Kearneyhelbo8901

OBJECTIVES We aimed to evaluate whether gadolinium-enhanced magnetic resonance imaging (MRI) in shoulders can contribute to more accurate diagnosis and prediction of recurrence in patients with polymyalgia rheumatica (PMR). METHODS Gadolinium-enhanced MRI and ultrasonography (US) in shoulders were performed in the patients who had bilateral shoulders pain and fulfilled the Bird's Classification Criteria between June 2012 and June 2018. PMR was clinically diagnosed by at least two rheumatologists. MRI and US findings assessed by independent radiologists were compared between the PMR or non-PMR patients. PMR patients were treated with 20 mg/day of prednisolone and were followed-up until June 2019 to determine any recurrences of the disease. RESULTS PMR was diagnosed in 58 of 137 patients received gadolinium-enhanced MRI and US examinations. Enhancement of joint capsule, enhancement of rotator cuff tendon and focal bone oedema in humerus heads were frequently found in the PMR patients. If the three findings were used in combination to diagnose PMR, MRI had 76% sensitivity and 85% specificity, higher compared to US findings, which had 50% sensitivity and 72% specificity. During follow-up, PMR recurred in 24 patients. Patients with recurrent PMR were younger in age, had less enhancement of rotator cuff tendon and more synovial hypertrophy findings on their MRI. CONCLUSIONS Gadolinium-enhanced MRI could display capsulitis, rotator cuff tendonitis and focal bone oedema in humerus heads that was sensitive and specific to patients with PMR, improving diagnostic accuracy in PMR. Rotator cuff tendonitis and synovial hypertrophy on MRI could help predict recurrence in PMR.OBJECTIVES We sought to analyse the expression characteristics of cytochrome C oxidase subunit I in mitochondrial of MRL/lpr lupus mice. METHODS The whole blood of MRL/lpr lupus mice was detected for whole mitochondrial genome sequencing performed by Illumina HiSeq PE150 instrument, compared with house mouse (NC_005089.1) and screened for the maximum difference gene, MT-CO1. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were used to detect the mRNA and protein expression of MT-CO1 in lupus mice and control mice. The total antioxidant capacities of lupus mice and control mice were measured using the rapid 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonate) (ABTS) method. RESULTS The mitochondrial genome sequencing showed that five mitochondrial genes had base differences and MT-CO1 was the maximum difference gene, 31 in total. Among the 31 base difference sites, 2 were missense mutations and 29 were synonymous_variant. qRT-PCR test results showed that the MT-CO1 expression in lupus mouse blood was statistically lower than that in control mice blood (t=4.333; p=0.0003). Western blot test results revealed that the expression of MT-CO1 was lower in the lupus mice compared with the control mice at the protein level. Serum total antioxidant capacity testing showed that the serum total antioxidant capacity of lupus mice was statistically lower than that of the control mice (t=9.957; p less then 0.0001). CONCLUSIONS High mutation rate and decreased expression of MT-CO1 in MRL/lpr lupus mice accompanied the decrease of antioxidant capacity, which indicated that abnormal MT-CO1 might be involved in the pathogenesis of SLE and the production of anti-dsDNA antibodies.OBJECTIVES The primary objective was to determine the impact of sharing musculoskeletal ultrasound (MUS) results with rheumatologists on worsening patient-reported outcomes (PROs) at 6 months of follow-up in rheumatoid arthritis (RA) patients with clinical remission. Secondary objectives were to describe MUS findings and to compare the proportion of patients with flares, according to the DAS28-ESR, following the intervention. METHODS Ninety-four consecutive outpatients with clinical remission had PROs and a treatment proposal recorded at study entry. MUS was then performed by trained specialists who were blinded to clinical assessments. Forty-seven patients were randomised (11) to either the intervention group (MUS data shared with the primary rheumatologist) or the control group (data not shared); changes in the treatment proposal were recorded. PROs worsening and the proportion of patients with ares were compared between both groups at 6±2 months of follow-up. The study received IRB approval. Appropriate statistics were used. RESULTS At baseline, patients from the intervention and control groups had similar characteristics; 43 and 41 patients, respectively, completed the 6-month follow-up period. PROs worsening at 6 months of follow-up were similar between groups, as were the DAS28-ESR and the proportion of patients who flared. In general, MUS findings were in accordance with the clinical remission status, although power Doppler synovitis was detected in up to 37% of the patients. RA-related treatment was increased in all the patients from the intervention group with discordant findings between clinical and MUS assessments. CONCLUSIONS The addition of MUS to clinical evaluation of RA outpatients in remission did not prevent worsening PROs at 6 months.OBJECTIVES We aimed to assess relationships between single Bath Ankylosing Spondylitis Metrology Index (BASMI) components and corresponding spinal segment magnetic resonance images (MRI) in anti-tumour-necrosis-factor-treated AS patients. METHODS Using available MRI and BASMI data from the GO-RAISE trial (n=91 patients), MRI scores for active inflammatory (ASspiMRI-a) and chronic structural (ASspiMRI-c) changes in cervical and lumbar spine segments were compared with BASMI cervical (cervical-rotation [CR] angle, tragus-to-wall [TTW] distance) and lumbar (lumbar flexion [LF], lateral-lumbar-flexion [LLF]) spine component scores (linear definition). Generalised linear models were employed to assess relationships between BASMI components and ASspiMRI-a/ASspiMRI-c measurements at baseline and for week-14 (golimumab/placebo groups) and week-104 (all golimumab-treated) change scores. RESULTS Baseline lumbar ASspiMRI-a scores correlated with LF and LLF (β=0.231 and 0.238, respectively; both p less then 0.01), while this was less prominent for ASspiMRI-c scores and LLF (β=0.142, p=0.04). A significant but weak correlation was found between changes from baseline to week 104 in cervical spine ASspiMRI-c score and TTW distance among all treated patients (β=0.161, p=0.003). CONCLUSIONS Detailed assessments indicated baseline spinal mobility impairment in patients with active AS correlated weakly with MRI-detected lumbar spinal inflammation; correlations with chronic, structural damage/changes were very weak. Improved, less variable MRI and spinal metrology assessments are needed for future clinical research.OBJECTIVES To investigate the role of body mass index (BMI) in the phenotypic and genotypic characteristics of early arthritis patients. METHODS We analysed the clinical and laboratory parameters from the baseline visit of patients (670 patients [78.51% women]) included in the PEARL study. The WHO definition for low weight, normal weight, overweight and obesity (BMI less then 18.5, 18.5-25, 25-30 or ≥30 kg/m2, respectively) was applied. Anticitrullinated protein antibodies (ACPA) were studied by ELISA and HLA-DRB1* were genotyped by sequence speci c oligonucleotide probes. The relationship between BMI classification and other variables was analysed using Kruskall-Wallis, Anova and Chi-Square tests. Then multivariate logistic regression was performed to establish the role of BMI in ACPA positivity and ordered logistic regression to establish its relationship with ACPA level. RESULTS Among the patients studied, 255 (38.06%) were considered overweight and 136 (20.3%) obese. High BMI patients had significantly more pain perception and disability than normal weight patients, whereas no clear differences in disease activity were observed between high BMI and normal weight patients. ACPA positivity was significantly less frequent in overweight and obese patients compared to normal BMI patients. This information was confirmed by adjusting for smoking habit and the presence of shared epitope. CONCLUSIONS Our data support the theory that high BMI patients suffer more frequently from ACPA-negative RA. Nevertheless, although no disease activity differences were observed, these patients showed higher pain and disability scores since the beginning of disease.OBJECTIVES Polymyalgia rheumatica (PMR) is an inflammatory rheumatic disease characterised by pain and stiffness of neck, shoulder- and hipgirdle, typically with elevated acute phase reactants (APR). However, patients may present with normal APR. Our aim was to explore whether normal APR were due to 1) 'caught early in the disease', 2) misdiagnosis, or 3) a distinct subset of PMR with different clinical presentation and prognosis. METHODS This was a retrospective cohort study on patients with clinical PMR diagnosis visiting the rheumatologists of the Sint Maartenskliniek from April 2008 to September 2017. RESULTS Of 454 patients, 62 patients had normal, and 392 elevated APR. Normal APR patients had longer symptom duration before diagnosis (13 vs. 10 weeks; p=0.02), however, during follow-up 31% developed elevated APR. In elevated APR patients with previous APR data available while already symptomatic, 58% had earlier normal APR. Fewer normal APR patients had peripheral arthritis (2% vs. 9%;p=0.04), and anaemia (17% vs. 43%; p=0.001). More often they had a previous PMR diagnosis (16% vs. 8%; p=0.057) and a shorter median time to glucocorticoid-free remission (552 vs. 693 days; n=36 vs. 160; p=0.02). Route of GC administration differed between groups (p=0.026). Fewer patients received methotrexate; 3 vs. 12%; p=0.046). No difference in alternative diagnosis was observed. CONCLUSIONS PMR patients with long-term normal APR seem to be a milder subset of PMR in clinical presentation and prognosis. Additionally, our data also suggest there is a subgroup with normal APR who are caught early in the disease. Misdiagnosis does not appear to play a role.OBJECTIVES Cytokines signaling pathway genes represent a key component of the genetic network implicated in the pathogenesis of immunoglobulin-A vasculitis (IgAV), an inflammatory vascular pathology. Interleukin (IL)17A is described as a genetic risk locus for some autoimmune diseases, such as giant cell arteritis and spondyloarthritis. Accordingly, we aimed to determine the potential influence of IL17A on the pathogenesis of IgAV. METHODS Five IL17A tag polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909), which cover the major variability of this gene, were genotyped in 360 Caucasian patients with IgAV and 1,003 sex and ethnically matched healthy controls using TaqMan probes. RESULTS No statistically significant differences between patients with IgAV and healthy controls were observed when each IL17A genetic variant was analysed independently. Similarly, no statistically significant differences between patients with IgAV and healthy controls were found when the five IL17A polymorphisms were evaluated combined conforming haplotypes. In addition, there were no statistically significant differences in genotype, allele and haplotype frequencies of IL17A when patients with IgAV were stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations. CONCLUSIONS Our results do not support an influence of IL17A on the pathogenesis of IgAV.