An overview of the Science and more at Eular 2014 at Paris. The overview was prepared during the congress based on twits, friends chat, the sessions I chaired and attended.
Lucknow Call girls - 8800925952 - 24x7 service with hotel room
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….
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”
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
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
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”
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”
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