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1
Nava, Tiziana. "Physiotherapy rehabilitation in patients with ankylosing spondylitis." Beyond Rheumatology 1, no. 2 (December 20, 2019): 37–46. http://dx.doi.org/10.4081/br.2019.6.
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Ankylosing spondylitis (AS) is a chronic immune-mediated inflammatory disease, it is a form of arthritis characterized by an autoimmune and genetic etiology, included in the group of chronic inflammatory, autoimmune, and diseases. One of the most frequent reasons for the long delay in diagnosis is represented by the AS main symptoms such as: chronic low back pain, very common in this kind of patients, followed by a diagnosis of degenerative disc pathologies, rheumatoid arthritis, and tuberculosis of the spine. Another reason is the quite late appearance of the radiographic signs in the sacroiliac region. The pain symptomatology manifesting itself from the onset of the pathology is the cause of an antalgic response. In this sense an early diagnosis is essential to avoid the establishment of deformities at the level of the spine and of the articular and peri-articular structures. Pharmacological treatment as well as a rehabilitation program are very important and effective in the early phase of the disease. In the most advanced phases, the spine presents an increasing stiffening, with dorsal hyperkyphosis and the abolition of the lumbar lordosis determining the typical postural alterations characteristic of the disease. Early diagnosis and timely delivery to rehabilitation and physiotherapy can significantly reduce disability and complications. The international guidelines and recommendations suggest the pharmacological treatment as well as the rehabilitation and physiotherapy program during the different stages of the disease. In the 2016 update of the ASAS-EULAR recommendations for axial AS, multidisciplinary, non-pharmacological (along with pharmacological) treatment is required to ensure optimal management of the disease. US-based recommendations also suggest the relevance of nonpharmacological therapies, along with recommended patient education, active physiotherapy and regular physical activity.
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Wielinska, Joanna, and Katarzyna Bogunia-Kubik. "miRNAs as potential biomarkers of treatment outcome in rheumatoid arthritis and ankylosing spondylitis." Pharmacogenomics 22, no. 5 (April 2021): 291–301. http://dx.doi.org/10.2217/pgs-2020-0148.
Full textAbstract:
Common autoimmune, inflammatory rheumatic diseases including rheumatoid arthritis and ankylosing spondylitis can lead to structural and functional disability, an increase in mortality and a decrease in the quality of a patient’s life. To date, the core of available therapy consists of nonsteroidal anti-inflammatory drugs, glucocorticoids and conventional synthetic disease-modifying antirheumatic drugs, like methotrexate. Nowadays, biological therapy including anti-TNF, IL-6 and IL-1 inhibitors, as well as antibodies targeting IL-17 and Janus kinase inhibitors have been found to be helpful in the management of rheumatic conditions. The review provides a summary of the current therapy strategies with a focus on miRNA, which is considered to be a potential biomarker and possible answer to the challenges in the prediction of treatment outcome in patients with rheumatoid arthritis and ankylosing spondylitis.
3
Antoniou, Antony N., Izabela Lenart, and David B. Guiliano. "Pathogenicity of Misfolded and Dimeric HLA-B27 Molecules." International Journal of Rheumatology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/486856.
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The association between HLA-B27 and the group of autoimmune inflammatory arthritic diseases, the spondyloarthropathies (SpAs) which include ankylosing spondylitis (AS) and Reactive Arthritis (ReA), has been well established and remains the strongest association between any HLA molecule and autoimmune disease. The mechanism behind this striking association remains elusive; however animal model and biochemical data suggest that HLA-B27 misfolding may be key to understanding its association with the SpAs. Recent investigations have focused on the unusual biochemical structures of HLA-B27 and their potential role in SpA pathogenesis. Here we discuss how these unusual biochemical structures may participate in cellular events leading to chronic inflammation and thus disease progression.
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Lai, Benjamin, Chien-Hsiang Wu, and Jenn-Haung Lai. "Activation of c-Jun N-Terminal Kinase, a Potential Therapeutic Target in Autoimmune Arthritis." Cells 9, no. 11 (November 12, 2020): 2466. http://dx.doi.org/10.3390/cells9112466.
Full textAbstract:
The c-Jun-N-terminal kinase (JNK) is a critical mediator involved in various physiological processes, such as immune responses, and the pathogenesis of various diseases, including autoimmune disorders. JNK is one of the crucial downstream signaling molecules of various immune triggers, mainly proinflammatory cytokines, in autoimmune arthritic conditions, mainly including rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis. The activation of JNK is regulated in a complex manner by upstream kinases and phosphatases. Noticeably, different subtypes of JNKs behave differentially in immune responses. Furthermore, aside from biologics targeting proinflammatory cytokines, small-molecule inhibitors targeting signaling molecules such as Janus kinases can act as very powerful therapeutics in autoimmune arthritis patients unresponsiveness to conventional synthetic antirheumatic drugs. Nevertheless, despite these encouraging therapies, a population of patients with an inadequate therapeutic response to all currently available medications still remains. These findings identify the critical signaling molecule JNK as an attractive target for investigation of the immunopathogenesis of autoimmune disorders and for consideration as a potential therapeutic target for patients with autoimmune arthritis to achieve better disease control. This review provides a useful overview of the roles of JNK, how JNK is regulated in immunopathogenic responses, and the potential of therapeutically targeting JNK in patients with autoimmune arthritis.
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Stevenson, John. "Inflammatory Arthritis." InnovAiT: Education and inspiration for general practice 2, no. 10 (September 22, 2009): 585–96. http://dx.doi.org/10.1093/innovait/inp149.
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Inflammatory arthritis is an umbrella term used to describe a range of conditions, including rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and reactive arthritis. These are autoimmune diseases in which joint and systemic features are present in varying degrees between disease processes and individuals. Delayed diagnosis can lead to irreversible joint destruction and dysfunction but a therapeutic revolution has transformed its prognosis. Ever-expanding therapeutic options require GPs to recognize these conditions, manage symptoms and undertake drug monitoring. The costs to individuals, their families and the National Health Service are high. There were 1.9 million GP consultations for inflammatory arthritis in 2000 and nearly 46000 hospital admissions. The challenge in primary care is to recognize an inflammatory arthritis early and refer to secondary care.
6
Strouse, Jennifer, Brittney M. Donovan, Munazza Fatima, Ruth Fernandez-Ruiz, Rebecca J. Baer, Nichole Nidey, Chelsey Forbess, et al. "Impact of autoimmune rheumatic diseases on birth outcomes: a population-based study." RMD Open 5, no. 1 (April 2019): e000878. http://dx.doi.org/10.1136/rmdopen-2018-000878.
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ObjectivesAutoimmune rheumatic diseases (ARDs) affect women of childbearing age and have been associated with adverse birth outcomes. The impact of diseases like ankylosing spondylitis and psoriatic arthritis (PsA) on birth outcomes remains less studied to date. Our objective was to evaluate the impact of ARDs on preterm birth (PTB), congenital anomalies, low birth weight (LBW) and small for gestational age (SGA), in a large cohort of women.MethodsWe conducted a propensity score-matched analysis to predict ARD from a retrospective birth cohort of all live, singleton births in California occurring between 2007 and 2012. Data were derived from birth certificate records linked to hospital discharge International Classification of Diseases, ninth revision codes.ResultsWe matched 10 244 women with a recorded ARD diagnosis (rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), antiphospholipid syndrome, PsA); ankylosing spondylitis and juvenile idiopathic arthritis (JIA) to those without an ARD diagnosis. The adjusted OR (aOR) of PTB was increased for women with any ARD (aOR 1.93, 95% CI 1.78 to 2.10) and remained significant for those with RA, SLE, PsA and JIA. The odds of LBW and SGA were also significantly increased among women with an ARD diagnosis. ARDs were not associated with increased odds of congenital anomalies.ConclusionConsistent with prior literature, we found that women with ARDs are more likely to have PTB or deliver an SGA infant. Some reassurance is provided that an increase in congenital anomalies was not found even in this large cohort.
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Amarasekara, Dulshara Sachini, Jiyeon Yu, and Jaerang Rho. "Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases." Journal of Immunology Research 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/832127.
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Bone remodeling is a lifelong process in vertebrates that relies on the correct balance between bone resorption by osteoclasts and bone formation by osteoblasts. Bone loss and fracture risk are implicated in inflammatory autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, and systemic lupus erythematosus. The network of inflammatory cytokines produced during chronic inflammation induces an uncoupling of bone formation and resorption, resulting in significant bone loss in patients with inflammatory autoimmune diseases. Here, we review and discuss the involvement of the inflammatory cytokine network in the pathophysiological aspects and the therapeutic advances in inflammatory autoimmune diseases.
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Chen, Chong, Tianhua Rong, Zheng Li, and Jianxiong Shen. "Noncoding RNAs Involved in the Pathogenesis of Ankylosing Spondylitis." BioMed Research International 2019 (July 7, 2019): 1–8. http://dx.doi.org/10.1155/2019/6920281.
Full textAbstract:
Ankylosing spondylitis (AS) is a form of arthritis that can lead to fusion of vertebrae and sacroiliac joints following syndesmophyte formation. The etiology of this painful disease remains poorly defined due to its complex genetic background. There are no commonly accepted methods for early diagnosis of AS, nor are there any effective or efficient clinical treatments. Several noncoding RNAs (ncRNAs) have been linked to AS pathogenesis and inflammation via selective binding of their downstream targets. However, major gaps in knowledge remain to be filled before such findings can be translated into clinical treatments for AS. In this review, we outline recent findings that demonstrate essential roles of ncRNAs in AS mediated via multiple signaling pathways such as the Wnt, transforming growth factor-β/bone morphogenetic protein, inflammatory, T-cell prosurvival, and nuclear factor-κB pathways. The summary of these findings provides insight into the molecular mechanisms by which ncRNAs can be targeted for AS diagnosis and the development of therapeutic drugs against a variety of autoimmune diseases.
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Tsukazaki, Hiroyuki, and Takashi Kaito. "The Role of the IL-23/IL-17 Pathway in the Pathogenesis of Spondyloarthritis." International Journal of Molecular Sciences 21, no. 17 (September 3, 2020): 6401. http://dx.doi.org/10.3390/ijms21176401.
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Spondyloarthritis (SpA) is a subset of seronegative rheumatic-related autoimmune diseases that consist of ankylosing spondylitis (AS), psoriatic spondylitis (PsA), reactive spondylitis (re-SpA), inflammatory bowel disease (IBD)-associated spondylitis, and unclassifiable spondylitis. These subsets share clinical phenotypes such as joint inflammation and extra-articular manifestations (uveitis, IBD, and psoriasis [Ps]). Inflammation at the enthesis, where ligaments and tendons attach to bones, characterizes and distinguishes SpA from other types of arthritis. Over the past several years, genetic, experimental, and clinical studies have accumulated evidence showing that the IL-23/IL-17 axis plays a critical role in the pathogenesis of SpA. These discoveries include genetic association and the identification of IL-23- and IL-17-producing cells in the tissue of mouse models and human patients. In this review, we summarize the current knowledge of the pathomechanism by focusing on the IL-23/IL-17 pathway and examine the recent clinical studies of biological agents targeting IL-23 and IL-17 in the treatment of SpA.
10
Granata, Guido, Dario Didona, Giuseppina Stifano, Aldo Feola, and Massimo Granata. "Macrophage Activation Syndrome as Onset of Systemic Lupus Erythematosus: A Case Report and a Review of the Literature." Case Reports in Medicine 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/294041.
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Macrophage activation syndrome (MAS) is a potentially fatal condition. It belongs to the hemophagocytic lymphohistiocytosis group of diseases. In adults, MAS is rarely associated with systemic lupus erythematosus, but it also arises as complication of several systemic autoimmune disorders, like ankylosing spondylitis, rheumatoid arthritis, and adult-onset Still’s disease. Several treatment options for MAS have been reported in the literature, including a therapeutic regimen of etoposide, dexamethasone, and cyclosporine. Here we report a case of 42-year-old woman in whom MAS occurred as onset of systemic lupus erythematosus.
11
Pérez-Fernández, Oscar M., Rubén D. Mantilla, Paola Cruz-Tapias, Alberto Rodriguez-Rodriguez, Adriana Rojas-Villarraga, and Juan-Manuel Anaya. "Spondyloarthropathies in Autoimmune Diseases and Vice Versa." Autoimmune Diseases 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/736384.
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Polyautoimmunity is one of the major clinical characteristics of autoimmune diseases (ADs). The aim of this study was to investigate the prevalence of ADs in spondyloarthropathies (SpAs) and vice versa. This was a two-phase cross-sectional study. First, we examined the presence of ADs in a cohort of patients with SpAs (N=148). Second, we searched for the presence of SpAs in a well-defined group of patients with ADs (N=1077) including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren’s syndrome (SS). Among patients with SpAs, ankylosing spondylitis was observed in the majority of them (55.6%). There were two patients presenting with SS in the SpA group (1.4%) and 5 patients with autoimmune thyroiditis (3.5%). The global prevalence of ADs in SpAs was 4.86%. In the ADs group, there were 5 patients with SpAs (0.46%). Our results suggest a lack of association between SpAs and ADs. Accordingly, SpAs might correspond more to autoinflammatory diseases rather than to ADs.
12
Aiba, Yoshihiro, and Minoru Nakamura. "The Role of TL1A and DR3 in Autoimmune and Inflammatory Diseases." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/258164.
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TNF-like ligand 1A (TL1A), which binds its cognate receptor DR3 and the decoy receptor DcR3, is an identified member of the TNF superfamily. TL1A exerts pleiotropic effects on cell proliferation, activation, and differentiation of immune cells, including helper T cells and regulatory T cells. TL1A and its two receptors expression is increased in both serum and inflamed tissues in autoimmune diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and ankylosing spondylitis (AS). Polymorphisms of theTNFSF15gene that encodes TL1A are associated with the pathogenesis of irritable bowel syndrome, leprosy, and autoimmune diseases, including IBD, AS, and primary biliary cirrhosis (PBC). In mice, blocking of TL1A-DR3 interaction by either antagonistic antibodies or deletion of the DR3 gene attenuates the severity of multiple autoimmune diseases, whereas sustained TL1A expression on T cells or dendritic cells induces IL-13-dependent small intestinal inflammation. This suggests that modulation of TL1A-DR3 interaction may be a potential therapeutic target in several autoimmune diseases, including IBD, RA, AS, and PBC.
13
Bank, Ilan. "The Role of Gamma Delta T Cells in Autoimmune Rheumatic Diseases." Cells 9, no. 2 (February 18, 2020): 462. http://dx.doi.org/10.3390/cells9020462.
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Autoimmune rheumatic diseases (ARDs), affecting ~1–1.5% of all humans, are associated with considerable life long morbidity and early mortality. Early studies in the 1990s showed numerical changes of the recently discovered γδ T cells in the peripheral blood and in affected tissues of patients with a variety of ARDs, kindling interest in their role in the immuno-pathogenesis of these chronic inflammatory conditions. Indeed, later studies applied rapid developments in the understanding of γδ T cell biology, including antigens recognized by γδ T cells, their developmental programs, states of activation, and cytokine production profiles, to analyze their contribution to the pathological immune response in these disorders. Here we review the published studies addressing the role of γδ T in the major autoimmune rheumatic diseases, including rheumatoid arthritis, juvenile idiopathic arthritis, ankylosing spondylitis, systemic lupus erythematosus and scleroderma, and animal models thereof. Due to their unique properties spanning adaptive and innate immune functions, the ever deeper understanding of this unique T cell population is shedding new light on the pathogenesis of, while potentially enabling new therapeutic approaches to, these diseases.
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Tizaoui, Kalthoum, Seon Kim, Gwang Jeong, Andreas Kronbichler, Kwang Lee, Keum Lee, and Jae Shin. "Association of PTPN22 1858C/T Polymorphism with Autoimmune Diseases: A Systematic Review and Bayesian Approach." Journal of Clinical Medicine 8, no. 3 (March 12, 2019): 347. http://dx.doi.org/10.3390/jcm8030347.
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The 1858T allele in the protein tyrosine phosphatase non-receptor type 22 (PTPN22) locus shows one of the strongest and most consistent genetic associations with autoimmune diseases. We synthesized all meta-analyses reporting a genetic association of the PTPN22 1858T C/T polymorphism with autoimmune diseases. This work examined their validity to discover false positive results under Bayesian methods. We conducted a PubMed search to identify relevant publications and extracted the respective results, published until 30 November 2018. In observational studies, the associations of 1858 C/T genetic variant were noteworthy for 12 autoimmune or autoimmunity-related diseases (rheumatoid arthritis, systemic lupus erythematosus, type 1 diabetes mellitus, juvenile idiopathic arthritis, Crohn’s disease, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, vitiligo, Graves’ disease, myasthenia gravis, Addison’s disease, giant cell arteritis, and endometriosis). In contrast, we could not confirm the noteworthiness for eight diseases (systemic sclerosis, psoriasis, Behçet’s disease, autoimmune thyroid disease, alopecia areata, Sjögren’s syndrome, inflammatory bowel disease, and ankylosing spondylitis). From the meta-analysis of genome-wide association studies (GWAS) with a p-value < 5 × 10−8, findings verified noteworthiness for all autoimmune diseases (psoriatic arthritis, myasthenia gravis, juvenile idiopathic arthritis and rheumatoid arthritis). The results from meta-analysis of GWAS showing a p-value ranging between 0.05 and 5 × 10−8 were noteworthy under both Bayesian approaches (ANCA-associated vasculitis, type 1 diabetes mellitus, giant cell arteritis and juvenile idiopathic arthritis). Re-analysis of observational studies and GWAS by Bayesian approaches revealed the noteworthiness of all significant associations observed by GWAS, but noteworthiness could not be confirmed for all associations found in observational studies.
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Adams, D. D., J. G. Knight, and A. Ebringer. "The Autoimmune Model of Schizophrenia." ISRN Psychiatry 2012 (April 30, 2012): 1–8. http://dx.doi.org/10.5402/2012/758072.
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Schizophrenia is of mysterious causation. It is not infectious, not congenital, but shows familial aggregation, the Mendelian genetics indicating involvement of multiple codominant genes with incomplete penetrance. This is the pattern for autoimmune diseases, such as Graves’ disease of the thyroid, where forbidden clones of B lymphocytes develop, and cause thyrotoxicosis by secreting autoantibodies that react with the thyroid gland’s receptor for thyroid-stimulating hormone from the pituitary gland. In 1982, Knight postulated that autoantibodies affecting the function of neurons in the limbic region of the brain are a possible cause of schizophrenia. Today, this is even more probable, with genes predisposing to schizophrenia having being found to be immune response genes, one in the MHC and two for antibody light chain V genes. Immune response genes govern the immune repertoire, dictating the genetic risk of autoimmune diseases. The simplest test for an autoimmune basis of schizophrenia would be trial of immunosuppression with prednisone in acute cases. The urgent research need is to find the microbial trigger, as done by Ebringer for rheumatoid arthritis and for ankylosing spondylitis. This could lead to prophylaxis of schizophrenia by vaccination against the triggering microbe.
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Rashid, Taha, and Alan Ebringer. "Autoimmunity in Rheumatic Diseases Is Induced by Microbial Infections via Crossreactivity or Molecular Mimicry." Autoimmune Diseases 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/539282.
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A general consensus supports fundamental roles for both genetic and environmental, mainly microbial, factors in the development of autoimmune diseases. One form of autoimmune rheumatic diseases is confined to a group of nonpyogenic conditions which are usually preceded by or associated with either explicit or occult infections. A previous history of clinical pharyngitis, gastroenteritis/urethritis, or tick-borne skin manifestation can be obtained from patients with rheumatic fever, reactive arthritis, or Lyme disease, respectively, whilst, other rheumatic diseases like rheumatoid arthritis (RA), ankylosing spondylitis (AS), and Crohn’s disease (CD) are usually lacking such an association with a noticeable microbial infection. A great amount of data supports the notion that RA is most likely caused byProteusasymptomatic urinary tract infections, whilst AS and CD are caused by subclinical bowel infections withKlebsiellamicrobes. Molecular mimicry is the main pathogenetic mechanism that can explain these forms of microbe-disease associations, where the causative microbes can initiate the disease with consequent productions of antibacterial and crossreactive autoantibodies which have a great impact in the propagation and the development of these diseases.
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Miranda-Hernández, Mariana P., Carlos A. López-Morales, Francisco C. Perdomo-Abúndez, Rodolfo D. Salazar-Flores, Nancy D. Ramírez-Ibanez, Nestor O. Pérez, Aarón Molina-Pérez, Jorge Revilla-Beltri, Luis F. Flores-Ortiz, and Emilio Medina-Rivero. "New Alternatives for Autoimmune Disease Treatments: Physicochemical and Clinical Comparability of Biosimilar Etanercept." Journal of Immunology Research 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/9697080.
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Etanercept is a recombinant fusion protein approved for the treatment of TNF-αmediated diseases such as rheumatoid arthritis (RA), psoriasis, psoriatic arthritis, and ankylosing spondylitis. Herein, we present an evaluation of the physicochemical and biological properties of a biosimilar etanercept and its reference product followed by a clinical study in patients diagnosed with RA intended to demonstrate comparability of their immunomodulatory activity. Identity analyses showed a total correspondence of the primary and higher-order structure between the two products. In regard to intrinsic heterogeneity, both products showed to be highly heterogenous; however the biosimilar etanercept exhibited similar charge and glycan heterogeneity intervals compared to the reference product. Apoptosis inhibition assay also showed that, despite the high degree of heterogeneity exhibited by both products, no significant differences exist in theirin vitroactivity. Finally, the clinical assessment conducted in RA-diagnosed patients did not show significant differences in the evaluated pharmacodynamic markers of both products. Collectively, the results from the comparability exercise provide convincing evidence that the evaluated biosimilar etanercept can be considered an effective alternative for the treatment of RA.
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Dantes, Elena, Doina Ecaterina Tofolean, Ariadna Petronela Fildan, Liviu Craciun, Elena Dumea, Ioan Tiberiu Tofolean, and Laura Mazilu. "Lethal disseminated tuberculosis in patients under biological treatment – two clinical cases and a short review." Journal of International Medical Research 46, no. 7 (May 23, 2018): 2961–69. http://dx.doi.org/10.1177/0300060518771273.
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Tumour necrosis factor (TNF)-α inhibitors are highly used in Romania for the treatment of autoimmune disorders, such as rheumatoid arthritis (RA), psoriasis, inflammatory bowel diseases, and ankylosing spondylitis. Biological therapy using TNF-α inhibitors is very effective but is associated with an increased risk of opportunistic infections, including active tuberculosis. Here, two cases are presented of patients with RA and psoriasis under biological therapy who developed very aggressive forms of disseminated tuberculosis, with a rapid progression to death. The authors conclude that patients undergoing biological therapy require thorough evaluation prior to initiating treatment, followed by continuous and rigorous monitoring by a multidisciplinary team during biological treatment, particularly in countries with a high incidence of tuberculosis.
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Xie, Lihui, Zhaohao Huang, He Li, Xiuxing Liu, Songguo Zheng, and Wenru Su. "IL-38: A New Player in Inflammatory Autoimmune Disorders." Biomolecules 9, no. 8 (August 5, 2019): 345. http://dx.doi.org/10.3390/biom9080345.
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Interleukin (IL)-38, a newly discovered IL-1 family cytokine, is expressed in several tissues and secreted by various cells. IL-38 has recently been reported to exert an anti-inflammatory function by binding to several receptors, including interleukin-36 receptor (IL-36R), interleukin-1 receptor accessory protein-like 1 (IL-1RAPL1), and interleukin-1 receptor 1 (IL-1R1) to block binding with other pro-inflammatory cytokines and inhibit subsequent signaling pathways; thereby regulating the differentiation and function of T cells, peripheral blood mononuclear cells, macrophages, and dendritic cells. Inflammatory autoimmune diseases, which are common immune-mediated inflammatory syndromes, are characterized by an imbalance between T helper cells (Ths), especially Th1s and Th17s, and regulatory T cells (Tregs). Recent findings have shown that abnormal expression of IL-38 in inflammatory autoimmune diseases, such as rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus, primary Sjogren’s syndrome, psoriasis, inflammatory bowel disease, hidradenitis suppurativa, ankylosing spondylitis, and glaucoma, involves Th1s, Th17s, and Tregs. In this review, the expression, regulation, and biological function of IL-38 are discussed, as are the roles of IL-38 in various inflammatory autoimmune disorders. Current data support that the IL-38/IL-36R and/or IL-38/IL-1RAPL1 axis primarily play an anti-inflammatory role in the development and resolution of inflammatory autoimmune diseases and indicate a possible therapeutic benefit of IL-38 in these diseases.
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Andreadou, E., E. Kemanetzoglou, Ch Brokalaki, M. E. Evangelopoulos, C. Kilidireas, A. Rombos, and E. Stamboulis. "Demyelinating Disease following Anti-TNFa Treatment: A Causal or Coincidental Association? Report of Four Cases and Review of the Literature." Case Reports in Neurological Medicine 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/671935.
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Tumor necrosis factor antagonists (anti-TNFa) are an established therapeutic option for several autoimmune and inflammatory bowel diseases. Despite their clinical effectiveness, neurological adverse events have been reported and literature data suggest a potential role of anti-TNFa in the induction of demyelination of the CNS. We present four patients treated with anti-TNFa who developed symptoms suggestive of CNS demyelination. The first patient, a 17-year-old male who received etanercept for psoriatic arthritis for eight months, presented with dysesthesias up to T4 level. The second patient, a 30-year-old male treated with adalimumab for three years due to ankylosing spondylitis, presented with right unilateral tinnitus. The third case, a 47-year-old female, received etanercept for four years because of psoriatic arthritis and developed persistent headache and left-sided face and head numbness. Finally, the fourth patient, a 57-years-old female treated with etanercept for six years due to ankylosing spondylitis, presented with difficulty in speech, swallowing, and ptosis of the right corner of the mouth. In all cases, brain MRI showed lesions suggestive of demyelination, while positive oligoclonal bands were detected in the CSF. Anti-TNFa treatments were discontinued and patients showed clinical improvement with pulsed intravenous corticosteroid therapy. CNS demyelination following anti-TNFa treatment represents a relatively rare but potential serious complication. Close follow-up and MRI monitoring of these patients is mandatory to elucidate whether the clinical manifestations represent adverse events occurring during anti-TNFa therapy or a first demyelinating episode.
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Wilbrink, R., A. Spoorenberg, S. Arends, F. G. M. Kroese, and G. M. Verstappen. "POS0412 CD21-/LOW B-CELLS ARE INCREASED IN PATIENTS WITH ANKYLOSING SPONDYLITIS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 435.2–436. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2957.
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Background:Ankylosing spondylitis (AS) is a chronic immune mediated inflammatory rheumatic disease, in which primarily the sacroiliac joints and the spine are affected. Extra-skeletal manifestations (ESM) include uveitis, psoriasis, inflammatory bowel disease and peripheral arthritis. In studies into the pathogenesis of AS, B-cells have received little attention most likely due to the lack of auto-antibodies1. A B-cell subset that has been particularly associated with autoreactivity is characterized by low expression of CD21. These CD21-/low B-cells are increased in systemic autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus and primary Sjögren syndrome (pSS)2. At least part of the CD21-/low B-cells are considered to represent anergic, autoreactive B-cells, that fail to become activated through conventional B-cell receptor and CD40 signaling2.Objectives:To phenotypically study the peripheral B-cell compartment in in the blood of AS patients compared to pSS patients, a typical B-cell-associated autoimmune disease, and healthy controls (HC). Special emphasis was given to the CD21-/low compartment.Methods:The proportions and phenotype of peripheral B-cells were assessed in cryopreserved peripheral blood mononuclear cells of 45 AS patients (62% male, mean age 49.2±13.2 years, mean ASDAS 2.5±1.0), 20 age-matched patients with pSS (20% male, mean age 50.6±12.0, median (IQR) ESSDAI 3±6.25) and 30 age- and sex-matched HCs, using 15-color flow-cytometry analysis. Differences between groups were tested using the Independent Samples t-test or Mann-Whitney U test depending on the distribution of variables. Associations between CD21-/low B-cells and clinical parameters were explored using the Pearson or Spearman correlation coefficient.Results:The percentage of total B-cells in AS patients did not differ from pSS patients and HCs. In AS patients, percentages of CD27+ memory B-cells and CD27-IgD+ naïve B-cells were also similar to HCs, whereas CD27+IgD- memory B-cells were significantly reduced in pSS patients, as expected. The proportions of CD27-CD38lowCD21-/low B-cells among total B-cells were significantly increased in both AS (median 6.4%, p<0.0001) and pSS patients (median 7.8%, p<0.0001) compared to HCs (median 4.9%). Interestingly, only in AS patients, expression of chemokine receptors CXCR3 and CXCR5 was significantly elevated on CD27-CD38lowCD21-/low B-cells compared to HCs (p<0.001 and p<0.01, respectively). In comparison to HCs the expression of the immune markers T-bet and CD11c by CD27-CD38lowCD21-/low B-cells was significantly lower in AS patients (p<0.01 and p<0.01, respectively). The distribution of IgM and IgD expression within the CD27-CD38lowCD21-/low B-cell population was similar between all three study groups. Regarding the association between CD27-CD38lowCD21-/low B-cells and clinical parameters in AS patients, we observed a positive correlation with age (r=0.347, p=0.02) and erythrocyte sedimentation rate (ρ=0.386, p=0.01). Furthermore, AS patients with ESM showed increased proportions of CD27-CD38lowCD21-/low B-cells compared to patients without ESM (p<0.05).Conclusion:In this cross-sectional study, we observed an increased proportion of circulating CD27-CD38lowCD21-/low B-cells in AS patients, similar as in patients with pSS, a typical B-cell-mediated autoimmune disease. The elevated expression of CXCR3 on CD27-CD38lowCD21-/low B-cells in AS patients is suggestive for active involvement in the inflammatory response. These findings are indicative of B-cell involvement in the pathogenesis of AS, against current dogma.References:[1]Ranganathan V et al. Nat Rev Rheumatol. 2017;13(6):359-367.[2]Thorarinsdottir K et al. Scand J Immunol. 2015;82(3):254-261.Disclosure of Interests:Rick Wilbrink: None declared, Anneke Spoorenberg: None declared, Suzanne Arends: None declared, Frans G.M. Kroese Speakers bureau: BMS, Roche, Janssen-Cilag, Consultant of: BMS, Grant/research support from: BMS, Gwenny M. Verstappen: None declared
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Perrotta, F. M., G. Guerra, A. De Socio, S. Scriffignano, and E. Lubrano. "Mesenchimal stem cells: a possible role in the pathogenesis and treatment of spondyloarthritis." Reumatismo 69, no. 1 (May 22, 2017): 1. http://dx.doi.org/10.4081/reumatismo.2017.976.
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Spondyloarthritis (SpAs) are a group of chronic inflammatory diseases that affect joints and enthesis with a possible involvement of other districts such as skin, eye and bowel. In SpAs, the inflammatory process could lead to both erosive damage (as in peripheral joint involvement of psoriatic arthritis), or bone formation (as in ankylosing spondylitis) with a reduction in function and quality of life. Recently, Mesenchimal stem cells (MSCs) transplant was used in different diseases, including autoimmune and inflammatory diseases, with the aim of repairing tissue damage, exploiting their regenerative capacity. However, MSCs also proved to have an immune-modulatory capacity due to their interaction with the cells of the immune system. The aim of this brief paper was to review the possible pathogenic role and the new perspective of MSCs use in SpAs.
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Zhao-wei, Gao, Guan-hua Zhao, Rui-cheng Li, Hui-ping Wang, Chong Liu, Hui-zhong Zhang, and Ke Dong. "Activities of Serum Adenosine Deaminase and its Isoenzymes in Patients with Systemic Lupus Erythematosus, Rheumatoid Arthritis, Ankylosing Spondylitis and Myasthenia Gravis." Aktuelle Rheumatologie 45, no. 04 (November 21, 2019): 348–55. http://dx.doi.org/10.1055/a-1024-3495.
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Abstract Objective The aim of this study was to evaluate the changes and diagnostic value of serum ADA activity in autoimmune diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), ankylosing spondylitis (AS), and myasthenia gravis (MG). Methods Serum ADA activity, including total ADA (tADA) and its isoenzymes (ADA1 and ADA2), was determined in patients with different autoimmune diseases (144 RA, 114 SLE, 55 AS, 68 MG). The changes in serum ADA activity in patients were analysed. A receiver operating characteristic (ROC) curve analysis was applied to evaluate the diagnostic performance of serum ADA activity. Results Compared with healthy controls, the serum tADA activity in SLE patients was significantly increased (p<0.001), while the serum tADA activity in patients with RA, AS and MG did not change (p>0.05). The ROC analysis showed that the optimal cut-off value of serum tADA activity for SLE diagnosis was 10.5 U/L (79.8% specificity and 74.6% sensitivity; likelihood ratio (LR): 3.693; p<0.001). Moreover, our results showed that there were no significant changes of ADA1 and ADA2 activity in RA, AS and MG patients, while the serum ADA2 activity was significantly increased in SLE patients. The ROC analysis showed that ADA2 activity could be used in diagnosing SLE with 75.4% specificity and 78.1% sensitivity (LR: 3.175). Based on the ROC curve analysis, serum tADA activity (79.8% specificity and 74.6% sensitivity; likelihood ratio (LR): 3.693) and ADA2 activity (75.4% specificity and 78.1% sensitivity; LR: 3.175) are unlikely to be used in diagnosing SLE. Furthermore, there was a positive correlation between tADA activity and SLE disease activity (r=0.303, p=0.010). Notably, serum tADA activity in SLE patients with arthritis was higher than in patients without arthritis (p=0.005), which suggests that tADA activity might be related to lupus arthritis. Conclusion These findings suggest that serum tADA and ADA2 activity might play an important role in SLE progression.
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Ma, Jun, Clare L. Abram, Yongmei Hu, and Clifford A. Lowell. "CARD9 mediates dendritic cell–induced development of Lyn deficiency–associated autoimmune and inflammatory diseases." Science Signaling 12, no. 602 (October 8, 2019): eaao3829. http://dx.doi.org/10.1126/scisignal.aao3829.
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CARD9 is an immune adaptor protein in myeloid cells that is involved in C-type lectin signaling and antifungal immunity. CARD9 is implicated in autoimmune and inflammatory-related diseases, such as rheumatoid arthritis, IgA nephropathy, ankylosing spondylitis, and inflammatory bowel disease (IBD). Given that Lyn-deficient (Lyn−/−) mice are susceptible to both autoimmunity and IBD, we investigated the immunological role of CARD9 in the development of these diseases using the Lyn−/− mouse model. We found that genetic deletion of CARD9 was sufficient to reduce the development of both spontaneous autoimmune disease as well as DSS- or IL-10 deficiency–associated colitis in Lyn−/− mice. Mechanistically, CARD9 was a vital component of the Lyn-mediated regulation of Toll-like receptor (TLR2 and TLR4) signaling in dendritic cells, but not in macrophages. In the absence of Lyn, signaling through a CD11b-Syk-PKCδ-CARD9 pathway was amplified, leading to increased TLR-induced production of inflammatory cytokines. Dendritic cell–specific deletion of CARD9 reversed the development of autoimmune and experimental colitis observed in dendritic cell–specific, Lyn-deficient mice. These findings suggest that targeting CARD9 may suppress the development of colitis and autoimmunity by reducing dendritic cell–driven inflammation.
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Kemeny-Beke, Adam, and Peter Szodoray. "Ocular manifestations of rheumatic diseases." International Ophthalmology 40, no. 2 (October 3, 2019): 503–10. http://dx.doi.org/10.1007/s10792-019-01183-9.
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Abstract Purpose Our aim was to summarize key aspects of the pathomechanism and the ocular involvements of rheumatic and systemic autoimmune diseases. Methods Apart from a paper in French (Morax V, Ann Oculist 109:368–370, 1893), all papers referred to in this article were published in English. All the materials were peer-reviewed full-text papers, letters, reviews, or book chapters obtained through a literature search of the PubMed database using the keywords ocular manifestations; pathogenesis; systemic inflammatory rheumatic diseases; rheumatoid arthritis; osteoarthritis; fibromyalgia; systemic lupus erythematosus; seronegative spondyloarthritis; ankylosing spondylitis; reactive arthritis; enteropathic arthritis; psoriatic arthritis; systemic sclerosis; polymyalgia rheumatica and covering all years available. Some statements articulated in this paper reflect the clinical experience of the authors in their tertiary-referral center. Results Ophthalmic disorders are categorized by anatomical subgroups in all rheumatic diseases. The most common ocular manifestations are diverse types of inflammations of different tissues and dry eye disease (DED). Conclusion The eye could be a responsive marker for the onset or aggravation of an immune reactivation in many rheumatic diseases, furthermore, ocular findings can antedate the diagnosis of the underlying rheumatic disease. By recognizing ocular manifestations of systemic rheumatic diseases it might be possible to avoid or at least delay many long term sequelae.
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Rosenzwajg, Michelle, Roberta Lorenzon, Patrice Cacoub, Hang Phuong Pham, Fabien Pitoiset, Karim El Soufi, Claire RIbet, et al. "Immunological and clinical effects of low-dose interleukin-2 across 11 autoimmune diseases in a single, open clinical trial." Annals of the Rheumatic Diseases 78, no. 2 (November 24, 2018): 209–17. http://dx.doi.org/10.1136/annrheumdis-2018-214229.
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ObjectiveRegulatory T cells (Tregs) prevent autoimmunity and control inflammation. Consequently, any autoimmune or inflammatory disease reveals a Treg insufficiency. As low-dose interleukin-2 (ld-IL2) expands and activates Tregs, it has a broad therapeutic potential.AimWe aimed to assess this potential and select diseases for further clinical development by cross-investigating the effects of ld-IL2 in a single clinical trial treating patients with 1 of 11 autoimmune diseases.MethodsWe performed a prospective, open-label, phase I–IIa study in 46 patients with a mild to moderate form of either rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, psoriasis, Behcet’s disease, granulomatosis with polyangiitis, Takayasu’s disease, Crohn’s disease, ulcerative colitis, autoimmune hepatitis and sclerosing cholangitis. They all received ld-IL2 (1 million IU/day) for 5 days, followed by fortnightly injections for 6 months. Patients were evaluated by deep immunomonitoring and clinical evaluation.Resultsld-IL2 was well tolerated whatever the disease and the concomitant treatments. Thorough supervised and unsupervised immunomonitoring demonstrated specific Treg expansion and activation in all patients, without effector T cell activation. Indication of potential clinical efficacy was observed.ConclusionThe dose of IL-2 and treatment scheme used selectively activate and expand Tregs and are safe across different diseases and concomitant treatments. This and preliminary indications of clinical efficacy should licence the launch of phase II efficacy trial of ld-IL2 in various autoimmune and inflammatory diseases.Trial registration numberNCT01988506.
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Voinescu, Doina Carina, Adrian Beznea, Ciprian Dinu, Camelia Ana Grigore, Silvia Fotea, Cristina Preda, Mihaela-Elena Zamfirescu, Daniela Laura Buruiana, and Aurel Nechita. "Reactive Arthritis The Reiter-Fiessinger-Leroy Syndrome." Revista de Chimie 71, no. 2 (March 3, 2020): 386–91. http://dx.doi.org/10.37358/rc.20.2.7941.
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The role of creating the expression of reactive arthritis rests with AHO in 1973, which defines reactive arthritis as an acute, unsupportive, sterile inflammatory arthropathy, arising from infections located at a distance in people with a certain genetic predisposition; the disease is systemic and, despite its name, is not limited to the joints. Reactive arthritis (RA), included in Reiter syndrome (with the classic triad of urethritis, conjunctivitis and arthritis), is a non-suppurative inflammatory joint pathology, with a minimal autoimmune component, which it is installed following intestinal or urogenital infections, mainly in people with genetic predisposition. Reactive arthritis is a form of arthritis that affects the joints, urethra, eyes and membranes and sometimes the skin and mucous membranes. This condition is also called Reiter`s syndrome, although this name only indicates a subtype. Reactive arthritis is a seronegative spondyloarthropathy, which brings together a group of disorders that cause inflammation in the body, especially in the spine - such as ankylosing spondylitis, and in the legs. The study covers a number of 20 patients (11 men, 9 women) admitted to the Rheumatology Service of the Clinical Recovery Hospital, between 2010 and 2011, aged over 20, who were diagnosed with reactive arthritis. The existence of a structural similarity between the etiological agent and the HLA-B27 molecule determines either the recognition of the disease-causing germ as a self, so that no immune response will be initiated against it and the antigen will be able to trigger the disease, or the recognition of the germ as nonself, with the triggering of an immune response aimed at both itself and against the HLA-B27 molecule carrying cells of similar structure. Reactive arthritis (RA), included in the Reiter syndrome (with the classic triad of urethritis, conjunctivitis and arthritis), is a non-suppurative inflammatory joint pathology, with a minimal autoimmune component, which is installed as a result of intestinal or urogenital infections, mainly in people with genetic predisposition.
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JUNG, KYONG-HEE, TAE-HWAN KIM, DONG-HYUK SHEEN, MI-KYOUNG LIM, SANG-KWANG LEE, JI-YOUNG KIM, HYO PARK, SOO-CHEON CHAE, and SEUNG-CHEOL SHIM. "Associations of Vitamin D Binding Protein Gene Polymorphisms with the Development of Peripheral Arthritis and Uveitis in Ankylosing Spondylitis." Journal of Rheumatology 38, no. 10 (August 15, 2011): 2224–29. http://dx.doi.org/10.3899/jrheum.101244.
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Objective.Genetic factors account for more than 90% of overall susceptibility to ankylosing spondylitis (AS), and recent studies have focused on non-major histocompatibility complex genes. Vitamin D binding protein (DBP) is a highly polymorphic protein that transports vitamin D and its metabolites. In addition to its sterol binding capacity, DBP has many other roles in the inflammatory and immune systems, and has been reported to be associated with autoimmune diseases. We investigated the association between DBP polymorphisms and susceptibility to AS.Methods.This case-control study was conducted in 223 patients with AS and 239 ethnically matched controls who were genotyped for 8 single-nucleotide polymorphisms (SNP) in the DBP and its promoter. Genomic DNA was isolated from peripheral blood leukocytes using the standard phenolchloroform method, and the GoldenGate assay was used for genotyping.Results.No significant association was found between the susceptibility to AS and DBP polymorphisms. In a subgroup analysis of patients with AS, G alleles at rs222016 and rs222020 (OR 0.63, 95% CI 0.42–0.95, p = 0.03; OR 0.63, 95% CI 0.42–0.95, p = 0.03, respectively) and A allele at rs3733359 (OR 0.59, 95% CI 0.39–0.90, p = 0.01) showed the decreased risk of peripheral arthritis. G allele at rs4752 showed increased risk of uveitis (OR 2.04, 95% CI 1.12–3.72, p = 0.02). On the haplotype analyses, haplotype 2 (AGGA) protected against the development of peripheral arthritis (p = 0.01) and haplotype 3 (GAAG) was associated with an increased likelihood of uveitis (p = 0.02).Conclusion.DBP gene polymorphisms are associated with the development of peripheral arthritis and uveitis in Korean patients with AS. Given the influence of different DBP variants on the immune system, larger-scale studies are warranted to elucidate the role of DBP in the pathogenesis of AS.
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Yao, Xuan, Megat Abd Hamid, Anand Sundaralingam, Alice Evans, Roshan Karthikappallil, Tao Dong, Najib M. Rahman, and Nikolaos I. Kanellakis. "Clinical perspective and practices on pleural effusions in chronic systemic inflammatory diseases." Breathe 16, no. 4 (December 2020): 200203. http://dx.doi.org/10.1183/20734735.0203-2020.
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Systemic inflammatory diseases are a heterogeneous family of autoimmune chronic inflammatory disorders that affect multiple systems within the human body. Connective tissue disease (CTD) is a large group within this family characterised by immune-mediated inflammation of the connective tissue. This group of disorders are often associated with pleural manifestations. CTD-induced pleuritis exhibits a wide variety of symptoms and signs including exudative pleural effusions and chest pain. Accurate estimation of prevalence for CTD-related pleuritis is challenging as small effusions are asymptomatic and remain undetected. Rheumatoid arthritis and systemic lupus erythematosus are frequent CTDs and present with pleural pathology in approximately 5–20% and 17–60% of cases, respectively. By contrast, pleural involvement in systemic sclerosis, eosinophilia–myalgia syndrome, mixed connective tissue disease, ankylosing spondylitis, polymyositis and dermatomyositis syndrome is rare. Clinical management depends on the severity of symptoms; however, most effusions resolve spontaneously. In this review we discuss the pathophysiological mechanisms and the clinical considerations of CTD-induced pleuritis.
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Baek, D., H. S. Lee, S. B. Park, H. K. Song, B. I. Jang, J. H. Bae, H. J. Goong, et al. "P816 Association of autoimmune rheumatic disease with inflammatory bowel disease: a nationwide population-based study." Journal of Crohn's and Colitis 14, Supplement_1 (January 2020): S635—S636. http://dx.doi.org/10.1093/ecco-jcc/jjz203.944.
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Abstract Background Increasing evidence demonstrated that inflammatory bowel disease (IBD) has a shared genetic background with autoimmune rheumatic diseases (ARDs). However, the association between these two disease entities is not vigorously elucidated. The aim of this study is to investigate the prevalence and association between IBD and ARDs. Methods A nationwide population-based cross-sectional study was performed using the Korean National Health Insurance Claims database according to ICD-10 codes (Table 1). The prevalence of ARDs, including systemic lupus erythematosus (SLE), inflammatory myositis (polymyositis (PM) and dermatomyositis (DM)), systemic sclerosis (SSc), Sjogren’s syndrome (SjS), ankylosing spondylitis (AS), and rheumatoid arthritis (RA), was determined in patients with inflammatory bowel disease, compared with general populations. Results A total of 82,480 IBD patients (57,382 patients with ulcerative colitis and 25,098 with Crohn’s disease) were enrolled. The analysis revealed that patient with IBD had higher risk of being concomitantly affected by AS and RA (Table 2). Other ARDs, such as SLE, inflammatory myositis, SSc, and SjS were not associated with IBD. Conclusion This nationwide population-based study demonstrated that RA and AS showed higher incidence in IBD patients. This result suggests that etiopathogenesis of IBD might be shared with RA and AS.
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Sarker, A., T. Shukla, A. Rostom, J. Sim, and J. D. McCurdy. "A194 A POSSIBLE ASSOCIATION BETWEEN SECUKINUMAB AND NEW-ONSET INFLAMMATORY BOWEL DISEASE: A CASE SERIES." Journal of the Canadian Association of Gastroenterology 4, Supplement_1 (March 1, 2021): 216–17. http://dx.doi.org/10.1093/jcag/gwab002.192.
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Abstract Background Secukinumab is a monoclonal antibody targeting interleukin-17A and is commonly used for managing autoimmune diseases such as, psoriasis, psoriatic arthritis, and ankylosing spondylitis. Prior studies have suggested that anti-IL17 therapy may worsen symptoms in patients with pre-existing inflammatory bowel disease (IBD). However, it remains unclear if secukinumab is associated with new-onset IBD or in provoking a flare of previously quiescent IBD. Aims We evaluated patients referred to our IBD clinic who developed intestinal inflammation after starting secukinumab for the management of autoimmune diseases. Methods We performed a retrospective, observational study at a single tertiary care center between 2017 and 2020. Patients referred to our IBD clinic who developed intestinal inflammation after starting secukinumab were included. We excluded patients with an established pre-existing diagnosis of IBD and patients who had positive stool testing for infectious organisms. Patient demographics, disease characteristics, distribution of intestinal inflammation and clinical outcomes were assessed. The pathology slides were reinterpreted by a single pathologist with a specialty in gastroenterology to determine the histologic characteristics of the inflammation. Results A total of 8 patients developed gastrointestinal symptoms after starting secukinumab: 4 (50%) males with a median age of 42.5 (IQR: 35–50 years old). Secukinumab was initiated for psoriasis in 3 (37.5%) patients, psoriatic arthritis in 2 (25%) patients, ankylosing spondylitis in 2 (25%) patients and juvenile idiopathic arthritis in 1 (12.5%) patient. The median time of onset for gastrointestinal symptoms after starting secukinumab was 7 months (IQR: 4–15 months). Of the patients who underwent testing for inflammatory biomarkers, the median CRP was 25.5 (IQR 25.4–34.2). Endoscopic disease distribution involved the colon in 5 (62.5%) patients and the ileum and colon in 3 (37.5%) patients. In this series of patients, the histologic characteristics demonstrated three patterns of colitis: IBD-like (ulcerative colitis or Crohn’s disease) in 6 (75%) patients based on mucosal granulomas and/or chronic inflammatory changes, MMF-like histology in 1 (12.5%) patient, characterized by an abundance of intraepithelial eosinophils in the lamina propria and numerous crypt apoptotic bodies, and finally active colitis in 1 (12.5%) patient characterized by an absence of chronic mucosal injury or granulomas. The treatment for these patients was cessation of secukinumab and initiating alternative therapies with close clinical monitoring. Conclusions In this small case series, Secukinumab was temporally associated with the development of gastrointestinal inflammation. Further larger studies are required to confirm this association and to determine if IL-17 contributes to the pathogenesis of IBD. Funding Agencies None
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Barton, James C., and J. Clayborn Barton. "Autoimmune Conditions in 235 Hemochromatosis Probands withHFEC282Y Homozygosity and Their First-Degree Relatives." Journal of Immunology Research 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/453046.
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We performed a retrospective study of autoimmune conditions (ACs) in 235 hemochromatosis probands at diagnosis by analyzing age, sex, ACs, history of first-degree family members with ACs (FH), diabetes, heavy ethanol consumption, elevated serum ALT/AST, nonalcoholic fatty liver disease, viral hepatitis, cirrhosis, iron removed to achieve iron depletion (QFe), and positivity for human leukocyte antigen (HLA) haplotypesA∗01,B∗08;A∗02,B∗44;A∗03,B∗07;A∗03,B∗14; andA∗29,B∗44. There were 138 men (58.7%). Median followup was 19.6 y. One or more of 19 ACs were diagnosed in each of 35 probands (14.9%). Prevalences of Hashimoto’s thyroiditis, rheumatoid arthritis, and ankylosing spondylitis were 8.1% (95% CI: [5.1, 12.5]), 1.7% [0.6, 4.6], and 0.0085 [0.0015, 0.0337], respectively. Eighteen probands (7.7%) had a FH. Eight probands with ACs had 9 family members with ACs. In a logistic regression, ACs were less likely in men (odds ratio (OR) 0.3 [0.1, 0.6]) and more likely in probands with a FH (OR 4.1 [1.4, 11.8]). Overall ACs risk was not significantly associated with QFe or HLA haplotypes. Estimated survival of probands with and without ACs did not differ significantly. We conclude that ACs are common in hemochromatosis probands, especially women and probands with a FH.
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Lorente, Elena, Miguel G. Fontela, Eilon Barnea, Antonio J. Martín-Galiano, Carmen Mir, Begoña Galocha, Arie Admon, Pilar Lauzurica, and Daniel López. "Modulation of Natural HLA-B*27:05 Ligandome by Ankylosing Spondylitis-associated Endoplasmic Reticulum Aminopeptidase 2 (ERAP2)." Molecular & Cellular Proteomics 19, no. 6 (April 7, 2020): 994–1004. http://dx.doi.org/10.1074/mcp.ra120.002014.
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The HLA-B*27:05 allele and the endoplasmic reticulum-resident aminopeptidases are strongly associated with AS, a chronic inflammatory spondyloarthropathy. This study examined the effect of ERAP2 in the generation of the natural HLA-B*27:05 ligandome in live cells. Complexes of HLA-B*27:05-bound peptide pools were isolated from human ERAP2-edited cell clones, and the peptides were identified using high-throughput mass spectrometry analyses. The relative abundance of a thousand ligands was established by quantitative tandem mass spectrometry and bioinformatics analysis. The residue frequencies at different peptide position, identified in the presence or absence of ERAP2, determined structural features of ligands and their interactions with specific pockets of the antigen-binding site of the HLA-B*27:05 molecule. Sequence alignment of ligands identified with species of bacteria associated with HLA-B*27-dependent reactive arthritis was performed. In the absence of ERAP2, peptides with N-terminal basic residues and minority canonical P2 residues are enriched in the natural ligandome. Further, alterations of residue frequencies and hydrophobicity profile at P3, P7, and PΩ positions were detected. In addition, several ERAP2-dependent cellular peptides were highly similar to protein sequences of arthritogenic bacteria, including one human HLA-B*27:05 ligand fully conserved in a protein from Campylobacter jejuni. These findings highlight the pathogenic role of this aminopeptidase in the triggering of AS autoimmune disease.
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Woo, Yu Ri, Hei Sung Kim, Se Hoon Lee, Hyun Jeong Ju, Jung Min Bae, Sang Hyun Cho, and Jeong Deuk Lee. "Systemic Comorbidities in Korean Patients with Rosacea: Results from a Multi-Institutional Case-Control Study." Journal of Clinical Medicine 9, no. 10 (October 17, 2020): 3336. http://dx.doi.org/10.3390/jcm9103336.
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Recent evidence links rosacea to systemic disease, but there are not enough methodologic studies addressing this association in Asians. Our aim was to identify rosacea comorbidities in Koreans and establish a reference database. A multi-center, case-control study was performed where a total of 12,936 rosacea patients and 12,936 age- and sex-matched control subjects were identified from 2007 to 2018. Logistic regression was performed to find significant association between rosacea and Sjögren syndrome (odds ratio [OR] 2.05; 95% confidence interval, 1.40–3.00), systemic sclerosis (OR 6.56; 95% CI, 1.50–28.7), rheumatoid arthritis (OR 1.72; 95% CI, 1.50–1.98), ankylosing spondylitis (OR 2.32; 95% CI, 1.42–3.84), autoimmune thyroiditis (OR 1.96; 95% CI, 1.40–2.73), alopecia areata (OR 1.77; 95% CI, 1.27–2.45), vitiligo (OR 1.90; 95% CI, 1.30–2.77), lung cancer (OR 1.54; 95% CI, 1.06–2.21), hepatobiliary cancer (OR 1.38; 95% CI, 1.06–1.77), alcohol abuse (OR 1.59; 95% CI, 1.05–2.39), diabetes mellitus (OR 1.11; 95% 1.02–1.19), obesity (OR 1.72; 95% CI, 1.22–2.41), allergic rhinitis (OR 1.65; 95% CI, 1.54–1.76), allergic conjunctivitis (OR 1.57; 95% CI, 1.27–1.94), chronic rhinosinusitis (OR 1.28; 95% CI, 1.14–1.42), herpes infection (OR 1.69; 95% CI, 1.53–1.86), and human papillomavirus infection (OR 2.50; 95% CI, 2.06–3.02). Higher odds for Sjogren syndrome, systemic sclerosis, ankylosing spondylitis, thyroiditis, vitiligo, hepatobiliary cancer, and obesity was exclusive in female subjects with rosacea, whereas increased prevalence of alopecia areata and alcohol abuse was confined to men. Only those who were 50 years and older exhibited higher odds for vitiligo, lung cancer, and gastroesophageal reflux disease while individuals younger than 50 were exclusively associated with hepatobiliary cancer, allergic conjunctivitis, and irritable bowel syndrome. Our study suggests that Koreans with rosacea are more likely to experience systemic comorbidity. Clinicians should acknowledge these interrelations and employ comprehensive care with an individual-based approach.
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Feiskhanova, L. I., and L. R. Khaliullina. "Cardiac involvement in some rheumatic diseases." Clinical Medicine (Russian Journal) 96, no. 7 (December 15, 2018): 597–603. http://dx.doi.org/10.18821/0023-2149-2018-96-7-597-603.
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The review covers the modern scientific literature about cardiovascular disease in patients with rheumatic diseases. Rheumatic diseases are associated with chronic inflammation, most often joints, skin, eyes, lungs, kidneys and circulatory system. Cardiovascular manifestations of autoimmune diseases can be mild and clinically silent; they can also increase morbidity and mortality. Defeat of cardiovascular system at patients with rheumatoid arthritis: myocarditis, a pericarditis, myocardial fibrosis, ventricular arrhythmias, a syndrome of the extended interval of QT, atrial fibrillation, valvulopathy, development of chronic heart failure, formation of heart disease. Cardiac involvement in systemic lupus erythematosus follows different pathophysiologic mechanisms and covers a wide spectrum of clinical phenotypes including pericarditis, myocarditis, valvular abnormalities, aseptic endocarditis, heartfailure, ischaemic heart disease and pulmonary hypertension. Valvular disease in systemic lupus erythematosus includes valvulitis, aortic and mitral regurgitation, aortic stenosis. For diagnosis of cardiovascular diseases are used clinical laboratory methods, the electrocardiogram, echocardiography, single-photon emission computed tomography, positron emission tomography/ computed tomography, computed coronary angiography, computed tomography, magnetic resonance imaging. The following echocardiographic abnormalities have been reported in ankylosing spondylitis: ascending aortitis, aortic and mitral regurgitation, mitral valve prolapse and diastolic dysfunction. The following echocardiographic abnormalities can be seen in psoriatic arthritis: fibrinous pericarditis, myocarditis and valvular disease.
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Lila, A. M., E. A. Galushko, A. V. Gordeev, and A. S. Semashko. "The role of microbiome in the pathogenesis of immune-mediated inflammatory diseases: controversial issues." Modern Rheumatology Journal 15, no. 1 (February 18, 2021): 15–19. http://dx.doi.org/10.14412/1996-7012-2021-1-15-19.
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Increasing attention in rheumatology is today paid to the detection of diseases at the earliest possible (preclinical) stages, which can contribute to a more favorable response to therapy. The preclinical period of a systemic autoimmune reaction is assumed to be related to dysregulation of immune interactions with the synanthropic microflora. A sequencing method was used to study deviations in the diversity of the gut microflora in patients with rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis. However, a number of unresolved issues remain, since the emphasis has been on the cataloguing of the microorganisms present and on the identification of correlations between microbial species and diseases. The main difference in future microbiome research in patients with immune-mediated inflammatory diseases should be a closer examination of the functions of microbiota components, and not just their description. Long-term studies with the collection of intestinal microbiome samples are required at several time intervals: before disease-modifying antirheumatic drug therapy and during ineffective therapy. Such studies will contribute to the development of new diagnostic and therapeutic interventions. Until they are completed, it is untimely to recommend microbiome analysis as a diagnostic or prognostic tool for the management of rheumatic diseases in clinical practice.
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Fayed, F., E. Abdelkarim, and M. Morsy. "AB1210 THE IMPACT OF EXAMINATION STRESS ON AUTOIMMUNE DISEASES AMONG UNIVERSITY STUDENTS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1896.3–1896. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4681.
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Background:Stress is a risk factor of various diseases including autoimmune diseases. Autoimmune diseases are one of the leading causes of morbidity in young adults.(1)Examination stress is a main concern nowadays due to the study style, lack of preparation, doctor- student relationship and family pressure.(2)The previous studies declared that stress may causes neuroendocrinal changes leading to immune dysregulations and cytokines production.(3)Objectives:The aim of study is to scope the light on the importance of stress as a predisposing factor in autoimmune disease flares particularly Examination stress.Methods:A three-year (2017-2019) cross-sectional prospective study conducted on 1365 students who presented to the Alexandria University rheumatology clinic during examinations. Clinical assessments, routine investigations, activity markers, activity indices, stress and anxiety questionnaires and perceived stress scale (PSS) were applied to all patients during consecutive visits.Results:Through 5800 visits in three years during examination sessions, patients age ranged from (17 -25) years with 76% females and 24% males. They grouped into SLE (31.35%), Rheumatoid arthritis (RA) (37.28%), Fibromyalgia (13.91%), FMF (2.63%), Ankylosing Spondylitis (1.75%), Psoriatic arthritis (0.73%), systemic sclerosis (0.58%), and undifferentiated connective tissue (11.73%). According to SLE patients, 43.92% were newly diagnosed whilst 54.16% of previously diagnosed SLE presented with Flare in particular lupus nephritis (56.33%), arthritis (43.22%), hematological (49.76%) and serositis (21.36%). Interestingly, RA patients who newly diagnosed were 35.16% of total RA patients while 42.42% of previously diagnosed RA patients presented with moderate and high DAS-28 due to incompliance with treatment in (64.37%) of patients, (11.53% on biological, 88.47% on conventional treatment). In addition, (49.36%) of FMF presented in recent attacks. It was also found that Arthralgia, bone aches and sleep deprivation are the main complaints. Concerning, A High perceived stress scale (PSS) was associated with High DAS28 and SLEDI-2K scores. (rs= 0.723, 0.865) (P<0.001)Conclusion:Examination stress is one of triggering factor for autoimmune disease flares. It is associated with high disease activities and ruthless outcomes.References:[1]Cooper, G. S., & Stroehla, B. C. The epidemiology of autoimmune diseases. Autoimmunity Reviews,2003:2(3);119–25.[2]Archana kumari, jagrati jain. Examination stress and anxiety: a study of college students. Global Journal of Multidisciplinary Studies 2014:4:ISSN 2348-0459Disclosure of Interests:None declared
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Monov, S., R. Shumnalieva, and D. Monova. "POS1184 AUTOIMMUNE SYSTEMIC DISEASES AND COVID-19 INFECTION." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 873.1–873. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1254.
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Background:Covid-19 infection poses a serious challenge for immune-compromised patients. This is likely due to a combination of immune dysfunction, immunosuppressive therapy and excess co-morbidities. Little is known about the impact of Coronavirus disease 2019 (COVID-19) in patients with inflammatory autoimmune systemic diseases.Objectives:The aim of this study is to describe clinical characteristics of patients with autoimmune systemic diseases and COVID-19, and to identify baseline variables associated with a severe infection requiring hospitalization.Methods:A telephone survey investigating the impact of COVID-19 on patients with systemic lupus erythematosus (SLE), systemic sclerosis (SSc), inflammatory arthritis (rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis), idiopathic inflammatory myopathies (IIM), ANCA-associated vasculitis (AAV) was administered. Data extraction included diagnosis, disease activity status, demographics, disease duration, occupational exposure, adherence to social distancing advise, therapy, comorbidities, and laboratory tests. Covid-19 was classified as definite diagnosis of Covid-19 disease: presence of symptomatic Covid-19 infection, confirmed by a nasopharyngeal SARS-CoV-2 polymerase chain reaction test. Comparisons between patients with or without hospitalization were performed.Results:512 patients (median age 53,4 ± 14,3 years) with autoimmune systemic diseases (234 IA, 182 SLE, 42 SSc, 31 IIM, 23 AAV) were included in the study. 89 patients (58 woman, 31 men) developed at least one symptom (fever, asthenia, chills, cough, sore throat, dyspnea, chest pain, headaches, arthralgias, myalgias, odynophagia, diarrhea, conjunctivitis, hypo-, ageusia, hypo-, anosmia) of COVID-19 and were PCR test positive. Of patients with COVID – 19 infection 54 patients were treated with methylprednisolone, 36 – with methotrexate, 34 – with hydroxychloroquine, 26- with biologics, 10 - with azathioprine, 6 - with cyclophosphamide prior to their COVID-19 illness.Conclusion:Covid-19 is more frequent in the subgroup of patients without therapy with modifying anti-rheumatic drugs, which might play some protective role against the most harmful manifestations of Covid-19. 21 patients required hospitalization - these were more frequently men, older and with comorbidities (cardio-respiratory illness, renal diseases, diabetes mellitus). Male sex, previous coronary and lung disease, serum creatinine level, proteinuria, glucocorticoids use > 5 mg/day, were associated to hospitalization. Patients with inflammatory arthritis do not seen to be at higher risk for infection or a severe course of COVID-19.References:[1]Monova, D., S. Monov. Mechanisms of kidney injury in patients with COVID-19. Nephrology, dialysis and transplantation, 2020; 26 (4): 5-15.[2]Monova, D., S. Monov. Kidney injures in COVID-19. Nephrology, dialysis and transplantation, 2020; 26 (4): 16-34.Disclosure of Interests:Simeon Monov Speakers bureau: AMGEN, PFIZER, NOVARTIS, ABBVIE, ROCHE, ASTRA-ZENECA, Russka Shumnalieva: None declared, Daniela Monova: None declared.
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Rafael-Vidal, Carlos, Nair Pérez, Irene Altabás, Samuel Garcia, and Jose M. Pego-Reigosa. "Blocking IL-17: A Promising Strategy in the Treatment of Systemic Rheumatic Diseases." International Journal of Molecular Sciences 21, no. 19 (September 26, 2020): 7100. http://dx.doi.org/10.3390/ijms21197100.
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Systemic rheumatic diseases are a heterogeneous group of autoimmune disorders that affect the connective tissue, characterized by the involvement of multiple organs, leading to disability, organ failure and premature mortality. Despite the advances in recent years, the therapeutic options for these diseases are still limited and some patients do not respond to the current treatments. Interleukin-17 (IL-17) is a cytokine essential in the defense against extracellular bacteria and fungi. Disruption of IL-17 homeostasis has been associated with the development and progression of rheumatic diseases, and the approval of different biological therapies targeting IL-17 for the treatment of psoriatic arthritis (PsA) and ankylosing spondylitis (AS) has highlighted the key role of this cytokine. IL-17 has been also implicated in the pathogenesis of systemic rheumatic diseases, including systemic lupus erythematosus (SLE), Sjögren’s syndrome (SS) and systemic sclerosis (SSc). The aim of this review is to summarize and discuss the most recent findings about the pathogenic role of IL-17 in systemic rheumatic and its potential use as a therapeutic option.
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Hammitzsch, Ariane, Cynthia Tallant, Oleg Fedorov, Alison O’Mahony, Paul E. Brennan, Duncan A. Hay, Fernando O. Martinez, et al. "CBP30, a selective CBP/p300 bromodomain inhibitor, suppresses human Th17 responses." Proceedings of the National Academy of Sciences 112, no. 34 (August 10, 2015): 10768–73. http://dx.doi.org/10.1073/pnas.1501956112.
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Th17 responses are critical to a variety of human autoimmune diseases, and therapeutic targeting with monoclonal antibodies against IL-17 and IL-23 has shown considerable promise. Here, we report data to support selective bromodomain blockade of the transcriptional coactivators CBP (CREB binding protein) and p300 as an alternative approach to inhibit human Th17 responses. We show that CBP30 has marked molecular specificity for the bromodomains of CBP and p300, compared with 43 other bromodomains. In unbiased cellular testing on a diverse panel of cultured primary human cells, CBP30 reduced immune cell production of IL-17A and other proinflammatory cytokines. CBP30 also inhibited IL-17A secretion by Th17 cells from healthy donors and patients with ankylosing spondylitis and psoriatic arthritis. Transcriptional profiling of human T cells after CBP30 treatment showed a much more restricted effect on gene expression than that observed with the pan-BET (bromo and extraterminal domain protein family) bromodomain inhibitor JQ1. This selective targeting of the CBP/p300 bromodomain by CBP30 will potentially lead to fewer side effects than with the broadly acting epigenetic inhibitors currently in clinical trials.
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Broyde, Adi, Uri Arad, Noa Madar-Balakirski, Daphna Paran, Ilana Kaufman, David Levartovsky, Irena Wigler, Dan Caspi, and Ori Elkayam. "Longterm Efficacy of an Antipneumococcal Polysaccharide Vaccine among Patients with Autoimmune Inflammatory Rheumatic Diseases." Journal of Rheumatology 43, no. 2 (January 15, 2016): 267–72. http://dx.doi.org/10.3899/jrheum.150397.
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Objective.To estimate the longterm humoral response of an antipneumococcal polysaccharide vaccine (PPSV23) in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), or inflammatory bowel disease (IBD)-associated spondyloarthropathy (SpA), and the effect of demographic and clinical factors and treatment on the longterm efficacy of the vaccine.Methods.A total of 145 consecutive patients treated with biologics [tumor necrosis factor-α (TNF-α) or interleukin 6 (IL-6) receptor inhibitors] or methotrexate (MTX) participated in this study. Fifteen were excluded because of absent information regarding their vaccination status (n = 9) or because of technical problems in obtaining their serum sample (n = 6). They were diagnosed with RA (n = 63, 48.5%), PsA (n = 29, 22.3%), AS (n = 28, 21.5%), or IBD-associated SpA (n = 3, 2.3%). Their mean age was 54.6 years, and 61.5% were women. Data were collected on the timing of vaccination, demographic and clinical characteristics, and treatment, and patients’ serum antipneumococcal antibody levels were tested.Results.Two-thirds of the patients (67.7%) had received PPSV23 45 months (mean) earlier. Treatment included TNF-α inhibitors (73.9%), IL-6 receptor inhibitors (13.1%), or MTX without a biological treatment (13%). The uptake of vaccination was significantly higher in the older population (> 65 yrs). Vaccinated patients had significantly higher antibody levels compared with vaccine-naive patients. The antibody levels had been preserved after 10 years. MTX use, but not biologics, was associated with significantly lower antibody levels.Conclusion.The longterm efficacy of the PPSV23 vaccination seems to be preserved among patients with RA, PsA, AS, and IBD-associated SpA for at least 10 years. Efficacy is slightly impaired by MTX, but it is not affected by biologics. These findings suggest that revaccination after 5 years might not be needed for all, and testing the antibody titers should be considered to identify those who may benefit from revaccination.
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Schulz, Martin, Helmut Dotzlaw, and Gunther Neeck. "Ankylosing Spondylitis and Rheumatoid Arthritis: Serum Levels of TNF-αand Its Soluble Receptors during the Course of Therapy with Etanercept and Infliximab." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/675108.
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The effects of the TNF-αblockers infliximab or etanercept on the levels of TNF-α, TNF-receptor 1 (TNF-R1), and TNF-receptor 2 (TNF-R2), as well as the levels of the inflammation markers CRP and IL-6, were measured in ankylosing spondylitis (AS) and rheumatoid arthritis (RA) patients receiving treatment with either compound. We found that RA patients tend to have higher levels of TNF-αthan both healthy individuals and AS patients prior to treatment (P<0.05). We measured greatly increased levels of TNF-αin both the AS and RA etanercept patient groups during the course of treatment, while in the infliximab treated patients, the amount of TNF-αmeasured remained unchanged. Elevated TNF-αin the etanercept treated patients does not appear to be a significant risk factor for the spontaneous development of further autoimmune diseases in our study group. Increased levels of TNF-R1 were determined in both AS (P<0.05) and RA (P<0.001) patients when compared to healthy controls. In AS patients, the levels of TNF-R1 dropped significantly when treated with either infliximab (P<0.01) or etanercept (P<0.001). In contrast, the levels of this receptor remained unchanged in RA patients treated with either compound.
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Krylov, M. Yu, A. S. Starkova, E. Yu Samarkina, T. V. Dubinina, and Sh F. Erdes. "Association of ankylosing spondylitis activity indicators in a Russian population of patients with STAT4 rs7574865 gene polymorphism." Modern Rheumatology Journal 13, no. 2 (May 20, 2019): 55–60. http://dx.doi.org/10.14412/1996-7012-2019-2-55-60.
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Family and twin studies have shown that ankylosing spondylitis (AS) has a hereditary nature that is based on a strong association with the leukocyte antigen HLA-B27. However, only 1–5% of HLA-B27 carriers develop AS, which indicates that there are other genetic markers involved in the formation of a predisposition to this disease. A number of genome-wide association studies have convincingly confirmed the role of the STAT4 gene. This gene encodes the protein – the signal transducer and activator of transcription (STAT) protein, which is a predisposing factor for the development of many autoimmune diseases. There are not so many studies of the relationship of STAT4 polymorphisms to the predisposition to AS, and there are no these studies regarding the Russian population.Objective: to study whether there is a possible association of STAT4 rs7574865 gene polymorphism with the predisposition to AS and to assess the activity of this disease using BASDAI and ASDAS scores in the Russian patient population.Patients and methods. A cohort of 203 individuals, including 100 patients (79 men and 21 women) with AS, and 103 healthy volunteers (a control group) was surveyed. Age, gender, duration, and specific features of AS onset, ESR, and CRP levels were assessed. BASDAI and ASDAS scores were calculated to evaluate disease activity.Results and discussion. There was a significant relationship between STAT4 polymorphism and C-reactive protein (CRP) levels and BASDAI and ASDAS-CRP scores. The TT genotype carriers had significantly higher mean activity indices compared to the GG (p=0.001) and GT (p=0.005) genotype carriers for CRP, BASDAI (p=0.0001 and p=0.009, respectively) and ASDAS-CRP (p=0.009 and p=0.001, respectively). High disease activity (BASDAI >4 and ASDAS-CRP >3.5) was also associated with the high frequency of the T allele (p=0.046 and p=0.004, respectively). The value of STAT4 rs7574865 gene polymorphism in the pathogenesis of autoimmune diseases is confirmed by a study in which the T allele in STAT4 rs7574865 enhances mRNA transcription and protein expression. Italian authors have shown that there is a relationship between the minor T allele of rs7574865 and the high risk of arthritis. We have previously established a relationship between the T allele and the predisposition to diffuse systemic scleroderma, interstitial lung damage, and elevated anti-topoisomerase I antibody levels.Conclusion. The present study has shown for the first time a significant association of STAT4 rs7574865 polymorphism with the main AS activity indicators: CRP levels, BASDAI and ASDAS-CRP scores. The studied polymorphism may be a new genetic marker for predicting the severity of AS.
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Varan, Özkan, Hakan Babaoğlu, and Berna Göker. "Associations between Depressive Disorders and Inflammatory Rheumatic Diseases." Current Topics in Medicinal Chemistry 18, no. 16 (November 26, 2018): 1395–401. http://dx.doi.org/10.2174/1568026618666180516100805.
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Depressive disorders, are not only common but also among the leading causes of disability worldwide. They are associated with increased incidences of various other diseases. It has been shown that in patients with autoimmune diseases, when depression coexists, the quality of life is worse and medical treatment and management is compromised. Depression-like symptoms, such as fatigue and disinterest are also common in inflammatory rheumatic diseases and often associated with poor quality of life. Medical therapy targeting inflammation results in alleviation of these symptoms in many patients. Interestingly, there is cumulating evidence suggesting potential roles of inflammatory cytokines in the pathogenesis of major depression. Effects of some of the biological agents used in rheumatic diseases have been studied on depressive disorders. Results have been controversial and further studies are needed in this area. These findings suggest associations between depression and inflammatory rheumatic diseases and raise the possibility that treatment of one of them might influence the outcome of the other. We have reviewed the current literature on associations between depression and inflammatory rheumatologic diseases, such as rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome and ankylosing spondylitis.
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Pacheco-Tena, César, and Susana Aideé González-Chávez. "The Danger Model Approach to the Pathogenesis of the Rheumatic Diseases." Journal of Immunology Research 2015 (2015): 1–23. http://dx.doi.org/10.1155/2015/506089.
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The danger model was proposed by Polly Matzinger as complement to the traditional self-non-self- (SNS-) model to explain the immunoreactivity. The danger model proposes a central role of the tissular cells’ discomfort as an element to prime the immune response processes in opposition to the traditional SNS-model where foreignness is a prerequisite. However recent insights in the proteomics of diverse tissular cells have revealed that under stressful conditions they have a significant potential to initiate, coordinate, and perpetuate autoimmune processes, in many cases, ruling over the adaptive immune response cells; this ruling potential can also be confirmed by observations in several genetically manipulated animal models. Here, we review the pathogenesis of rheumatic diseases such as systemic lupus erythematous, rheumatoid arthritis, spondyloarthritis including ankylosing spondylitis, psoriasis, and Crohn’s disease and provide realistic approaches based on the logic of the danger model. We assume that tissular dysfunction is a prerequisite for chronic autoimmunity and propose two genetically conferred hypothetical roles for the tissular cells causing the disease: (A) the Impaired cell and (B) the paranoid cell. Both roles are not mutually exclusive. Some examples in human disease and in animal models are provided based on current evidence.
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Efremova, Ulyana, Nataliya Lychkovska, Roman Fafula, and Zinoviy Vorobets. "Characteristic of no-synthase of peripheral blood lymphocytes of patients with rheumatic pathology." Journal of Medical Science 84, no. 1 (March 30, 2015): 46–54. http://dx.doi.org/10.20883/medical.e35.
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It is known that NO is a ubiquitous mediator which acts as a universal modulator of various functions in organism and is produced by three isoforms of NO synthase. Nowadays the role of NO in the development of autoimmune diseases is actively studied. However, it remains unclear the biochemical and biophysical mechanisms of disturbances of NOS activity in blood lymphocytes at autoimmune process. The aim of present work is to study the kinetic properties of NO-synthase of peripheral blood lymphocytes of patients with rheumatic pathology. The study was carried out on peripheral blood lymphocytes isolated from patients with rheumatoid arthritis and ankylosing spondylitis. NOS activity was determined on the saponin-permeabilized blood lymphocytes. The difference between the values of NADPH oxidation with L-Arg and with inhibitor L-NAME reflects the value of the NADPH oxidation, ie total NOS activity. The kinetic properties of NO-synthase in peripheral blood lymphocytes of patients with rheumatic pathology were studied. It was found that the development of rheumatic pathology is associated with an imbalance in the NO synthesis and changes of kinetic parameters of NOS. It was shown that reduction in eNOS activity is accompanied by a sharp increase in activity of its inducible form. It was established that inhibition of eNOS occurs by noncompetitive type. NO production in lymphocytes of patients with rheumatic diseases is mainly realized by iNOS, whereas under normal physiological conditions endothelial form of the enzyme is being involved.
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Morenkova, A. Yu, M. A. Tikhonova, T. V. Tyrinova, E. V. Batorov, A. E. Sizikov, O. A. Chumasova, A. E. Sulutian, A. A. Ostanin, and E. R. Chernykh. "Expansion of myeloid-derived suppressor cells in the peripheral blood of patients with ankylosing spondylitis." Medical Immunology (Russia) 23, no. 2 (May 3, 2021): 327–38. http://dx.doi.org/10.15789/1563-0625-eom-2143.
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Expansion of myeloid-derived suppressor cells (MDSCs) due to impaired differentiation of myeloid progenitor cells under conditions of inflammation was described in a number of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, and type 1 diabetes mellitus. Studying the role of MDSCs in ankylosing spondylitis is an important issue, given that increased concentration of proinflammatory mediators in this pathology can also cause myelopoiesis disorders. The aim of present work was to study the quantitative content of MDSC subpopulations in patients with different clinical phenotypes and activity of AS. 37 patients, including 10 patients without peripheral skeletal lesions (axial form) and 27 patients with simultaneous lesions of spine and peripheral joints (peripheral form) were recruited into the study. The control group consisted of 32 age/sex-related healthy donors. Evaluation of granulocytic (LinHLA-DRCD33+CD66b+; G-MDSC), monocytic (CD14+HLA-DRlow/-; M-MDSC) and early-stage MDSCs (LinHLA-DRCD33+CD66b- ; E-MDSC) was performed using corresponding antibodies (BD Biosciences, USA) in the population of peripheral blood mononuclear cells by flow cytometry. In general, the AS patients were characterized by an increased relative and absolute amount of M-MDSC (p = 0.00002 and p = 0.00003, respectively) and G-MDSC (p = 0.0002 and p = 0.0006, respectively). Patient gender, age, and HLA-B27 expression did not significantly affect the content of these cells in peripheral blood. An increase in the median values of M-MDSC was detected both in patients with axial (Ме 5.0 (3.2-6.3) versus 2.4 (1.7-3.5) %; p = 0.001) and peripheral form (Ме 5.0 (3.0-7.0) versus 2.4 (1.7-3.5) %; p = 0.0002) AS. At the same time, the G-MDSC expansion was observed only in patients with involvement of peripheral joints (Ме 0.16 (0.07-0.3) % versus 0.05 (0.04-0.09) %; p = 0.0001). The relative contents of E-MDSC, M-MDSC and G-MDSC in the axial form of AS was in direct correlation with the activity of the disease (R = 0.58, p = 0.02; R = 0.73, p = 0.08 and R = 0.65 p = 0.04, respectively). This relationship was not observed in peripheral form of AS. The data obtained suggest a potential involvement of MDSCs in pathogenesis and phenotypic heterogeneity of AS. Simultaneously, the revealed direct correlation between the MDSC contents and the disease activity suggests a decrease in suppressive activity and/or appearance of pro-inflammatory activity in MDSC, thus requiring further research in the field.
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Saad, Carla G. S., Eduardo F. Borba, Nadia E. Aikawa, Clovis A. Silva, Rosa M. R. Pereira, Ana Luisa Calich, Julio C. B. Moraes, et al. "Immunogenicity and safety of the 2009 non-adjuvanted influenza A/H1N1 vaccine in a large cohort of autoimmune rheumatic diseases." Annals of the Rheumatic Diseases 70, no. 6 (May 2, 2011): 1068–73. http://dx.doi.org/10.1136/ard.2011.150250.
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BackgroundDespite the WHO recommendation that the 2010–2011 trivalent seasonal flu vaccine must contain A/California/7/2009/H1N1-like virus there is no consistent data regarding its immunogenicity and safety in a large autoimmune rheumatic disease (ARD) population.Methods1668 ARD patients (systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), ankylosing spondylitis (AS), systemic sclerosis, psoriatic arthritis (PsA), Behçet's disease (BD), mixed connective tissue disease, primary antiphospholipid syndrome (PAPS), dermatomyositis (DM), primary Sjögren's syndrome, Takayasu's arteritis, polymyositis and Granulomatosis with polyangiitis (Wegener's) (GPA)) and 234 healthy controls were vaccinated with a non-adjuvanted influenza A/California/7/2009(H1N1) virus-like strain flu. Subjects were evaluated before vaccination and 21 days post-vaccination. The percentage of seroprotection, seroconversion and the factor increase in geometric mean titre (GMT) were calculated.ResultsAfter immunisation, seroprotection rates (68.5% vs 82.9% p<0.0001), seroconversion rates (63.4% vs 76.9%, p<0.001) and the factor increase in GMT (8.9 vs 13.2 p<0.0001) were significantly lower in ARD than controls. Analysis of specific diseases revealed that seroprotection significantly reduced in SLE (p<0.0001), RA (p<0.0001), PsA (p=0.0006), AS (p=0.04), BD (p=0.04) and DM (p=0.04) patients than controls. The seroconversion rates in SLE (p<0.0001), RA (p<0.0001) and PsA (p=0.0006) patients and the increase in GMTs in SLE (p<0.0001), RA (p<0.0001) and PsA (p<0.0001) patients were also reduced compared with controls. Moderate and severe side effects were not reported.ConclusionsThe novel recognition of a diverse vaccine immunogenicity profile in distinct ARDs supports the notion that a booster dose may be recommended for diseases with suboptimal immune responses. This large study also settles the issue of vaccine safety.(ClinicalTrials.gov #NCT01151644)
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APPEL, HEINER, PEIHUA WU, REBECCA SCHEER, CLAUDIA KEDOR, BIRGIT SAWITZKI, ANDREAS THIEL, ANDREAS RADBRUCH, JOACHIM SIEPER, and UTA SYRBE. "Synovial and Peripheral Blood CD4+FoxP3+ T Cells in Spondyloarthritis." Journal of Rheumatology 38, no. 11 (September 15, 2011): 2445–51. http://dx.doi.org/10.3899/jrheum.110377.
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Objective.Regulatory T cells are characterized by expression of the transcription factor FoxP3 and are thought to be involved in the pathogenesis of autoimmune diseases. We determined the frequency and phenotypic characteristics of CD4+FoxP3+ T cells in the blood and synovial fluid (SF) of patients with inflammatory joint diseases.Methods.SF from 10 patients with ankylosing spondylitis (AS), 20 patients with other spondyloarthritides or with peripheral arthritis (pSpA), and 12 patients with rheumatoid arthritis (RA), and peripheral blood (PB) from 22 patients with AS, 19 with pSpA, 15 with RA, and 12 healthy controls were stained for CD4, FoxP3, CD25, and CD127 and different effector cytokines and then analyzed by flow cytometry. Methylation pattern of the Treg-specific demethylated region (TSDR) was determined after bisulfite treatment by quantitative polymerase chain reaction.Results.In all groups of patients we observed higher frequencies of Foxp3+ cells/CD4+ T cells within SF compared to PB. The frequency of synovial Foxp3+ cells/CD4+ T cells was significantly higher in patients with pSpA (18.79% ± 6.41%) compared to patients with AS (9.69% ± 4.11%) and patients with RA (5.95% ± 2.21%). CD4+FoxP3+ T cells were CD25+ and CD127− and lacked effector cytokine production in any of the different patient groups. The majority of the CD4+CD25+CD127− T cells showed demethylation of the TSDR within the Foxp3 locus, confirming its regulatory phenotype.Conclusion.Our data show accumulation of Foxp3+ T cells within inflamed joints. These Foxp3+ T cells are mainly of stable T regulatory phenotype. The high frequency of Foxp3+ T cells in pSpA might contribute to the spontaneous resolution and remitting course of arthritis in pSpA as compared to the more persistent joint inflammation in RA.
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Guarene, M., C. Capittini, A. De Silvestri, A. Pasi, C. Badulli, I. Sbarsi, A. L. Cremaschi, et al. "Targeting the Immunogenetic Diseases with the Appropriate HLA Molecular Typing: Critical Appraisal on 2666 Patients Typed in One Single Centre." BioMed Research International 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/904247.
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We compared the immunogenetic data from 2666 patients affected by HLA-related autoimmune diseases with those from 4389 ethnically matched controls (3157 cord blood donors CBD, 1232 adult bone marrow donors BMD), to verify the appropriateness of HLA typing requests received in the past decade. The frequency of HLA-B*27 phenotype was 10.50% in 724 ankylosing spondylitis, 16.80% in 125 uveitis (3.41% BMD, 4.24% CBD,P<0.0001); HLA-B*51 allele was 15.57% in 212 Behçet’s disease (12.91% BMD, 9.88% CBD,P<0.0001); the HLA-DRB1-rheumatoid arthritis (RA) shared epitope was 13.72% in 554 RA (10.85% BMD, 13.48% CBD,P=0.016); the carriers of almost one of HLA-DQB1 susceptibility alleles were 84.91% in 795 celiac disease (CD) and 59.37% in 256 insulin-dependent diabetes mellitus (IDDM) (46.06% in 875 CBD, 42.75% in 662 BMDP<0.0001). Overall, our results show that the HLA marker frequencies were higher in patients than controls, but lower than expected from the literature data (excluding CD and IDDM) and demonstrate that, in complex immunogenetic conditions, a substantial number of genetic analyses are redundant and inappropriate, burdening to the public health costs. For this reason, we suggest the Italian Scientific Society of Immunogenetics to establish guidelines to improve the appropriateness of typing requests.