Downloaded from http://ard.bmj.com/ on December 6, 2017 - Published by group.bmj.com
2
Speaker Presentations
Wednesday, 12 June 2013
Wednesday, 12 June 2013
Looking forward to EULAR Madrid 2013 _____
Psoriatic arthritis - new outcomes and therapy options __________________________
SP0001
FINDING YOUR WAY AROUND EULAR HOT TIPS FOR A SUCCESSFUL CONFERENCE
SP0004
P. Cornell . Poole Hospital NHS Foundation Trust, Poole, United Kingdom 1 1
Abstract: This year we’ve decided to present a preliminary session on getting the best out of EULAR for health professionals. This will be a short introduction to the logistics in Madrid, provide details of the health professional programme and the various study groups. This introductory session will include a presentation from the new EULAR president Maurizio Cutolo who will give a presidents perspective for the future of health professionals in EULAR. Disclosure of Interest: None Declared Wednesday, 12 June 2013
WIN session 1 ___________________________ SP0002
THERAPY OF RHEUMATOID ARTHRITIS
C. Gabay . University Hospitals of Geneva, Geneva, Switzerland 1 1
Abstract: The objective of the lecture is to provide up-to-date information on the therapy of rheumatoid arthritis, including the results of clinical trials comparing different treatment strategies, novel data on different biological agents as well as on small molecules targeting intracellular signaling pathways, the results of head to head clinical trials comparing biological agents, and the safety data from patient’s registries. Disclosure of Interest: C. Gabay Grant/research support from: Roche, Abbvie, MSD, Consultant for: Roche, Abbvie, MSD, Pfizer, BMS
SP0003
WHAT IS NEW IN SPONDYLOARTHRITIS
R. Lories 1. 1Department of Development and Regeneration, KU Leuven, Leuven, Belgium Abstract: The recent seminal discovery that an interleukin-23 (IL23) receptor positive T cell population is present in tendon and ligament attachment sites and that these cells contribute to spondyloarthritis-like joint inflammation in mice, has transformed current paradigms of the human disease. These attachment sites, commonly referred to as entheses, were earlier suggested as primary disease localization in SpA but their role in the development of chronic inflammation remained elusive. The IL23 responsive T cell population identified by Sherlock et al., is proposed as a key mediator or masterswitch in the disease process by triggering downstream inflammatory cascades as well as joint remodeling, the Janus-faced characteristics of spondyloarthritis. Interestingly the novel paradigm centered around this unexpected cell population is corroborated by further progress in genetics of spondyloarthritis, highlighted by clearly mapped molecular interactions and pathway integration. From the clinical perspective, accumulating datasets on non-radiographic axial spondyloarthritis not only support the success of anti-TNF strategies in case of failure to achieve symptom control with classical anti-inflammatory drug, but additionally trigger novel questions on the epidemiology of disease. Data obtained in cohorts of early disease patients shed new light on the demographics and likely evolution of the disease. Biomarker research is rapidly growing and a number of novel molecules may find their way into clinical practice over time provided that the original datasets linking serum levels to radiographic progression of disease can be confirmed. With regards to the much feared radiographic progression and evolution towards ankylosis, additional evidence for a structural effect associated with nonsteroidal anti-inflammatory drugs has been presented. From the therapeutic perspective, novel strategies are eagerly awaited with preliminary evidence suggesting clinical responses in patients treated with anti-interleukin 17 strategies. Early phase clinical trial data also point towards apremilast, a phosphodiesterase inhibitor as a drug that needs to be further studied. In summary, over the last year, paradigm-shifting data have been published in the field of spondyloarthritis not only leading to novel insights into the pathophysiology but also defining novel and attractive therapeutic targets thereby suggesting that the next phase in spondyloarthritis research and therapy may be on the horizon. Disclosure of Interest: None Declared
HOW TO ASSESS DISEASE ACTIVITY AND SEVERITY IN CLINICAL PRACTICE
O. Fitzgerald1. 1Rheumatology, St Vincent’s University Hospital, Dublin, Ireland Abstract: Psoriatic Arthritis (PsA) is a complex multisystem disease with involvement of synovial structures, entheseal sites, spine, and skin and nails all common features. The extended clinical phenotype has recently received some attention with obesity, hypertension, Type 2 Diabetes Mellitus, hypercholesterolemia and metabolic syndrome all found more frequently in PsA as compared to controls. An excess of cardiovascular-related events including early mortality is a likely consequence. Radiographic change is also heterogeneous with features including erosive disease and osteolysis and also new bone formation, sacroiliitis and ankylosis. Disease activity measures in PsA have either focused on joint or skin disease or have been borrowed from rheumatoid arthritis. The Psoriatic Arthritis Response Criteria (PsARC) was developed as a specific PsA response measure but the measure is dichotomous and poorly discriminates responders from placebo. More recently, a number of composite disease activity measures have been proposed. These measures are designed to capture disease activity across all of the involved domains; as not all domains are active in all individuals with PsA and as there may be a differential treatment response, ideally it should also be possible to access disease activity and response in individual domains as well. The individual composite measures and their relative performance in clinical trial data to date will be presented and discussed. Measuring disease severity may well relate to disease activity but this is yet to be clearly demonstrated. There would be little argument with the statement that patients with the arthritis mutilans phenotype have severe disease but there are many patients with polyarticular disease and high inflammatory markers who do not develop this severe phenotype. Severe disease whether it is defined on the basis of radiographic change, severe skin/nail disease, some of the cardiovascular risk factors such as presence of the metabolic syndrome or even some composite score requires further study in order to identify as early as possible risk factors which predict its development. Some recent results based on analysis of detailed clinical and genetic data will be presented. If risk factors are modifiable or if early treatment intervention for patients with potentially severe disease can bring about a change in outcome, then some progress for PsA patients will have been made. Disclosure of Interest: O. Fitzgerald Grant/research support from: Pfizer, Abbott, BMS, Roche, Merck
SP0005
IS IT TIME TO AIM FOR REMISSION IN PSA AND HOW SHOULD IT BE MEASURED?
P. Helliwell1. 1University of Leeds, Keighley, United Kingdom Abstract: Psoriatic arthritis is a multifaceted disease and it provides a challenge to outcome methodologists. A number of measures have been used to define remission in PsA but they have been mostly articular. Composite measures of disease activity and low disease states are now emerging but further work is required to assess the implication of achieving these goals and in developing cost-effective treatment strategies to achieve them. Disclosure of Interest: None Declared Wednesday, 12 June 2013
Chronic gout: imaging, diagnosis, treatment__ SP0006
VISUALISING CRYSTALS: DECT AND MORE
B. Manger1. 1 Medizinische Klinik 3, Erlangen, Germany Abstract: The first human to see monosodium urate (MSU) crystals in his newly invented microscope was the Dutch researcher Antoni van Leeuwenhoek in 1679. Since then, the gold standard to establish the diagnosis of gout arthritis is the detection of these crystals, phagocytosed by leukocytes contained in the synovial fluid of an inflamed joint. However, various obstacles may interfere with arthrocentesis individual cases: (i) Gout patients frequently carry a high cardiovascular risk and are on anticoagulant therapy or they do not consent to an invasive procedure due to the extreme pain level of their condition. (ii) In addition, diffuse soft tissue swelling without clearly detectable
Downloaded from http://ard.bmj.com/ on December 6, 2017 - Published by group.bmj.com
SP0001 Finding your Way Around Eular Hot Tips for a Successful Conference P. Cornell Ann Rheum Dis 2013 72: A2
doi: 10.1136/annrheumdis-2013-eular.1 Updated information and services can be found at: http://ard.bmj.com/content/72/Suppl_3/A2.1
These include:
Email alerting service
Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
2
Speaker Presentations
Wednesday, 12 June 2013
Wednesday, 12 June 2013
Looking forward to EULAR Madrid 2013 _____
Psoriatic arthritis - new outcomes and therapy options __________________________
SP0001
FINDING YOUR WAY AROUND EULAR HOT TIPS FOR A SUCCESSFUL CONFERENCE
SP0004
P. Cornell . Poole Hospital NHS Foundation Trust, Poole, United Kingdom 1 1
Abstract: This year we’ve decided to present a preliminary session on getting the best out of EULAR for health professionals. This will be a short introduction to the logistics in Madrid, provide details of the health professional programme and the various study groups. This introductory session will include a presentation from the new EULAR president Maurizio Cutolo who will give a presidents perspective for the future of health professionals in EULAR. Disclosure of Interest: None Declared Wednesday, 12 June 2013
WIN session 1 ___________________________ SP0002
THERAPY OF RHEUMATOID ARTHRITIS
C. Gabay . University Hospitals of Geneva, Geneva, Switzerland 1 1
Abstract: The objective of the lecture is to provide up-to-date information on the therapy of rheumatoid arthritis, including the results of clinical trials comparing different treatment strategies, novel data on different biological agents as well as on small molecules targeting intracellular signaling pathways, the results of head to head clinical trials comparing biological agents, and the safety data from patient’s registries. Disclosure of Interest: C. Gabay Grant/research support from: Roche, Abbvie, MSD, Consultant for: Roche, Abbvie, MSD, Pfizer, BMS
SP0003
WHAT IS NEW IN SPONDYLOARTHRITIS
R. Lories 1. 1Department of Development and Regeneration, KU Leuven, Leuven, Belgium Abstract: The recent seminal discovery that an interleukin-23 (IL23) receptor positive T cell population is present in tendon and ligament attachment sites and that these cells contribute to spondyloarthritis-like joint inflammation in mice, has transformed current paradigms of the human disease. These attachment sites, commonly referred to as entheses, were earlier suggested as primary disease localization in SpA but their role in the development of chronic inflammation remained elusive. The IL23 responsive T cell population identified by Sherlock et al., is proposed as a key mediator or masterswitch in the disease process by triggering downstream inflammatory cascades as well as joint remodeling, the Janus-faced characteristics of spondyloarthritis. Interestingly the novel paradigm centered around this unexpected cell population is corroborated by further progress in genetics of spondyloarthritis, highlighted by clearly mapped molecular interactions and pathway integration. From the clinical perspective, accumulating datasets on non-radiographic axial spondyloarthritis not only support the success of anti-TNF strategies in case of failure to achieve symptom control with classical anti-inflammatory drug, but additionally trigger novel questions on the epidemiology of disease. Data obtained in cohorts of early disease patients shed new light on the demographics and likely evolution of the disease. Biomarker research is rapidly growing and a number of novel molecules may find their way into clinical practice over time provided that the original datasets linking serum levels to radiographic progression of disease can be confirmed. With regards to the much feared radiographic progression and evolution towards ankylosis, additional evidence for a structural effect associated with nonsteroidal anti-inflammatory drugs has been presented. From the therapeutic perspective, novel strategies are eagerly awaited with preliminary evidence suggesting clinical responses in patients treated with anti-interleukin 17 strategies. Early phase clinical trial data also point towards apremilast, a phosphodiesterase inhibitor as a drug that needs to be further studied. In summary, over the last year, paradigm-shifting data have been published in the field of spondyloarthritis not only leading to novel insights into the pathophysiology but also defining novel and attractive therapeutic targets thereby suggesting that the next phase in spondyloarthritis research and therapy may be on the horizon. Disclosure of Interest: None Declared
HOW TO ASSESS DISEASE ACTIVITY AND SEVERITY IN CLINICAL PRACTICE
O. Fitzgerald1. 1Rheumatology, St Vincent’s University Hospital, Dublin, Ireland Abstract: Psoriatic Arthritis (PsA) is a complex multisystem disease with involvement of synovial structures, entheseal sites, spine, and skin and nails all common features. The extended clinical phenotype has recently received some attention with obesity, hypertension, Type 2 Diabetes Mellitus, hypercholesterolemia and metabolic syndrome all found more frequently in PsA as compared to controls. An excess of cardiovascular-related events including early mortality is a likely consequence. Radiographic change is also heterogeneous with features including erosive disease and osteolysis and also new bone formation, sacroiliitis and ankylosis. Disease activity measures in PsA have either focused on joint or skin disease or have been borrowed from rheumatoid arthritis. The Psoriatic Arthritis Response Criteria (PsARC) was developed as a specific PsA response measure but the measure is dichotomous and poorly discriminates responders from placebo. More recently, a number of composite disease activity measures have been proposed. These measures are designed to capture disease activity across all of the involved domains; as not all domains are active in all individuals with PsA and as there may be a differential treatment response, ideally it should also be possible to access disease activity and response in individual domains as well. The individual composite measures and their relative performance in clinical trial data to date will be presented and discussed. Measuring disease severity may well relate to disease activity but this is yet to be clearly demonstrated. There would be little argument with the statement that patients with the arthritis mutilans phenotype have severe disease but there are many patients with polyarticular disease and high inflammatory markers who do not develop this severe phenotype. Severe disease whether it is defined on the basis of radiographic change, severe skin/nail disease, some of the cardiovascular risk factors such as presence of the metabolic syndrome or even some composite score requires further study in order to identify as early as possible risk factors which predict its development. Some recent results based on analysis of detailed clinical and genetic data will be presented. If risk factors are modifiable or if early treatment intervention for patients with potentially severe disease can bring about a change in outcome, then some progress for PsA patients will have been made. Disclosure of Interest: O. Fitzgerald Grant/research support from: Pfizer, Abbott, BMS, Roche, Merck
SP0005
IS IT TIME TO AIM FOR REMISSION IN PSA AND HOW SHOULD IT BE MEASURED?
P. Helliwell1. 1University of Leeds, Keighley, United Kingdom Abstract: Psoriatic arthritis is a multifaceted disease and it provides a challenge to outcome methodologists. A number of measures have been used to define remission in PsA but they have been mostly articular. Composite measures of disease activity and low disease states are now emerging but further work is required to assess the implication of achieving these goals and in developing cost-effective treatment strategies to achieve them. Disclosure of Interest: None Declared Wednesday, 12 June 2013
Chronic gout: imaging, diagnosis, treatment__ SP0006
VISUALISING CRYSTALS: DECT AND MORE
B. Manger1. 1 Medizinische Klinik 3, Erlangen, Germany Abstract: The first human to see monosodium urate (MSU) crystals in his newly invented microscope was the Dutch researcher Antoni van Leeuwenhoek in 1679. Since then, the gold standard to establish the diagnosis of gout arthritis is the detection of these crystals, phagocytosed by leukocytes contained in the synovial fluid of an inflamed joint. However, various obstacles may interfere with arthrocentesis individual cases: (i) Gout patients frequently carry a high cardiovascular risk and are on anticoagulant therapy or they do not consent to an invasive procedure due to the extreme pain level of their condition. (ii) In addition, diffuse soft tissue swelling without clearly detectable
Downloaded from http://ard.bmj.com/ on December 6, 2017 - Published by group.bmj.com
SP0001 Finding your Way Around Eular Hot Tips for a Successful Conference P. Cornell Ann Rheum Dis 2013 72: A2
doi: 10.1136/annrheumdis-2013-eular.1 Updated information and services can be found at: http://ard.bmj.com/content/72/Suppl_3/A2.1
These include:
Email alerting service
Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.
Notes
To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/
