sjogren's disease. Case report

Sjogren's disease is an immunoinflammatory rheumatic disease that is characterized by damage to the secreting epithelial glands with the development of parenchymal sialadenitis with xerostomia and keratoconjunctivitis sicca with hypolacrymia. Due to the high heterogeneity of clinical manifestations of this disease, diagnosis is difficult. This article presents a clinical case of a patient with a detailed description of the manifestation, course, and treatment of Sjogren's disease with a rare combination of extraglandular complications in the form of polymyositis and secondary polyneuropathy.

Coronavirus disease 2019 (COVID-19) pandemic and autoimmune rheumatic diseases: Outcomes and prospects

The pandemic of coronavirus disease 2019 (COVID-19), etiologically related to the SARS-CoV-2 virus (severe acute respiratory syndrome coronavirus-2), has drawn attention to new clinical and fundamental problems in the immunopathology of human diseases associated with virus-induced autoimmunity and autoinflammation. The provision that “the experience gained in rheumatology in the process of studying the pathogenetic mechanisms and pharmacotherapy of immunoinflammatory rheumatic diseases as the most common and severe forms of autoimmune and autoinflammatory pathology in humans will be in demand for deciphering the nature of the pathological processes underlying COVID-19 and developing approaches to effective pharmacotherapy” was confirmed in numerous studies conducted over the next 3 years in the midst of the COVID-19 pandemic. The main focus will be on a critical analysis of data regarding the role of autoimmune inflammation, which forms the basis of the pathogenesis of immune-mediated rheumatic diseases in the context of the immunopathology of COVID-19.