Open Rheumatology Journal最新文献

Systemic sclerosis (SSc) is a complex disease involving multiple genetic factors. A recent genome-wide association study (GWAS) indicated that CD247 was strongly associated with SSc, which was subsequently confirmed in a SSc cohort of European population. However, genetic heterogeneity in different ethnic populations may significantly impact the complex trait of SSc. The studies herein aimed to examine whether the SSc-associated SNP rs2056626 of CD247 identified in Caucasian is also associated with Han Chinese SSc. A Han Chinese cohort consisting of 387 SSc patients and 523 healthy controls were examined in the studies. TaqMan assays were performed to examine the SNP. Exact p-values were obtained (Fisher's test) from 2x2 tables of allele counts and disease status. The results showed that there was no association between rs2056626 of CD247 and SSc or any SSc subtypes of Han Chinese. The negative results are important in understanding genetics of SSc in different ethnic populations, which further suggest complex nature of genetics of SSc.

Systemic sclerosis (SSc) is a fibrotic and autoimmune disease characterized clinically by skin and internal organ fibrosis and vascular damage, and serologically by the presence of circulating autoantibodies. Although etiopathogenesis is not yet well understood, the results of numerous genetic association studies support genetic contributions as an important factor to SSc. In this paper, the major genes of SSc are reviewed. The most recent genome-wide association studies (GWAS) are taken into account along with robust candidate gene studies. The literature search was performed on genetic association studies of SSc in PubMed between January 2000 and March 2014 while eligible studies generally had over 600 total participants with replication. A few genetic association studies with related functional changes in SSc patients were also included. A total of forty seven genes or specific genetic regions were reported to be associated with SSc, although some are controversial. These genes include HLA genes, STAT4, CD247, TBX21, PTPN22, TNFSF4, IL23R, IL2RA, IL-21, SCHIP1/IL12A, CD226, BANK1, C8orf13-BLK, PLD4, TLR-2, NLRP1, ATG5, IRF5, IRF8, TNFAIP3, IRAK1, NFKB1, TNIP1, FAS, MIF, HGF, OPN, IL-6, CXCL8, CCR6, CTGF, ITGAM, CAV1, MECP2, SOX5, JAZF1, DNASEIL3, XRCC1, XRCC4, PXK, CSK, GRB10, NOTCH4, RHOB, KIAA0319, PSD3 and PSOR1C1. These genes encode proteins mainly involved in immune regulation and inflammation, and some of them function in transcription, kinase activity, DNA cleavage and repair. The discovery of various SSc-associated genes is important in understanding the genetics of SSc and potential pathogenesis that contribute to the development of this disease.

Serum adenosine deaminase (ADA) has been previously proposed to predict disease activity in patients with rheumatoid arthritis (RA). The aim of this study was to investigate the level of serum ADA, and the relationship between ADA and disease activity markers, in a group of patients with RA. A hundred and 10 patients with a diagnosis of RA were recruited from outpatient clinic of Rheumatology Unit. Demographic properties comprising age, gender, disease duration and drugs were recorded. Disease activity based on disease activity score (DAS)28-erythrocyte sedimentation rate (ESR) and DAS28- C reactive protein (CRP,) ESR, CRP levels, as well as pain by visual analog scale and rheumatoid factor (RF) were recorded. Serum ADA levels (IU/L) were determined in all RA patients and in 55 age and sex similar healthy control subjects. Ninety-six female and 14 male RA patients with a mean age of 54.32±11.51, and with a mean disease duration of 11.5±9.13 years were included to the study. The control group comprised of 48 female and 7 male healthy subjects. 35.5% of the patients were on methotrexate (MTX) and 64.5% of patients were on combined DMARDs or combined MTX and anti-TNF therapies. The mean serum ADA level was statistically higher in RA patients than in control subjects (27.01±10.6 IU/L vs 21.8 ±9.9 IU/L). The mean values of ESR (23.2±14.8 mm/h), CRP (1.71±1.11mg/dL), pain by VAS (37.2±27.1), DAS28-ESR (2.72±0.77), DAS28 CRP (1.37±0.5) were not correlated with ADA levels (p>0.05). Our results have shown that serum ADA levels are higher in RA patients than in controls but were not related with any of the disease activity markers. We conclude that ADA in the serum may not be a reliable biochemical marker to predict disease activity in patients with RA.

Osteonecrosis (ON), subchondral insufficiency fracture (SIF), and rapidly destructive coxopathy (RDC) are considered to be clinically different disorders despite exhibiting several overlapping features. We encountered an elderly female patient with an atypical clinical course who was radiographically diagnosed as having osteoarthritis (OA), ON, SIF, and/or RDC over a long-term follow-up. In this case, radiographic diagnosis was apparently affected by the timing of imaging evaluation and was challenging because of radiographic overlap and atypical disease progression. The disorders of OA, SIF, ON, and RDC might share a similar pathophysiology.

To our knowledge, the possible unveiled interaction between adult-onset Still's disease (AOSD) with autoimmune thyroid disease (AITD) has never been reported although it is well established that systemic autoimmune disease may usually occur in relation to AITD. As increasingly clear links of AITD with other autoimmune disease such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and primary Sjögren's syndrome (pSS) have been reported, and the incidence of AOSD concurrent AITD draws our attention rapidly. In this study, we searched relevant literatures published in the past 30 years to explore that condition.

Introduction: Adult-onset Still's disease (AOSD) is a systemic inflammatory disorder characterized by rash, leukocytosis, fevers, and arthralgias. Pulmonary involvement has been reported rarely in AOSD, but acute respiratory distress syndrome (ARDS) is extremely rare and potentially fatal and must be recognized as potential manifestation of underlying AOSD.

Methods: We present a case of AOSD manifested by ARDS and review the previously reported cases in Medline/Pub med.

Results: Including this case, 19 cases of AOSD complicated with ARDS have been reported in the literature.

Conclusions: It is important to recognize ARDS as a manifestation of AOSD so that proper diagnostic and therapeutic management can be initiated promptly.

Equisetum giganteum is a plant used in traditional medicine as diuretic. From our knowledge this is the first time this plant is tested in an in vivo model of acute inflammation. To evaluate the effect of aqueous extract of giant horsetail (AEGH) as immunomodulatory therapy, antigen-induced arthritis (AIA) was generated in mice with methylated bovine serum albumin (mBSA). Inflammation was evaluated by articular nociception, leukocytes migration and lymphocyte proliferation. AEGH reduced nociception at 3, 6 and 24 h (P < 0.01), decreased leukocyte migration (P < 0.015), and inhibited lymphocyte proliferation stimulated with Concanavalin A and Lipopolysaccharide (P < 0.05). In conclusion, AEGH has an anti-inflammatory potential in acute model of inflammation, as well as immunomodulatory effect on both B and T lymphocytes, with an action independent of cytotoxicity.

Objectives: Determine risk factors for infection following hip or knee total joint arthroplasty in patients with rheumatoid arthritis.

Methods: All rheumatoid arthritis patients with a hip or knee arthroplasty between years 2000 and 2010 were identified from population-based administrative data from the Calgary Zone of Alberta Health Services. Clinical data from patient charts during the hospital admission and during a one year follow-up period were extracted to identify incident infections.

Results: We identified 381 eligible procedures performed in 259 patients (72.2% female, mean age 63.3 years, mean body mass index 27.6 kg/m2). Patient comorbidities were hypertension (43.2%), diabetes (10.4%), coronary artery disease (13.9%), smoking (10.8%) and obesity (32%). Few infectious complications occurred: surgical site infections occurred within the first year after 5 procedures (2 joint space infections, 3 deep incisional infections). Infections of non-surgical sites (urinary tract, skin or respiratory, n=4) complicated the hospital admission. The odds ratio for any post-arthroplasty infection was increased in patients using prednisone doses exceeding 15 mg/day (OR 21.0, 95%CI 3.5-127.2, p=<0.001), underweight patients (OR 6.0, 95%CI 1.2-30.9, p=0.033) and those with known coronary artery disease (OR 5.1, 95%CI 1.3-19.8, p=0.017). Types of disease-modifying therapy, age, sex, and other comorbidities were not associated with an increased risk for infection.

Conclusion: Steroid doses over 15 mg/day, being underweight and having coronary artery disease were associated with significant increases in the risk of post-arthroplasty infection in rheumatoid arthritis. Maximal tapering of prednisone and comorbidity risk reduction must be addressed in the peri-operative management strategy.

Objectives: The aim of this study was to investigate whether bone alterations detected by hip magnetic resonance imaging (MRI) were associated with subsequent primary hip OA.

Methods: We enrolled 7 patients with hip joint pain from their first visit, at which hip joints were classified as grade 0 or I on the Kellgren-Lawrence grading scale. Plain radiographs and magnetic resonance imaging (MRI) were performed on all cases, and pain was assessed with the Denis pain scale. Average age, height, weight, body mass index, bone mineral density (L1-4), central edge angle, Sharp's angle, and acetabular hip index were calculated.

Results: Within two months of the onset of pain, 4 of the 7 cases showed broad bone signal changes, while 3 cases showed local signal changes in the proximal femur on hip MRI. Three to 6 months after the onset of pain, in all patients whose pain was much improved, plain radiographs showed progression to further-stage OA.

Conclusion: Our findings suggest that bone abnormalities in the proximal femur might be involved in the pathogenesis of primary hip OA.