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Artykuły w czasopismach na temat "Spondyloarthrites"
Haddouche, Assia. "Brèves de l’EULAR 2015 Les spondyloarthrites". Batna Journal of Medical Sciences (BJMS) 2, nr 1 (15.09.2015): S10—S15. http://dx.doi.org/10.48087/bjms.2015.s215.
Pełny tekst źródłaBarry, A., AI Baldé, AB Kamissoko, M. Ndong Obiang, M. Sanda, K. Condé i M. Touré. "Manifestations oculaires au cours des spondyloarthrites en Guinée". Rhumatologie Africaine Francophone 3, nr 2 (16.10.2022): 6–12. http://dx.doi.org/10.62455/raf.v3i2.34.
Pełny tekst źródłaWendling, Daniel. "L’intestin des spondyloarthrites". Revue du Rhumatisme 82 (listopad 2015): A19—A22. http://dx.doi.org/10.1016/s1169-8330(16)30068-0.
Pełny tekst źródłaLacout, A., C. Le Breton, I. Peretti, R. Carlier, N. Amoretti, C. Meunier, C. Tamas i P. Y. Marcy. "Imagerie des spondyloarthrites". Feuillets de Radiologie 56, nr 3 (czerwiec 2016): 133–50. http://dx.doi.org/10.1016/j.frad.2016.03.008.
Pełny tekst źródłaDamiano, Joël. "Le pied des spondyloarthrites". Revue du Podologue 13, nr 78 (listopad 2017): 9. http://dx.doi.org/10.1016/j.revpod.2017.09.003.
Pełny tekst źródłaPialat, J. B., L. Di Marco, A. Feydy, C. Peyron, B. Porta, P. H. Himpens, A. Ltaief-Boudrigua i S. Aubry. "Sacro-iliaques et spondyloarthrites". Journal de Radiologie Diagnostique et Interventionnelle 97, nr 3 (sierpień 2016): 229–41. http://dx.doi.org/10.1016/j.jradio.2016.02.014.
Pełny tekst źródłaRahmouni, S., M. Slouma, R. Dhahri, L. Metoui, N. Boussetta, N. H. Guediche, S. Sayhi, F. Ajili, I. Gharsallah i B. Louzir. "La coxite des spondyloarthrites". La Revue de Médecine Interne 39 (czerwiec 2018): A169—A170. http://dx.doi.org/10.1016/j.revmed.2018.03.120.
Pełny tekst źródłaHamdi, O., K. Maatallah, H. Ferjani, D. Kaffel i W. Hamdi. "La coxite des spondyloarthrites". La Revue de Médecine Interne 40 (grudzień 2019): A111. http://dx.doi.org/10.1016/j.revmed.2019.10.139.
Pełny tekst źródłaMougui, A., M. Belaabid, S. Ait Malek, R. Abouqual, L. Achemlal, F. Allali, R. Bahiri i in. "Les spondyloarthrites à début tardif". Revue du Rhumatisme 88 (grudzień 2021): A274. http://dx.doi.org/10.1016/j.rhum.2021.10.462.
Pełny tekst źródłaHaddouche, Assia. "Brèves de l’EULAR 2014 Spondyloarthrites". Batna Journal of Medical Sciences (BJMS) 1, S1 (30.09.2014): S12—S15. http://dx.doi.org/10.48087/bjms.2014.1s05.
Pełny tekst źródłaRozprawy doktorskie na temat "Spondyloarthrites"
Grandon, Benjamin. "La drosophile transgénique HLA-B27 : un nouveau modèle pour l'étude des spondyloarthrites". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLV051/document.
Pełny tekst źródłaSpondyloarthritis (SpA) is a chronic inflammatory rheumatic disorder characterized by joint manifestations affecting the spine, peripheral joints and entheses, as well as extra-articular manifestations such as psoriasis, uveitis, or intestinal inflammation. This complex disorder has a strong genetic component dominated by the HLA-B27 antigen of the major histocompatibility complex class I (MHC-I), which is present in more than 80% of SpA patients. Discovered 45 years ago, the association between HLA-B27 and SpA development remains unexplained. Several hypotheses have been proposed to explain this association at the molecular level, but all face experimental inconsistencies that seem to invalidate them. Therefore, it appeared to us essential to elaborate new and yet unexplored approaches in order to better understand the molecular role of HLA-B27 in SpA development. Drosophila melanogaster is a powerful genetic model that has led to considerable advances in understanding numerous functions of metazoan cells, as well as in describing the cellular and molecular processes of many human pathologies. To elucidate the molecular pathogenic mechanisms associated with HLA-B27, we have established several transgenic Drosophila lines for SpA-associated and non-associated of HLA-B alleles, as well as for the MHC-I invariant chain, the human 2-microglobulin (hβ2m). Expression of the HLA-B27 alleles, in the presence of hβ2m, in the Drosophila wing and eye led to two specific phenotypes. The crossveinless wing phenotype is due to a disturbance in the Bone Morphogenetic Protein (BMP) signaling pathway. Interestingly, this misregulation is associated with a co-localization of HLA-B27 and the BMP type I receptor named Sax. Our preliminary results obtained in SpA patient cells suggest that HLA-B27 also colocalizes with ALK2 receptor, which is ortholog to Sax. Altogether, our results suggest that the pathogenic role of HLA-B27 in SpA may depend on a BMP signaling misregulation at the crosstalk between ossification and inflammation
Miralles, Daniel. "Troubles de l'avant-pied dans les spondylarthropathies". Montpellier 1, 1989. http://www.theses.fr/1989MON11184.
Pełny tekst źródłaLauraine, Marc. "Effets d'HLA-B27 sur la voie BMP/TGFbeta dans les lymphocytes T CD4+, dans le contexte de la spondyloarthrite". Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL130.
Pełny tekst źródłaSpondyloarthritis (SpA) is a common chronic inflammatory disease. In human, the association between the HLA-B27 allele of the class-I major histocompatibility complex (MHC-I) and the development of this disease was demonstrated 50 years ago, with 70-90% of SpA patients carrying this allele. However, the exact role of HLA-B27 in the pathophysiology of SpA remains unknown. The model of rat transgenic for HLA-B27 and the human β2-microglobulin (hβ2m) (B27 rat), which develops manifestations similar to the human disease, has shed light on certain aspects of the question. In particular, the involvement of CD4+ T lymphocytes in SpA has been demonstrated. In the B27 rat, regulatory CD4+ T lymphocytes (Treg) exhibit an imbalance of the interleukin-10/interleukin-17 (IL-10/IL-17) ratio, which are anti-inflammatory and pro-inflammatory, respectively. On the other hand, an expansion of the sub-population of pro-inflammatory CD4+ T helper 17 (lymphocytes Th17), which produce IL-17, was observed in both B27 rats and SpA patients. To study the non-canonical effects of HLA-B27, a Drosophila melanogaster model transgenic for HLA-B27 and hβ2m was developed and demonstrated that an interaction between HLA-B27 and type I receptors of the BMP/TGFβ pathway (BMPR1s) altered the formation of the wing transverse veins. In this model, an interaction between HLA-B27 and the Saxophone (Sax) receptor has previously been shown to lead to increased BMP signalling. Our study complemented these results by showing that aberrant signaling via the BMPR1 Baboon (Babo) of the activin/TGFβ pathway also contributed to the abnormal phenotype induced by HLA-B27 expression. In an attempt to extrapolate these results to a mechanism of HLA-B27 pathogenicity in SpA, we first demonstrated that there was a specific interaction between HLA-B27 and activin receptor-like kinase 2 (ALK2), the orthologue of Sax, and also with ALK5, the type 1 receptor for TGFβ orthologue of Babo, in rat B27 lymphocytes. Study of SMAD2/3, the main transducer of the TGFβ signal, in T lymphocytes from B27 and nontransgenic rats revealed a lower basal phosphorylation and a higher amplitude of phosphorylation after stimulation by TGFβ1. Concordantly, we observed that several genes induced by TGFβ signaling and involved in Treg and Th17 differentiation (Foxp3, Rorc, Runx1) had increased expression in naive CD4+ T lymphocytes (Tn) from B27 rats. Taken together, these results indicate a possible early activation of the TGFβ pathway in B27 rat Tn followed by a negative feedback loop. Interestingly, the Tgfb1 gene itself was decreased. Given the importance of autocrine TGFβ1 produced by T lymphocytes in preventing chronic inflammation, these observations open up prospects for a better understanding of the role of HLA-B27 in the development of SpA. In particular, we propose to study in greater depth the response of Tn from B27 rats to TGFβ1 using multi-omics methods (transciptomic, phosphoproteomic, proteomic). Finally, given the essential role of autocrine TGFβ1 in the maintenance of Treg and Th17 profiles, a study of the plasticity of Treg and Th17 in B27 rat would be relevant to a better understanding of the pathophysiology of SpA
Rupp, Paul-Antoine. "Spondylarthropathie destructive découverte par une paraplégie progressive chez un patient dialysé depuis 12 ans, évolution favorable aprés chirurgie". Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M119.
Pełny tekst źródłaMambu, Mambueni Hendrick. "Identification de nouveaux variants rares associés à la spondyloarthrite par séquençage haut-débit". Electronic Thesis or Diss., université Paris-Saclay, 2022. http://www.theses.fr/2022UPASL064.
Pełny tekst źródłaSpondyloarthritis (SpA) is a multifactorial disease with an estimated heritability of over 90%, mainly related to HLA-B27. All identified susceptibility factors, including HLA-B27, explain less than one third of the heritability. The involvement of rare variants could explain part of this missing heritability. The aim of this work was to identify rare variants associated with SpA via a combined family analysis and high-throughput sequencing approach. First, we sequenced a 1.4 Mb region significantly linked to SpA at 13q13 in 71 patients and 21 healthy controls from families with a high linkage score in this region. We identified a rare variant in the FREM2 gene present in 9 patients from a family with high linkage to the region and not found in other families or isolated cases of SpA. We then sequenced the exome of 48 patients from 20 multiplex families. Unfortunately, we did not observe any recurrent variants between families. We then focused on a second, previously known genetic linkage peak on chromosome 9. The study of the family most linked to this region, which includes 12 patients, led to the identification of several rare coding variants segregating with the disease. However, subsequent studies have shown equivalent allelic frequencies of these variants between cases and controls. Finally, whole genome sequencing of 413 patients from 76 multiplex families with 4 or more patients was performed. We identified 1203 rare, coding, non-synonymous variants shared by at least all affected family members. Genetic and functional validation analyses of these variants are underway, as is the analysis of non-coding variants. In conclusion, these different approaches suggest significant genetic heterogeneity in SpA and also highlight the difficulty of confirming the involvement of rare variants in complex diseases
Chaplais, Emmanuel. "Une approche de modélisation de biologie des systèmes sur la spondylarthrite". Thesis, Versailles-St Quentin en Yvelines, 2015. http://www.theses.fr/2015VERS035V/document.
Pełny tekst źródłaSpondyloarthritis is a frequent chronic inflammatory rheumatism, with a prevalence of 0.43 % in France. This disease presents axial skeleton injuries, but also on peripheral joints, and can results in a total spinal and sacro-iliac motility loss. Extra-articular features including uveitis, psoriasis and inflammatory bowel disease are frequent. Current SpA treatments are only symptomatic, relieving inflammatory symptoms. SpA etiology is largely multifactorial with a genetic component dominated by the long-known strong association with the HLA-B27 allele. This allele, however, is not sufficient for the disease to occur. This thesis project objective was then to identify other genetic factors in the origin of SpA.My work was mainly divided in two complementary data analyses, in a way to get a systems biology approach. The first one consisted in proceed linking analyses on data from Affymetrix genotyping chips gathered from DNA of 1310 people grouped in 210 families. This study allowed notably to detect a new significantly linked region to SpA : 13q13, with an interval of 1.3 Mb. This part of genome is currently being sequenced to allow a better causal SNP identification.Secondly, an Affymetrix HumanGene 1.0 st transcriptomic chips analysis was performed on MD-DCs extracted from 68 people, stimulated or not by LPS during 6 or 24 hours. This cohort was grouped between 23 patients HLA-B27+, 23 healthy controls HLA-B27+ and 21 healthy controls HLA-B27-. I could notice that HLA-B27 allele is farly enough to considerably affect cell transcriptomic profiles, which encourages to include HLA-B27+ healthy controls. Otherwise, a gene network analysis allowed me to highlight on an inhibition of early steps of cholesterol biosyntthesis
Al-Mossawi, Mohammad Hussein. "Pathogenic immune responses in spondyloarthritis". Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:eab12909-6af6-4269-85de-69fa99d11af7.
Pełny tekst źródłaHaibel, Hildrun [Verfasser]. "Therapie der axialen Spondyloarthritis / Hildrun Haibel". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1075757673/34.
Pełny tekst źródłaEl, Jamal Alaeddine. "Implication du métabolisme de la sphingosine 1-phosphate dans les mécanismes biochimiques et cellulaires de la minéralisation dans la spondylarthrite ankylosante". Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1169.
Pełny tekst źródłaSpondyloarthritis (SpA) is a rheumatic disease characterized in particular by enthesis ectopic ossification and inflammation. Enthesis is a zone of concentration of mechanical stresses where ligaments and tendons attach to bone through fibrocartilaginous connections. Sphingosine 1-phosphate (S1P) is a bioactive lipid that plays an important role in both bone remodelling and in inflammatory response. Our aim was to explore the role of S1P in SpA excessive ossification. We observed that serum S1P concentrations in SpA patients are significantly higher compared to control donors. We used primary mouse osteoblasts, chondrocytes and tenocytes as cellular models and organotypic cultures of mice enthesis. We observed that S1P synthetizing enzymes, sphingosine kinases 1 and 2, stimulate osteoblasts’ and chondrocytes’ mineralizing process. S1P pro-mineralizing effect was partially mediated by two of the S1P receptors (S1P1 and S1P3). Moreover, S1P production was enhanced by cyclic strain in osteoblasts and chondrocytes and by pro-inflammatory cytokines (TNF-α and IL-17) in chondrocytes. Finally, the inhibition of S1P metabolic pathway by Fingolimod reduced the mineralization in cultured osteoblasts and even more in chondrocytes. These results suggest that S1P metabolism participates in SpA excessive ossification. In vivo studies are now needed to validate this possibility
Jarvis, Lorna Beth. "Autoreactive CD8+ regulatory T cells in spondyloarthritis". Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.605067.
Pełny tekst źródłaKsiążki na temat "Spondyloarthrites"
Nicknam, Mohammad Hossein, red. Ankylosing Spondylitis - Axial Spondyloarthritis. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-4733-8.
Pełny tekst źródłaSieper, Joachim, i Jürgen Braun. Clinician’s Manual on Axial Spondyloarthritis. Tarporley: Springer Healthcare Ltd., 2014. http://dx.doi.org/10.1007/978-1-907673-85-6.
Pełny tekst źródłaGarrido-Cumbrera, Marco, Victoria Navarro-Compán, Christine Bundy, Raj Mahapatra, Souzi Makri, Carlos J. Delgado-Domínguez, Pedro Plazuelo-Ramos i Denis Poddubnyy. Axial Spondyloarthritis: Patient-Reported Impact in Europe. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-97606-4.
Pełny tekst źródłaSheldon, Peter John. Lymphocyte responses in rheumatoid reactive and spondyloarthritis. Birmingham: University of Birmingham, 1987.
Znajdź pełny tekst źródłaSiebert, Stefan, Raj Sengupta i Alexander Tsoukas, red. Axial Spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.001.0001.
Pełny tekst źródłaAxial Spondyloarthritis. Elsevier, 2020. http://dx.doi.org/10.1016/c2017-0-01005-4.
Pełny tekst źródłaKhan, Muhammad Asim, i Philip Mease. Axial Spondyloarthritis. Elsevier - Health Sciences Division, 2019.
Znajdź pełny tekst źródłaSiebert, Stefan, Raj Sengupta i Alexander Tsoukas. Axial Spondyloarthritis. Oxford University Press, 2016.
Znajdź pełny tekst źródłaBrown, Matthew A., i John Reveille. Genetics of spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0005.
Pełny tekst źródłaLeirisalo-Repo, Marjatta, i John D. Carter. Infection and spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0009.
Pełny tekst źródłaCzęści książek na temat "Spondyloarthrites"
Ermann, Joerg. "Spondyloarthritis". W Neurorheumatology, 87–91. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16928-2_9.
Pełny tekst źródłaCypers, Heleen, S. Louis Bridges i Dirk Elewaut. "Spondyloarthritis". W The Microbiome in Rheumatic Diseases and Infection, 201–20. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-79026-8_16.
Pełny tekst źródłaSommefleck, Fernando A., Emilce E. Schneeberger i Gustavo Citera. "Spondyloarthritis". W Compendium of Inflammatory Diseases, 1210–21. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_191.
Pełny tekst źródłaEder, Lihi, i Dafna D. Gladman. "Spondyloarthritis". W Handbook of Clinical Gender Medicine, 367–79. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000336430.
Pełny tekst źródłaSyed, Nilofar, Fatemah Ezzati i Lesley Davila. "Spondyloarthritis". W Multidisciplinary Spine Care, 109–19. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04990-3_5.
Pełny tekst źródłaNagaratnam, Nages, Kujan Nagaratnam i Gary Cheuk. "Spondyloarthritis". W Geriatric Diseases, 1–4. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-32700-6_55-1.
Pełny tekst źródłaNagaratnam, Nages, Kujan Nagaratnam i Gary Cheuk. "Spondyloarthritis". W Geriatric Diseases, 513–16. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-33434-9_55.
Pełny tekst źródłaSommefleck, Fernando A., Emilce E. Schneeberger i Gustavo Citera. "Spondyloarthritis". W Encyclopedia of Inflammatory Diseases, 1–12. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-0348-0620-6_191-1.
Pełny tekst źródłaHanda, Rohini. "Spondyloarthritides". W Clinical Rheumatology, 67–80. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4885-1_7.
Pełny tekst źródłaJagpal, Aprajita, Surahbhi S. Vinod i S. Louis Bridges. "Seronegative Spondyloarthritis". W Orthopedic Surgery Clerkship, 729–34. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52567-9_150.
Pełny tekst źródłaStreszczenia konferencji na temat "Spondyloarthrites"
Shatunova, E. A., M. A. Korolev i M. A. Vorobyeva. "COLORIMETRIC APTAMER-BASED TEST SYSTEMS FOR THE DETECTION OF SERUM DKK-1 PROTEIN IN SPONDYLOARTHRITIS". W X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-147.
Pełny tekst źródłaSelvarajah, Uma, Jesus Miguens Blanco, Shiva Radhakrishnan, Sam Powles, Julie McDonald, Alex Pechlivanis, Julian Marchesi i in. "PTH-123 Is axial spondyloarthritis in IBD different to axial spondyloarthritis without IBD?" W British Society of Gastroenterology Annual Meeting, 17–20 June 2019, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-bsgabstracts.182.
Pełny tekst źródłaTenorio, Ariane, José Ferreira Junior, Vitor Dalto, Matheus Faleiros, Rodrigo Assad, Marcello Nogueira-Barbosa i Paulo Azevedo-Marques. "Radiomics Assessment of SPAIR and STIR MRI Sequences to Predict Axial and Peripheral Spondyloarthritis". W Anais Principais do Simpósio Brasileiro de Computação Aplicada à Saúde. Sociedade Brasileira de Computação - SBC, 2020. http://dx.doi.org/10.5753/sbcas.2020.11532.
Pełny tekst źródłaVukić, Vana, Mandica Vidović, Miroslav Harjaček i Lovro Lamot. "448 Treatment of juvenile spondyloarthritis". W 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.448.
Pełny tekst źródłaMaksymowych, W. P., D. Loeuille, S. Wichuk, J. Paschke, O. Judet, M. Breban, M. A. D’Agostino i R. G. Lambert. "FRI0218 Validation of assessments in spondyloarthritis international society (ASAS) mri lesion definitions in axial spondyloarthritis: data from the echography in spondyloarthritis cohort (ECHOSPA)". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7278.
Pełny tekst źródłaDiniz Araújo Teixeira, Matheus, i Sandra Lúcia Euzébio Ribeiro. "PREVALENCE OF OPHTHALMIC MANIFESTATIONS IN SPONDYLOARTHRITIS". W Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17437.
Pełny tekst źródłaROGOWSKI, PEDRO OTAVIO, LUIZ FELIPE BECKER i TIAGO OSTERNACK MALUCELLI. "SEVERE AND TREATMENT RESISTANT UNDIFFERENTIATED SPONDYLOARTHRITIS". W 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-244.
Pełny tekst źródłaSerrano-Benavente, B., C. M. González Fernández, L. Valor, J. C. Nieto-González, R. D. González-Benítez, I. Janta, C. Sáenz Tenorio i in. "SAT0273 Golimumab retention rate in patients with spondyloarthritis. differences between ankylosing spondylitis and non-radiographic axial spondyloarthritis". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4135.
Pełny tekst źródłaOcaña Garcia, Omar Enrique, Sergio Cerpa-Cruz, Sergio Gutierrez-Ureña, Gloria Martinez-Bonilla, Ana Guilaisne Bernard Medina, Veronica Gonzalez-Diaz, Jose Antonio Velarde Ruiz Velazco i Liliana Ivett Hernandez Cruz. "THU0396 SMALL INTESTINAL BACTERIA OVERGROWTH IN SPONDYLOARTHRITIS". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5215.
Pełny tekst źródłaDougados, M. "SP0004 Extra spinal manifestations in axial spondyloarthritis". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7651.
Pełny tekst źródłaRaporty organizacyjne na temat "Spondyloarthrites"
Spitsina, S. S. Assessment of pain syndrome in patients with spondyloarthritic psoriatic arthritis. DOI CODE, 2021. http://dx.doi.org/10.18411/wco-iof-esceo-2021-390-2.
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