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ID PMID Title PublicationDate abstract
22776315 The most reliable probe position in the ultrasonographic examination of the wrist in rheum 2012 Jul OBJECTIVES: This study aims to evaluate the inter-observer reliability of the ultrasonographic examination of the wrist in RA patients between 3 examiners and 3 probe positions. METHODS: Fifty-three RA patients were recruited at the University Clinical Hospital of Santiago de Compostela in Spain for ultrasonographic examination of the wrist. Ultrasonography (US) was performed on both wrists using a GE LOGIQ 9 machine, using three probe positions: Lister's Tubercle to digit II (position 1), Lister's Tubercle to digit III (position 2) and ulnocarpal (position 3), from the anatomic medial orientation. Three examiners (2 experienced ultrasonographers and 1 junior ultrasonographer) scored synovitis according to a 0-3 semiquantitative scoring system. Inter-observer reliability was expressed using the ICC (A,1). RESULTS: For grey-scale ultrasound (GSUS) the inter-observer reliability (ICC(A,1)) (single measure, agreement definition) ranged from 0.35 for the ulnocarpal joint, position 3, to 0.60 in both position 1 for the radiocarpal joint and position 2 for the inter-carpal joint. Using power Doppler ultrasound (PDUS) the inter-observer reliability (ICC(A,1)) ranged from 0.36 in position 3, to 0.52 both in position 1 and 2 for the radiocarpal joint. CONCLUSIONS: The reliability of the GSUS-examination of the wrist joints of RA patients with GSUS shows highest, moderate reliability using the anatomical landmarks Tubercle of Lister and digit III (position 2). The reliability of the PDUS examination was similar and moderate in both position 1 (Lister's Tubercle to digit II) and position 2 (Lister's Tubercle to digit III). The reliability was poorest for position 3 (the anatomic medial view of the ulnocarpal joint) in both the GSUS and PDUS examination. This study suggests that position 2 should be used in clinical trials and daily practice.
22340319 Adiponectin receptor 1 mediates the difference in adiponectin- induced prostaglandin E2 pr 2011 Dec BACKGROUND: The synovial fluid concentrations of adiponectin are significantly higher in patients with rheumatoid arthritis (RA) than in patients with osteoarthritis (OA). Accumulating evidence suggests that adiponectin may be an inducer of inflammation in arthritis, but the mechanism remains unclear. The objectives of this study were to compare the expression levels of adiponectin receptors in rheumatoid arthritis synovial fibroblasts (RASF) and osteoarthritis synovial fibroblasts (OASF), evaluate the roles of adiponectin receptors in adiponectin-induced prostaglandin E(2) (PGE(2)) production, and then investigate the effects of a nonsteroidal anti-inflammatory drug (NSAID) and a cyclooxygenase (COX)-2-selective inhibitor on adiponectin-induced PGE(2) release. METHODS: The expressions of adiponectin receptor 1 (AdipoR1) and AdipoR2 mRNA and protein in synovial fibroblasts from seven patients with RA and eight patients with OA undergoing total knee replacement were evaluated by real-time polymerase chain reaction, immunofluorescence microscopy and Western blotting analysis. Adiponectin-induced PGE(2) production was detected by enzyme-linked immunosorbent assay. RNA interference against the AdipoR1 and AdipoR2 genes was performed to investigate the effects of the adiponectin receptors on adiponectin-induced PGE(2) production in both RASF and OASF. RESULTS: AdipoR1 and AdipoR2 mRNA and protein were expressed by both RASF and OASF. Compared with OASF, RASF exhibited higher levels of AdipoR1, but there was no significant difference for AdipoR2. Adiponectin induced the production of PGE(2) by the synovial fibroblasts in a concentration-dependent manner, and this was more obvious in RASF. RNA interference showed that the difference may be mediated by the diverse distribution of AdipoR1. The adiponectin-induced PGE(2) production was efficiently relieved by the NSAID and COX-2-selective inhibitor. CONCLUSION: The present findings suggest that AdipoR1 may mediate the difference in adiponectin-induced PGE(2) production in RASF and OASF.
21109521 Changes in expression of membrane TNF, NF-{kappa}B activation and neutrophil apoptosis dur 2011 Mar BACKGROUND: Tumour necrosis factor (TNF) is central to the pathophysiological process of rheumatoid arthritis (RA), whether as soluble cytokine or membrane-expressed pro-TNF (mTNF). OBJECTIVES: To determine whether neutrophils, which can express TNF, are activated in the blood of patients with RA compared with healthy controls. To investigate, by focusing on mTNF expression, if the functions of RA neutrophils change in response to therapeutic TNF inhibition. METHODS: TNF was measured by flow cytometry and qPCR in neutrophils from 20 patients with RA before and after the start of TNF inhibitor therapy. Apoptosis was measured by morphology, and western blotting of pro- and antiapoptotic proteins in cell lysates. Nuclear factor κB (NF-κB) activation was determined by western blotting of phosphorylated NF-κB (p65). RESULTS: Before treatment RA neutrophils exhibited increased TNF mRNA expression, elevated mTNF levels and NF-κB activity compared with controls. They also underwent delayed apoptosis as shown by altered expression of anti- and proapoptotic proteins, such as Mcl-1 and caspases. Neutrophil TNF expression returned to baseline levels during successful treatment with anti-TNF biological agents, and there was a close correlation between clinical disease improvement and changes in neutrophil function. CONCLUSIONS: Neutrophils express elevated levels of TNF in RA and the transcription factor, NF-κB, a target of TNF, is activated. This mechanism could lead to a self-sustained inflammatory process. These data point to an important role of neutrophils in the abnormal TNF signalling pathways activated in RA and provide new evidence that neutrophils actively contribute to altered cytokine signalling in inflammatory diseases.
22366857 From HLA association to function. 2012 Feb 27 A new study refines the association signals for rheumatoid arthritis susceptibility in the major histocompatibility complex (MHC) region to five amino-acid positions encoded in three HLA genes, all within peptide-binding grooves. By adapting statistical methods from genome-wide association studies (GWAS) and using imputation from a large reference panel, they demonstrate the potential for this approach to identify functional variants in associated regions.
22411424 Cost per treated patient for etanercept, adalimumab, and infliximab across adult indicatio 2012 Mar INTRODUCTION: This paper aims to estimate the annual cost of etanercept, adalimumab, and infliximab per treated patient across adult indications using US-managed care drug use data. METHODS: Adult patients who used etanercept, adalimumab, or infliximab were identified in the Thomson Reuters MarketScan® Commercial Claims and Encounters Database (Thomson Reuters Healthcare, Ann Arbor, MI, USA) between January 1, 2005 and June 30, 2009. The index event was the first use of etanercept, adalimumab, or infliximab preceded by a diagnosis for rheumatoid arthritis, psoriasis, psoriatic arthritis, or ankylosing spondylitis. Patients were defined as either newly initiating or continuing tumor necrosis factor (TNF) blocker treatment based on their use during the 6 months before the index event. Annual cost per treated patient was the sum of the etanercept, adalimumab, and infliximab medication and administration costs during the 12 months following the index claim. Annual costs were calculated across all patients as well as within each indication group and patient type (new initiator or continuing). RESULTS: In total, 21,652 patients met the study criteria (etanercept n = 12,065; adalimumab n = 5,685; infliximab n = 3,902); 43% of patients were new initiators. Patient characteristics were similar across treatment groups in terms of age (mean = 49, SD = 10) and gender (66% female). Across indications, the mean annual TNF-blocker cost per treated patient was $15,345 for etanercept, $18,046 for adalimumab, and $24,018 for infliximab. In new initiators, the TNF-blocker cost per treated patient across indications was $14,543 for etanercept, $16,978 for adalimumab, and $21,086 for infliximab; among patients continuing therapy, annual costs were $15,836 for etanercept, $19,457 for adalimumab, and $25,748 for infliximab. CONCLUSION: Patients on etanercept had the lowest TNF-blocker cost per treated patient for adult indications when applying actual drug use from a US-managed care population. TNF-blocker costs per treated patient on adalimumab and infliximab were approximately 18% and 57% higher than etanercept, respectively, using real-world drug use data.
22718219 Over-expression of extracellular superoxide dismutase in mouse synovial tissue attenuates 2012 Sep 30 Oxidative stress such as reactive oxygen species (ROS) within the inflamed joint have been indicated as being involved as inflammatory mediators in the induction of arthritis. Correlations between extracellular- superoxide dismutase (EC-SOD) and inflammatory arthritis have been shown in several animal models of RA. However, there is a question whether the over-expression of EC-SOD on arthritic joint also could suppress the progression of disease or not. In the present study, the effect on the synovial tissue of experimental arthritis was investigated using EC-SOD over-expressing transgenic mice. The over-expression of EC- SOD in joint tissue was confirmed by RT-PCR and immunohistochemistry. The degree of the inflammation in EC-SOD transgenic mice was suppressed in the collagen-induced arthritis model. In a cytokine assay, the production of pro-inflammatory cytokines such as, IL-1β, TNFα, and matrix metalloproteinases (MMPs) was decreased in fibroblast-like synoviocyte (FLS) but not in peripheral blood. Histological examination also showed repressed cartilage destruction and bone in EC-SOD transgenic mice. In conclusion, these data suggest that the over-expression of EC-SOD in FLS contributes to the activation of FLS and protection from joint destruction by depressing the production of the pro-inflammatory cytokines and MMPs. These results provide EC-SOD transgenic mice with a useful animal model for inflammatory arthritis research.
22664499 Serum interleukin-17 & nitric oxide levels in patients with primary Sjögren's syndrome. 2012 Apr BACKGROUND & OBJECTIVES: The interleukin (IL)-17 producing T-helper cells have been linked to pathogenesis of autoimmunity and mostly investigated in rheumatoid arthritis (RA). In this study we tested the IL-17 levels, as well as the levels of nitric oxide (NO) as possible IL-17-induced product, in patients with primary Sjögren's syndrome (pSS), an intricate and complex chronic autoimmune disorder of exocrine glands. METHODS: Serum IL-17 levels and nitrite concentrations determined in patients with pSS (n=30) were compared with the values obtained in patients with RA (n=10) and healthy controls (n=15). The values obtained for IL-17 in pSS patients were also associated with the patients' clinical characteristics, particularly the rheumatoid factor (RF) and total antinuclear antibodies (tANA) levels. RESULTS: Serum concentrations of IL-17 were significantly (P<0.01) higher in patients with pSS (12.9 ± 28.0 pg/ml) as compared to those obtained in healthy individuals (0.2 ± 0.6 pg/ml), but not as high as the values obtained for the patients with RA (34.5 ± 56.2 pg/ml). The mean IL-17 levels were significantly (P<0.05) higher in the pSS patients positive for rheumatoid factor (20.3 ± 33.3 pg/ml) than in RF-negatives (0.3 ± 0.6 pg/ml). Mean serum concentrations of IL-17 were also higher in antinuclear antibody (ANA)-positive samples (19.8 ± 33.5 pg/ml) in comparison to ANA-negative sera (1.1 ± 3.1 pg/ml) (P<0.05). The NO levels also showed elevated values in both pSS and RA patients, as compared to the healthy controls, since mean nitrite levels in patients with pSS and RA were 38.2 ± 29.2 μM and 41.7 ± 21.1 μM, respectively, while those in healthy controls were significantly lower, at 19.2 ± 10.5 μM. INTERPRETATION & CONCLUSIONS: The findings of this study showed that there was increased IL-17 and NO production in patients with primary SS, especially if they had associated elevated rheumatoid factor and antinuclear antibody values.
21382268 Impact of IL-18 on inflammation. 2011 Jan IL-18 is produced by many cell types, such as Kupffer cells, keratinocytes, macrophages, dendritic cells, and activated T cells stimulated by LPS. It is an important regulator of both innate and acquired immune responses. IL-18 plays a central role in rheumatoid arthritis since the T cells and macrophages that invade the synovial. These finding support a role for IL-18 in inflammation, allergy and immune diseases.
22813350 Risk factors for reported influenza and influenza-like symptoms in patients with rheumatoi 2012 Oct OBJECTIVES: To determine the prevalence and predictors of influenza and influenza-like symptoms in patients with rheumatoid arthritis (RA). METHOD: Questionnaires were sent to patients registered as having RA and they were asked to fill in per month any period and details of influenza-like symptoms and vaccination. An experienced rheumatologist assessed the level of disease activity and use of anti-rheumatic medication. The prevalence of reported influenza (fever > 38°C, headache, muscle soreness, and coughing and/or dyspnoea) and influenza-like symptoms was determined and risk factors were identified by logistic regression analysis. RESULTS: Of the 1692 patients approached, 783 (46%) patients were eligible for follow-up. Fifty per cent of the patients reported influenza-like symptoms, 5.9% had symptoms suggesting influenza, and 74% reported vaccination. The prevalence of influenza and influenza-like symptoms per month ranged from 0.0% to 2.3% and from 10.4% to 19.7%, respectively. Anti-tumour necrosis factors (anti-TNFs) [odds ratio (OR) 2.4, 95% confidence interval (CI) 1.2-4.8] and body mass index (BMI) (OR 1.06, 95% CI 1.0-1.1) were independently associated with symptoms of influenza. A trend was found for patients not in remission, patients using leflunomide, and patients with previous lung conditions. Independent risk factors of influenza-like symptoms were age (OR 0.98, 95% CI 0.97-0.99), female gender (OR 1.8, 95% CI 1.3-2.5), influenza vaccination (OR 1.6, 95% CI 1.1-2.4), and previous lung condition (OR 1.7, 95% CI 1.2-2.4). CONCLUSIONS: In 2009-2010, the prevalence of reported influenza in patients with RA was 5.9%. Patients using anti-TNFs and with higher BMI seemed to be more at risk for influenza symptoms. Milder upper respiratory tract infections were reported more often by females, younger patients, and those vaccinated against influenza or with previous lung conditions.
22516984 [Survey of tumor necrosis factor inhibitors application in patients with rheumatoid arthri 2012 Apr 18 OBJECTIVE: To investigate the current status of tumor necrosis factor (TNF) inhibitors application in rheumatoid arthritis (RA) patients in China and to analyze the related factors. METHODS: A retrospective survey was conducted in 21 hospitals from different parts of China. The patients with RA were randomly enrolled. Data of their social backgrounds, clinical conditions, usage and adverse effects of TNF inhibitors were collected. The costs of TNF inhibitors and the indirect costs of the disease were calculated. A multivariate Logistic regression analysis was performed to analyze the factors related to TNF inhibitors application. RESULTS: In the study, 1 095 RA patients from July 2009 to November 2010 were enrolled, of whom 112 had received TNF inhibitors, representing 10.2% of the total patients. The patients who received etanercept and infliximab were 7.4% (86/1 095) of the patients and 2.4% (26/1 095), respectively. There were 0.5% of the patients (5/1 095) who had received both of the TNF inhibitors. The patients who had accepted etanercept and treatment duration for less than 3 months and 3-6 months accounted for 38.5% and 25.0% respectively, while those treated with Infliximab were 38.1%. Their health assessment questionnaire (HAQ) scores were 1.1, 0.5 and 0.1, corresponding to treatment duration of infliximab for less than 3, 3-6 and 6-9 months and those were 1.3, 1.0, 0.3 corresponding to treatment duration of etanercept, respectively. Infliximab costs were RMB 24 525.0, 69 300.0 and 96 800.0 Yuan and etanercept costs were RMB 7 394.8, 9 158.6, 54 910.9 Yuan, respectively. Indirect costs for RA patients who accepted infliximab for less than 3, 3-6 and 6-9 months were RMB 365.6, 0 and 158.9 Yuan and those who accepted etanercept were RMB 2 158.4, 288.5 and 180.1 Yuan, respectively. Allergy and infection were the main side-effects of etanercept and both happened in 3.5% of all the patients. Liver damage happened in 2.3% of all the patients, while allergy and infection happened in 6.5% of all the patients who accepted infliximab. Logistic regression analysis showed that patients with higher education experience increased the odds of entering the TNF inhibitors group (OR: 1.292, 95%CI: 1.132-1.473, P=0.000). CONCLUSION: About one-tenth of RA patients in China have accepted TNF inhibitors. Higher education experience is the key factor for using TNF inhibitors.
22037282 Chemerin induces CCL2 and TLR4 in synovial fibroblasts of patients with rheumatoid arthrit 2012 Feb INTRODUCTION: Chemerin stimulates migration of leukocytes to sites of inflammation and also increases inflammatory signaling in chondrocytes suggesting a function of chemerin in joint inflammation. Synovial fibroblasts (SF) are critically involved in synovitis and subsequent cartilage destruction. Here, we analyzed whether synovial fibroblasts express chemerin and its receptor CMKLR1. Further, the role of chemerin in synovial fibroblast chemotaxis, proliferation, insulin response and release of inflammatory proteins was studied. METHODS: Synovial tissue sections were labeled with chemerin antibody and chemerin was measured in synovial fluid by ELISA. Chemerin mRNA and protein as well as CMKLR1 expression were determined in SFs from patients with osteoarthritis (OA) and rheumatoid arthritis (RA). Effects of chemerin on cytokines, chemokines and matrix metalloproteinases (MMP), and on proliferation, migration and insulin signaling were analyzed appropriately. RESULTS: SFs expressed CMKLR1 and chemerin mRNA, and chemerin protein was found in cell supernatants of synovial fibroblasts. Immunohistochemistry detected chemerin in synovial tissue predominantly localized within the lining layer. Chemerin was present in synovial fluids of RA, OA and psoriatic arthritis patients in similar concentrations. Chemerin neither increased IL-6 levels nor MMP-2 or -9 activity in SFs. Also, it did not act as a chemoattractant for these cells. With respect to intracellular signaling, neither basal nor insulin-mediated phosphorylation of Akt was affected. However, chemerin significantly increased TLR4 mRNA and synthesis of CCL2 in SFs while CCL4 and -5 were not altered. Cell proliferation of SFs, however, was modestly reduced by chemerin. CONCLUSIONS: These data show that human SFs express both chemerin and its receptor. As chemerin enhanced expression of TLR4 and induced release of CCL2 in SFs, a role of this protein in innate immune system-associated joint inflammation is proposed.
22943199 Differential effects of infliximab on absolute circulating blood leucocyte counts of innat 2012 Oct Anti-tumour necrosis factor (TNF) biologics have revolutionized therapy of rheumatoid arthritis (RA). We compared the effects of infliximab on numbers of circulating leucocyte subsets in early RA (disease/symptom duration of ≤1 year) and late RA patients (>1 year). A control group consisted of early RA patients treated with a combination of methotrexate (MTX) and methylprednisolone. Blood samples were obtained at baseline (pre-therapy) from all RA patients, divided into three groups: (i) late RA receiving infliximab/MTX, (ii) early RA-infliximab/MTX, (iii) early RA-steroid/MTX, and also from follow-up patients at 2 and 14 weeks. Significant differences in absolute counts of monocytes and granulocytes were observed between healthy controls and RA patients. At baseline CD14(bright) monocytes and CD16(+) granulocytes were increased in both early RA and late RA patients. CD4(+) T cells, CD8(+) T cells and B cells were all increased at baseline in early RA, but not in late RA. At 2 weeks following infliximab treatment decreased granulocytes were observed in both early and late RA and decreased natural killer (NK) cells in late RA. CD16(+) granulocytes and NK cells were also decreased at 14 weeks post-infliximab in early RA. Biotinylated infliximab was used to detect membrane-associated TNF (mTNF)-expressing leucocytes in RA patients. CD16(+) granulocytes, NK cells and CD14(dim) monocytes all expressed higher levels of mTNF in RA patients. In summary infliximab is associated with decreased CD16(+) granulocyte and NK cell counts, possibly through binding of mTNF. Differential effects of infliximab between early and late RA suggest that pathogenic mechanisms change as disease progresses.
21449161 [Clostridium difficile-associated diarrhea: causes and relationship to reactive arthritis] 2011 Jan We present a patient treated with methotrexate (MTX] for rheumatoid arthritis, in whom clostridium difficile-associated colitis has developed, without preceding antibiotic treatment. Two weeks later, the patient was admitted with knee arthritis. Reactive arthritis was diagnosed and treated successfully with the naproxen. The article discusses risk factors for Clostridium difficile-associated diarrhea [CDAD] other than antibiotics, and the relation of this pathogen to the development of reactive arthritis. It seems to be the first report of the association of MTX treatment with CDAD.
21569351 Are patients' judgments of health status really different from the general population? 2011 May 11 BACKGROUND: Many studies have found discrepancies in valuations for health states between the general population (healthy people) and people who actually experience illness (patients). Such differences may be explained by referring to various cognitive mechanisms. However, more likely most of these observed differences may be attributable to the methods used to measure these health states. We explored in an experimental setting whether such discrepancies in values for health states exist. It was hypothesized that the more the measurement strategy was incorporated in measurement theory, the more similar the responses of patients and healthy people would be. METHODS: A sample of the general population and two patient groups (cancer, rheumatoid arthritis) were included. All three study groups judged the same 17 hypothetical EQ-5D health states, each state comprising the same five health domains. The patients did not know that apart from these 17 states their own health status was also included in the set of states they were assessing. Three different measurement strategies were applied: 1) ranking of the health states; 2) placing all the health states simultaneously on a visual analogue scale (VAS); 3) separately assessing the health states with the time trade-off (TTO) technique. Regression analyses were performed to determine whether differences in the VAS and TTO can be ascribed to specific health domains. In addition, effect of being member of one of the two patient groups and the effect of the assessment of the patients' own health status was analyzed. RESULTS: Except for some moderate divergence, no differences were found between patients and healthy people for the ranking task or for the VAS. For the time trade-off technique, however, large differences were observed between patients and healthy people. The regression analyses for the effect of belonging to one of the patient groups and the effect of the value assigned to the patients' own health state showed that only for the TTO these patient-specific parameters did offer some additional information in explaining the 17 hypothetical EQ-5D states. CONCLUSIONS: Patients' assessment of health states is similar to that of the general population when the judgments are made under conditions that are defended by modern measurement theory.
22198693 Optic neuritis after infliximab therapy. 2013 Apr Demyelinating diseases were described in patients receiving anti-TNF agents. Optic neuritis (ON) induced by TNF blockers was already described in 22 cases in the literature. In this article, the authors report a 53-year-old woman with refractory rheumatoid arthritis that developed neuritis optica after the fourth dose of infliximab and had a good outcome after anti-TNF withdrawal, associated with glucocorticoid treatment. In addition, the previous cases of ON induced by anti-TNF agents were reviewed.
22389903 New onset sarcoid-like granulomatosis developing during anti-TNF therapy: an under-recogni 2012 Jan Tumour necrosis factor-alpha (TNF-a) antagonists have advanced the treatment of inflammatory arthropathies, and are even considered for use in refractory sarcoidosis with some success. Paradoxically, cases of new onset sarcoidosis-like diseases are increasingly reported in patients receiving TNF-a antagonists. Here, we report three cases of sarcoid-like granulomatosis that developed during treatment with TNF-a antagonists. Review of the Biologics clinic data base at Westmead, Sydney, Australia identified three patients whom, during anti-TNF therapy, developed non-caseating granulomas consistent with sarcoidosis. These three cases are described with review of the literature from 2000 to 2009 using PubMed. One hundred and sixty-nine patients within our data base were reviewed for the period 2003–2009. Sarcoidosis-like granulomas developed in three patients within a period of 3 to 36 months of treatment with etanercept and/or adalimumab. All cases demonstrated non-infective, non-caseating granulomas on renal or lymph node biopsy. Improvement was seen in two cases upon cessation of TNF-a antagonist and steroid therapy. Interestingly, clinical deterioration was noted upon re-challenge with the same TNF-a antagonist in one patient. To date, a total of 37 cases of sarcoid-like granuloma development after anti-TNF therapy have been reported in the literature. Development of sarcoidosis-like granulomatosis in patients treated with TNF-a antagonists is a phenomenon previously under-recognised. All three anti-TNF agents have been observed to cause this phenomenon, suggesting a ‘class effect’ rather than being drug specific.
22258456 Interferon-gamma induced nitric oxide-mediated apoptosis of anemia of chronic disease in r 2013 Jan Proinflammatory cytokines play a role in the pathogenesis of anemia of chronic disease (ACD), which is a common cause of anemia in rheumatoid arthritis (RA). Anemia in RA is associated with increased apoptosis of erythroid cells. However, there is unclear information on the mechanism of ACD in the disease. The purpose of this study is to investigate the role of cytokines on nitric oxide-mediated apoptosis in erythroid progenitor cells of ACD in RA patients. Erythroid progenitor cells from healthy subjects and RA patients with ACD were treated with cytokines like interleukin-1β, tumor necrosis factor-α, and interferon-γ at concentrations of 2, 20, and 40 ng/ml for 14 days. Cell viability and cell apoptosis were analyzed by trypan blue staining and flow cytometry, respectively. The results showed that the highest effect of cytokines on reduction cell viability and induction cell apoptosis was found in 20 ng/ml IFN-γ-treated cells of RA patients. In addition, IFN-γ showed significantly increased nitric oxide production and iNOS mRNA expression, which was measured by Griess assay and real-time PCR, respectively. The percentage of cell apoptosis and NO production was reduced after an inducible nitric oxide synthase inhibitor, SMT, treatment. In conclusion, IFN-γ could induce nitric oxide production-mediated apoptosis process, which might be involved in the pathogenesis of ACD in RA patients.
21106403 Radial nerve palsy after humeral revision in total elbow arthroplasty. 2011 Mar HYPOTHESIS: The Mayo Clinic database was queried for all humeral component revision elbow arthroplasties complicated by radial nerve palsy. MATERIALS AND METHODS: Multiple variables were analyzed to determine their impact on patient outcomes. RESULTS: Of 258 humeral component revisions, 7 (2.7%) were complicated by radial nerve palsy. The mean follow-up was 84 months (range, 24-233 months). Only 3 of 7 patients (43%) regained function. There was no recovery in 4 out of the 5 patients in whom power instruments or ultrasound was used for cement removal. Two of three patients who underwent exposure of the radial nerve had return of function at most recent follow-up. CONCLUSIONS: Radial nerve palsy is an uncommon complication after humeral revision in total elbow arthroplasty but is not necessarily associated with full recovery. Return of function is less likely when power instruments or ultrasound is used for cement removal. Formal exposure and protection of the radial nerve are predictive of recovery.
22171710 Frequency of Th17 CD20+ cells in the peripheral blood of rheumatoid arthritis patients is 2011 INTRODUCTION: Rheumatoid arthritis (RA) is considered a T cell driven autoimmune disease, therefore, the ability of B cell depleting biologics, e.g., anti-CD20 antibodies, to alleviate RA is unclear. This study examined the proportions of IL-17-secreting lymphocytes in the blood of healthy subjects and RA patients and determined if Th17 cells belong to a CD20+ subset of T cells. METHODS: Fluorescence-activated cell sorting and confocal microscopy verified CD3, CD4/CD8 and CD20-staining of T cells. IL-17 secretion was determined using a commercial assay. RESULTS: In healthy subjects and RA patients blood, the median percentage of total CD20+ lymphocytes was similar (7.5%; n = 6 and 10.3%; n = 9, respectively) and comprised predominantly of B cells (~ 86%). However, 2-4% of CD3+ T cells from both healthy subjects (n = 7) and RA (n = 8) individuals co-expressed CD20. The peripheral blood of healthy subjects contained few IL-17-secreting CD20+ T cells (< 0.1%; n = 6). In contrast, in RA blood a median and interquartile range % of, 24.2%; IQR 28.5 of IL-17-secreting T cells were CD20+ (n = 9; p = 0.02). CONCLUSIONS: In the blood of RA patients, a greater proportion of Th17 cells are of a CD20+ phenotype compared to healthy individuals. These cells may represent an additional target for anti-CD20 therapies.
20676645 White cells count in smokers affected by rheumatic diseases. 2012 Jan Evidence shows that tobacco smoking interacts with development of rheumatic diseases. Increase in white cells count (leukocytosis) is frequently present, and in smokers, it is considered a biomarker of cardiovascular risk. Aim of the study is to evaluate this biomarker in smokers with rheumatic diagnosis. We carried out an observational study on 115 rheumatic outpatients (26 men and 89 women) divided into two groups according to their smoking habit: one composed of 56 smokers, the other of 59 not smokers. Diagnosis and common routinary clinical parameters were collected. In the total sample, smokers were 48.69%. Most common diagnosis was osteoarthritis (OA) (40.87% of the total); smokers in OA women were 36.11%, smokers in OA men were 54.55%. Second most common diagnosis was rheumatoid arthritis (RA) (23.48% of the total); smokers in RA women were 40.91%; smokers in RA men were 80%. OA smokers showed a significant increase (P < 0.05) in white cells count when compared with OA not smokers. Between RA smokers and not smokers, any clinical difference was found. RA subjects following regular pharmacological treatment in the last 2 months were 84.61%. OA patients treated with drugs in the last 2 months were only 22.2%. Results seem to confirm that smoking habit may influence the development as well as gender distribution of rheumatic diseases. They show also that in absence of pharmacological treatment in smokers affected by OA leukocytosis (biomarker of cardiovascular risk) is observed.