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ID PMID Title PublicationDate abstract
20697789 Adrenomedullin inhibits IL-1β-induced rheumatoid synovial fibroblast proliferation and MM 2011 Oct To determine the effects of adrenomedullin (AM) on interleukin (IL)-1β-induced proliferation of rheumatoid synovial fibroblasts (RASFs) and production of matrix metalloproteinases (MMPs), cyclooxygenase (COX) and prostaglandin E2 (PGE2) by RASFs. The RASFs proliferation was evaluated with CCK-8 reagent in the presence of IL-1β with/without AM (1-52) and AM inhibitor (AM (22-52)). MMPs, tissue inhibitor of metalloproteinase (TIMP-1), COXs, PGE2 and intracellular mitogen-activated protein kinase (MAPK) signalings, including p-ERK, p-p38, p-JNK were examined by immunoblotting or semiquantitative RT-PCR and ELISA. AM (1-52) inhibited IL-1β-induced RASFs proliferation and inhibited MMP-1, 3, COX-2 and PGE2 production. AM (1-52) also inhibited IL-1β-induced phosphorylation of ERK-1/2, p38, JNK. AM 22-52 inhibited the effects of AM (1-52) on proliferation of RASFs and production of MMP-1, 3, COX-2 via MAPKs. These results suggest that AM might involved joint destruction in rheumatoid arthritis and indicate that it might be a new therapeutic modality for management of this disease.
21556937 Elevated Th22 cells correlated with Th17 cells in patients with rheumatoid arthritis. 2011 Aug BACKGROUND: T-helper (Th) 22 and Th17 cells are implicated in the pathogenesis of autoimmune diseases. The roles of Th22 cells in the pathophysiology of rheumatoid arthritis (RA) remain unsettled. MATERIALS AND METHODS: CD4(+)IFNγ(-)IL17(-)IL-22(+) T cells (Th22 cells), CD4(+)IFNγ(-)IL-22(-)IL17(+) T cells (pure Th17 cells), CD4(+)IL17(+) T cells (Th17 cells), and CD4(+)IFNγ(+) T cells (Th1 cells) in RA, osteoarthritis patients, and healthy controls were examined by flow cytometry. Plasma IL-22 and IL-17 levels were examined by enzyme-linked immunosorbent assay. RESULTS: Th22 cells, pure Th17 cells, Th17 cells, and interleukin-22 were significantly elevated in RA patients compared with osteoarthritis and healthy controls, but there were no significant differences regarding Th1 cells and interleukin-17. Th22 cells showed a positive correlation with interleukin-22 as well as pure Th17 cells or Th17 cells in RA patients. Additionally, the percentages of Th22 cells, pure Th17 cells as well as Th17 cells correlated positively with both C-reactive protein levels and 28-joints disease activity score. CONCLUSION: Together, our results indicated a possible role of Th22 pure Th17 cells and Th17 cells in RA, and blockade of the interleukin-22 may be a reasonable therapeutic strategy for RA.
22196377 Influence of TRAF1/C5 and STAT4 genes polymorphisms on susceptibility and severity of rheu 2012 Rheumatoid arthritis (RA) is the most common cause of adult inflammatory arthritis. Recent genome-wide association scans have disclosed several single-nucleotide polymorphisms associated with RA susceptibility. The aim of this study was to determine whether the polymorphisms of TRAF1/C5 (tumor necrosis factor (TNF)-receptor associated factor 1)/(complement component 5) and STAT4 (signal transducers and activators of transcription 4) confer susceptibility, activity and severity to RA in Egyptian populations. One hundred and seventy-two RA patients and 160 controls were enrolled in the study. Polymorphisms of TRAF1/C5 and STAT4 genes were determined using restriction fragment length polymorphism-polymerase chain reaction. The TRAF1/C5 A and STAT4 T alleles were significantly associated with RA in Egyptian population. TRAF1/C5 A allele and STAT4 TT genotype were significantly associated with RA severity. In conclusion the mutant alleles or genotypes of both examined polymorphisms are associated with the development of RA in Egyptian population.
22139200 [The other opinion: nephrotoxicity of low-dose methotrexate - a problem which does not exi 2011 Dec The nephrotoxicity of methotrexate (MTX) is a phenomenon which is observed in high-dose therapy for treatment of malignant diseases. Even low-dose MTX therapy for treatment of rheumatic diseases is claimed to cause impairment in renal function. The necessity to adapt the dosage of MTX therapy for renal function disorders due to other causes however has first priority. The following article describes why nephrotoxicity of low-dose MTX has no clinical relevance and why in contrast non-steroidal anti-rheumatic drugs (NSARDs) are a problematic nephrotoxic group of substances and a long-term elimination from the therapeutic armamentarium for rheumatoid arthritis (RA) should be instigated.
21515916 Discontinuation of infliximab and potential predictors of persistent low disease activity 2011 Aug OBJECTIVE: To describe the disease course after the cessation of infliximab in early rheumatoid arthritis patients with disease activity score (DAS)-steered treatment and to identify predictors of persistent low disease activity. METHODS: In a post-hoc analysis of the BeSt study, disease activity and joint damage progression were observed in patients treated with methotrexate plus infliximab, who discontinued infliximab after achieving low disease activity (DAS ≤2.4) for 6 months. Predictors were identified using Cox regression analysis. RESULTS: 104 patients discontinued infliximab, of whom 77 had received infliximab plus methotrexate as initial treatment. Mean DAS at the time of infliximab cessation was 1.3, median symptom duration was 23 months and median Sharp/van derHeijde score was 5.5. The median follow-up was 7.2 years. Infliximab was re-introduced after loss of low disease activity in 48%, after a median of 17 months. The joint damage progression rate did not increase in the year after cessation, regardless of flare. After re-introduction of infliximab, 84% of these patients again achieved a DAS ≤2.4. In the multivariable model, smoking, infliximab treatment duration ≥18 months and shared epitope (SE) were independently associated with the re-introduction of infliximab: 6% of the non-smoking, SE-negative patients treated <18 months needed infliximab re-introduction. CONCLUSION: Cessation of infliximab was successful in 52%, with numerically higher success rates in patients initially treated with infliximab. Of the 48% who flared, 84% regained low disease activity. The joint damage progression rate did not increase in the year after cessation. Smoking, long infliximab treatment duration and SE were independently associated with re-introduction of infliximab.
22403267 Risk of atrial fibrillation and stroke in rheumatoid arthritis: Danish nationwide cohort s 2012 Mar 8 OBJECTIVES: To determine if patients with rheumatoid arthritis have increased risk of atrial fibrillation and stroke. DESIGN: Longitudinal nationwide register based cohort study. SETTING: Inpatient and outpatient hospital care in Denmark from 1997 to 2009. PARTICIPANTS: Entire Danish population aged over 15 years without rheumatoid arthritis, atrial fibrillation, or stroke before 1997. Participants with rheumatoid arthritis were identified by individual level linkage of diagnoses and rheumatoid arthritis treatment. MAIN OUTCOME MEASURES: Rates of atrial fibrillation and stroke. RESULTS: Of 4,182,335 participants included in the cohort, 18,247 were identified as having rheumatoid arthritis during follow-up, with a mean age at disease onset of 59.2 years and a median follow-up of 4.8 years. A total of 156,484 people, including 774 with rheumatoid arthritis, were diagnosed as having atrial fibrillation (age and sex matched event rates of 8.2 per 1000 person years in rheumatoid arthritis patients and 6.0 per 1000 person years in the general population), with an adjusted incidence rate ratio of 1.41 (95% confidence interval 1.31 to 1.51). In addition, 165,343 people, including 718 with rheumatoid arthritis, had a stroke (7.6 per 1000 person years in rheumatoid arthritis and 5.7 per 1000 person years in the general population), with a resultant rate ratio of 1.32 (1.22 to 1.42). For both atrial fibrillation and stroke, relative risks were increased in all strata based on thirds of sex and age, with higher relative risks in younger patients but higher absolute risk differences in older patients. CONCLUSIONS: Rheumatoid arthritis was associated with an increased incidence of atrial fibrillation and stroke. The novel finding of increased risk of atrial fibrillation in rheumatoid arthritis suggests that this arrhythmia is relevant in cardiovascular risk assessment of these patients.
23202996 [Risk of atherosclerosis mediated by inflammation in rheumatoid arthritis]. 2012 Dec Systemic inflammation is one of the pivotal pathogenetic principles in atherogenesis and progression of atherosclerosis. Patients with rheumatoid arthritis (RA) exhibit an increased cardiovascular risk that is not explained by traditional cardiovascular risk factors but rather by a chronic systemic inflammatory reaction. Reduction of inflammatory activity in RA patients was shown to reduce cardiovascular morbidity and mortality. Besides this specific approach traditional cardiovascular risk factors need to be carefully controlled in order to improve mortality in RA patients; however, this task is difficult to implement in everyday practice as RA patients usually have decisively different medical needs that need to be addressed irrespective of the well-acknowledged limitations of medical resources, such as time and costs.
22427364 Associations between the p53 codon 72 polymorphisms and susceptibility to systemic lupus e 2012 Apr OBJECTIVE: The aim of this study was to determine whether the p53 codon 72 polymorphism confers susceptibility to systemic lupus erythematous (SLE) and rheumatoid arthritis (RA). METHODS: A meta-analysis was conducted on the associations between the p53 codon 72 polymorphism and SLE or RA using: 1) allele contrast; 2) the recessive model; 3) the dominant model; and 4) the additive model. RESULTS: A total of 10 studies, that is, 6 SLE and 4 RA studies, involving 1578 patients and 3138 controls were considered in the meta-analysis. Meta-analysis of the p53 codon 72 polymorphism showed no association between patients and the C allele (odds ratio (OR) = 0.834, 95% confidence interval (CI) = 0.599-1.161, p = 0.282), or between SLE and the p53 C allele (OR = 0.998, 95% CI = 0.765-1.302, p = 0.989). However, stratification by ethnicity showed an association between the p53 C allele and SLE in Asians (OR = 1.410, 95% CI = 1.044-1.906, p = 0.025), but not in Europeans (OR = 0.871, 95% CI = 0.625-1.214, p = 0.415). Furthermore, an association was found between the polymorphism and SLE in Asians using recessive and additive models. However, no association was found between RA and the p53 codon 72 polymorphism in all study subjects or in Europeans. CONCLUSIONS: This meta-analysis demonstrates that the p53 codon 72 polymorphism may confer susceptibility to SLE in Asians, but not in Europeans.
21597950 Leuconostoc bacteremia in a patient with amyloidosis secondary to rheumatoid arthritis and 2011 Dec Leuconostoc infections are rare and usually occur in immunocompromised patients. This report describes a case of Leuconostoc lactis bacteremia in a patient with coexisting rheumatoid arthritis and tuberculosis arthritis. A disrupted gastrointestinal barrier due to gastrointestinal amyloidosis in long-standing rheumatoid arthritis and tuberculosis arthritis could be a risk factor for Leuconostoc bacteremia. Despite aggressive antibiotic treatment, the patient progressed to septic shock and multi-organ failure. The fatal course might have been caused by rapid progression of gastrointestinal pathology, which could be a risk factor for Leuconostoc bacteremia.
23088220 CARD8 rs2043211 (p.C10X) polymorphism is not associated with disease susceptibility or car 2013 Jan Rheumatoid arthritis (RA) is a complex polygenic inflammatory disease associated with accelerated atherosclerosis, which is the main cause of increased cardiovascular (CV) morbidity and mortality in RA patients. CARD8 is a constituent of inflammasome, which regulates interleukin 1-beta production, and has been associated with a worse disease course in early RA. One thousand six hundred twenty-one patients fulfilling the 1987 ACR classification criteria for RA and 1300 matched controls, were genotyped for the CARD8 rs2043211 (30T>A, p.C10X) single-nucleotide polymorphism (SNP) using predesigned TaqMan SNP genotyping assay. The genotyping success rate in our study was greater than 94%. We assessed CARD8 rs2043211 gene polymorphism results in 1530 Spanish RA patients in whom information on CV disease and CV risk factors was available at the time of the study. Also, a subgroup of patients with no history of CV events (n=276) was assessed for the potential influence of the rs2043211 variant in the development of subclinical atherosclerosis, by measurement of carotid intima-media thickness (IMT) and presence of carotid plaques. No statistically significant differences in allele or genotype frequencies for the rs2043211 CARD8 gene variant between patients with RA and controls were seen. Similarly, CARD8 rs2043211 (30T>A, p.C10X) SNP did not influence the development of CV events or the risk of CV events throughout the time. Likewise, no significant association between this gene variant and carotid IMT or the presence of plaques was found. In summary, our results do not support a role of the CARD8 rs2043211 gene variant in susceptibility to RA or in the development of CV disease in patients with RA.
22549098 Plasma asymmetric dimethylarginine in active rheumatoid arthritis: links with oxidative st 2012 INTRODUCTION:  Endothelial dysfunction and accumulation of asymmetric dimethylarginine (ADMA) have been identified as independent predictors of future cardiovascular events in patients with coronary artery disease. OBJECTIVES:  The aim of the study was to investigate the factors that determine increased accumulation of ADMA, an endogenous inhibitor of nitric oxide synthesis, in patients with rheumatoid arthritis (RA). PATIENTS AND METHODS:  We studied 46 consecutive patients with RA (39 women, 7 men; mean age, 57 years [range, 23-75 years]) with active disease (mean Disease Activity Score 28 [DAS28], 5.2), without clinically overt cardiovascular disease and 50 controls matched for age, sex, hypertension, blood cholesterol, and glucose. We assessed the plasma levels of ADMA, symmetric dimethylarginine (SDMA), L‑arginine, and the marker of oxidative stress, 8‑iso‑prostaglandin F2α (8‑iso‑PGF2α).  RESULTS:  ADMA and SDMA levels were significantly higher in the RA group than in controls (0.58 ±0.081 vs. 0.46 ±0.045 μmol/l, P <0.0001; 0.45 ±0.07 vs. 0.36 ±0.046 μmol/l, P <0.0001; respectively). ADMA levels in the RA group correlated positively with fibrinogen (r = 0.70, P <0.00001), C‑reactive protein (CRP; r = 0.88, P <0.00001), DAS28 (r = 0.44, P = 0.002) and Health Assessment Questionnaire scores (r = 0.39, P = 0.008), but not with age, renal function, or the medications used. 8‑iso‑PGF2α correlated positively with ADMA (r = 0.82), SDMA (r = 0.72), CRP (r = 0.76), fibrinogen (r = 0.57) (all, P <0.0001) and DAS28 (r = 0.44, P = 0.003). Regression analysis models showed that CRP was the only independent predictor of 8‑iso‑PGF2α and ADMA levels in RA. CONCLUSIONS:  Our study is the first to show positive associations between plasma ADMA levels and the production of 8‑isoprostanes and CRP in RA.
22021897 Treating to target matrix metalloproteinase 3 normalisation together with disease activity 2012 Apr OBJECTIVES: To assess whether therapy to achieve both a disease activity score in 28 joints (DAS28) less than 2.6 and matrix metalloproteinase (MMP) 3 normalisation offers better outcomes than either target alone in early rheumatoid arthritis (RA) at 56 weeks: Treating to Twin Targets (T-4) Study. METHODS: 243 early RA patients were randomly allocated to one of four strategy groups: routine care (R group; n=62); DAS28-driven therapy (D group; n=60); MMP-3-driven therapy (M group; n=60); or both DAS28 and MMP-3-driven therapy group (twin; T group; n=61). Medication was started with sulfasalazine (1 g/day) in all intervention groups. Targets were DAS28 less than 2.6 for the D group, MMP-3 normalisation for the M group and both DAS28 less than 2.6 and MMP-3 normalisation for the T group. If the value in question did not fall below the previously measured level, medication was intensified, including methotrexate, other disease-modifying antirheumatic drugs and biological agents. Primary, secondary and outcome measures consisted of the proportions of patients showing clinical remission (DAS28 <2.6), radiographic non-progression (Δmodified total Sharp score ≤0.5), normal physical function (modified health assessment questionnaire score 0), or comprehensive disease remission defined as the combination of clinical remission, radiographic non-progression and normal physical function. RESULTS: Clinical remission at 56 weeks was achieved by more patients in the T group (56%) than in the R group (p<0.0005) or M group (p<0.0005). CONCLUSIONS: Results of the T-4 Study reveal that a twin target strategy can achieve a high clinical remission rate in early RA.
21981985 PADI4 polymorphisms and related haplotype in rheumatoid arthritis patients. 2012 Mar OBJECTIVE: To investigate whether peptidyl arginine deiminase type IV gene (PADI4) polymorphisms contribute to rheumatoid arthritis (RA) susceptibility in Egyptians, whether they influence disease severity and activity, and whether they affect anti-mutated citrullinated vimentin antibodies (anti-MCV) level. METHODS: Three PADI4 single nucleotide polymorphisms (SNPs) (PADI4-92, PADI4-96, and PADI4-102) were screened in 275 RA patients and 275 unaffected controls by polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) method. Serum anti-MCV levels were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: There were significant associations between RA susceptibility with the minor alleles of PADI4-92 and PADI4-102 [odds ratio (OD) and 95% confidence interval (CI) for the minor alleles of PADI4-92 and PADI4-102: 1.48 (1.17-1.88) and 2.05 (1.61-2.61) respectively] but not with PADI4-96 [OD and 95% CI for the C allele: 1.09 (0.86-1.39)]. PADI4 haplotypes 2 (GCC) and 3 (GCT) were also associated with RA susceptibility while PADI4 haplotypes 1 (CTC) may be protective against developing of this disease. A significant association was detected between PADI4 haplotypes and RA severity. CONCLUSIONS: The PADI4 SNPs and haplotypes were associated with RA susceptibility, although no relation was observed between the PADI4 haplotypes and anti-MCV levels.
22037510 A comparative study of serum and synovial fluid lipoprotein levels in patients with variou 2012 Jan 18 The aim of this study was to investigate apolipoprotein (apo) A-I, apo B, lipoprotein (Lp) (a), HDL-cholesterol (C), LDL-C, triglycerides (TG) and total cholesterol (TC) values in the serum and synovial fluid (SF) of untreated rheumatoid arthritis (RA), psoriatic arthritis (PsA), and osteoarthritis (OA) patients. METHODS: Paired SF and serum samples were collected simultaneously from 14 patients with RA, 14 with PsA, and 16 with OA and tested for apo A-I, apo B, HDL-C, LDL-C, Lp(a), TC and TG. Serum C reactive protein (CRP) and amyloid A (SAA) levels were also determined. RESULTS: The inflammatory arthritis patients had higher SF lipid levels with the exception of HDL. Reflecting increased synovial permeability, the lipid SF/serum ratio was always higher in RA and PsA with respect to OA patients. The positive correlation between serum and SF apo A-I, apo B, HDL-C, TG, and Lp(a) levels confirmed that there is lipoprotein diffusion into the SF. RA and PsA patients had lower concentrations of all serum lipids except for Lp(a) with respect to OA patients. The levels in the RA patients were similar to those in healthy matched controls, while the PsA patients had significantly lower apo A-I and HDL levels and higher apo B and LDL values. CONCLUSIONS: Lipid diffusion into the joint cavity, which largely depends on the degree of inflammation, may contribute to modulating local inflammatory processes.
21253435 Rodent preclinical models for developing novel antiarthritic molecules: comparative biolog 2011 Rodent models of immune-mediated arthritis (RMIA) are the conventional approach to evaluating mechanisms of inflammatory joint disease and the comparative efficacy of antiarthritic agents. Rat adjuvant-induced (AIA), collagen-induced (CIA), and streptococcal cell wall-induced (SCW) arthritides are preferred models of the joint pathology that occurs in human rheumatoid arthritis (RA). Lesions of AIA are most severe and consistent; structural and immunological changes of CIA best resemble RA. Lesion extent and severity in RMIA depends on experimental methodology (inciting agent, adjuvant, etc.) and individual physiologic parameters (age, genetics, hormonal status, etc.). The effectiveness of antiarthritic molecules varies with the agent, therapeutic regimen, and choice of RMIA. All RMIA are driven by overactivity of proinflammatory pathways, but the dominant molecules differ among the models. Hence, as with the human clinical experience, the efficacy of various antiarthritic molecules differs among RMIA, especially when the agent is a specific cytokine inhibitor.
23046371 Gene expression analysis using a high-resolution DNA microarray of peripheral whole blood 2012 Oct Leukocytapheresis (LCAP) is a safe, unique therapy pertaining to intractable rheumatoid arthritis (RA) even in cases of drug allergy or infectious states. To investigate how to represent LCAP efficacy, we have conducted gene expression analyses from the peripheral blood of RA patients treated with non-woven polyethylene terephthalate filters. Peripheral blood samples were collected immediately before and after treatment from eight RA patients who received LCAP. Among these patients, all of them achieved 20% improvement in the core set of the American College of Rheumatology (ACR20), and thus, they were confirmed as LCAP responders. Gene expression analysis was done with a high-resolution DNA microarray. The results of each of the two groups' gene expression values (immediately before and after LCAP) were calculated using Welch's t-test. Calculations were performed with a statistical software R.basic package: if the P-value was less than 0.05, this was seen as a significant change. In a comparison of 25,370 gene expressions, the number of genes showing a P-value < 0.05 in the upregulating group was 2110, and in the downregulating group it was 1864. The results of pathway analysis using the MetaCore program indicate that gene groups work for cytoskeletal remodeling are upregulated, and genes related to immune responses, such as antigens presenting via major histocompatibility complex class I and II, are downregulated just after LCAP. These findings may relate to LCAP efficacy for RA patients, but this needs further investigation.
21755815 Risk of hepatotoxicity with add-on leflunomide in rheumatoid arthritis patients. 2011 Combination of disease-modifying antirheumatic drugs (DMARDs) is increasingly used in the treatment of rheumatoid arthritis (RA) patients. Hepatotoxicity has been an important safety concern with DMARDs therapy. Though leflunomide (CAS 75706-12-6) has emerged as an effective oral DMARD, its use is associated with hepatotoxicity. Limited data is available regarding hepatotoxic risk when leflunomide is used in combination therapy in RA patients. An open-label, prospective study was conducted to evaluate the hepatotoxic risk after addition of leflunomide with other DMARDs in RA patients, who did not respond to their ongoing DMARD therapy. A total of 46 patients were enrolled and leflunomide was given as add-on therapy with earlier DMARDs. Biochemical parameters of serum aminotransferase levels (AST and ALT) were estimated at the baseline and then every month after addition of leflunomide. Study results showed that 13.0% patients developed > 1.5 to < 2 times upper limit of normal (ULN) elevation; 6.5% patients developed > 2 to < 3 times the ULN elevation and 2.2% patients developed > 3 times the ULN elevation. In 20% of the patients with hepatic enzyme elevations, enzyme levels returned to normal within 4-6 weeks after discontinuation of leflunomide therapy, whereas in 50% of patients the dose of leflunomide was reduced from 20 mg/day to 10 mg/day for normalization of enzymes levels. 30% of patients were continued with leflunomide without dose reduction. None of the patients showed clinical signs and symptoms of hepatotoxicity. Leflunomide therapy with other DMARDs requires strict monitoring of serum aminotransferases.
22273590 Up-regulated dipeptidyl-peptidase IV (CD26) on monocytes was unaffected by effective DMARD 2012 Jan OBJECTIVES: To study the CD26 density on monocytes and CD4+ T-lymphocytes in steroid and DMARD-naïve, early rheumatoid arthritis (RA) patients and to analyse for correlations with disease activity, including long-term radiographic progression. METHODS: Forty patients with active, early steroid and DMARD naïve RA (<6 months' duration) were randomised to treatment with methotrexate (MTX) versus MTX and cyclosporine A (CYA). Controls were 15 healthy age and gender matched subjects. Peripheral blood mononuclear cells were analysed for CD26 density by flow cytometry at baseline and after 52 weeks. Radiographic progression was scored by delta total Sharp-van der Heijde score (TSS) from 0 to 5 years. RESULTS: The density of CD26 on monocytes (CD3-CD14+) in RA was up-regulated compared to healthy controls (p<0.0001) and remained unaffected by clinically effective DMARD treatment after 52 weeks. In anti-CCP positive RA patients (n=18) baseline CD26 density on monocytes correlated to 5-year radiographic progression (p=0.008, r=0.60). The density of CD26 did not correlate to DAS28, the swollen or tender joint count or CRP-level at baseline or at year one. The CD26 density on CD4+ T-lymphocytes at week 0 was comparable to healthy controls (p=0.34). CONCLUSIONS: The up-regulated density of CD26 on monocytes in steroid and DMARD naïve active early RA was unaffected by 52 weeks of effective DMARD treatment and correlated to 5-year radiographic progression.
22626639 Improved detection of synovial boundaries in ultrasound examination by using a cascade of 2013 Feb Rheumatoid arthritis (RA) is a chronic multisystemic autoimmune disease, with an unclear etiopathogenesis. Its early diagnosis and activity assessment are essential to adjust the proper therapy. Among the different imaging techniques, ultrasonography (US) allows direct visualization of early inflammatory joint changes as synovitis, being also rapidly performed and easily accepted by patients. We propose an algorithm to semi-automatically detect synovial boundaries on US images, requiring minimal user interaction. In order to identify the synovia-bone and the synovia-soft tissues interfaces, and to tackle the morphological variability of diseased joints, a cascade of two different active contours is developed, whose composition corresponds to the whole synovial boundary. The algorithm was tested on US images acquired from proximal interphalangeal (PIP) and metacarpophalangeal (MCP) finger joints of 34 subjects. The results have been compared with a consensus manual segmentation. We obtained an overall mean sensitivity of 85±13%, and a mean Dice's similarity index of 80±8%, with a mean Hausdorff distance from the manual segmentation of 28±10 pixels (approximately 1.4±0.5mm), that are a better performance than those obtained by the raters with respect to the consensus.
22867933 Tai Chi and yoga as complementary therapies in rheumatologic conditions. 2012 Jun Tai Chi and yoga are complementary therapies which have, during the last few decades, emerged as popular treatments for rheumatologic and musculoskeletal diseases. This review covers the evidence of Tai Chi and yoga in the management of rheumatologic diseases, especially osteoarthritis of the knee, hip and hand, and rheumatoid arthritis. There is evidence that Tai Chi and yoga are safe, and some evidence that they have benefit, leading to reduction of pain and improvement of physical function and quality of life in patients. Recommendations for Tai Chi in knee osteoarthritis have recently been issued by the American College of Rheumatology. To allow broader recommendations for the use of Tai Chi and yoga in rheumatic diseases, there is a need to collect more evidence researched with larger randomised controlled trials.