scholarly journals Comparison between 1.5T and 3.0T MRI: both field strengths sensitively detect subclinical inflammation of hand and forefoot in patients with arthralgia

Author(s):  
DI Krijbolder ◽  
M Verstappen ◽  
F Wouters ◽  
LR Lard ◽  
PDM de Buck ◽  
...  
2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 978.1-978
Author(s):  
D. Krijbolder ◽  
M. Verstappen ◽  
F. Wouters ◽  
L. R. Lard ◽  
P. D. De Buck ◽  
...  

Background:Magnetic resonance imaging (MRI) of small joints sensitively detects inflammation. MRI-detected subclinical inflammation, and tenosynovitis in particular, has been shown predictive for RA development in patients with arthralgia. These scientific data are mostly acquired on 1.0T-1.5T MRI scanners. However, 3.0T MRI is nowadays increasingly used in practice. Evidence on the comparability of these field strengths is scarce and it has never been studied in arthralgia where subclinical inflammation is subtle. Moreover, comparisons never included tenosynovitis, which is, of all imaging features, the strongest predictor for progression to RA.Objectives:To determine if there is a difference between 1.5T and 3.0T MRI in detecting subclinical inflammation in arthralgia patients.Methods:2968 locations (joints, bones or tendon sheaths) in hands and forefeet of 28 arthralgia patients were imaged on both 1.5T and 3.0T MRI. Two independent readers scored for erosions, osteitis, synovitis (according to RAMRIS) and tenosynovitis (as described by Haavaardsholm et al.). Scores were also summed as total inflammation (osteitis, synovitis and tenosynovitis) and total RAMRIS (erosions, osteitis, synovitis and tenosynovitis) scores. Interreader reliability (comparing both readers) and field strength agreement (comparing 1.5T and 3.0T) was assessed with interclass correlation coefficients (ICCs). Next, field strength agreement was assessed after dichotomization into presence or absence of inflammation. Analyses were performed on patient- and location-level.Results:ICCs between readers were excellent (>0.90). Comparing 1.5 and 3.0T revealed excellent ICCs of 0.90 (95% confidence interval 0.78-0.95) for the total inflammation score and 0.90 (0.78-0.95) for the total RAMRIS score. ICCs for individual inflammation features were: tenosynovitis: 0.87 (0.74-0.94), synovitis 0.65 (0.24-0.84) and osteitis 0.96 (0.91-0.98). The field strength agreement on dichotomized scores was 83% for the total inflammation score and 89% for the total RAMRIS score. Of the individual features, agreement for tenosynovitis was the highest (89%). Analyses on location- level showed similar results.Conclusion:Agreement of subclinical inflammation scores on 1.5T and 3.0T were good to excellent, in particular for tenosynovitis. This suggests that scientific evidence on predictive power of MRI in arthralgia patients, obtained on 1.5T, can be generalized to 3.0T when this field strength would be used for diagnostic purposes in daily practice.Disclosure of Interests:None declared


2015 ◽  
Vol 43 (2) ◽  
Author(s):  
Uday Krishnamurthy ◽  
Jaladhar Neelavalli ◽  
Swati Mody ◽  
Lami Yeo ◽  
Pavan K. Jella ◽  
...  

Abstract: Our two objectives were to evaluate the feasibility of fetal brain magnetic resonance imaging (MRI) using a fast spin echo sequence at 3.0T field strength with low radio frequency (: T2 weighted images of the fetal brain at 1.5T were compared to similar data obtained in the same fetus using a modified sequence at 3.0T. Quantitative whole-body SAR and normalized image signal to noise ratio (SNR), a nominal scoring scheme based evaluation of diagnostic image quality, and tissue contrast and conspicuity for specific anatomical structures in the brain were compared between 1.5T and 3.0T.: Twelve pregnant women underwent both 1.5T and 3.0T MRI examinations. The image SNR was significantly higher (P=0.03) and whole-body SAR was significantly lower (P<0.0001) for images obtained at 3.0T compared to 1.5T. All cases at both field strengths were scored as having diagnostic image quality. Images from 3.0T MRI (compared to 1.5T) were equal (57%; 21/37) or superior (35%; 13/37) for tissue contrast and equal (61%; 20/33) or superior (33%, 11/33) for conspicuity.It is possible to obtain fetal brain images with higher resolution and better SNR at 3.0T with simultaneous reduction in SAR compared to 1.5T. Images of the fetal brain obtained at 3.0T demonstrated superior tissue contrast and conspicuity compared to 1.5T.


1967 ◽  
Vol 31 ◽  
pp. 381-383
Author(s):  
J. M. Greenberg

Van de Hulst (Paper 64, Table 1) has marked optical polarization as a questionable or marginal source of information concerning magnetic field strengths. Rather than arguing about this–I should rate this method asq+-, or quarrelling about the term ‘model-sensitive results’, I wish to stress the historical point that as recently as two years ago there were still some who questioned that optical polarization was definitely due to magnetically-oriented interstellar particles.


2020 ◽  
Vol 92 (2) ◽  
pp. 20401
Author(s):  
Evgeniy Dul'kin ◽  
Michael Roth

In relaxor (1-x)SrTiO3-xBiFeO3 ferroelectrics ceramics (x = 0.2, 0.3 and 0.4) both intermediate temperatures and Burns temperatures were successfully detected and their behavior were investigated in dependence on an external bias field using an acoustic emission. All these temperatures exhibit a non-trivial behavior, i.e. attain the minima at some threshold fields as a bias field enhances. It is established that the threshold fields decrease as x increases in (1-x)SrTiO3-xBiFeO3, as it previously observed in (1-x)SrTiO3-xBaTiO3 (E. Dul'kin, J. Zhai, M. Roth, Phys. Status Solidi B 252, 2079 (2015)). Based on the data of the threshold fields the mechanisms of arising of random electric fields are discussed and their strengths are compared in both these relaxor ferroelectrics.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 277.1-278
Author(s):  
C. Diaz-Torne ◽  
M. A. Ortiz ◽  
S. Jeria Navarro ◽  
A. Garcia-Gullien ◽  
L. Sainz ◽  
...  

Background:Gout is the most prevalent inflammatory arthritis. Gout is chronic inflammatory deposition disease related to an increase of cardiovascular (CV) events and mortality. Subclinical chronic inflammation has been demonstrated in this patients but not its relation with the monosodium urate (MSU) crystal deposit size and the number of CV risk factors.Objectives:To study the subclinical inflammation in intercritical gout patients and its possible relation to the estimated size of the crystal deposition and the number of CV risk factors.Methods:To analyze subclinical inflammation we performed a secretome analysis and a cytokine and adiponektine plasma levels quantification (IL-1β, IL-18, IL-6, sIL-6R, TNFα, CXCL-5, RANTES, leptin, resistin and adiponectin) in a cohort of gout patients. As nowadays it is not feasible to determinate the whole body deposit of MSU crystals we created three different MSU crystal deposit size patient groups using an indirect clinical and analytical classification to estimate it. Then we compared cytokine levels between healthy donors and gout patients. We also compared cytokine levels between the different crystal size deposition groups and studied its association to the number of CV risk factors.Results:Ninety consecutive patients attending a Crystal Arthritis Unit were studied. Mean age was 68.27 (28-101) years. 81.1% were male. Clinical gout evolution was of 10.1±9.8 years. 77.5% were on urate lowering treatment. 24% had tophaceous gout. Mean uric acid was 6.3±2.1 mg/dl with 47.1% of them being on target. Hypertension was present in 68.9%, diabetes mellitus in 18.9%, dislipemia in 48.9%, BMI>30 in 32.9%, abdominal obesity in 50% and 16.1% suffered from ischemic heart disease. From the 102 molecules studied in the secretome analysis in 56 there was at least a 20% difference between donors group and any of the deposition groups. In 74% of them gout patients secreted lower levels. IL-18, sIL-6R, RANTES, leptin and adiponectin were higher in patients than in healthy donors. IL-18, sIL6-R, RANTES and CXCL5 levels were associated to the size of the crystal deposits. IL-18, sIL-6R, RANTES and leptin were higher in gout groups with CV risk factors. IL-18, sIL6-R, RANTES and leptin were higher in gout patients with no risk factors when compared to healthy donors with no risk factors. We found no differences when comparing urate lowering treated and non-treated patients.Conclusion:Our results demonstrate that some proinflammatory cytokines and metabolic proteins are raised in intercritical gout patients. Some of them are different from the flare/inflammasome expected ones. In some cytokines this elevation is related to the size of the monosodium urate crystal deposit and/or to the number of cardiovascular risk factors. This cytokine changes could help to explain the increase of the cardiovascular events in gout patients.Disclosure of Interests:Cesar Diaz-Torne Grant/research support from: Received a grant from Grünenthal, Maria Angels Ortiz: None declared, Sicylle Jeria Navarro: None declared, Andrea Garcia-Gullien: None declared, Lluis Sainz: None declared, Hector Corominas: None declared, Silvia Vidal: None declared


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 200.2-200
Author(s):  
A. Krishnamurthy ◽  
Y. Kisten ◽  
A. Circiumaru ◽  
K. Sakurabas ◽  
P. Jarvolli ◽  
...  

Background:In rheumatoid arthritis (RA), anti-citrullinated protein antibodies (ACPAs) are associated with bone loss and pain. Recently, tenosynovitis has been suggested as a predicting factor for arthritis progression in individuals at-risk for RA.Objectives:We aimed to investigate if transfer of human ACPAs into mice could induce tenosynovitis and/or subclinical inflammation.Methods:Monoclonal ACPA (1325:04C03 and 1325:01B09) and control (1362:01E02) antibodies (mAbs) were generated from synovial plasma or memory B cells of RA patients. 2mg of combination of monoclonal ACPAs or control antibody were injected in BALB/c female mice (age 12-16 weeks) (n= 9). Pain-like behavior was monitored by measuring mechanical hypersensitivity using von Frey filaments every 3 days and estimation by up-down Dixon method. Bone morphometrics was analyzed by micro-CT. Using specially designed mobilization casts, dedicated mouse MRI coils, and gadolinium enhanced contrast medium, the hind limbs of these mice were scanned in a 9.4 T scanner and resulting T1-weighted images were evaluated for signs of soft tissue joint inflammation. The MRI images were scored for the presence of joint involvement and tendon inflammatory changes by 3 readers in a blinded manner.Figure 1.NAPA performed on healthy donor mo-DCs incubated with native, PAD2-citrullinated, and PAD4-citrullinated fibrinogen. Alpha, beta, and gamma chains of fibrinogen are shown separately. Each colored line represents a unique peptide. Nested peptides with a common core motif are shown in the same color. Grey bar denotes peptides with identical core motif between samples.Results:ACPAs (1325:04C03 and 1325:01B09) induced pain-like behavior (lasting for at least 4 weeks) and reduction of the trabecular and cortical bone thickness in the hind limbs as compared to control monoclonal antibodies (p<0.05). While no macroscopic or MRI signs of synovial inflammation were detected, MRI subclinical inflammation of the tendon sheaths was present in mice injected with ACPAs, but not in those injected with control mAb. Semi-quantitative scoring of the inflammatory tendon changes showed significant higher values in mice injected with ACPA (median of 1, range 0 to 2) than those injected with control mAb (median of 0, range 0 to 1).Conclusion:We show that ACPA induces pain-like behavior, bone loss and tendon sheath inflammation in mice, a model that mimics the preclinical state of ACPA positive RA.References:[1]Harre, U. et al. J Clin Invest (2012)[2]Krishnamurthy, A. et al. Ann Rheum Dis (2016, 2019), JI 2019[3]Wigerblad, G. et al. Ann Rheum Dis (2016, 2019)[4]KleyerA, Seminars in Arthritis and Rheumatism (2016)Disclosure of Interests:Akilan Krishnamurthy: None declared, Yogan Kisten: None declared, Alexandra Circiumaru: None declared, Koji Sakurabas: None declared, Patrik Jarvolli: None declared, Juan Jimenez Jimenez Andrade: None declared, Peter Damberg: None declared, Heidi Wähämaa: None declared, Vivianne Malmström Grant/research support from: VM has had research grants from Janssen Pharmaceutica, Lars Klareskog: None declared, Camilla Svensson: None declared, Bence Réthi: None declared, Anca Catrina: None declared


2021 ◽  
Vol 10 (9) ◽  
pp. 1934
Author(s):  
Domingo Hernández ◽  
Teresa Vázquez ◽  
Juana Alonso-Titos ◽  
Myriam León ◽  
Abelardo Caballero ◽  
...  

The impact of human leukocyte antigen (HLA)-mismatching on the early appearance of subclinical inflammation (SCI) in low-immunological-risk kidney transplant (KT) recipients is undetermined. We aimed to assess whether HLA-mismatching (A-B-C-DR-DQ) is a risk factor for early SCI. As part of a clinical trial (Clinicaltrials.gov, number NCT02284464), a total of 105 low-immunological-risk KT patients underwent a protocol biopsy on the third month post-KT. As a result, 54 presented SCI, showing a greater number of total HLA-mismatches (p = 0.008) and worse allograft function compared with the no inflammation group (48.5 ± 13.6 vs. 60 ± 23.4 mL/min; p = 0.003). Multiple logistic regression showed that the only risk factor associated with SCI was the total HLA-mismatch score (OR 1.32, 95%CI 1.06–1.64, p = 0.013) or class II HLA mismatching (OR 1.51; 95%CI 1.04–2.19, p = 0.032) after adjusting for confounder variables (recipient age, delayed graft function, transfusion prior KT, and tacrolimus levels). The ROC curve illustrated that the HLA mismatching of six antigens was the optimal value in terms of sensitivity and specificity for predicting the SCI. Finally, a significantly higher proportion of SCI was seen in patients with >6 vs. ≤6 HLA-mismatches (62.3 vs. 37.7%; p = 0.008). HLA compatibility is an independent risk factor associated with early SCI. Thus, transplant physicians should perhaps be more aware of HLA mismatching to reduce these early harmful lesions.


Nature ◽  
1964 ◽  
Vol 201 (4922) ◽  
pp. 911-912 ◽  
Author(s):  
J. A. WHITE
Keyword(s):  

2021 ◽  
pp. annrheumdis-2021-220884
Author(s):  
Kulveer Mankia ◽  
Heidi J Siddle ◽  
Andreas Kerschbaumer ◽  
Deshire Alpizar Rodriguez ◽  
Anca Irinel Catrina ◽  
...  

BackgroundDespite growing interest, there is no guidance or consensus on how to conduct clinical trials and observational studies in populations at risk of rheumatoid arthritis (RA).MethodsAn European League Against Rheumatism (EULAR) task force formulated four research questions to be addressed by systematic literature review (SLR). The SLR results informed consensus statements. One overarching principle, 10 points to consider (PTC) and a research agenda were proposed. Task force members rated their level of agreement (1–10) for each PTC.ResultsEpidemiological and demographic characteristics should be measured in all clinical trials and studies in at-risk individuals. Different at-risk populations, identified according to clinical presentation, were defined: asymptomatic, musculoskeletal symptoms without arthritis and early clinical arthritis. Study end-points should include the development of subclinical inflammation on imaging, clinical arthritis, RA and subsequent achievement of arthritis remission. Risk factors should be assessed at baseline and re-evaluated where appropriate; they include genetic markers and autoantibody profiling and additionally clinical symptoms and subclinical inflammation on imaging in those with symptoms and/or clinical arthritis. Trials should address the effect of the intervention on risk factors, as well as progression to clinical arthritis or RA. In patients with early clinical arthritis, pharmacological intervention has the potential to prevent RA development. Participants’ knowledge of their RA risk may inform their decision to participate; information should be provided using an individually tailored approach.ConclusionThese consensus statements provide data-driven guidance for rheumatologists, health professionals and investigators conducting clinical trials and observational studies in individuals at risk of RA.


NeuroImage ◽  
2012 ◽  
Vol 60 (2) ◽  
pp. 940-951 ◽  
Author(s):  
Adolf Pfefferbaum ◽  
Torsten Rohlfing ◽  
Margaret J. Rosenbloom ◽  
Edith V. Sullivan

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