Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
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25016432 | Exploiting endogenous anti-inflammatory pathways as a therapeutic approach to multiorgan i | 2014 Aug | This Commentary highlights the article by Montero-Melendez et al, revealing novel protective properties of endogenous melanocortin receptor 3 on periodontal status in health and disease and suggesting a new genus of anti-arthritic bone-sparing therapeutics. | |
24295560 | Pharmacogenomics of biological treatment in rheumatoid arthritis. | 2014 Feb | INTRODUCTION: Rheumatoid arthritis (RA) demonstrates a high heterogeneity in clinical responses to treatment. Although the efficacy of biological therapy has undoubtedly been established, the response differs considerably between individuals. This variability between individuals has aroused the research for biomarkers predictive of treatment response. Pharmacogenomics underlying individual responses to drugs is rapidly developed and has the potential of realizing the personalized therapy in RA. This review will summarize the pharmacogenomics of biological therapies approved for clinical RA treatment. AREAS COVERED: The pharmacogenomics underlies individual responses to biological drugs in RA. Current studies on pharmacogenomics of biological therapy in RA are presented. EXPERT OPINION: The personalized treatment in RA according to pharmacogenomics is promising, but the available pharmacogenomic data on biological treatment in RA are not adequate and consistent and still require further larger sample studies to corroborate. | |
24556692 | HMGB1-LPS complex promotes transformation of osteoarthritis synovial fibroblasts to a rheu | 2014 Feb 20 | It is generally believed that some inflammatory antigens can recognize Toll-like receptors on synovial fibroblasts (SFs) and then activate downstream signals, leading to the formation of RASFs and inducing rheumatoid arthritis (RA). The objective of the current work was to study on the hypothesis that outer PAMP (LPS) binds to the inner DAMP (HMGB1) and becomes a complex that recognizes TLRs/RAGE on SFs, thus initiating a signaling cascade that leads to the secretion of inflammatory cytokines and chemokines, production of tissue-destructive enzymes, and formation of RASFs, finally resulting in RA. Osteoarthritis synovial fibroblasts (OASFs) were co-cultured with HMGB1-LPS complex in vitro for five generations to induce the transformation of human SFs to RA-like SFs (tOASFs). Then, changes of tOASFs in cell cycle and apoptosis-autophagy balance were investigated in vitro, and the pathogenicity of tOASFs was evaluated in a SCID mouse model in vivo. In vitro cell cycle analysis showed more tOASFs passing through the G1/S checkpoint and moving to S or G2 phase. Flow cytometry and confocal microscopy showed that apoptosis was reduced and autophagy was enhanced significantly in tOASFs as compared with those in OASFs. The expression of certain receptors and adhesion molecules in tOASFs was upregulated. In vivo experiments showed that tOASFs attached to, invaded, and degraded the co-implanted cartilage. In addition, histochemistry showed excessive proliferation of tOASFs and the expression of matrix metalloproteinases (MMPs). Based on the above findings, we conclude that HMGB1-LPS complex could promote the formation of RASFs. | |
24405620 | In vivo movement of femoral flexion axis of a single-radius total knee arthroplasty. | 2014 Dec | The objective of this study was to investigate in vivo femoro-tibial motion using the movement of femoral flexion axis of a single-radius TKA. We examined 20 clinically successful knees with a single-radius posterior stabilized TKA to evaluate the kinematics of deep knee flexion using 2-3-dimensional registration techniques. The mean knee flexion range of motion was 117.8°. The mean rotation of the femoral component was 7.6° external rotation. The mean knee flexion angle at initial post-cam engagement was 55.2°. No paradoxical movement of femoral component was shown until 70° flexion, afterward the femoral component rolled back with flexion. The data showed that the design of this prosthesis might contribute to reduce the paradoxical anterior femoral movement and provide stability in mid-flexion ranges. | |
22807253 | Increase of body mass index in a tight controlled methotrexate-based strategy with prednis | 2013 Jan | OBJECTIVE: To clarify whether increase of body weight in patients with early rheumatoid arthritis (RA) upon administration of prednisone is a side effect of prednisone or a result of better control of disease activity, we examined the association of prednisone and disease activity with a subsequent change in body mass index (BMI). METHODS: In the Computer Assisted Management in Early Rheumatoid Arthritis Trial-II, patients ages ≥18 years with early RA (disease duration <1 year and no prior use of disease-modifying antirheumatic drugs) had been randomized to a methotrexate (MTX)-based tight control strategy with either 10 mg of prednisone (MTX + prednisone) or placebo (MTX + placebo). The MTX + prednisone group had lower disease activity, but gained more weight than the MTX + placebo group (mean ± SD 2.9 ± 4.2 kg versus 1.3 ± 5.3 kg; P = 0.03). Data from patients with monthly measurements of disease activity (Disease Activity Score in 28 joints [DAS28]) and BMI were analyzed with a longitudinal regression (mixed model) analysis with BMI as the dependent variable and treatment strategy and DAS28 as the independent variables, correcting for baseline BMI and possible confounders (sex, age, and rheumatoid factor status). RESULTS: There was no independent association of glucocorticoid therapy with a change in BMI, but a lower DAS28 was associated with an increased BMI 6 months later. The association of the DAS28 with BMI was most strongly present in postmenopausal women. Clinical cutoff points showed a clear association between DAS28 level and the change in BMI 6 months later. CONCLUSION: Weight gain during treatment with prednisone seems attributable to a reduction of disease activity and is probably, at least partly, regained weight. | |
22527141 | Successful childbearing in two women with rheumatoid arthritis and a history of miscarriag | 2013 Sep | Two women with rheumatoid arthritis who had experienced miscarriages became pregnant while they were under etanercept treatment. One stopped etanercept after 3 weeks with increased doses of prednisolone, and the other restarted etanercept at a half doses 3 months later. They delivered a healthy baby at full term, and no problems in both expecting mothers and babies were observed. The use of etanercept in patients with rheumatoid arthritis seemed safe for pregnant mothers and their fetuses. | |
24614280 | Rheumatoid arthritis medications and lactation. | 2014 May | PURPOSE OF REVIEW: In contrast to the disease remission enjoyed by a majority of rheumatoid arthritis (RA) patients during pregnancy, the immediate postpartum period is generally characterized by flare. Managing symptoms during this time is challenging because the potential transfer of medication into the breast milk of nursing mothers may limit which antirheumatic drugs can be safely used. The benefits of breastfeeding are significant, however, so an understanding of how to adjust medications to permit lactation and nursing is important for rheumatologists. RECENT FINDINGS: Although nonsteroidal antiinflammatory drugs (NSAIDs) in general are passed into milk in low doses, shorter acting NSAIDs are preferred, with caution for premature infants. Prednisone can be taken by nursing mothers, although when used at doses higher than 20 mg/day an interval of 4 h after dosing and prior to breastfeeding is recommended. Hydroxychloroquine and sulfasalazine are compatible with nursing. Cyclosporine is generally allowed in lactating women, although a single infant was reported to develop therapeutic drug levels. Azathioprine (AZA) and tissue necrosis factor-α-inhibitors have little to no transfer into breast milk, with negligible levels measured in infant sera, and thus may be considered for use in lactating mothers. Methotrexate and leflunomide should not be used. Other biological RA medications have not been evaluated, and are, therefore, best avoided by breastfeeding patients. SUMMARY: Many but not all RA medications may be used during lactation with low risk to the nursing infant; this review summarizes the available data for commonly used medications in order to help guide therapy during the postpartum period. | |
24610702 | Spleen tyrosine kinase inhibitors for rheumatoid arthritis: where are we now? | 2014 Mar | The development of small-molecule inhibitors of inflammatory cascade signaling kinases offers a potential approach to treating rheumatoid arthritis (RA). Spleen tyrosine kinase is one such tyrosine kinase. Recent research efforts have focussed on the development and testing of a spleen tyrosine kinase inhibitor, fostamatinib. We reviewed the results of the clinical trials of fostamatinib in RA with the aim of outlining its clinical efficacy and the nature and frequency of its main adverse events. To date, this drug has been evaluated in over 3,200 RA patients enrolled in three phase II, one phase IIb and three phase III trials. These studies showed fostamatinib was effective. In four trials in which patients received 100Â mg twice daily, fostamatinib reduced inflammatory synovitis; the relative risks of achieving American College of Rheumatology Responder rates compared with placebo in the combined studies ranged from 1.6 for 20Â % of responders to 3.7 for 70Â % of responders. There was a similar relative risk of achieving a clinically meaningful reduction in disability of 1.6 for the chance of patients achieving a reduction in health assessment questionnaire scores of 0.22 or more. Three of the trials examined the impact of fostamatinib on erosive radiographic damage using changes in the modified total Sharp score. None of them provided any evidence for a significant effect of fostamatinib on erosive damage over 6Â months. All the trials included descriptions of adverse events. Hypertension was common, involving over 40Â % of patients treated. Other common adverse events included diarrhoea, neutropenia and increases in hepatic enzyme levels. Some patients developed infections. On the conclusion of the phase III trials, one of the main pharmaceutical sponsors decided not to further develop fostamatinib for RA. | |
24465901 | A potential role of myeloid DAP12-associating lectin (MDL)-1 in the regulation of inflamma | 2014 | The pathogenic roles of myeloid DAP12-associating lectin-1(MDL-1) and DAP12 in human rheumatoid arthritis (RA) remain unknown. Frequencies of MDL-1-expressing monocytes in 22 active RA patients, 16 inactive RA patients, 12 osteoarthritis (OA) patients and 10 healthy controls (HC) were determined by flow-cytometry analysis. The mRNA expression levels of MDL-1 and DAP12 on PBMCs were evaluated by quantitative PCR, and their protein expression levels in the synovium were examined by immunohistochemistry. Significantly higher median percentages of circulating MDL-1-expressing monocytes were observed in active RA patients (53.6%) compared to inactive RA patients (34.1%), OA patients (27.9%), and HC (21.2%). Levels of MDL-1 and DAP12 gene expression in PBMCs and their protein expression in the synovium were significantly higher in active RA patients than in inactive RA or OA patients. MDL-1 levels were positively correlated with parameters of disease activity, articular damage, and levels of proinflammatory cytokines. MDL-1 activator (Dengue virus type 2 antigen) stimulation on PBMCs resulted in significantly enhanced levels of proinflammatory cytokines in RA patients compared to those in OA patients or HC, indicating that MDL-1 activation is functional. Frequencies of MDL-1-expressing monocytes and levels of MDL-1 and DAP12 gene expression significantly decreased after effective therapy. Concordant overexpression of MDL-1 and DAP12 were correlated with increased production of proinflammatory cytokines in RA patients, suggesting their roles in regulating articular inflammation. | |
24517052 | [Treatment of rheumatoid arthritis by xinfeng capsule: an efficacy observation]. | 2013 Dec | OBJECTIVE: To observe the curative effect of Xinfeng Capsule (XC) in treatment of rheumatoid arthritis (RA). METHODS: Recruited were 80 active RA patients, who were randomly assigned to the normal control group and the treatment group, 40 in each group. All patients received the same routine anti-rheumatic treatment: Methotrexate 10 mg per week; Diclofenac 50 mg when pain was obvious, twice daily. Patients in the treatment group took XC 3 tablets each time, thrice daily. All treatment lasted for 12 consecutive weeks. Serum iron (SI), serum ferritin (SF), transferrin (TRF); and RA disease activity index (DAS-28) were detected in all patients. RESULTS: XC could improve HAQ, DAS-28, hypersensitive C reactive protein (hs-CRP), prostaglandins A (PGA), erythrocyte sedimentation rate (ESR), number of swelling joints, number of tender joints, and morning stiffness time in acute RA patients, showing statistical difference when compared with those of the control group (P < 0.01, P < 0.05). Compared with the control group, SI, SF, DAS-28, and TRF significantly decreased in the treatment group (P < 0.05). CONCLUSION: XC could improve DAS-28, and SI reserve in patients with active RA, and lower DAS-28 related indicators. | |
24758887 | Rheumatoid arthritis-related interstitial lung disease: associations, prognostic factors a | 2014 Sep | OBJECTIVES: The prevalence of interstitial lung disease (ILD) in RA is ∼5%. Previous work identified increasing age, active articular disease and articular damage as risk factors for RA-associated ILD (RA-ILD). The roles of high-resolution CT (HRCT) and lung function testing in defining the nature and extent of pulmonary involvement have recently been explored. This study is the first to examine predictive and prognostic factors for the development of RA-ILD and to report on the physiological and radiological characteristics of the condition from a large multicentre UK network. METHODS: We collected data from centres across the UK on patients with both RA and ILD (proved on HRCT) diagnosed over a 25-year period from 1987 to 2012 using a standard pro forma. Potential predictors of RA-ILD were analysed. Baseline lung function data were recorded and related to HRCT findings. We analysed HRCT for subtype and extent of lung involved and examined the relationship between these and both all-cause and pulmonary mortality. We compared our results with case controls matched for age and gender using computer-generated selection from the RA population from one contributing centre. RESULTS: A total of 230 patients were identified from across the UK with proven RA-ILD diagnosed over 25 years. Median age at diagnosis was 64 years and the male:female ratio was 1:1.09. Univariate analysis showed anti-CCP antibody titres to be the single most strongly associated predictor of RA-ILD. Male gender, age at onset, smoking and RF were all independently associated with RA-ILD on multivariate analysis. Vital capacity (VC) was preserved in limited disease but reduced in extensive disease, while gas transfer was reduced in both. Usual interstitial pneumonia (UIP) was the most common subtype on HRCT and both this and extensive disease were associated with increased all-cause mortality. CONCLUSION: This is the largest study of RA-ILD in the UK. Anti-CCP antibodies were strongly associated with RA-ILD in both sexes. Smoking was strongly associated with ILD in males, which may explain the higher frequency of RA-ILD in men. The predominant HRCT pattern was UIP and most patients had limited disease at presentation. The presence of UIP and extensive disease are associated with increased mortality. Baseline gas transfer is a useful screening tool for ILD, while the preservation of VC at baseline might predict limited disease on HRCT. | |
25986347 | Periprosthetic Joint Infection in Patients Receiving TNFα Antagonists. | 2014 | Tumor necrosis factor-α antagonists (anti-TNFα) have become increasingly more common as a treatment for rheumatoid arthritis (RA). However, there has been an increased incidence of severe infections in patients taking anti-TNFα therapy. We present a case series of RA patients treated with anti-TNFα therapy that had previously underwent TJA and subsequently developed periprosthetic infections. All patients had a well-functioning implant for a period of 1 to 14 years prior to the development of infection. Each patient underwent two to five different joint replacements, and four patients developed infection in multiple sites. The infections proved difficult to eradicate with four patients requiring multiple procedures, and one patient ultimately requiring a hemipelvectomy. This study suggests that periprosthetic infections acquired by patients on anti-TNFα therapy are challenging to eradicate and treat; highlighting the need for the establishment of guidelines for perioperative and long-term management of anti-TNFα therapy, and infection monitoring in joint replacement patients. | |
23436223 | Inhibition of connective tissue growth factor ameliorates disease in a murine model of rhe | 2013 Jun | OBJECTIVE: We have shown that connective tissue growth factor (CTGF) plays an important role in the pathogenesis of rheumatoid arthritis (RA). This study was undertaken to evaluate the effects of blockade of the CTGF pathway on the development of collagen-induced arthritis (CIA) in mice. METHODS: Arthritis was induced in DBA/1J mice by immunization with a combination of type II collagen (CII) and Freund's complete adjuvant. We evaluated the development of arthritis in mice with CIA left untreated versus treated with neutralizing anti-CTGF monoclonal antibody (mAb). RESULTS: Inhibition of CTGF in mice treated with neutralizing anti-CTGF mAb significantly ameliorated arthritis compared to the untreated mice with CIA. Serum levels of matrix metalloproteinase 3 were reduced by anti-CTGF mAb treatment. Moreover, blockade of CTGF decreased interleukin-17 expression on purified CD4+ T lymphocytes. Although the expression of the retinoic acid receptor-related orphan receptor γt gene was not suppressed by anti-CTGF mAb treatment, that of interferon regulatory factor 4 (IRF-4) and IκBζ (Nfkbiz), which are other important molecules for the differentiation of Th17 cells, was suppressed. In addition, blockade of CTGF inhibited pathologic proliferation of T lymphocytes in response to CII restimulation in vitro. Moreover, aberrant osteoclastogenesis in mice with CIA was restored by anti-CTGF mAb treatment. CONCLUSION: Our findings indicate that blockade of CTGF prevents the progression of arthritis in mice with CIA. Anti-CTGF mAb treatment suppresses pathologic T cell function and restores aberrant osteoclastogenesis in mice with CIA. CTGF may become a new target for the treatment of RA. | |
24501248 | Distinct arthropathies of the hands in patients with anti-aminoacyl tRNA synthetase antibo | 2014 Jun | OBJECTIVE: The aim of this study was to characterize arthropathies of the hands associated with antiaminoacyl tRNA synthetase (ARS) autoantibodies. METHODS: Fifty-six patients with anti-ARS antibodies were selected from consecutive patients who visited Keio University Hospital between1983 and 2011, based on their joint symptoms and the availability of hand X-rays. Their clinical characteristics, anti-CCP antibodies, RF, and hand X-ray findings were retrospectively examined. RESULTS: Based on characteristic hand X-ray findings, the anti-ARS-positive patients with joint symptoms could largely be categorized into three groups. The predominant group (64%) was patients with no significant X-ray findings. The remaining patients with destructive changes were classified into two distinct groups. One group had mainly erosions in the PIP and MCP joints and/or ankylosis of the wrists with anti-CCP and RF, which is consistent with the features of RA. The other group showed subluxation of the thumbs and periarticular calcification that was independent of anti-CCP or RF, which is exclusively found in anti-Jo-1-positive patients. CONCLUSION: Autoantibody profiles, including anti-CCP, RF and individual anti-ARS specificities, are useful in classifying anti-ARS-associated arthropathies of the hands into RA or anti-Jo-1-related disorders. | |
24569640 | Rheumatoid arthritis in the Women's Health Initiative: methods and baseline evaluation. | 2014 Apr 1 | Second-generation assays for anti-cyclic citrullinated peptide (anti-CCP), a highly sensitive and specific marker for rheumatoid arthritis (RA), have redefined the epidemiology of RA. In the Women's Health Initiative (WHI) RA study (2009-2011), we evaluated the prevalence of anti-CCP positivity among 15,691 (10.2% of 161,808) WHI participants aged 50-79 years who reported RA. Using stored baseline specimens, we measured serum anti-CCP, rheumatoid factor (RF), and antinuclear antibody in a defined sample of 9,988 of black, white, and Hispanic women. In a subset of women, we measured plasma cytokine levels and number of copies of the human leukocyte antigen (HLA)-DRB1 (HLA-DRB1) shared epitope in DNA by means of Luminex polymerase chain reaction typing (Luminex Corporation, Austin, Texas). We validated classification of probable clinical RA in 2 clinics as anti-CCP positivity or self-reported validated use of disease-modifying antirheumatic drugs (DMARDs). The prevalence of anti-CCP positivity was 8.1%, and the prevalence of RF positivity was approximately 16.0%. DMARD use including prednisone was reported by 1,140 (11.4%) participants (841 excluding prednisone) but by 57.5% of anti-CCP-positive women. The prevalence of 2 shared epitopes was also much higher for anti-CCP-positive women (18.2%, as opposed to only 5.5% for women with anti-CCP-negative DMARD-positive RA and 6.6% for anti-CCP-negative, RF-negative DMARD nonusers). Median cytokine levels were much higher for anti-CCP-positive/RF-positive women. Women with anti-CCP-positive RA and anti-CCP-negative RA had different characteristics with regard to HLA shared epitope, cigarette smoking, and inflammation (cytokines). | |
23052484 | The levels of β-thromboglobulin in female rheumatoid arthritis patients as activation cri | 2013 May | The activation of the platelets plays a key role in the formation of thrombosis. The variables such as mean platelet volume, platelet factor 4 and β-thromboglobulin have been used in the demonstration of the platelet activation. However, when the literature was reviewed, there was not found any study investigating the level of β-thromboglobulin in patients with rheumatoid arthritis. Our goal is to evaluate the β-thromboglobulin levels together with mean platelet volume in patients with arthritis. This study is a clinical study which has a control group that has been designed prospectively, and in this study, Rheumatology Outpatient Clinic follow-up patients with rheumatoid arthritis and healthy control group were studied. All patients and healthy volunteers were examined β-thromboglobulin and mean platelet volume. Twenty-two patients with rheumatoid arthritis and 21 healthy volunteers participated in the study. β-Thromboglobulin mean was found as 98.00 ± 60.49 ng/mL in rheumatoid arthritis group and it was 62.38 ± 30.41 ng/mL in healthy control group. The differences between these groups were significant in terms of the levels of β-thromboglobulin (p = 0.02). We found significant differences between the groups in terms of mean platelet volume (p = 0.049). In this study, the level of β-thromboglobulin was found significantly higher in patients with rheumatoid arthritis, which is a chronic inflammatory disease. This result could be an indicator, such as platelet activation in patients with rheumatoid arthritis, or it may be a helper marker in the follow-up and treatment of developing cardiovascular risk. | |
24095938 | Identification of small molecule inhibitors of RANKL and TNF signalling as anti-inflammato | 2015 Jan | INTRODUCTION: Inflammatory joint diseases such as rheumatoid arthritis are associated with local bone erosions and systemic bone loss, mediated by increased osteoclastic activity. The receptor activator of nuclear factor (NF) κB ligand (RANKL) plays a key role in mediating inflammation-induced bone loss, whereas tumour necrosis factor (TNF) plays a central role in the inflammatory process. Here we tested whether a recently identified class of small molecule inhibitors of RANKL signalling (ABD compounds) also affect TNF signalling and whether these compounds inhibit inflammation in an animal model of rheumatoid arthritis. METHODS: The inhibitory effects of the ABD compounds on TNF-induced signalling were tested in mouse macrophage cultures by western blotting and in an NFκB luciferase-reporter cell line. The anti-inflammatory effects of the compounds were tested in the mouse collagen-induced arthritis model of rheumatoid arthritis. RESULTS: The ABD compounds ABD328 and ABD345 both inhibited TNF-induced activation of the NFκB pathway and the extracellular signal-regulated kinase (ERK) and Jun kinase (JNK) mitogen activated protein kinases (MAPKs). When tested in the mouse collagen-induced arthritis model of rheumatoid arthritis, the compounds suppressed inflammatory arthritis, inhibited joint destruction and prevented systemic bone loss. Furthermore, one of the compounds (ABD328) showed oral activity. CONCLUSIONS: Here we describe a novel class of small molecule compounds that inhibit both RANKL- and TNF-induced NFκB and MAPK signalling in osteoclasts and macrophages, and inflammation and bone destruction in a mouse model of rheumatoid arthritis. These novel compounds therefore represent a promising new class of treatments for inflammatory diseases, such as rheumatoid arthritis. | |
22975732 | Efficacy of adjunct tacrolimus treatment in patients with rheumatoid arthritis with inadeq | 2013 Jul | OBJECTIVES: We aimed to assess the efficacy of tacrolimus (TAC) as an add-on therapy in patients with rheumatoid arthritis (RA) who were previously treated with methotrexate (MTX) but not with biologics. METHODS: The study group (MTX + TAC group) consisted of 157 patients (selected from among the patients in the Institute of Rheumatology, Rheumatoid Arthritis [IORRA] RA cohort from April 2005 to October 2009) who received add-on therapy with TAC in addition to MTX, but without biologics. A propensity score (PS) for the use of TAC was derived, and 471 PS-matched patients who received MTX alone or MTX with other non-biologic disease-modifying antirheumatic drugs (except for TAC), but not with biologics, were selected and served as the control group. Changes in disease activity in the two groups during three consecutive IORRA phases were analyzed by adjusting for confounding factors. RESULTS: The median 28-joint disease activity score (DAS28) decreased from 4.58 to 3.70 in the MTX + TAC group and from 4.12 to 3.61 in the control group. After adjusting for confounding factors, the decrease in the DAS28 score in the MTX + TAC group was significantly larger (by 0.273 points) than that in the control group (P < 0.05). CONCLUSION: This study demonstrated the efficacy of add-on therapy with TAC to MTX in patients with RA in daily practice. | |
23554040 | Infliximab-induced discoid lupus erythematosus. | 2013 Apr | Anti-tumor necrosis factor-alpha (TNF-α) immunotherapy is currently used in the treatment of various inflammatory diseases such as rheumatoid arthritis, psoriasis, psoriatic arthritis, ankylosing spondylitis and Crohn's disease. Infliximab is a chimeric monoclonal antibody that binds to transmembrane-bound and soluble TNF-α. Previously, a discoid lupus erythematosus-like eruption linked to its use was rarely reported in patients with rheumatoid arthritis. We present a case of rheumatoid arthritis which developed such an eruption after treatment with infliximab. The lesions resolved after the discontinuation of infliximab. In the present case, the clinical, serological and immunohistochemical features of our patient are discussed with the literature. | |
23856916 | Computer-aided diagnosis of rheumatoid arthritis with optical tomography, Part 2: image cl | 2013 Jul | This is the second part of a two-part paper on the application of computer-aided diagnosis to diffuse optical tomography (DOT) for diagnosing rheumatoid arthritis (RA). A comprehensive analysis of techniques for the classification of DOT images of proximal interphalangeal joints of subjects with and without RA is presented. A method for extracting heuristic features from DOT images was presented in Part 1. The ability of five classification algorithms to accurately label each DOT image as belonging to a subject with or without RA is analyzed here. The algorithms of interest are the k-nearest-neighbors, linear and quadratic discriminant analysis, self-organizing maps, and support vector machines (SVM). With a polynomial SVM classifier, we achieve 100.0% sensitivity and 97.8% specificity. Lower bounds for these results (at 95.0% confidence level) are 96.4% and 93.8%, respectively. Image features most predictive of RA are from the spatial variation of optical properties and the absolute range in feature values. The optimal classifiers are low-dimensional combinations (<7 features). These results underscore the high potential for DOT to become a clinically useful diagnostic tool and warrant larger prospective clinical trials to conclusively demonstrate the ultimate clinical utility of this approach. |