Journal articles: 'Arthritis Molecular aspects'

1

Gross, D. M., and B. T. Huber. "Cellular and molecular aspects of Lyme arthritis." Cellular and Molecular Life Sciences 57, no. 11 (October 2000): 1562–69. http://dx.doi.org/10.1007/pl00000641.

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Chetina, E. V., and E. P. Sharapova. "Rheumatic pain management: molecular aspects." Modern Rheumatology Journal 14, no. 1 (March 22, 2020): 93–100. http://dx.doi.org/10.14412/1996-7012-2020-1-93-100.

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Rheumatic diseases (RDs), including osteoarthritis and rheumatoid arthritis, are non-infectious slowly progressive incurable inflammatory diseases that lead to prolonged disability due to damage to the musculoskeletal system. Pain is a dominant symptom at any stage of these diseases, is directly related to joint functioning, and determines the quality of life in patients. Moreover, despite the significant successes of studying the role of inflammation and regulation of autoimmune processes, the pathogenetic mechanisms for the development and maintenance of pain in RDs are little investigated. The nociceptive mechanisms due to inflammation and/or joint structural impairment are involved in the development of rheumatic pain. In addition, the latter is also associated with impaired signaling in the nervous system and with psychological problems in patients.At the present stage, pain treatment includes non-pharmacological interventions, as well as the use of certain pharmacological agents, in particular opioids and narcotic drugs. However, despite significant successes in the design of drugs that relieve pain, at present, a significant proportion of patients with RDs still experience pain after therapy. When designing novel drugs for the treatment of pain, it is necessary to take into account the molecular mechanisms of its development in RDs. This review considers the features of the manifestations of pain, its molecular markers and mechanisms at different stages of the disease in patients with the two most common RDs, such as rheumatoid arthritis and osteoarthritis.

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Neeck, Gunther, Rainer Renkawitz, and Martin Eggert. "Molecular aspects of glucocorticoid hormone action in rheumatoid arthritis." Cytokines, Cellular & Molecular Therapy 7, no. 2 (January 2002): 61–69. http://dx.doi.org/10.1080/13684730412331302081.

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Kobayashi, Shu, Shigeki Momohara, Naoyuki Kamatani, and Hiroshi Okamoto. "Molecular aspects of rheumatoid arthritis: role of environmental factors." FEBS Journal 275, no. 18 (July 25, 2008): 4456–62. http://dx.doi.org/10.1111/j.1742-4658.2008.06581.x.

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Okamoto, Hiroshi, Thomas P. Cujec, Hisashi Yamanaka, and Naoyuki Kamatani. "Molecular aspects of rheumatoid arthritis: role of transcription factors." FEBS Journal 275, no. 18 (July 25, 2008): 4463–70. http://dx.doi.org/10.1111/j.1742-4658.2008.06582.x.

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García-Hernández, Mariana H., Roberto González-Amaro, and Diana Patricia Portales-Pérez. "Specific therapy to regulate inflammation in rheumatoid arthritis: molecular aspects." Immunotherapy 6, no. 5 (May 2014): 623–36. http://dx.doi.org/10.2217/imt.14.26.

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Lotz, M., and J. Roudier. "Epstein-Barr virus and rheumatoid arthritis: cellular and molecular aspects." Rheumatology International 9, no. 3-5 (November 1989): 147–52. http://dx.doi.org/10.1007/bf00271872.

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Sacre, Sandra M., Evangelos Andreakos, Peter Taylor, Marc Feldmann, and Brian M. Foxwell. "Molecular therapeutic targets in rheumatoid arthritis." Expert Reviews in Molecular Medicine 7, no. 16 (August 24, 2005): 1–20. http://dx.doi.org/10.1017/s1462399405009488.

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In an attempt to combat the pain and damage generated by rheumatoid arthritis (RA), new drugs are being developed to target molecular aspects of the disease process. Recently, a major development has been the use of biologicals (antibodies and soluble receptors) that neutralise the activity of tumour necrosis factor α (TNF-α) and interleukin 1 (IL-1), both of which are involved in disease progression. An increase in our understanding of cell and molecular biology has resulted in the identification and investigation of potential new targets, and also the refinement and improvement of current therapeutic modalities. This review describes therapies that are approved, in clinical trials or under pre-clinical investigation at the laboratory level, particularly focusing on cytokines, although other therapeutic targets of interest are mentioned.

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RULLI, NESTOR E., JULIAN MELTON, ANJA WILMES, GARY EWART, and SURESH MAHALINGAM. "The Molecular and Cellular Aspects of Arthritis Due to Alphavirus Infections." Annals of the New York Academy of Sciences 1102, no. 1 (April 2007): 96–108. http://dx.doi.org/10.1196/annals.1408.007.

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Okamoto, Hiroshi. "Molecular aspects of rheumatoid arthritis: chemokines, environmental factors and transcription factors." FEBS Journal 275, no. 18 (July 25, 2008): 4447. http://dx.doi.org/10.1111/j.1742-4658.2008.06579.x.

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Iwamoto, Takuji, Hiroshi Okamoto, Yoshiaki Toyama, and Shigeki Momohara. "Molecular aspects of rheumatoid arthritis: chemokines in the joints of patients." FEBS Journal 275, no. 18 (July 25, 2008): 4448–55. http://dx.doi.org/10.1111/j.1742-4658.2008.06580.x.

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Dulyapin, V. A. "Morphological aspects of chondroclasis in rheumatoid arthritis." Bulletin of Experimental Biology and Medicine 112, no. 1 (July 1991): 1040–44. http://dx.doi.org/10.1007/bf00841168.

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Stoustrup, P., K. D. Kristensen, A. Küseler, T. K. Pedersen, and T. Herlin. "AB1210 Aspects of temporomandibular joint arthritis-related orofacial symptoms in juvenile idiopathic arthritis." Annals of the Rheumatic Diseases 71, Suppl 3 (June 2013): 707.2–707. http://dx.doi.org/10.1136/annrheumdis-2012-eular.1208.

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Ishikawa, Larissa Lumi Watanabe, Priscila Maria Colavite, Larissa Camargo da Rosa, Bianca Balbino, Thais Graziela Donegá França, Sofia Fernanda Gonçalves Zorzella-Pezavento, Fernanda Chiuso-Minicucci, and Alexandrina Sartori. "Commercial Bovine Proteoglycan Is Highly Arthritogenic and Can Be Used as an Alternative Antigen Source for PGIA Model." BioMed Research International 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/148594.

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Rheumatoid arthritis (RA) is the most common systemic autoimmune disease. It affects mainly the joints, causing synovitis, cartilage destruction, and bone erosion. Many experimental models are used to study the mechanisms involved in immunopathogenesis and new therapies for this disease. Proteoglycan-induced arthritis (PGIA) is a widely used model based on the cross-reactivity of injected foreign (usually human) PG and mice self-PG. Considering the complexity of the extraction and purification of human PG, in this study we evaluated the arthritogenicity of bovine PG that is commercially available. Bovine PG was highly arthritogenic, triggering 100% incidence of arthritis in female BALB/c retired breeder mice. Animals immunized with bovine PG presented clinical symptoms and histopathological features similar to human RA and other experimental models. Moreover, bovine PG immunization determined higher levels of proinflammatory and anti-inflammatory cytokines in arthritic mice compared to healthy ones. As expected, only the arthritic group produced IgG1 and IgG2a antibodies against PG. Thus, commercial bovine PG can be used as an alternative antigenic source to PGIA for the study of many RA aspects, including the immunopathogenesis of the disease and also the development of new therapies.

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Visser, H. "Sarcoid arthritis: clinical characteristics, diagnostic aspects, and risk factors." Annals of the Rheumatic Diseases 61, no. 6 (June 1, 2002): 499–504. http://dx.doi.org/10.1136/ard.61.6.499.

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Askari, Gholamreza, Abdolreza Norouzy, Vahid Hadi, Naseh Pahlavani, Mahsa Malekahmadi, Elyas Nattagh-Eshtivani, JamshidGholizadeh Navashenaq, Saeid Hadi, GordonA Ferns, and Majid Ghayour-Mobarhan. "Nigella sativa in controlling Type 2 diabetes, cardiovascular, and rheumatoid arthritis diseases: Molecular aspects." Journal of Research in Medical Sciences 26, no. 1 (2021): 20. http://dx.doi.org/10.4103/jrms.jrms_236_20.

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Márquez, Ana, Javier Martín, and F. David Carmona. "Emerging aspects of molecular biomarkers for diagnosis, prognosis and treatment response in rheumatoid arthritis." Expert Review of Molecular Diagnostics 16, no. 6 (April 18, 2016): 663–75. http://dx.doi.org/10.1080/14737159.2016.1174579.

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Macaubas, Claudia, Khoa Nguyen, Kuang-Hung Pan, Tzielan Lee, Chetan Deshpande, Christy Sandborg, Stanley Cohen, and Elizabeth Mellins. "Distinct Molecular and Cellular Aspects of Systemic Juvenile Idiopathic Arthritis (SJIA) and Polyarticular (PolyJIA)." Clinical Immunology 123 (2007): S94—S95. http://dx.doi.org/10.1016/j.clim.2007.03.450.

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Hoffmann, Henrik, and Cordelia Schiene-Fischer. "Functional aspects of extracellular cyclophilins." Biological Chemistry 395, no. 7-8 (July 1, 2014): 721–35. http://dx.doi.org/10.1515/hsz-2014-0125.

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Abstract The cyclophilin family of peptidyl prolyl cis/trans isomerases includes several isoforms found to be secreted in response to different stimuli, thus existing both in the interior and the exterior of cells. The extracellular fractions of the cyclophilins CypA and CypB are involved in the control of cell-cell communication. By binding to the cell membrane receptor CD147 and cell surface heparans they elicit a variety of intracellular signaling cascades involved in inflammatory processes. Increased levels of cyclophilins in inflammatory tissues and body fluids are considered as an inflammatory response to injury. Thus, the extracellular portion of cyclophilins probably plays an important role in human diseases associated with acute or chronic inflammation like rheumatoid arthritis, sepsis, asthma and cardiovascular diseases. Specific inhibition of the cyclophilins in the extracellular space may open an effective therapeutic approach for treating inflammatory diseases.

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Laragione, Teresina, Max Brenner, Amit Lahiri, Erjing Gao, Carolyn Harris, and Percio S. Gulko. "Huntingtin-interacting protein 1 (HIP1) regulates arthritis severity and synovial fibroblast invasiveness by altering PDGFR and Rac1 signalling." Annals of the Rheumatic Diseases 77, no. 11 (July 26, 2018): 1627–35. http://dx.doi.org/10.1136/annrheumdis-2018-213498.

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ObjectivesWhile new treatments for rheumatoid arthritis (RA) have markedly improved disease control by targeting immune/inflammatory pathways, current treatments rarely induce remission, underscoring the need for therapies that target other aspects of the disease. Little is known about the regulation of disease severity and joint damage, which are major predictors of disease outcome, and might be better or complementary targets for therapy. In this study, we aimed to discover and characterise a new arthritis severity gene.MethodsAn unbiased and phenotype-driven strategy including studies of unique congenic rat strains was used to identify new arthritis severity and joint damage genes. Fibroblast-like synoviocytes (FLS) from rats and patients with RA expressing or not Huntingtin-interacting protein 1 (HIP1) were studied for invasiveness, morphology and cell signalling. HIP1 knockout mice were used in in vivo confirmatory studies. Paired t-test was used.ResultsDNA sequencing and subcongenic strains studied in pristane-induced arthritis identified a new amino acid changing functional variant in HIP1. HIP1 was required for the increased invasiveness of FLS from arthritic rats and from patients with RA. Knocking down HIP1 expression reduced receptor tyrosine kinase-mediated responses in RA FLS, including RAC1 activation, affecting actin cytoskeleton and cell morphology and interfering with the formation of lamellipodia, consistent with reduced invasiveness. HIP1 knockout mice were protected in KRN serum-induced arthritis and developed milder disease.ConclusionHIP1 is a new arthritis severity gene and a potential novel prognostic biomarker and target for therapy in RA.

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Galozzi, Paola, Sara Bindoli, Andrea Doria, Francesca Oliviero, and Paolo Sfriso. "Autoinflammatory Features in Gouty Arthritis." Journal of Clinical Medicine 10, no. 9 (April 26, 2021): 1880. http://dx.doi.org/10.3390/jcm10091880.

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In the panorama of inflammatory arthritis, gout is the most common and studied disease. It is known that hyperuricemia and monosodium urate (MSU) crystal-induced inflammation provoke crystal deposits in joints. However, since hyperuricemia alone is not sufficient to develop gout, molecular-genetic contributions are necessary to better clinically frame the disease. Herein, we review the autoinflammatory features of gout, from clinical challenges and differential diagnosis, to the autoinflammatory mechanisms, providing also emerging therapeutic options available for targeting the main inflammatory pathways involved in gout pathogenesis. This has important implication as treating the autoinflammatory aspects and not only the dysmetabolic side of gout may provide an effective and safer alternative for patients even in the prevention of possible gouty attacks.

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Boers, M., A. M. Croonen, B. A. Dijkmans, F. C. Breedveld, F. Eulderink, A. Cats, and J. J. Weening. "Renal findings in rheumatoid arthritis: clinical aspects of 132 necropsies." Annals of the Rheumatic Diseases 46, no. 9 (September 1, 1987): 658–63. http://dx.doi.org/10.1136/ard.46.9.658.

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van de Laar, M. A., M. Aalbers, F. G. Bruins, A. C. van Dinther-Janssen, J. K. van der Korst, and C. J. Meijer. "Food intolerance in rheumatoid arthritis. II. Clinical and histological aspects." Annals of the Rheumatic Diseases 51, no. 3 (March 1, 1992): 303–6. http://dx.doi.org/10.1136/ard.51.3.303.

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Cavagna, Lorenzo, Sara Monti, Vittorio Grosso, Nicola Boffini, Eva Scorletti, Gloria Crepaldi, and Roberto Caporali. "The Multifaceted Aspects of Interstitial Lung Disease in Rheumatoid Arthritis." BioMed Research International 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/759760.

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Interstitial lung disease (ILD) is a relevant extra-articular manifestation of rheumatoid arthritis (RA) that may occur either in early stages or as a complication of long-standing disease. RA related ILD (RA-ILD) significantly influences thequoad vitamprognosis of these patients. Several histopathological patterns of RA-ILD have been described: usual interstitial pneumonia (UIP) is the most frequent one, followed by nonspecific interstitial pneumonia (NSIP); other patterns are less commonly observed. Several factors have been associated with an increased risk of developing RA-ILD. The genetic background plays a fundamental but not sufficient role; smoking is an independent predictor of ILD, and a correlation with the presence of rheumatoid factor and anti-cyclic citrullinated peptide antibodies has also been reported. Moreover, bothexnovooccurrence and progression of ILD have been related to drug therapies that are commonly prescribed in RA, such as methotrexate, leflunomide, anti-TNF alpha agents, and rituximab. A greater understanding of the disease process is necessary in order to improve the therapeutic approach to ILD and RA itself and to reduce the burden of this severe extra-articular manifestation.

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Brand, Linda, De Wet Wolmarans, and Sarel J. Brand. "A Quick and Painless Reminder: The Pharmacotherapy of Rheumatoid Arthritis in Primary Practice." South African Family Practice 60, no. 2 (June 7, 2018): 38–42. http://dx.doi.org/10.4102/safp.v60i2.4839.

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Rheumatoid arthritis, an auto-immune disorder, is characterized by chronic inflammation of the joints, synovial hyperplasia and bone erosion. These pathological features are promoted by a synovial microenvironment featuring B-cell and T-cell infiltrate, synovial fibroblasts and an intricate network of pro-inflammatory cellular messengers – prominent molecular role-players that represent critical targets in the pharmacotherapy of the disease. This review offers a brief overview of the etiopathology of rheumatoid arthritis while focussing on the practical aspects of methotrexate and glucocorticoid use that are of relevance for primary practice.

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Sha, Naijun, Marina Vannucci, Philip J. Brown, Michael K. Trower, Gillian Amphlett, and Francesco Falciani. "Gene Selection in Arthritis Classification with Large-Scale Microarray Expression Profiles." Comparative and Functional Genomics 4, no. 2 (2003): 171–81. http://dx.doi.org/10.1002/cfg.264.

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The use of large-scale microarray expression profiling to identify predictors of disease class has become of major interest. Beyond their impact in the clinical setting (i.e. improving diagnosis and treatment), these markers are also likely to provide clues on the molecular mechanisms underlining the diseases. In this paper we describe a new method for the identification of multiple gene predictors of disease class. The method is applied to the classification of two forms of arthritis that have a similar clinical endpoint but different underlying molecular mechanisms: rheumatoid arthritis (RA) and osteoarthritis (OA). We aim at both the classification of samples and the location of genes characterizing the different classes. We achieve both goals simultaneously by combining a binary probit model for classification with Bayesian variable selection methods to identify important genes.We find very small sets of genes that lead to good classification results. Some of the selected genes are clearly correlated with known aspects of the biology of arthritis and, in some cases, reflect already known differences between RA and OA.

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Loréal, Olivier, Thibault Cavey, François Robin, Moussa Kenawi, Pascal Guggenbuhl, and Pierre Brissot. "Iron as a Therapeutic Target in HFE-Related Hemochromatosis: Usual and Novel Aspects." Pharmaceuticals 11, no. 4 (November 26, 2018): 131. http://dx.doi.org/10.3390/ph11040131.

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Genetic hemochromatosis is an iron overload disease that is mainly related to the C282Y mutation in the HFE gene. This gene controls the expression of hepcidin, a peptide secreted in plasma by the liver and regulates systemic iron distribution. Homozygous C282Y mutation induces hepcidin deficiency, leading to increased circulating transferrin saturation, and ultimately, iron accumulation in organs such as the liver, pancreas, heart, and bone. Iron in excess may induce or favor the development of complications such as cirrhosis, liver cancer, diabetes, heart failure, hypogonadism, but also complaints such as asthenia and disabling arthritis. Iron depletive treatment mainly consists of venesections that permit the removal of iron contained in red blood cells and the subsequent mobilization of stored iron in order to synthesize hemoglobin for new erythrocytes. It is highly efficient in removing excess iron and preventing most of the complications associated with excess iron in the body. However, this treatment does not target the biological mechanisms involved in the iron metabolism disturbance. New treatments based on the increase of hepcidin levels, by using hepcidin mimetics or inducers, or inhibitors of the iron export activity of ferroportin protein that is the target of hepcidin, if devoid of significant secondary effects, should be useful to better control iron parameters and symptoms, such as arthritis.

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Hashimoto, Teppei, Kohsuke Yoshida, Akira Hashiramoto, and Kiyoshi Matsui. "Cell-Free DNA in Rheumatoid Arthritis." International Journal of Molecular Sciences 22, no. 16 (August 19, 2021): 8941. http://dx.doi.org/10.3390/ijms22168941.

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Endogenous DNA derived from the nuclei or mitochondria is released into the bloodstream following cell damage or death. Extracellular DNA, called cell-free DNA (cfDNA), is associated with various pathological conditions. Recently, multiple aspects of cfDNA have been assessed, including cfDNA levels, integrity, methylation, and mutations. Rheumatoid arthritis (RA) is the most common form of autoimmune arthritis, and treatment of RA has highly varied outcomes. cfDNA in patients with RA is elevated in peripheral blood and synovial fluid and is associated with disease activity. Profiling of cfDNA in patients with RA may then be utilized in various aspects of clinical practice, such as the prediction of prognosis and treatment responses; monitoring disease state; and as a diagnostic marker. In this review, we discuss cfDNA in patients with RA, particularly the sources of cfDNA and the correlation of cfDNA with RA pathogenesis. We also highlight the potential of analyzing cfDNA profiles to guide individualized treatment approaches for RA.

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Poddighe, Dimitri, Micol Romano, Maurizio Gattinara, and Valeria Gerloni. "Biologics for the Treatment of Juvenile Idiopathic Arthritis." Current Medicinal Chemistry 25, no. 42 (February 6, 2019): 5860–93. http://dx.doi.org/10.2174/0929867325666180522085716.

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Juvenile Idiopathic Arthritis (JIA) is one of the most common chronic diseases in children. Recently, the management of JIA has substantially changed, thanks to the availability of new treatment options, represented by biological drugs or biologics. These drugs modulate the specific mechanisms of the immune systems, such as TNF-α, IL-1 and IL-6 signaling, or lymphocyte activation and/or functioning. In this review, we provide a comprehensive discussion on the current recommendations and clinical evidence regarding the use of the available biologics in the treatment of JIA; moreover, the main pharmacokinetic and pharmacodynamic aspects of any specific biologic drug have been summarized.

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Berardi, S., A. Corrado, N. Maruotti, D. Cici, and F. P. Cantatore. "Osteoblast role in the pathogenesis of rheumatoid arthritis." Molecular Biology Reports 48, no. 3 (March 2021): 2843–52. http://dx.doi.org/10.1007/s11033-021-06288-y.

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AbstractIn the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-α, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid arthritis showed that complete resolution of inflammation (with maximal reduction in the expression of pro-inflammatory factors) is crucial for bone healing, performed by osteoblasts activity. In fact, abnormal activity of factors and systems involved in osteoblast function in these patients has been described. A better understanding of the pathogenic mechanisms involved in osteoblast dysregulation could contribute to explain the generalized and focal articular bone loss found in rheumatoid arthritis. Nevertheless, these aspects have not been frequently and directly evaluated in studies. This review article is focused on analysis of the current knowledge about the role of osteoblast dysregulation occurring in rheumatoid arthritis: a better knowledge of these mechanisms could contribute to the realization of new therapeutic strategies.

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Caporali, Roberto, and Josef S. Smolen. "Back to the future: forget ultrasound and focus on clinical assessment in rheumatoid arthritis management." Annals of the Rheumatic Diseases 77, no. 1 (August 2, 2017): 18–20. http://dx.doi.org/10.1136/annrheumdis-2017-211458.

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Ultrasound (US) unquestionably improves many aspects of rheumatoid arthritis (RA) diagnosis and management, but no consensus has been reached regarding the optimal US methodology that should be used, and high levels of standardisation have not yet been attained. Current evidence from two randomised controlled trials does not support the US in directing treatment decisions. A return to the endorsement of clinical assessment and the adoption of T2T strategies aiming at ACR/EULAR remission still represent the standard of care for RA and should be pursued through appropriate educational programmes. Thus, for now, the major application of sonography in arthritis should have a focus on diagnostic and especially differential diagnostic aspects.

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Inman, R. D. "Immunogenetic aspects of host immune response." Canadian Journal of Microbiology 34, no. 3 (March 1, 1988): 319–22. http://dx.doi.org/10.1139/m88-058.

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The central role of histocompatibility leukocyte antigens (HLA) class II molecules in antigen presentation has received great attention in recent years, yet class I molecules have been defined as primarily functioning as a restriction element for cytotoxic T cell killing of virus-infected cells. Extensive clinical evidence, however, indicates that the HLA class I genes are strongly associated with nonseptic complications of enteric and genitourinary bacterial infections. Ninety percent of patients with Reiter's syndrome and reactive arthritis are positive for HLA-B27, yet the mechanism of disease susceptibility conferred by this gene remains obscure. Hypotheses concerning this interaction include (i) class I antigens functioning as receptors for microbial antigens; (ii) class I antigens expressing determinants that cross-react with microbial antigens; and (iii) class I genes controlling immunoregulatory functions that dictate qualitative differences in immune response to pathogenic organisms. These hypotheses await formal testing and hold great promise for understanding immunogenetic control of immune responses in general.

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Kreutz, G. "European regulatory aspects on new medicines targeted at treatment of rheumatoid arthritis." Annals of the Rheumatic Diseases 58, Supplement 1 (November 1, 1999): i92—i95. http://dx.doi.org/10.1136/ard.58.2008.i92.

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Doghish, Ahmed S., Ahmed Ismail, Hesham A. El-Mahdy, Samy Y. Elkhawaga, Elsayed G. E. Elsakka, Eman A. Mady, Mahmoud A. Elrebehy, Mahmoud A. F. Khalil, and Hussein M. El-Husseiny. "miRNAs insights into rheumatoid arthritis: Favorable and detrimental aspects of key performers." Life Sciences 314 (February 2023): 121321. http://dx.doi.org/10.1016/j.lfs.2022.121321.

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Pandolfi, Franco, Laura Franza, Valentina Carusi, Simona Altamura, Gloria Andriollo, and Eleonora Nucera. "Interleukin-6 in Rheumatoid Arthritis." International Journal of Molecular Sciences 21, no. 15 (July 23, 2020): 5238. http://dx.doi.org/10.3390/ijms21155238.

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The role of interleukin (IL)-6 in health and disease has been under a lot of scrutiny in recent years, particularly during the recent COVID-19 pandemic. The inflammatory pathways in which IL-6 is involved are also partly responsible of the development and progression of rheumatoid arthritis (RA), opening interesting perspectives in terms of therapy. Anti-IL-6 drugs are being used with variable degrees of success in other diseases and are being tested in RA. Results have been encouraging, particularly when anti-IL-6 has been used with other drugs, such as metothrexate (MTX). In this review we discuss the main immunologic aspects that make anti-IL-6 a good candidate in RA, but despite the main therapeutic options available to target IL-6, no gold standard treatment has been established so far.

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Doumen, M., S. Pazmino, D. Bertrand, D. De Cock, J. Joly, R. Westhovens, and P. Verschueren. "POS0266-HPR PATIENT-PERCEIVED ASPECTS OF RA FLARE EVOLVE OVER TIME, AS REFLECTED BY THE FLARE-RA QUESTIONNAIRE: POST-HOC ANALYSIS OF TAPERA." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 356.1–356. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2003.

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Background:Flares are common in rheumatoid arthritis (RA). While flares negatively impact clinical and patient-reported outcomes, different aspects of disease activity may constitute a flare to patients. Flare Assessment in RA (FLARE-RA) is a patient-reported questionnaire aiming to detect active or recent RA flares (1). During its validation, arthritis and general health subscales were identified and the instrument was adapted from 13 questions (1-6 Likert scale) to 11 questions (0-10).Objectives:To investigate which patient-perceived aspects of flare are assessed by FLARE-RA in the context of a TNFi-tapering trial, using exploratory factor analysis (EFA).Methods:Patients with RA in DAS28CRP/ESR-remission (≥6 months) and treated with etanercept 50 mg weekly (≥1 year) were included in the 12-month TapERA (Tapering Etanercept in Rheumatoid Arthritis) trial between 2012 and 2014. Participants completed 3-monthly FLARE-RA questionnaires.The first and final follow-up visits (M3 & M12) were analyzed. Missing data were imputed with multiple imputation (n = 10). Sampling adequacy was assessed by Kaiser-Meyer-Olkin (KMO) and correlations between variables were evaluated with Bartlett’s sphericity test. Spearman correlation matrices were constructed in each of the 10 imputed datasets. The pooled matrix was then analyzed by EFA with principal component extraction and promax-rotation. EFA aims to identify clusters of questions that elicit similar responses because of association with the same underlying latent (not observable) constructs/factors.Results:Sixty-six patients (68% female) with a mean age of 55 years (SD 13) and a mean disease duration of 14.8 years (SD 9) completed a total of 330 FLARE-RA questionnaires. Sampling adequacy was acceptable (KMO = 0.94) and correlation between items was sufficient for factor analysis (p < 0.001).Table 1 shows the results of EFA in TapERA compared to the validation study (1). Factor loadings indicate how strongly each item correlates with its underlying factor. EFA of the full 13-item FLARE-RA at M3 revealed 3 factors: Arthritis, General health and a Medication factor relating to management of flare. The Arthritis factor explained the largest proportion of variance (31%). EFA at M12 showed the same underlying factors, but a less robust factor structure (cross-loadings >0.3) and a larger proportion of variance explained by the General health factor (33%).Conclusion:FLARE-RA assessed similar patient-perceived aspects of RA flare within the context of a TNFi-tapering trial when compared to the validation study, including a Medication factor reflecting use of both glucocorticoids and analgesics. This underlines the usefulness of FLARE-RA in providing a multi-faceted view of patients’ conceptions of RA flare. However, these aspects and their relative importance do seem to evolve over time. Further research is needed to assess if this is due to the influence of time or specific to the studied population/tapering setting.References:[1]Fautrel B, et al. Validation of FLARE-RA, a Self-Administered Tool to Detect Recent or Current Rheumatoid Arthritis Flare. Arthritis Rheumatol. 2017;69(2):309–19Table 1.Factor loadings (>0.3) from exploratory factor analysis of the 13-question FLARE-RA collected in TapERA, compared to results from the FLARE-RA validation study (1). Factors presented in descending order of % variance explained. Q5 & Q7 were removed in the final FLARE-RA.ITEMFLARE-RA ValidationTapERA M3TapERA M12GFAFAFGFMFGFAFMFQ1: stiffness0.330.750.930.73Q2: pain0.470.650.911.00Q3: swelling0.350.800.920.93Q4: nocturnal pain0.390.820.670.76Q5: overall0.390.840.860.86Q6: analgesics0.360.810.680.470.51Q7: glucocorticoids0.910.96Q8: fatigue0.680.510.700.87Q9: limitation0.730.480.300.750.74Q10: irritability0.850.390.770.69Q11: mood0.830.440.970.79Q12: withdrawal0.900.891.06Q13: needing help0.810.380.720.600.30Variance explained (%)6610313112333110AF = arthritis factor, GF = general health factor, MF = medication factorDisclosure of Interests:None declared

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Zheng, Yijun, and Duming Zhu. "Molecular Hydrogen Therapy Ameliorates Organ Damage Induced by Sepsis." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/5806057.

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Since it was proposed in 2007, molecular hydrogen therapy has been widely concerned and researched. Many animal experiments were carried out in a variety of disease fields, such as cerebral infarction, ischemia reperfusion injury, Parkinson syndrome, type 2 diabetes mellitus, metabolic syndrome, chronic kidney disease, radiation injury, chronic hepatitis, rheumatoid arthritis, stress ulcer, acute sports injuries, mitochondrial and inflammatory disease, and acute erythema skin disease and other pathological processes or diseases. Molecular hydrogen therapy is pointed out as there is protective effect for sepsis patients, too. The impact of molecular hydrogen therapy against sepsis is shown from the aspects of basic vital signs, organ functions (brain, lung, liver, kidney, small intestine, etc.), survival rate, and so forth. Molecular hydrogen therapy is able to significantly reduce the release of inflammatory factors and oxidative stress injury. Thereby it can reduce damage of various organ functions from sepsis and improve survival rate. Molecular hydrogen therapy is a prospective method against sepsis.

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Shadnoush, Mahdi, Vida Nazemian, Homa Manaheji, and Jalal Zaringhalam. "Research Paper: The Effect of Orally Administered Probiotics on the Behavioral, Cellular, and Molecular Aspects of Adjuvant-Induced Arthritis." Basic and Clinical Neuroscience Journal 9, no. 5 (September 30, 2018): 325–36. http://dx.doi.org/10.32598/bcn.9.5.325.

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Nazemian, Vida, Homa Manaheji, Ali Mohammad Sharifi, and Jalal Zaringhalam. "Long term treatment by mesenchymal stem cells conditioned medium modulates cellular, molecular and behavioral aspects of adjuvant-induced arthritis." Cellular and Molecular Biology 64, no. 1 (January 31, 2018): 19. http://dx.doi.org/10.14715/cmb/2018.64.2.5.

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Corbet, Marlene, Miguel A. Pineda, Kun Yang, Anuradha Tarafdar, Sarah McGrath, Rinako Nakagawa, Felicity E. Lumb, Colin J. Suckling, William Harnett, and Margaret M. Harnett. "Suppression of inflammatory arthritis by the parasitic worm product ES-62 is associated with epigenetic changes in synovial fibroblasts." PLOS Pathogens 17, no. 11 (November 8, 2021): e1010069. http://dx.doi.org/10.1371/journal.ppat.1010069.

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ES-62 is the major secreted protein of the parasitic filarial nematode, Acanthocheilonema viteae. The molecule exists as a large tetramer (MW, ~240kD), which possesses immunomodulatory properties by virtue of multiple phosphorylcholine (PC) moieties attached to N-type glycans. By suppressing inflammatory immune responses, ES-62 can prevent disease development in certain mouse models of allergic and autoimmune conditions, including joint pathology in collagen-induced arthritis (CIA), a model of rheumatoid arthritis (RA). Such protection is associated with functional suppression of “pathogenic” hyper-responsive synovial fibroblasts (SFs), which exhibit an aggressive inflammatory and bone-damaging phenotype induced by their epigenetic rewiring in response to the inflammatory microenvironment of the arthritic joint. Critically, exposure to ES-62 in vivo induces a stably-imprinted CIA-SF phenotype that exhibits functional responses more typical of healthy, Naïve-SFs. Consistent with this, ES-62 “rewiring” of SFs away from the hyper-responsive phenotype is associated with suppression of ERK activation, STAT3 activation and miR-155 upregulation, signals widely associated with SF pathogenesis. Surprisingly however, DNA methylome analysis of Naïve-, CIA- and ES-62-CIA-SF cohorts reveals that rather than simply preventing pathogenic rewiring of SFs, ES-62 induces further changes in DNA methylation under the inflammatory conditions pertaining in the inflamed joint, including targeting genes associated with ciliogenesis, to programme a novel “resolving” CIA-SF phenotype. In addition to introducing a previously unsuspected aspect of ES-62’s mechanism of action, such unique behaviour signposts the potential for developing DNA methylation signatures predictive of pathogenesis and its resolution and hence, candidate mechanisms by which novel therapeutic interventions could prevent SFs from perpetuating joint inflammation and destruction in RA. Pertinent to these translational aspects of ES-62-behavior, small molecule analogues (SMAs) based on ES-62’s active PC-moieties mimic the rewiring of SFs as well as the protection against joint disease in CIA afforded by the parasitic worm product.

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Schoels, Monika, John Wong, David L. Scott, Angela Zink, Pamela Richards, Robert Landewé, Josef S. Smolen, and Daniel Aletaha. "Economic aspects of treatment options in rheumatoid arthritis: a systematic literature review informing the EULAR recommendations for the management of rheumatoid arthritis." Annals of the Rheumatic Diseases 69, no. 6 (May 6, 2010): 995–1003. http://dx.doi.org/10.1136/ard.2009.126714.

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ObjectiveTo review the cost effectiveness of rheumatoid arthritis (RA) treatments and inform the clinical recommendations by the European League Against Rheumatism.MethodsA systematic literature search and review of the health economic evidence on RA treatment options was performed.ResultsDespite diverse methodological approaches, health economic analyses are concordant: at onset of disease, traditional disease-modifying antirheumatic drugs (DMARDs) are cost effective—that is, treatment merits outweigh treatment costs. If DMARDs fail, therapeutic escalation with tumour necrosis factor α inhibitors (TNFi) is cost effective when standard dosing schemes are employed. If TNFi fail, rituximab or abatacept is cost effective. Economic evidence for switching TNFi remains sparse.ConclusionsThe costly sequelae of insufficiently controlled RA justify intensive escalations of treatment in this disease. By maintaining function, patients are kept in the work process, reducing indirect costs. Quality of life is improved at an expense commonly accepted for chronic diseases. Effective control of disease activity seems to be a prudent use of societal resources.

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Deng, Jing, Handan Tan, Jiayue Hu, Guannan Su, Qingfeng Cao, Xinyue Huang, Chunjiang Zhou, Yao Wang, Aize Kijlstra, and Peizeng Yang. "Genetic aspects of idiopathic paediatric uveitis and juvenile idiopathic arthritis associated uveitis in Chinese Han." British Journal of Ophthalmology 104, no. 3 (April 2, 2019): 443–47. http://dx.doi.org/10.1136/bjophthalmol-2018-313200.

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BackgroundIdiopathic paediatric uveitis (IPU) and juvenile idiopathic arthritis associated uveitis (JIA-U) are the two most common entities in paediatric uveitis. This study addressed the possible association of IPU and JIA-U with genes that had been shown earlier to be associated with juvenile idiopathic arthritis.MethodsWe carried out a case-control association study involving 286 IPU, 134 JIA-U patients and 743 healthy individuals. A total of 84 candidate single nucleotide polymorphisms (SNPs) in 60 genes were selected for this study. The MassARRAY platform and iPLEX Gold Genotyping Assay was used to genotype 83 candidate SNPs and the remaining SNP (rs27293) was analysed using the TaqMan SNP Genotyping Assay.ResultsNo evidence was found for an association of the candidate polymorphisms tested with IPU. Six SNPs (PRM1/rs11074967, JAZF1/rs73300638, IRF5/rs2004640, MEFV/rs224217, PSMA3/rs2348071 and PTPN2/rs7234029) showed an association with JIA-U (p<1.0×10−2).ConclusionOur findings showed associations of six SNPs (PRM1/rs11074967, JAZF1/rs73300638, IRF5/rs2004640, MEFV/rs224217, PSMA3/rs2348071 and PTPN2/rs7234029) with JIA-U. No association was detected between the 84 tested SNPs and IPU.

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Kostine, Marie, Léa Rouxel, Thomas Barnetche, Rémi Veillon, Florent Martin, Caroline Dutriaux, Léa Dousset, et al. "Rheumatic disorders associated with immune checkpoint inhibitors in patients with cancer—clinical aspects and relationship with tumour response: a single-centre prospective cohort study." Annals of the Rheumatic Diseases 77, no. 3 (November 16, 2017): 393–98. http://dx.doi.org/10.1136/annrheumdis-2017-212257.

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ObjectivesTo evaluate the prevalence and type of rheumatic immune-related adverse events (irAEs) in patients receiving immune checkpoint inhibitors (ICIs), as well as the correlation with tumour response.MethodsThis was a single-centre prospective observational study including all cancer patients receiving ICIs. The occurrence of irAEs and tumour response was assessed on a regular basis. Patients who experienced musculoskeletal symptoms were referred to the department of rheumatology for clinical evaluation and management.ResultsFrom September 2015 to May 2017, 524 patients received ICIs and 35 were referred to the department of rheumatology (6.6%). All but one of the rheumatic irAEs occurred with anti-programmed cell death protein 1(PD-1)/PD-1 ligand 1(PD-L1) antibodies, with a median exposure time of 70 days. There were two distinct clinical presentations: (1) inflammatory arthritis (3.8%) mimicking either rheumatoid arthritis (n=7), polymyalgia rheumatica (n=11) or psoriatic arthritis (n=2) and (2) non-inflammatory musculoskeletal conditions (2.8%; n=15). One patient with rheumatoid arthritis was anti-cyclic citrullinated peptide (anti-CCP) positive. Nineteen patients required glucocorticoids, and methotrexate was started in two patients. Non-inflammatory disorders were managed with non-steroidal anti-inflammatory drugs, analgesics and/or physiotherapy. ICI treatment was pursued in all but one patient. Patients with rheumatic irAEs had a higher tumour response rate compared with patients without irAEs (85.7% vs 35.3%; P<0.0001).ConclusionSince ICIs are used with increasing frequency, knowledge of rheumatic irAEs and their management is of major interest. All patients were responsive either to low-to-moderate doses of prednisone or symptomatic therapies and did not require ICI discontinuation. Furthermore, tumour response was significantly higher in patients who experienced rheumatic irAEs.

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Nikitina, N., I. Afanaciev, and A. Rebrov. "AB0410 Use of disease-modifying treatment (dmard) in patients with rheumatoid arthritis: clinical aspects." Annals of the Rheumatic Diseases 71, Suppl 3 (June 2013): 661.1–661. http://dx.doi.org/10.1136/annrheumdis-2012-eular.410.

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Louis-Sidney, F., D. Morillon, M. Blettery, L. Brunier, P. Numeric, and M. De Bandt. "POS0945 NON-RADIOGRAPHIC AXIAL SPONDYLOARTHRITIS IN THE AFRO-CARIBBEAN POPULATION, CLINICAL ASPECTS AND PARTICULARITIES." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 735.2–736. http://dx.doi.org/10.1136/annrheumdis-2021-eular.260.

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Background:Spondyloarthritis is a polymorphic disease and the absence of diagnostic marker has led to propose diagnostic criteria for recognition. All the criteria, established in Caucasian populations, place at the center of the approach sacroiliac imaging and genetic terrain (HLA B27). For this reason, these criteria are not appropriate in populations lacking HLA B27. SPA is known to be rare in African populations and this rarity correlates with that of HLA B27.Prevalence of B27 in French West Indies is 2% (identical to the African populations).Objectives:We report clinical manifestations of SpA seen at the Fort de France University Hospital, with an emphasis on the so-called “non-radiographic SpA” (NRSPA).Methods:Adult patients with spondyloarthritis seen over a period of three consecutive months, were invited to participate in a survey and filled-in a self-administered questionnaire. The consulting rheumatologist specified the rheumatologic and extra-articular involvement, BASDAI score, HLAB27 data, markers of inflammation and imaging.Results:There were 93 patients, 47 with radiographic sacroilitis (RSPA) and 46 patients without but all - these 46 - had magnetic sacroilitis. This population is Afro-Caribbean for 98%. Mean age at onset of clinical signs is 38.5 ± 15.0 years and median age is 37.0 (13-77). An evocative family history is noted in 37%. All these 93 patients suffer from rachialgia.But the axial complaint is often secondary to the peripheral involvement. 3 patients have a mechanical spinal complaint. All the others have intermittent inflammatory complaint evolving by flares affecting all the spinal stages. 15/93 patients have isolated axial complain without peripheral disease. Enthesopathies are seen in 70%.Peripheral inflammatory joint complain is observed in 78 patients (84%), it is a bilateral and symmetrical chronic polyarticular pattern affecting (70/78) the small joints of the hands, forefeet and wrists. Ankle bi-arthritis is almost systematic and is observed in 71/78 patients; 8 patients with RSPA had no polyarthritis but oligo (6) or monoarthritis (2). Peripheral inflammatory joint is more frequent in NRSPA than in RSPA (98% vs 70%). Ultrasound individualises grade II synovitis (78/78), rarely with a Doppler effect (5/78). On average, more painful and swollen joints are observed in NRSPA than in RSPA. Extra articular and immunological aspects and activity scores are in table 1.Good sensitivity of peripheral arthritis to NSAIDs and MTX is noted in 94 and 91%.Conclusion:NRSpA are not uncommon in the Afro-Caribbean population, but are distinct from Caucasian SpA by several points: female predominance, rarity of B27 and syndesmophytes, frequency of polyalgic pattern, frequency of peripheral arthritis, rarity of extra-articular manifestations, more frequent but less marked inflammation, good response of arthritis to NSAIDs and MTX. Appropriate classification criteria for Afro-descendant populations is an urgent unmet need.References:[1](López-Medina C, et al. RMD Open 2019;5:e001108).Table 1.Extra articular manifestations, activity scores and immunological aspects of the patients.ItemResults (%)NRSPA n=46Results (%)RSPA n=47Dactylitis11 (23 %)13 (27 %)Uvéïtis5 (11 %) (p 0.02)15 (32%)Psoriasis1 (2 %)1 (2 %)IBD4 (9 %) (p 0.02)10 (21 %)Balanitis00Non gonococcal urethritis00Non gonococcal cervicitis00High CRP (at least 2 measure)21 (45%) (p 0.03)30 (63%)Mean CRP mg/l6 ± 4 17 ± 7BASDAI4.1 ± 0.24 ± 0.2EVA pain4.5 ± 0.44,5 ± 0.2HAQ0.6 ± 0.30,5 ± 0.2EVA Global4.9 ± 0.84,8 + 0.8EVA Spine5 ± 0.54,1 + 0.9FIRST score >55 /46 patients (10.9%)6 / 47 patients (12.5%)HLA B27 presence4/46 (8.7%) (p 0.01)14/47 (29.8%)Sexemale 10 (21.3%) (p 0.001)male 19 (51.3%)ACPA00Latex Waaler-Rose1 (low titer, > 65 years)1 (low titer, > 65 years)ANA2 (low titer, < 1/320°)3 (low titer, < 1/320°)Disclosure of Interests:None declared

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Pelosi, Andrea, Claudio Lunardi, Piera Filomena Fiore, Elisa Tinazzi, Giuseppe Patuzzo, Giuseppe Argentino, Francesca Moretta, Antonio Puccetti, and Marzia Dolcino. "MicroRNA Expression Profiling in Psoriatic Arthritis." BioMed Research International 2018 (2018): 1–15. http://dx.doi.org/10.1155/2018/7305380.

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Background. Psoriatic arthritis (PsA) is an inflammatory arthritis, characterized by bone erosions and new bone formation. MicroRNAs (miRNAs) are key regulators of the immune responses. Differential expression of miRNAs has been reported in several inflammatory autoimmune diseases; however, their role in PsA is not fully elucidated. We aimed to identify miRNA expression signatures associated with PsA and to investigate their potential implication in the disease pathogenesis. Methods. miRNA microarray was performed in blood cells of PsA patients and healthy controls. miRNA pathway analyses were performed and the global miRNA profiling was combined with transcriptome data in PsA. Deregulation of selected miRNAs was validated by real-time PCR. Results. We identified specific miRNA signatures associated with PsA patients with active disease. These miRNAs target pathways relevant in PsA, such as TNF, MAPK, and WNT signaling cascades. Network analysis revealed several miRNAs regulating highly connected genes within the PsA transcriptome. miR-126-3p was the most downregulated miRNA in active patients. Noteworthy, miR-126 overexpression induced a decreased expression of genes implicated in PsA. Conclusions. This study sheds light on some epigenetic aspects of PsA identifying specific miRNAs, which may represent promising candidates as biomarkers and/or for the design of novel therapeutic strategies in PsA.

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Rodríguez, Sandra, Andrés Muñoz, Rosa-Helena Bustos, and Diego Jaimes. "Pharmacovigilance of Biopharmaceuticals in Rheumatic Diseases, Adverse Events, Evolution, and Perspective: An Overview." Biomedicines 8, no. 9 (August 23, 2020): 303. http://dx.doi.org/10.3390/biomedicines8090303.

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Since we have gained an understanding of the immunological pathophysiology of rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus, treatment based on biological drugs has become a fundamental axis. These therapies are oriented towards the regulation of cytokines such as tumour necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1, and the modulation of cell-mediated immunity (B cells and T cells) by anti CD20 or anti CTAL-4 agents, and can increase the risk of associated infections or adverse events (AE). In this context, the entry of biotherapeutics represented a challenge for pharmacovigilance, risk management and approval by the main global regulatory agencies regarding biosimilars, where efficacy and safety are based on comparability exercises without being an exact copy in terms of molecular structure. The objective of this review is divided into three fundamental aspects: (i) to illustrate the evolution and focus of pharmacovigilance at the biopharmaceutical level, (ii) to describe the different approved recommendations of biopharmaceuticals (biological and biosimilars) and their use in rheumatic diseases (RDs) such as rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), systemic lupus erythematosus (SLE) and other less frequent RD like cryopyrin-associated autoinflammatory syndromes (CAPS), and (iii) to identify the main AE reported in the post-marketing phase of RD biopharmaceuticals.

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Gerami, Reza, Ramezan Jafari, Niloufar Nazeri, and Amin Saburi. "The Anti-inflammatory Role of Curcumin in Osteoarthritis: An Overview of Molecular and Radiologic Changes." Hospital Practices and Research 7, no. 1 (December 1, 2021): 1–3. http://dx.doi.org/10.34172/hpr.2022.01.

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Osteoarthritis (OA) is the most common form of arthritis, causing pain and progressive disability in millions of people worldwide. The commonly prescribed medications for OA, including non-steroidal anti-inflammatory drugs, have many side effects which has led the scientists to consider safer drugs as an alternative. Therapeutic effects of Curcumin on OA are increasingly declared, and its various aspects in suppressing inflammation and reducing the disease progression are examined more thoroughly. This study aims to discuss curcumin and OA to help scientists working in these fields. In this brief review, we took a look at OA pathogenesis, the role of the immune system, and the biomarkers involved in the onset and progression of the disease. We focused on available data on the anti-inflammatory effect and mechanism of treatment by curcumin on OA.

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Skovsgaard Itenov, K., N. Søe, E. M. Bartels, H. Bliddal, and M. Andersen. "AB0103 SITE SPECIFICITY OF RHEUMATOID ARTHRITIS INFLAMMATION: A SECONDARY ANALYSIS OF BIOPSIES FROM RADIAL AND ULNAR ASPECTS OF MCP JOINTS." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1182.2–1182. http://dx.doi.org/10.1136/annrheumdis-2022-eular.5196.

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BackgroundUlnar drift is a common complication of Rheumatoid Arthritis (RA) (1,2). There is no clear consensus regarding the etiology of the hand deformity. Observations from corrective hand surgery and other studies have noted more pronounced inflammation in the radial site of the MCP-joints (3,4). This could partly explain the pathophysiology behind the ulnar deviation.ObjectivesTo determine if there is more pronounced inflammation, measured by increased CD-68 expression (5) and Krenn-synovitis score (6), at the radial side of the MCP joints when compared to the ulnar side, in patients with verified RA.MethodsWe included RA patients from a previous study who had biopsies taken from the most affected joints based on clinical examination and ultrasound (7). Twenty-nine PIP-, MCP- and wrist-joints were biopsied. Biopsies from the MCP-joints were taken from the dorso-ulnar and dorso-radial concavity. Inflammation was graded by the Krenn-synovitis score (0-9) and the density of CD-68-positive cells (%). The difference between radial and ulnar joint inflammation was calculated by paired t-test. P-value <0.05 was considered statistically significant.ResultsIn 8 patients biopsies were taken from both the ulnar and the radial site of the same MCP-joint. The mean difference in inflammation on the radial and ulnar site of MCP-joints was based on differences in CD-68 density: 0,67% (95%-CI -4,77 to 6,10; P = 0,77) (Figure 1) and Krenn-score: 0,83 (95%-CI -1,31 to 2,98; P = 0,36), respectively.Figure 1.Paired data on CD-68 percentage in radial and ulnar sitesConclusionThere was no difference in concentration of inflammatory cells or overall synovial pathology between the radial and ulnar site of MCP-joints in RA patients. The impression of a more pronounced inflamed synovium on the radial site of MCP joints, as observed during surgery, does not seem to arise from an immunological preference, but rather to be linked to a larger synovial volume.References[1]Wise KS: The anatomy of the metacarpo-phalangeal joints, with observations of the aetiology of ulnar drift. J. Bone Joint Surg. Br. 1975; 57:485–90[2]Johnsson PM, Eberhardt K: Hand deformities are important signs of disease severity in patients with early rheumatoid arthritis. Rheumatology 2009; 48:1398–1401[3]Philpott H.T. Synovial tissue perivascular edema is associated with altered gait patterns in patients with knee osteoarthritis, Osteoarthritis and Cartilage. 2022; 30(1): 42-51[4]Tan AL, Tanner SF, Conaghan PG, et al.: Role of metacarpophalangeal joint anatomic factors in the distribution of synovitis and bone erosion in early rheumatoid arthritis. Arthritis Rheum. 2003; 48:1214–22[5]Zhang X.-P: Addition of Fibroblast-Stromal Cell Markers to Immune Synovium Pathotypes Better Predicts Radiographic Progression at 1 Year in Active Rheumatoid Arthritis, Frontiers in Immunology 2021; 12: 778480[6]Krenn V, Morawietz L, Burmester G-R, et al.: Synovitis score: discrimination between chronic low-grade and high-grade synovitis. Histopathology 2006; 49:358–364[7]Andersen M, Ellegaard K, Hebsgaard JB, et al.: Ultrasound colour Doppler is associated with synovial pathology in biopsies from hand joints in rheumatoid arthritis patients: a cross-sectional study. Ann. Rheum. Dis. 2014; 73:678–683AcknowledgementsThe authors would like to thank the study participants as well as Inger Wätjen, Eva Littrup Andersen, Mette Okkels, Jette Møller Frøsig and Suzi Høeg Madsen for technical assistance. I have no acknowledgements to declare.Disclosure of InterestsKatrine Skovsgaard Itenov: None declared, Niels Søe: None declared, Else Marie Bartels: None declared, Henning Bliddal: None declared, Martin Andersen Grant/research support from: The primary study was supported by unrestricted grants from Novo Nordisk, Employee of: Was employed at Novo Nordisk A/S during the conduction of the study.

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Patenaude, S., and W. Gerhart. "AB0923-PARE WHAT IS THE IMPACT ON THE QUALITY OF LIFE (QOL) OF PEOPLE LIVING WITH SPONDYLOARTHRITIS (SPA*)?" Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1482.1–1483. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1615.

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Background:SpA describes a group of chronic inflammatory arthritic diseases with common features including inflammation of the spine, eyes, skin and gastrointestinal tract. These conditions can be painful and debilitating for many. Delayed diagnosis and treatment can lead to irreversible damage to the spine and other joints. Diagnosis of these conditions can take, on average, 7 years or more. We don’t know what causes SpA and there is no cure. The onset of symptoms can be in early childhood and expands throughout one’s lifespan. It affects children, women and men worldwide.Objectives:To understand how living with SpA impacts QOL (including relationships, work and day-to-day life) and what is important to patients in order to help the CSA** prioritize advocacy focus and resource development.Methods:The CSA surveyed the community virtually from 11/19/19 to 01/21/20. The results of 838 respondents were analyzed after the survey closed.Results:66% of respondents had been diagnosed with Ankylosing Spondylitis and 24% with Psoriatic Arthritis. 22% were diagnosed with more than one form of SpA.Over 70% reported their day-to-day life was negatively impacted by SpA. Only 7% indicated no impact on their daily life and 22% said it was somewhat impacted. Ability to remain in the workplace was impacted and 16% reported being on long-term disability and 4% on short-term disability. There were 7% who retired early due to their disease.Sleep loss/interruption was reported by 89% and 74% said they avoid social events. 41% of participants are highly restricted by SpA when it comes to tasks like outdoor yard work. Other highly restricted tasks include exercise (36%) and cleaning (31%). Tasks of medium restriction include preparing meals (31%) and engaging in intimate relations (30%).Upon diagnosis and disease progression, many reported less frequent participation in exercise, travel, intimate relationships, social outings and family activities. Some even said they stopped participating in these all together.When asked to rank what was most important regarding QOL, most ranked living with no/reduced pain as most important, followed by improved sleep/no fatigue. The least important were returning to work and going out with friends.Conclusion:SpA conditions have a negative impact on QOL and are a burden causing patients to constantly assess their situation, worry about tomorrow and adjust different aspects of their lives. Results confirmed every aspect of life is impacted, both physically and mentally, leaving people feeling hopeless and without a purpose. Many can no longer work or do their favorite hobbies which leads to emotional and mental difficulties. People struggle with maintaining social and intimate relationships, intensifying social isolation and low self-confidence. Many indicated that their loved ones have difficulties understanding chronic pain and illness, making patients feel like a burden. This may be attributed to general lack of knowledge about SpA. The unpredictability of the disease impacts QOL leaving patients hesitant to make social plans in advance. Even those who are undergoing successful treatment and have improved QOL worry about the future. QOL can be improved with proper treatment, management and support.Many expressed frustrations of being limited by their disease and indicated that it is often the chronic pain that causes these limits. It is clear that by living with less pain, patients can improve all aspects of their lives and be happier.The CSA is committed to educating, supporting and advocating on behalf of Canadians impacted by SpA to improve health outcomes and QOL.It doesn’t have to be visible to be real. Together we are stronger!Footnotes:*SpA conditions include: Ankylosing Spondylitis, Psoriatic Arthritis, non-radial SpA, Axial and Peripheral Spondyloarthritis, Enteropathic Arthritis, Reactive Arthritis and Juvenile Onset Arthritis**The Canadian Spondylitis Association (CSA) is a national non-profit patient association supporting and advocating for those living with SpA.Disclosure of Interests:None declared

Journal articles on the topic 'Arthritis Molecular aspects'

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