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27th November 2024
Personalised treatment innovations in the field of rheumatology are transforming patient care and outcomes, driven by significant advances in understanding the origins of rheumatological diseases. Professor Xenofon Baraliakos, president-elect of EULAR, speaks to Helen Quinn about the biggest challenges and opportunities in the field and where he sees rheumatology advancing to next.
Scientific advancements in rheumatology are shifting treatment from a one-size-fits-all approach towards more patient-centred care. Inflammation can show up differently across individuals, arising from a variety of causes. Targeted therapies now offer more effective and individualised options for patients, marking the beginning of a new era in rheumatologic care.
Within this exciting landscape of research innovation and clinical advancement, Professor Xenofon Baraliakos will take over the European Alliance of Associations for Rheumatology (EULAR) presidency in June 2025, having recently been voted as the Alliance’s president-elect.
Professor Baraliakos is a world-leading expert in rheumatology and is currently seeing out his term as president of the Assessment of Spondyloarthritis International Society alongside his roles as medical director at Rheumazentrum Ruhrgebiet in Herne, Germany, and full professor of internal medicine and rheumatology at Ruhr-University Bochum, Germany.
‘We are at a pretty advanced stage when it comes to now being able to have the right techniques to understand where diseases come from,’ Professor Baraliakos explains. ‘In the last 20 to 25 years, we have seen a huge development with biologics, which was a revolution.’
Indeed, biologics have transformed the treatment of inflammation, offering a safer and more effective options compared to traditional medications such as prednisone and cortisone, which reduce inflammation but can have unwanted side effects.
The rise of personalised therapies means there has been a step away from broad treatment options like TNF blockers, IL-6 blockers and IL-17 blockers, which treat everything rather than specific cytokines. Alongside this, advancements have also been made in tissue and blood analysis, allowing researchers to gain further insights into the causes of inflammation and select treatments based on an individual’s needs.
‘We understand better why one [patient] is getting a response and one is not and what this means. We understand better how diseases occur and how they develop over time. Now that means we also have a big unmet need: to translate that basic science back to clinical outcomes,’ Professor Baraliakos says. ‘Before, we just didn’t know where the disease came from. I think now we are in a very good position in terms of developing the field further – even faster.’
It is hoped that this additional knowledge will lead to fewer treatment failures for patients, as clinicians can identify the most effective treatment for each individual. In addition, Professor Baraliakos explains that by borrowing treatments from fields such as oncology and haematology and developing them further for their own needs in rheumatology, certain treatments may even be able to give the hope of a cure.
‘We are now also in the position to speak about possibilities to cure rheumatological diseases,’ he says. ‘This of course may take time, but curing is now, I believe, in reach, as compared to not being an option 10 years ago.’
Professor Baraliakos has contributed extensively to imaging research in rheumatology, and he says the first 10 years of this century saw the MRI and ultrasound becoming standard tools for diagnosing rheumatic diseases. But the biggest changes have come through recent improvements in image quality, with clinicians now able to get much greater detail of information from the images, allowing them to read and understand the progression of the disease more accurately.
‘We’ve learned how to interpret the images better in the clinical context. Something showing as ‘positive’ on imaging does not always mean the presence of a disease. We’ve learned to make that differentiation: that signal of inflammation may not be rheumatological, the inflammation may be something else. [It’s a] distinction between pathology and a coincidental finding,’ he explains.
In addition to advancements in imaging and the understanding of pathology, Professor Baraliakos emphasises the critical role of artificial intelligence (AI) in driving the future of rheumatology. Screening for diseases using AI is enabling early and accurate diagnosis, reducing the risk of misdiagnosis and unnecessary treatment while also ensuring patients are directed to the right clinician without losing time.
‘AI will change everything,’ he says. ‘It will make us aware of things we’re not really seeing that much. AI will be much more sensitive to [pathological] change, so the sensitivity of image interpretation will be improved beyond the human eye and human understanding.’
Coupled with AI’s ability to identify images with greater speed and accuracy, Professor Baraliakos believes these advancements will play an essential role in enhancing patient-centred treatment models. ‘I would see AI as a tool and not as a threat,’ he says.
Professor Baraliakos hopes to use his platform as the future president of EULAR to expand the Alliance’s global outreach and education initiatives, leveraging recent scientific advancements and enhancing interdisciplinary collaboration to ensure optimal treatment for all patients no matter where they live.
‘I think EULAR is on a very good track,’ he says. ‘We are already the number one global rheumatology organisation worldwide. But of course, we need to develop and go with the science of the times. We need to invest in improving the patients’ situation because there are big differences between countries and continents.’
To this end, Professor Baraliakos hopes to extend the EULAR’s reach ‘to provide research, but also educational activities that are for everyone,’ whether they are based in Europe or further afield.
One of his first tasks as president will be to oversee the Alliance’s annual Congress and he is keen to make it ‘the place to be’ in the rheumatology calendar and ‘where you really see the most recent rheumatological status, what is moving the field, and where the field will be moving towards’.
While the focuses of next year’s Congress remain safely under wraps for the time being, Professor Baraliakos is resolute that it will cover the most recent research and innovations in the field at a time of such exciting progress. He believes that being flexible in the structure and forward-looking in the content is the key to achieving this goal.
‘We are trying new formats to attract people and implement their ideas where possible. Content wise, we’re concentrating on what’s hot and what’s important. I think that makes it attractive for everyone, and also really exciting, but suited to the times we’re living in,’ he says.
Reflecting on his work and plans for the future, Professor Baraliakos says that at the heart of his ambitions is a strong desire to understand rheumatological diseases even better and to champion translational research and bring it back to the patient.
‘The most rewarding part of my work is to really see ideas coming into life,’ he says. ‘I feel the responsibility, but I’m also looking forward to really applying my plans to reach the goal, to improve patients’ lives and improve outreach overall.’
19th July 2023
A series of points to consider to help define the clinical and imaging features of people with psoriasis who transition to psoriatic arthritis (PsA) have been developed by the European Alliance of Associations for Rheumatology (EULAR) in order to identify those who might benefit from a therapeutic intervention.
The fact that psoriasis typically develops some 10 years before PsA, provides an opportunity for clinicians to investigate risk factors and predictors for PsA in those with the skin disease. Now, with the help of both dermatologists and rheumatologists, a EULAR multidisciplinary taskforce of 30 members and from 13 European countries has produced five overarching principles and a total of 10 points to consider.
Published in the Annals of the Rheumatic Diseases, these principles acknowledge that not everyone with psoriasis will go on to develop PsA, and even among those who do develop the arthritis, this can occur at different times. The taskforce also stress the importance of being able to identify specific risk factors for PsA and how these could influence the choice of treatment, which is crucial given that some systemic psoriasis treatments might reduce the risk of transitioning to PsA.
The 10 points highlight that arthralgia, together with abnormalities seen on ultrasound or magnetic resonance imaging scans, represent key elements of subclinical PsA that could serve as short-term predictors. Additionally, the more traditional risk factors for PsA – such as psoriasis severity, obesity and nail involvement – can be seen as more long-term disease predictors.
EULAR suggests standard naming to define the three distinct stages relevant to the prevention of PsA: people with psoriasis at higher risk of PsA, subclinical PsA and clinical PsA. This, the EULAR group felt, was important because in other inflammatory rheumatic musculoskeletal diseases, such as rheumatoid arthritis, the clinical onset is usually preceded by a preclinical phase encompassing arthralgia and immunological or imaging abnormalities, but without a clinical diagnosis.
A definition for early psoriatic arthritis was proposed by EULAR based on the development of joint swelling as a clinical outcome measure for trials of PsA prevention.
EULAR believes that the points to consider will help to define the clinical and imaging features of those with psoriasis that raise the index of suspicion for progression to PsA. Furthermore, these points could be used to identify people who could benefit from a therapeutic intervention to delay or prevent PsA.
An additional and important practice issue, is that clinicians inform patients with psoriasis about the risk of developing PsA and encourage them to report any joint-related symptoms to facilitate early diagnosis. Previous studies have shown that even a diagnostic delay as short as six months can lead to significantly more severe radiographic joint damage, worse physical function and decrease the changes of therapeutic success
3rd December 2021
For further information on rheumatology, please click here for the latest clinical news and updates’.
28th June 2021
The European Alliance of Associations for Rheumatology (EULAR) is the organisation that represents the people with arthritis/rheumatism, health professions in rheumatology and scientific societies of rheumatology of all the European nations. With immune mechanisms clearly involved in the evolution of more severe COVID-19, there is a potentially important role for immunotherapy in those infected with the virus. As a result, EULAR convened a task force to develop overarching principles (OPs) and points to consider (PtC) on the pathophysiology of COVID-19 from a rheumatological perspective through a systematic review of the available evidence. The task force included 24 members from 8 different countries and comprised rheumatologists, translational immunologists, haematologists, paediatric rheumatologists and a patient representative. Based on the evidence from the literature, a series of statements were prepared and circulated to members, discussed and voted on. Initially EULAR sought at least 75% agreement on statement wording from members but where this did not occur, refinements were made and the revised statement re-circulated and the accepted level of acceptance was set at 67% for this second round.
The task force defined two overarching principles. The first was that the phenotype of COVID-19 infection is heterogenous and ranged from asymptomatic to lethal disease as a result of multi-organ failure. The second highlighted the need for different treatment approaches to manage an infection and that these were required at different stages of the disease.
The task force also approved 14 PtC, with a view to offering guidance on the management COVID-19 with immunotherapy. Six of the PtC covered aspects of the pathophysiology of COVID-19 with the remainder discussing the use of immunotherapy. For example, it was recognised that while cellular and humoral immune responses to COVID-19 were highly variable in patients, there was insufficient evidence to associate these differing responses directly with patient outcomes. The first PtC for immunotherapy noted the absence of evidence supporting a role for this treatment modality among non-hospitalised patients, or for the value of initiating such treatment. In contrast, given the evidence on oral corticosteroids, there was a recommendation to use these drugs (in particular dexamethasone and which has the strongest evidence), in patients receiving supplemental oxygen, non-invasive or mechanical ventilation. While the evidence base continued to change rapidly, another PtC was that it was still inappropriate to offer a formal recommendation for the routine use of tocilizumab in hospitalised COVID-19 patients requiring either supplemental oxygen, non-invasive or mechanical ventilation. The final PtC was that there was a lack of evidence to recommend the use of immunomodulators including convalescent plasma, interferon kappa, interferon beta, lenzilumab, cyclosporin or canakinumab.
An important caveat with the EULAR document is that it is not intended to undermine or override local regulations or guidelines produced by bodies such as the World Health Organization. Rather the purpose is to provide recommendations of good practice to help clinicians analyse their own therapeutic strategy and inspire change were appropriate. The authors concluded that given how knowledge around COVID-19 changes quickly, these PtCs will be updated as and when appropriate.
Citation
Aluno A et al. EULAR points to consider on pathophysiology and use of immunomodulatory therapies in COVID-19. Ann Rheum Dis 2021; 80(6): 698-706
16th April 2020
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with variable presentation, course and prognosis.
Recommendations for its management, endorsed by the European League Against Rheumatism (EULAR), were first published in 2008. Due to the emergence of new data on treatment strategies and goals of treatment, an update of these recommendations was deemed appropriate. This involved a multidisciplinary task force and was based on combination of evidence base (in the form of a systematic literature review, period 01/2007-12/2017, to address 15 different research questions) and expert opinion.1
Treatment in SLE should aim at remission or at least low disease activity in all organ systems, and prevention of flares. The latter can be treated according to the severity of organ involvement, either by adjusting current therapies to higher doses or switching to alternative drugs.
Hydroxychloroquine (HCQ) is recommended for all patients with SLE, in the absence of contraindications, at a dose not exceeding 5mg/kg real body weight. Ophthalmological screening for retinal toxicity should be performed at baseline, after 5 years and yearly thereafter, by means of optical coherence tomography, 10-2 visual fields, or both (fundoscopy may be sufficient only for the baseline examination).
Glucocorticoid (GC) dose for chronic treatment should be minimised to less than 7.5mg/d prednisone equivalent or, when possible, withdrawn. To this end, use of pulse intravenous methylprednisolone may allow for a lower starting dose of oral GC, whereas early initiation of immunosuppressive (IS) drugs may assist in tapering and ultimately discontinuing GC.
Methotrexate (MTX), azathioprine (AZA), mycophenolate mofetil (MMF), or belimumab should be considered in patients not responding to HCQ in combination with GC, or in patients unable to reduce GC below 7.5-10 mg/d. Cyclophosphamide (CYC) should be reserved for organ- or life-threatening disease, and as a rescue therapy in refractory non-major organ manifestations.
Regarding biologic agents, belimumab should be considered in extrarenal disease with inadequate control to standard of care (combination of HCQ with GC with or without IS agents), frequent flares, and/or inability to taper GC. Patients with refractory cutaneous and musculoskeletal manifestations who are serologically active may respond better to the drug. In organ-threatening disease refractory or contraindicated to standard immunosuppressive agents (including CYC), rituximab (RTX) can be considered, despite its off-label status.
For skin manifestations of SLE, effective protection from ultraviolet exposure with sunscreens and smoking cessation are strongly recommended. First-line treatment includes topical agents (GC, calcineurin inhibitors) and antimalarials, with or without systemic GC. In non-responding cases, MTX, retinoids, dapsone, or MMF can be added.
Attribution of neuropsychiatric manifestations to SLE requires a multidisciplinary approach to rule out mimics (infections, malignancy and others). Neuroimaging, cerebrospinal fluid analysis, consideration of risk factors (type and timing of the manifestation in relation to the onset of lupus, patient age, non-neurological disease activity, presence of antiphospholipid antibodies (aPL)) are essential in the diagnostic process.
Treatment of SLE-related neuropsychiatric disease includes GC and IS agents for a presumed inflammatory process (for example, psychosis, myelopathy, acute confusional state) and antiplatelet/anticoagulants for atherothrombotic/aPL-related manifestations, especially stroke. Targeted symptomatic therapy is indicated according to the type of manifestation (for example, antipsychotics for psychosis, anxiolytics for anxiety disorders).
Haematological disorders needing IS treatment are thrombocytopenia and autoimmune haemolytic anaemia. Lupus thrombocytopenia warrants therapy for platelet counts <20-30000/mm³. First-line treatment consists of high dose GC (including pulses of intravenous methylprednisolone) with or without intravenous immunoglobulin (IVIG). For the sustainment of response, MMF, AZA or cyclosporine can be used. In refractory cases, RTX or CYC should be considered. The same general principles apply for the treatment of autoimmune haemolytic anaemia.
Vigilance for early recognition of signs of kidney involvement and performance of kidney biopsy for the diagnosis of lupus nephritis (LN) are essential to ensure better outcomes. For initial (“induction”) treatment, MMF and low-dose CYC (Euro-Lupus regimen) are recommended, as they have the best efficacy/toxicity ratio.
In severe forms of LN, associated with increased risk of progression into end-stage kidney disease (reduced glomerular filtration rate, histological presence of fibrous crescents or fibrinoid necrosis, or tubular atrophy/interstitial fibrosis), high-dose intravenous CYC can also be considered. For subsequent (“maintenance”) therapy, MMF or AZA should be used, the former being associated with fewer relapses. MMF may be combined with low dose of a calcineurin inhibitor (especially tacrolimus) in class V LN, podocytopathy or in proliferative disease with refractory nephrotic syndrome.
In cases with incomplete renal response (persistent proteinuria> 0.8-1gr/24h after at least one year of IS treatment) or nephritic flares, repeat biopsy can distinguish chronic from active lesions or a possible histologic transition, respectively.
All patients with SLE should be screened for aPL at diagnosis. Patients with SLE and high-risk aPL profile (persistently positive medium/high titres or multiple positivity), should receive primary prophylaxis with antiplatelet agents, especially if additional atherosclerotic/thrombophilic factors are present. For secondary prevention, treatment should not differ from the treatment of primary antiphospholipid syndrome (APS).2
Increased risk of infection in SLE is attributed to both disease-related and treatment-related factors. High-dose GC therapy, CYC, MMF and RTX are related with an increased risk of infection, as is the case with high disease activity, severe leukopenia and kidney involvement. General preventive measures, including vaccinations, and early recognition and treatment of infection are recommended.
SLE is an independent risk factor for cardiovascular disease (CVD) and patients should undergo regular assessment for traditional and disease-related risk factors such as persistent disease activity, history of LN, presence of aPL and use of GC. Lupus patients may be candidates for CVD-preventive strategies, including lipid-lowering agents and low-dose aspirin, based on individual risk stratifications and calculation of the 10-year cardiovascular risk.
Sofia Koutsoviti MD
Antonis Fanouriakis MD, PhD
Department of Rheumatology, “Asklepieion” General Hospital, Athens, Greece
21st February 2020
Antiphospholipid syndrome (APS) is a systemic autoimmune disorder manifesting as venous and/or arterial thrombosis or obstetric complications, secondary to elevated production of antiphospholipid antibodies (aPL).
APS can occur in a primary form (primary APS, PAPS), in combination with other autoimmune diseases such as systemic lupus erythematosus (SLE) or in the rare, fulminant, form of catastrophic APS (CAPS) leading to multiorgan failure. The three types of aPL included in the most recent classification criteria for APS are the anticardiolipin (aCL) and anti-beta2 glycoprotein (anti-β2GPI) antibodies, as well as the lupus anticoagulant (LA).1
Due to the rarity of the syndrome, its wide clinical spectrum involving several thrombotic and pregnancy morbidity complications, and the lack of high-quality, randomised clinical trials, the formulation of guidelines for the management of APS has been both a dire necessity and a difficult task.
EULAR recommendations for the management of APS in adults were developed to address this issue, aiming to provide evidence-based recommendations for APS stemming from a combination of expert opinion and a systematic review of the relevant literature.
A task force comprised of specialists from 11 European countries tackled four pivotal questions regarding the prevention and treatment of different forms of APS. These were risk stratification and modification in asymptomatic individuals with positive aPL; primary and secondary prevention of thrombosis in APS; management of obstetric APS; and CAPS treatment.2
The qualitative and quantitative characterisation of aPL such as their type, single-, double- or triple-positivity, titre, and persistence of positivity in repeat measurements formulate the ‘aPL profile’. Stratification of patients into those having low- and high-risk aPL profiles is considered as one of the main pillars on which the varying recommendations are based.
High-risk aPL profile was defined as the presence of LA or double or triple aPL positivity (any combination of the three aPL or all three aPL) or of high aPL titres. Isolated aCL or anti-β2GPI antibodies at low-medium titres, particularly if transiently positive, are defined as low-risk aPL. Proposed risk attenuation measures are comprised of lifestyle modifications, emphasising the importance of treatment adherence and eliminating cardiovascular and venous thrombosis risk factors.2
As far as pharmacological treatment of APS is concerned, different substances including low-dose aspirin (LDA), vitamin K antagonists (VKA), heparin, hydroxychloroquine (HCQ) or immunosuppressive agents can be used variably in accordance to each different clinical scenario.
Administration of LDA was recommended for asymptomatic aPL carriers, patients with SLE without history of thrombotic or obstetric APS, and non-pregnant women with prior obstetric APS, if high-risk aPL profiles are present. Patients with first unprovoked venous thrombosis should receive VKA with a target international normalised ratio (INR) of 2–3, while in those with first arterial thrombosis VKA treatment of a target INR of 2–3 or 3–4 can be considered, according to each individual bleeding/thrombosis risk. In patients with recurrent thrombotic events despite an appropriate treatment, either adding LDA to the treatment regimen, increasing the target INR to 3–4 or using low molecular weight heparin are effective alternatives.2,3
Based on current evidence from the recent TRAPS randomised controlled trial that showed a higher percentage of thrombotic relapses in APS patients with triple aPL positivity treated with rivaroxaban versus those treated with warfarin,4 use of rivaroxaban is not recommended in patients with a history of vascular thrombosis and triple aPL positivity, especially in those with arterial thrombosis history. New evidence from ongoing trials on direct oral anticoagulants is anticipated that will help to better understand their efficacy and safety in thrombotic APS.
In pregnant women with a history of foetal loss after the 10th week, or delivery before the 34 weeks of gestation due to eclampsia or severe pre-eclampsia or placental insufficiency, a prophylactic dose of heparin should be considered in conjunction with LDA. In women with recurring pregnancy complications despite a combination treatment with prophylactic dose heparin and low dose aspirin, therapeutic dose of heparin plus LDA, or add-on therapy with either HCQ or low-dose prednisone during the first trimester, are appropriate treatment options.2,3 First-line treatment of CAPS includes a combination therapy with glucocorticoids, heparin and plasma exchange or intravenous immunoglobulins.
Following the formulation of the current recommendations for APS in adults, an emerging need for more high-quality studies is evident. To this end, a plan in the form of a research agenda has been drafted by the task force, underlining the main points on which future studies should be focused.
Further clarification of the pathogenetic mechanisms of APS along with studies focusing on how the different phenotypes of the syndrome may respond to various treatment types are necessary in order to facilitate the expansion and improvement of the current recommendations so as to achieve better quality of care for individuals with APS.
Maria Tektonidou MD PhD
Associate professor of rheumatology, head of the Rheumatology Unit, First Department of Propaedeutic Internal Medicine, School of Medicine, National and Kapodistrian University of Athens, Greece
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