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Ninth International Congress on Spondyloarthritis Ninth International Congress on Spondyloarthritis October 23–25, 2014 Gent, Belgium Presidents Martin Rudwaleit Dept. of Internal Medicine and Rheumatology Klinikum Bielefeld Bielefeld, Germany John D. Reveille Division of Rheumatology The University of Texas Health Science Center at Houston Houston, USA Local Organisers Herman Mielants Dirk Elewaut Filip Van den Bosch Dept. of Rheumatology, University of Gent Gent, Belgium Abstracts Page no. Invited Lectures (INV1 – INV25) 766 Oral Presentations (O1 – O12) 771 Short Oral Presentations (SO1 – SO5) 775 Poster Presentations (P1 – P182) 776 Author Index 835 Clinical and Experimental Rheumatology 2014; 32: 765-838. Invited Lectures Ninth International Congress on Spondyloarthritis Invited Lectures (SCORE), which are based on CV risk factors. Statin and/or antihypertensive treatment is then only initiated above a certain threshold, e.g. a 10-year CV mor- tality risk of 10% or more or a 10 year CV morbidity of 20% or more. EULAR recommendations for CV-RM in patients with IJD advised yearly CV INV1 risk screening For RA it is recommended to adapt existing risk functions, such as SCORE, by a multiplier of 1.5 to achieve a more appropriate estimation of THE INTESTINAL MICROBIOME AND THE IMMUNE SYSTEM the 10 years CV risk (9). Obviously, effective suppression on the inflammatory process is necessary to further decrease the CV-risk. For SLE it is recommended Eberl G. the LDL-cholesterol levels should below 2.6 mmol/L and blood pressure levels Lymphoid Tissue Development Unit, Institut Pasteur, Paris, France be lower than 130/80 mmHg. When there are no contraindications, aspirin should be given to patients with a history of CV events (including myocardial infarction, RORγt+ T cells and RORγt+ innate lymphoid cells (ILCs) play central roles in angina or stroke), the presence of antiphospholipid antibodies, hypertension, dia- the development of the immune system, in homeostasis of the host with its sym- betes, hypercholesterolemia, or smoking (10). Also for SLE the EULAR recom- biotic microbiota, in defence against invasive microbes and in inflammatory pa- mends yearly CV-risk screening (11). + thology. The cytokines produced by RORγt cells, including the lymphotoxins References LTα 1ß2 and LTα3, GM-CSF, IL-17 and IL-22, elicit innate defence mechanisms 1. HAHN BH, GROSSMAN J, CHEN W, MCMAHON M: The pathogenesis of atheroscle- in mucosal tissues, activate and regulate lymphocytes and antigen presenting rosis in autoimmune rheumatic diseases: roles of inflammation and dyslipidemia.J + cells, and recruit myeloid cells. We have shown that RORγt ILCs, or ILC3s, are Autoimmun 2007; 28: 69-75 cardiovascular disease (CVD), particularly of athero- programmed to express high levels of IL-22, and that microbiota regulate this sclerotic origin such as ischemic heart disease. + activity during homeostasis. In contrast, the activity of RORγt T cells is induced 2. O’NEILL TW, BRESNIHAN B: The heart in ankylosing spondylitis. Ann Rheum Dis. by microbiota. RORγt+ T cells not only include pro-inflammatory Th17 cells 1992; 51: 705-6. expressing IL-17, but also FoxP3+ regulatory T cells (Tregs). We find that FoxP3+ 3. BREMANDER A, PETERSSON IF, BERGMAN S, ENGLUND M: Population-based esti- RORγt+ Tregs express high levels of IL-10, but not IL-17, and are induced by the mates of common comorbidities and cardiovascular disease in ankylosing spondy- symbiotic microbiota through pro-inflammatory pathways that normally induce litis. Arthritis Care Res 2011; 63: 550-6. Th17 cells. However, in the colon, these pathways lead to the preferential induc- 4. KANG JH, CHEN YH, LIN HC: Comorbidity profiles among patients with ankylosing tion of Tregs in a vitamin A-dependent pathway, and play an important role in the spondylitis: a nationwide population-based study. Ann Rheum Dis 2010; 69: 1165- microbiota-controlled development of a balanced immune system. 8. 5. MATHIEU S, GOSSEC L, DOUGADOS M, SOUBRIER M: Cardiovascular profile in an- kylosing spondylitis: a systematic review and meta-analysis. Arthritis Care Res 2011; 63: 557-63. 6. DIVECHA H, SATTAR N, RUMLEY A et al.: Cardiovascular risk parameters in men INV3 with ankylosing spondylitis in comparison with non-inflammatory control sub- jects: relevance of systemic inflammation.Clin Sci 2005; 109: 171-6. CV RISK AND OTHER RISK FACTORS: A VIEW OF AXIAL SPA, 7. BOERS M, NURMOHAMED MT, DOELMAN CJA et al.: Influence of glucocorticoids RA, AND SLE and disease activity on total and high density lipoprotein cholesterol in patients with rheumatoid arthritis. Ann Rheum Dis 2003; 62: 842-45. Nurmohamed M.T. 8. MCMAHON M, GROSSMAN J, FITZGERALD J et al.: Proinflammatory high-density Dept. of Rheumatology, VU University Medical Centre, Amsterdam, The Nether- lipoprotein as a biomarker for atherosclerosis in patients with systemic lupus ery- thematosus and rheumatoid arthritis. Arthritis Rheum 2006; 54: 2541-49. lands 9. PETERS MJ, SYMMONS DP, MCCAREY D et al.: EULAR evidence-based recommen- dations for cardiovascular risk management in patients with rheumatoid arthritis There is accumulating evidence that patients with inflammatory joint diseases and other forms of inflammatory arthritis.Ann Rheum Dis 2010; 69: 325-31. (IJD) such as axial SpA (particularly ankylosing spondylitis (AS)) and RA suffer 10. WAJED J, AHMAD Y, DURRINGTON PN, BRUCE IN: Prevention of cardiovascular dis- from an increased cardiovascular (CV) risk in comparison to the general popula- ease in systemic lupus erythematosus--proposed guidelines for risk factor manage- tion. The magnitude is approximately doubled in IJD whereas in SLE the risk ment. Rheumatology (Oxford) 2004; 43: 7-12. appears to be increased at least four-fold in comparison the general population. 11. MOSCA M, TANI C, ARINGER M et al.: European League Against Rheumatism rec- There are several potential explanations for the higher CV risk in these patients ommendations for monitoring patients with systemic lupus erythematosus in clini- categories but inflammation itself appears to play a pivotal role (1). Inflammation cal practice and in observational studies. Ann Rheum Dis 2010; 69: 1269-74. accelerates atherosclerosis directly, but also mediates CV risk factors, such as lipid profile, blood pressure, and insulin resistance. The increased CV-risk in AS is not only due to atherosclerotic disease, but also due to the “AS-specific” cardiac manifestations. Well-known lesions are conduc- INV5 tion defects and aortic insufficiency. Less common CV-diseases include peri- carditis, cardiomyopathy, mitral valve disease and ventricular dysfunction (2). MAPPING THE IL-23/IL-17 AXIS Conduction disturbances are due to inflammation-induced fibrosis of the inter- ventricular septum, thereby affecting the atrioventricular node and prevalences Elewaut D. are reported up to 35%, and there might be an relationship with the HLA-B27 Dept. of Rheumatology, University Hospital Ghent, Ghent, Belgium antigen. However, these data are based on studies conducted several decades ago, hence there is a clear need for contemporary studies assessing the current Inflammatory responses in rheumatic diseases are steered by hierarchical cy- contribution of AS-related cardiac manifestations towards the increased CV-risk tokine cascades. In spite of the marked therapeutic success of TNF blockade in in AS. Hypertension occurs between 50 – 100% more frequent than in the general SpA and PsA, there is a particular need for new mode of action drugs. Evidence population (3, 4). Dyslipidemia is related to disease activity and patients with ac- has emerged that in SpA and PsA, IL-17 and IL-17 steering responses may rep- tive disease have decreased HDL-cholesterol and total cholesterol levels (5, 6). resent another dominating cytokine cascade. In the skin, IL-17 blockade in pso- Furthermore, there is some evidence that patients with AS smoke twice as much riasis has marked efficacy and in PsA significant impact on arthritic disease. Also in comparison to the general population. in axial disease, blocking IL-17 driven responses induces therapeutic responses. An inverse relationship between lipid levels and disease activity, i.e. a higher By contrast, in inflammatory bowel disease, lack of benefit was observed. These disease activity is related with a lower TC but even more depressed HDL-cho- observations highlight that IL-17 driven responses appear to be distinctly fine lesterol, resulting in a higher (unfavorable) atherogenic index (TC/HDL-C ratio) tuned in different organs. is also observed in RA (7). Smoking and insulin resistance are more frequent in RA in comparison to the general population, data about hypertension are contra- dictory whereas no conclusions can be drawn with respect to the contribution of “body mass” index and physical fitness towards the increased CV risk in RA. It is important to realize that in an inflammatory situation the normally anti- inflammatory and ant-atherogenic HDL-cholesterol becomes pro-inflammatory and pro-atherogenic. For instance, these dysfunctional HDL particles were ob- served in approximately 50% of SLE patients, compared with 5–7% in healthy controls and are associated with a more than 15-fold increased risk of carotid plaque in SLE (8). Nowadays, there is no doubt that CV risk management is necessary for patients with IJD as well as SLE. This is generally done on the basis of the 10 years abso- lute risk for a (fatal) CV-event, which is calculated from a CV-risk formula, such as the Framingham risk calculator and the Systematic Coronary Risk Evaluation 766 Ninth International Congress on Spondyloarthritis Invited Lectures INV7 sacroiliitis on MRI” as applied in the ASAS classification criteria for axial SpA. The ASAS classification is a practical and widely used definition that has been THERAPIES FOR NON-RADIOGRAPHIC AXIAL SPA – FROM very important in helping to advance research and therapy in early disease but CLINICAL TRIALS TO CLINICAL PRACTICE in subtle or challenging cases, the definition remains controversial. How much BMO is required to be “highly suggestive”? How many lesions are required or what size do they need to be? What is the role of the structural damage lesions Dougados M.
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