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Eular 2014
Highlights from the Scientific
Programme
Loreto Carmona
Instituto de Salud Musculoesquelética
Madrid, SPAIN
Disclosures
• I was not paid by a drug company to come here.
• I have no actions neither special interests in any
drug company.
• I have my own company of research on
musculoskeletal health, but will not present
anything related to our results (despite it’s
nothing on medications).
• I have received money sometimes for
conferences or courses on mtehodology from
drug companies, such as Pfizer, MSD, Abbvie,
BMS
Highlights from the Scientific
Programme
Tweets, pictures, facebook, e-mails….
EULAR Science
Methodology
Public
health
Children
Basic science
Clinical
science
Education
Diseases
Pain – Gary MacFarlane
OA - twitter
Osteoarthritis
Also Jessica Bertrand (WIN OA):
“Verapamil [used in hypertension] reduces
inflammation in OA models in mice”
“Clues to early OA:
- Alteration of lymphatic vessels around
knee joint
- Infrapatellar fat pad related to
inflammatory processes in knee OA
“news in genetics of OA:
- Evidence on interaction gene-
environment
- COLL1A1 and VEGF genes related to hip
OA
- BMP4 (involved in retinoid signaling)
related to hand OA
Psoriatic arthritis
Harald Burkhardt (WIN on PsA):
“We now know much more on underlying
mechanisms in PsA. The recently untangled
TH17-driven effector pathways (IL-12/IL-23)
are being targeted by therapies.”
“Three new drugs have been approved for
PsA (ustekinumab, certolizumab,
apremilast) after years of desert, and many
are coming”
“The TICOPA study in the UK shows that
the use of early and intensive treatment in
PsA in routine clinical care leads to an
improved clinical and radiographic
outcome”
RA - twitter
RA – guidelines
José María Álvaro-Gracia
• “There are up and downs in guidelines”
• “We may not adhere to them because we
have no time, we don’t know them, or…
yes, because we disagree”
• “Sometimes it is very difficult to apply to
individual patients: it is the patient’s
social situation, his mode of life,
limitations in measuring tools, patient
profile, comorbidities…”
RA – Strategy trials
If you start early enough with
treatment, whatever you do is
efficacious
SLE - twitter
SLE – Jaime Calvo
• “It is possible to stop
(slowly) the corticoids”
• “Triple therapy with
MMF + tracholimus +
GC is the present”
• “Check the sunscreen
whether the SPF/PPD is
less than 3”
Gout – twitter & Fernando Pérez
Gout
PMR – GCA
MA González-Gay
• “Maria Cid talked on the pathogenesis. It is
not only TH-17 cells but the TH-1- IFN-
gamma axis is now playing a key role in the
risk of ischemic events associated with GCA.”
• “Dr Pipitone highlighted the importance of
new imaging techniques, such as FDG-PET, in
the diagnosis of aortitis in the setting of large
vessel vasculitis. He also made clear that
temporal artery doppler US is a
complementary technique to the temporal
artery biopsy for the diagnosis.”
PMR – GCA
MA González-Gay
• “I discussed the pivotal role of steroids as the
cornerstone of the therapy in the management of
giant cell arteritis, and the potential use of
biologic therapies, in particular anti-IL6
(tocilizumab), in the management of large vessel
vasculitis refractory to conventional therapy.
•Hydroxychloroquine in Giant Cell Arteritis
NCT00430807
•HECTHOR: Humira to Spare Steroids in Giant Cell Arteritis
NCT00305539
•A Study of the Safety and Effectiveness of Infliximab (Remicade) in Patients With GCA
NCT00076726
•Abatacept for Treating Adults With Giant Cell Arteritis and Takayasu's Arteritis
NCT00556439
•Tocilizumab for Patients With Giant Cell Arteritis
NCT01450137
•Tocilizumab Effect iN pOlymyalgia Rheumatica (TENOR)
NCT0171384
•A 3-arm Proof of Concept Study of AIN457 (secukinumab), ACZ885 (canakinumab) or
Corticosteroids in Patients With Polymyalgia Rheumatica
NCT01364389
http://www.clinicaltrials.gov
GCA THERAPY
the new & the old
Scleroderma
Children
Children – Dani Clemente
• “We need criteria that take into account
some aspects of the clinical picture not
included now” (Alberto Martini)
• “Regulatory-T-cells are involved in the
pathogenesis of JIA” (Berent J Prakken)
• “Alarmins (Danger-associated molecular
patterns (DAMPS) molecules) regulate
inflammation in JIA”(Johanes Roth)
• “Four years results of the Strive register:
Treatment modulates genetic expression”
PReS session (15:00-16:30) on advances in pathogenesis and classification criteria in JIA
Children – Seza Ozen
• “Management of patients with Familial
Mediterranean Fever can be “tuned-up”
safely by genotype”.
• “Lots of large studies going on: EULAR
Projects in paediatric Rheumatology,
PRINTO, Pharmachild, Eurofever, EPOCA…”
• “Lots of new criteria: Pediatric Behçet’s,
macrophage activating syndrome,
response criteria for polymyositis-
dermatomyositis, autoinflamatory disease
activity index…”
Autoimmflamatory diseases (13:30-15:00)
“Check
IgG4
abstracts!”
IgG4 related disease
• A systemic disease
• Affects glands
• Similar to Sjögren’s
• May cause aorta
rupture or liver failure
• Treated with corticoids
and IM
The “battle” on corticoids
Glucocorticoids
Maarten Boers
• “Good news: the bone loss after a year
due to glucocorticoids in RA is much
lower than what they used to say”
Bad news?
Glucocorticoids as confounders
Frank Buttgereit talked about how good steroids could be to bone.
Will Dixon talked about the complexity of corticoid-related infections.
Angela Zink
playing petanq
Comorbidity
Comorbidity
Nemanja Damjanov
Comorbidity – Will Dixon
• Things can be good in a
patient and bad in other.
• It is important to
understand the context
and to know the strength
of association
• What association is
stronger?
– Statins protective effect?
– NSAIDs effect on CV
health?
Comorbidity – Will Dixon
• “Data is clear: Stop
smoking is much a
stronger protective
factor than statins”
• “Very few clinics have
a program to quit
smoking”
Comorbidity – Will Dixon
• “Dual benefits: corticoids may be good for
many things; quit smoking also”
• “COMORA showed that depression is very
frequent.”
• “Depression has an important impact on
RA.”
• “We do not know how to detect and to
diagnose depression.”
Measurement
Biomarkers
Biomarkers: useful or a waste of resources
Ted Pincus making his point that no good
biomarker yet exists. Only what the patient says is
still the best biomarker
Imaging
Imaging - Esperanza Naredo
The youngsters and the
methodologists
“René Toes explained the inflammation
process and where do therapies act.”
“Helen Leavis explained the microbiome
its functions. Disbiosis [aletartion of
bacteria in the gut] may alter
equilibrium among Treg and Th17 cells
and cause diseases”
Trials today
Basic Epidemiology explained
Johan Askling
1
2
3
Patient  Primary care 
Rheuma
• “Talk to your GP” (Christian Mallen)
• “Some strategies to reduce delay are
more cost-effective than others” (Bruno
Fautrel)
• “Yes, but it may be worth it to know why
patients do not come earlier”
Public health – GBD session
Thank you all!
2014 PARE highlights

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2014 PARE highlights

  • 1. Eular 2014 Highlights from the Scientific Programme Loreto Carmona Instituto de Salud Musculoesquelética Madrid, SPAIN
  • 2. Disclosures • I was not paid by a drug company to come here. • I have no actions neither special interests in any drug company. • I have my own company of research on musculoskeletal health, but will not present anything related to our results (despite it’s nothing on medications). • I have received money sometimes for conferences or courses on mtehodology from drug companies, such as Pfizer, MSD, Abbvie, BMS
  • 3. Highlights from the Scientific Programme Tweets, pictures, facebook, e-mails….
  • 4.
  • 7. Pain – Gary MacFarlane
  • 9. Osteoarthritis Also Jessica Bertrand (WIN OA): “Verapamil [used in hypertension] reduces inflammation in OA models in mice” “Clues to early OA: - Alteration of lymphatic vessels around knee joint - Infrapatellar fat pad related to inflammatory processes in knee OA “news in genetics of OA: - Evidence on interaction gene- environment - COLL1A1 and VEGF genes related to hip OA - BMP4 (involved in retinoid signaling) related to hand OA
  • 10. Psoriatic arthritis Harald Burkhardt (WIN on PsA): “We now know much more on underlying mechanisms in PsA. The recently untangled TH17-driven effector pathways (IL-12/IL-23) are being targeted by therapies.” “Three new drugs have been approved for PsA (ustekinumab, certolizumab, apremilast) after years of desert, and many are coming” “The TICOPA study in the UK shows that the use of early and intensive treatment in PsA in routine clinical care leads to an improved clinical and radiographic outcome”
  • 12. RA – guidelines José María Álvaro-Gracia • “There are up and downs in guidelines” • “We may not adhere to them because we have no time, we don’t know them, or… yes, because we disagree” • “Sometimes it is very difficult to apply to individual patients: it is the patient’s social situation, his mode of life, limitations in measuring tools, patient profile, comorbidities…”
  • 13. RA – Strategy trials If you start early enough with treatment, whatever you do is efficacious
  • 15. SLE – Jaime Calvo • “It is possible to stop (slowly) the corticoids” • “Triple therapy with MMF + tracholimus + GC is the present” • “Check the sunscreen whether the SPF/PPD is less than 3”
  • 16. Gout – twitter & Fernando Pérez
  • 17. Gout
  • 18. PMR – GCA MA González-Gay • “Maria Cid talked on the pathogenesis. It is not only TH-17 cells but the TH-1- IFN- gamma axis is now playing a key role in the risk of ischemic events associated with GCA.” • “Dr Pipitone highlighted the importance of new imaging techniques, such as FDG-PET, in the diagnosis of aortitis in the setting of large vessel vasculitis. He also made clear that temporal artery doppler US is a complementary technique to the temporal artery biopsy for the diagnosis.”
  • 19. PMR – GCA MA González-Gay • “I discussed the pivotal role of steroids as the cornerstone of the therapy in the management of giant cell arteritis, and the potential use of biologic therapies, in particular anti-IL6 (tocilizumab), in the management of large vessel vasculitis refractory to conventional therapy.
  • 20. •Hydroxychloroquine in Giant Cell Arteritis NCT00430807 •HECTHOR: Humira to Spare Steroids in Giant Cell Arteritis NCT00305539 •A Study of the Safety and Effectiveness of Infliximab (Remicade) in Patients With GCA NCT00076726 •Abatacept for Treating Adults With Giant Cell Arteritis and Takayasu's Arteritis NCT00556439 •Tocilizumab for Patients With Giant Cell Arteritis NCT01450137 •Tocilizumab Effect iN pOlymyalgia Rheumatica (TENOR) NCT0171384 •A 3-arm Proof of Concept Study of AIN457 (secukinumab), ACZ885 (canakinumab) or Corticosteroids in Patients With Polymyalgia Rheumatica NCT01364389 http://www.clinicaltrials.gov GCA THERAPY the new & the old
  • 23. Children – Dani Clemente • “We need criteria that take into account some aspects of the clinical picture not included now” (Alberto Martini) • “Regulatory-T-cells are involved in the pathogenesis of JIA” (Berent J Prakken) • “Alarmins (Danger-associated molecular patterns (DAMPS) molecules) regulate inflammation in JIA”(Johanes Roth) • “Four years results of the Strive register: Treatment modulates genetic expression” PReS session (15:00-16:30) on advances in pathogenesis and classification criteria in JIA
  • 24. Children – Seza Ozen • “Management of patients with Familial Mediterranean Fever can be “tuned-up” safely by genotype”. • “Lots of large studies going on: EULAR Projects in paediatric Rheumatology, PRINTO, Pharmachild, Eurofever, EPOCA…” • “Lots of new criteria: Pediatric Behçet’s, macrophage activating syndrome, response criteria for polymyositis- dermatomyositis, autoinflamatory disease activity index…” Autoimmflamatory diseases (13:30-15:00) “Check IgG4 abstracts!”
  • 25. IgG4 related disease • A systemic disease • Affects glands • Similar to Sjögren’s • May cause aorta rupture or liver failure • Treated with corticoids and IM
  • 26. The “battle” on corticoids
  • 27. Glucocorticoids Maarten Boers • “Good news: the bone loss after a year due to glucocorticoids in RA is much lower than what they used to say” Bad news?
  • 28. Glucocorticoids as confounders Frank Buttgereit talked about how good steroids could be to bone. Will Dixon talked about the complexity of corticoid-related infections. Angela Zink playing petanq
  • 31. Comorbidity – Will Dixon • Things can be good in a patient and bad in other. • It is important to understand the context and to know the strength of association • What association is stronger? – Statins protective effect? – NSAIDs effect on CV health?
  • 32. Comorbidity – Will Dixon • “Data is clear: Stop smoking is much a stronger protective factor than statins” • “Very few clinics have a program to quit smoking”
  • 33. Comorbidity – Will Dixon • “Dual benefits: corticoids may be good for many things; quit smoking also” • “COMORA showed that depression is very frequent.” • “Depression has an important impact on RA.” • “We do not know how to detect and to diagnose depression.”
  • 35. Biomarkers Biomarkers: useful or a waste of resources Ted Pincus making his point that no good biomarker yet exists. Only what the patient says is still the best biomarker
  • 38. The youngsters and the methodologists
  • 39.
  • 40. “René Toes explained the inflammation process and where do therapies act.” “Helen Leavis explained the microbiome its functions. Disbiosis [aletartion of bacteria in the gut] may alter equilibrium among Treg and Th17 cells and cause diseases”
  • 41. Trials today Basic Epidemiology explained Johan Askling 1 2 3
  • 42. Patient  Primary care  Rheuma • “Talk to your GP” (Christian Mallen) • “Some strategies to reduce delay are more cost-effective than others” (Bruno Fautrel) • “Yes, but it may be worth it to know why patients do not come earlier”
  • 43. Public health – GBD session

Editor's Notes

  1. Abstract#: 2368 Tocilizumab in Refractory Takayasu’s Arteritis: 7 Patients Followed At a Single Italian Centre Background/Purpose: Takayasu arteritis (TA) is a rare chronic-relapsing vasculitis involving primarily the aorta and its major branches.TA is associated with considerable morbidity and mortality. Therapy is based on corticosteroids (CS) but steroid-sparing immunosuppressive drugs are required in most patients to minimize CS adverse events and to control progressive vascular disease. However, about 25% of patients relapse when CS are tapered. In this setting, previous works showed that tocilizumab (TCZ), an humanized anti-IL6 receptor antibody may be useful. Objectives To evaluate the safety and efficacy of TCZ in the treatment of refractory TA. Methods: We retrospectively studied 7 TA patients (pts) treated with TCZ (8 mg/kg monthly) between 2010 and 2012 at a single academic Italian center. All pts satisfied ACR criteria for TA classification and had active refractory TA. Treatment efficacy was evaluated as: i) reduction of signs and symptoms of active disease, ii) steroid sparing activity (assessed as reduction in the average daily dose measured within the 12 month period preceding each medical evaluation, iii) angio-MRI assessment of vascular lesions evolution, iv) decrease in CRP and ESR. Results: All 7 pts were female, with a median age at the beginning of TCZ therapy of 35 years (range 32-46), median duration of disease 66 months (range 17-101). Before TCZ therapy, they were taking a median of 4 (range 1-8) immunosuppressive agents. Four pts had been previously treated with anti-TNF agents. Median FU on TCZ therapy was 14 months (range 9-24). Mean duration of CS therapy before TCZ was 37 months. Two pts did not show signs or symptoms of active disease during FU while 3 pts satisfied NIH criteria of active disease. During FU, average prednisone daily dose decreased from a median value of 8.3 mg (range 5.9–29) to 8.0 mg (range 5.0-16): however, the dose could be reduced more than 3 mg/day in 4 patients. The median number of vascular lesions was unchanged (8, range 4-12) at baseline and at the end of FU. In one pt vascular lesions improved during FU and in another did not progress, while in the other 5 pts there was worsening of at least one vascular lesion. Median values of ESR and CRP decreased from 34 (range 8.0-76) to 4.0 (range 2.0-45) mm/h and from 13 (range 10-35) to 2.0 (range 1.0-44) mg/l, respectively. TCZ was stopped in 4 pts because of suboptimal disease control. During FU one pt had severe pneumonia, requiring TCZ interruption, another had relapsing upper respiratory infections and a third developed pytiriasis rosea, that subsided after TCZ interruption. Conclusion: In this study of refractory TA, TCZ showed efficacy only in a minority of pts. Our data do not confirm the positive results of TCZ therapy reported in previous studies . However, our pts may have had more severe disease, as suggested by the higher number of immunosuppressive agents at baseline compared to previous reports. Finally, it should be noted that ESR and CRP do not appear to correlate reliably with disease activity during TCZ therapy. Further studies are necessary to better define the role of TCZ in TA therapy. Enrico Tombetti, Elena Baldissera, Stefano Franchini, Patrizia Aiello, Francesca Motta, Barbara Gulgielmi and Maria Grazia Sabbadini, Vita-Salute San Raffaele University, Milan, Italy