Clinical paradigms and pathogenetic explanations.

Slides:



Advertisements
Similar presentations
H&E and immunohistochemical (IHC) staining for CD68/CD21, CD3/CD20 and CD117 on colonic mucosa of patients with inflammatory bowel disease (IBD) in disease.
Advertisements

Immunohistochemical (IHC) staining for CD68/CD21 and CD3/CD20 on synovial tissue (ST) of patients with inflammatory bowel disease (IBD) with onset of peripheral.
Multivariable model of abatacept retention in biologic-naïve patients.
European League Against Rheumatism/American College of Rheumatology classification criteria probability of having idiopathic inflammatory myopathies (IIMs)
Multivariable model of abatacept retention by RF and anti-CCP status in biologic-naïve patients with or without radiographic erosion at baseline. Multivariable.
(A) EULAR response based on DAS28 (ESR, otherwise CRP) and (B) Boolean remission, at 6 months in patients treated with abatacept as a first-line biologic.
Immunohistochemical (IHC) staining for CD117 on synovial tissue (ST) of patients with inflammatory bowel disease (IBD) with onset of peripheral arthritis.
Main fields of interest.
Conversion to ACPA and RF seronegative status in patients with early RA treated with abatacept+MTX compared with MTX alone. Conversion to ACPA and RF seronegative.
Mean DAS (A), HAQ (B) and percentages in low disease activity, DAS remission and drug-free DAS remission (C) during 5 years in the DAS ≤2.4 steered (BeSt)
Kaplan-Meier survival plots for survival without: (A) progression to RA according to the number of joints with significant synovitis defined by GS≥ grade.
Percentage of patients achieving EULAR response
Flow diagram of the literature search process, including exclusions and reasons for exclusions. *Population of pregnant women (n=2), asymptomatic antiphospholipid.
Clinical, functional and radiographic outcomes following up to 3 years of open-label adalimumab as monotherapy after 2 years of adalimumab+methotrexate.
Cells and mediators of the immune-inflammatory ‘cascade’ leading to overt clinical rheumatoid arthritis are described. Cells and mediators of the immune-inflammatory.
The patient profiles presented to rheumatologists in the discrete choice experiment (DCE). aCCP, anti-cyclic citrullinated peptide; DAS28, 28-joint Disease.
Frequency of patients in flare at each time point over 3 months
Cumulative incidence of tuberculosis (TB) in certolizumab pegol (CZP)-treated patients with rheumatoid arthritis (RA) in the pooled RA safety database.
The severity of fatigue over 8 years of disease in early rheumatoid arthritis patients. The severity of fatigue over 8 years of disease in early rheumatoid.
Efficacy outcomes in patients aged ≥65 years versus younger patients: ACR outcomes at (A) week 12 and (B) week 24. Efficacy outcomes in patients aged ≥65.
Ratings of core domains stratified by stakeholder group in the second Delphi round. Ratings of core domains stratified by stakeholder group in the second.
Effect of collagen-induced arthritis (CIA) and 3,4-dichloropropionaniline (DCPA) on osteoclast bone interface density determined by ATPa3 (TCIRG) labelling,
Cumulative probability of time to achieve first sustained DAS28 (CRP) remission by conversion to ACPA seronegative status. Cumulative probability of time.
(A) Reduction of circulating stromal cell-derived factor (SDF)-1 levels over time in patients with rheumatoid arthritis (RA) and ankylosing spondylitis.
Relationships between the baseline disease activity scores and scintigraphic sum scores for the patients with RA, pSpA and axSpA. Relationships between.
Different treatment strategies in rheumatoid arthritis in relation to radiographic progression (A) number of swollen joints (B) and fatigue severity over.
Column bar graphs showing Health Assessment Questionnaire (HAQ) scores and pain score on Visual Analogue Scale (VAS) (scale 0–10) that were collected at.
Bold diamonds are the mean percentage of time with inactive disease during the first 12 months within the subgroup. Bold diamonds are the mean percentage.
EULAR-defined characteristics describing arthralgia at risk for RA
Prescription rates of (A) NSAIDs, glucocorticoids and analgaesics, (B) TNF inhibitors and synthetic DMARDs and (C) combination therapy of NSAIDs with TNF.
Low-dose glucocorticoid chronotherapy in rheumatoid arthritis (RA) include the night-time-release prednisone, a timing drug release formulation with administration.
The association between alcohol consumption and the severity of MRI-detected inflammation in hand and foot joints of (A) patients with RA and (B) asymptomatic.
Matrix risk model showing the probability of SRP in patients with moderate disease activity after 3 years of MTX treatment. Matrix risk model showing the.
Multivariate analysis for SRP after 3 years in patients with moderate disease activity despite MTX treatment. Multivariate analysis for SRP after 3 years.
Clinical response in patients with early and established RA at month 24. *p
Clinical expertise of GPs and rheumatologists in differentiating patients with arthralgia. Clinical expertise of GPs and rheumatologists in differentiating.
Patients with RA on csDMARDs with and without GC, bDMARDs/tofacitinib with and without GC on the x axis. Patients with RA on csDMARDs with and without.
Examples of MRI at presentation with clinically suspect arthralgia (CSA) (top panel) and at IA development (bottom panel), showing joints (A) from no inflammation.
The clinical and histological changes of arthritis in gp130F759.
Percentage of patients with RA achieving DAS28(CRP)<2
JSN and SvdH damage and progression scores with and without the CMC3-5 joints. JSN and SvdH damage and progression scores with and without the CMC3-5 joints.
Cox proportional-hazards model of time to first RA flare after treatment withdrawal for patients who entered the re-treatment period (n=146). Cox proportional-hazards.
Distribution of swelling and tenderness in joints with or without x-ray progression. Distribution of swelling and tenderness in joints with or without.
MRI, STIR sequence of sacroiliac joints (SIJs): minimal localised signal increase on both sides of the upper part of the left SIJ (arrows), which does.
Percentage of patients achieving 20% improvement in the American College of Rheumatology criteria at week 12 by patient demographic and disease characteristics.
The effect of 3,4-dichloropropionaniline (DCPA) treatment on collagen-induced arthritis (CIA) at 40 days. The effect of 3,4-dichloropropionaniline (DCPA)
Ultrasonographic characteristics and synovitis pattern of patients with inflammatory bowel disease (IBD) with onset of peripheral arthritis under tumour.
Patient disposition after 2 years of treatment.
Study design. *Randomisation stratified by corticosteroid use at baseline. Study design. *Randomisation stratified by corticosteroid use at baseline. DAS28-CRP,
Satisfaction with control of RA
The proportions (and 95% CIs) of anti-CCP+/RF+, anti-CCP+/RF- anti-CCP-/RF+ and anti-CCP-/RF- patients receiving tofacitinib 5 or 10 mg two times a day.
The proportions (and 95% CIs) of anti-CCP+/RF+, anti-CCP+/RF-, anti-CCP-/RF+ and anti-CCP-/RF- patients receiving tofacitinib 5 or 10 mg two times a day.
Classification tree with the selected characteristics.
Mean profiles over 1 year from the observed Disease Activity Score 28 (DAS28) data for the methotrexate (MTX)-exposed patients after stratifying by predicted.
(A) NKG2A and (B) NKG2C expression on NK cells in subjects with AS and HCs. The upper figure represents % of NK positive cells; the lower figure represents.
Cardiovascular disease risk assessment capture rates in the NOCAR project, evaluated across diagnosis groups and participating centre. Cardiovascular disease.
Patient-level radiographic progression of structural joint damage at year 1 and year 2 by original randomisation. Patient-level radiographic progression.
Patient disposition over the 52-week study period
Joint pain location and severity.
Forest plot showing the results of the meta-analysis on the effect of strength exercise on M.quadriceps femoris in people with rheumatoid arthritis and.
Forest plot showing the results of the meta-analysis on the effect of aerobic exercise on measured on VO2max in people with rheumatoid arthritis, spondyloarthritis.
ACPA and RF titres in patients with early RA treated with abatacept+MTX compared with MTX alone. ACPA and RF titres in patients with early RA treated with.
Improvement in BASDAI score in patients with normal or elevated CRP at baseline through week 156. *p
Traditional cardiovascular risk factors can cause cardiac disease in patients with IIM. Systemic and local inflammation may either have a direct effect.
ACR20, ACR20 and ACR70 response rates (proportions of patients meeting ACR 20, 50% or 70% improvement criteria) in patients with rheumatoid arthritis randomised.
Percentage of patients achieving remission by conversion to ACPA seronegative status. Percentage of patients achieving remission by conversion to ACPA.
NRDC and TNF-α increase in synovial fluid from patients with RA
Changes in non-classical (CD11b+CD14+CD163−CD16+) and classical (CD11b+CD14+CD163+CD16−) monocytes over time in patients with rheumatoid arthritis (RA)
Kaplan-Meier failure curves with development of RA stratified by depression exposure. Kaplan-Meier failure curves with development of RA stratified by.
Distribution of points (%) across the ESSDAI domains in patients with neurological involvement and in those with non-neurological systemic involvement.
Presentation transcript:

Clinical paradigms and pathogenetic explanations. Clinical paradigms and pathogenetic explanations. The well-established clinical sequence of disease activity and structural damage is in the centre of the figure. At the same time, in clinical studies, rheumatoid factor (RF) has been shown to be linked to damage of rheumatoid arthritis via increasing disease activity, but also directly (blue arrows). Antibodies against citrullinated peptides/proteins (ACPA) is also associated with structural outcomes (solid green arrow). However, ACPA have not been shown to be associated with clinical disease activity. Vice versa, disease activity might even be lower in ACPA-positive patients (broken green arrow; see also, section ‘ACPA paradox’). Since this finding needs further confirmation, it is marked with a ‘?’. The panels around the central sequence are pathogenetic explanations for these clinical links; these links are quite well established for RF and the inflammatory disease processes (A), RF and direct effects on progression (B), as well as ACPA and its direct links to progression (D). They are hypothetical for the (paradoxic) link between APCA and disease activity (C). For details on the links and references see respective sections in the text. Daniel Aletaha, and Stephan Blüml RMD Open 2016;2:e000009 Copyright © BMJ Publishing Group & EULAR. All rights reserved.