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ID PMID Title PublicationDate abstract
22177434 [Medium and long-term clinical results of using Zweymüller cup to treat protrusio acetabu 2011 Sep 1 OBJECTIVE: To discuss long-term clinical results of using Zweymüller cup to treat protrusio acetabuli. METHODS: From May 1998 to September 2006, 31 patients with 39 hips diagnosed protrusio acetabuli were treated with Zweymüller cup in total hip arthroplasties or revisions. There were 12 men and 19 women with average age of 57.6 years (from 30 to 82 years). The reasons causing protrusio acetabuli were as followed: rheumatoid arthritis 3 cases 6 hips, osteoarthritis followed femoral head necrosis 7 cases 12 hips, acetabular wear after hemi-arthroplasty 11 cases 11 hips and acetabular component loosening 10 cases 10 hips. During all operations, Zweymüller cup was used to fix the acetabular part. RESULTS: All cases were followed up 6 months and one year after operations. Two patients with 3 hips were died for lung cancer and acute myocardial infarction respectively. Twenty-four cases with 31 hips got recent follow-up with average 7.4 years (from 5.0 to 11.5 years). The average Harris score improved from 31.0 (from 14 to 61) preoperatively to 84.7 (from 70 to 95) postoperatively. There was one infection in right hip after bilateral hip arthroplasty treating by removal prosthesis and cement spacer insert. But until now this patient still did not get revision for her internal medicine. One rheumatoid arthritis patient with two-stage bilateral hip arthroplasty was found slight internal migration and loosening line of left acetabular component, but the patient had no pain with good hip function. All other cases had good hip functions and were very satisfied with clinical results. CONCLUSION: Using Zweymüller cup to treat protrusion acetabuli can get strong fixations and perfect medium and long-term clinical results for over 7.4 years.
21641829 Incidence and implications of early postoperative wound complications after total elbow ar 2011 Sep HYPOTHESIS: Other than an awareness, there is little detailed information regarding wound problems after total elbow arthroplasty. The purpose of this study was to (1) determine the incidence of wound complications after elbow arthroplasty, (2) document the long-term implications, (3) characterize risk factors, and (4) discuss a management strategy. We hypothesize that the incidence of this complication can be reduced with careful preoperative planning. MATERIALS AND METHODS: We reviewed 1749 total elbow arthroplasties. The average patient age was 61.5 years (range; 30-91 years). Wound complications were diagnosed according to the criteria of the Centers for Disease Control and Prevention. RESULTS: We identified and studied 97 patients (5.5%) from the 1749 procedures. The most common problems were delayed healing and drainage in 34 and wound hematoma in 33, of which 9 (27%) progressed to secondary deep infection. Of the 97 patients, 86 (88.7%) healed with the retention of the implant, 24 (∼25%) progressed to a septic elbow, and 11 (∼50%) required resection. Patients with rheumatoid arthritis represented 33% of the entire sample, but represented 45.8% of those with septic complications. Posttraumatic arthritis patients represented 58% of the entire sample and only 33% of those with septic problems (P < .05). CONCLUSIONS: The overall incidence of serious wound complications was slightly less than anticipated; however, the significance was considerable. Patients with rheumatoid arthritis are most vulnerable. Persistent wound drainage showed a high correlation for deep infection and subsequent implant removal. Anticipation of potential problems and appropriate prophylactic management may avoid wound complications.
22378812 Sixty years after Hench--corticosteroids and chronic inflammatory disease. 2012 May CONTEXT: Proinflammatory cytokines activate the hypothalamic pituitary adrenal axis in the acute phase but not with chronic inflammation; indeed, the hypothalamic pituitary adrenal axis is subtly subnormal, with apparently low ACTH and cortisol secretion. This paper reviews evidence that suggests that this is not simply an adaptation to chronic stress. These patients have increased conversion of inactive cortisone (E) to cortisol (F) by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Expression of this enzyme is markedly enhanced by TNF, an important autocrine protective mechanism at the inflammatory site. EVIDENCE ACQUISITION AND SYNTHESIS: This report reviews the current understanding of the interaction between TNF and 11β-HSD1 in patients with chronic inflammatory disease. It is based on publications from PubMed and the Science Citation Index. CONCLUSIONS: The systemic effects of enhancing 11β-HSD1 activity may amplify the inflammatory response. Thus, increased conversion of cortisone to cortisol can alter the circadian rhythm of cortisol secretion (lower nadir, later rise, impaired stress response) with consequent relative nocturnal cortisol deficiency when inflammatory cytokines are highest. This could contribute to the circadian symptomatology in rheumatoid arthritis, the effectiveness of early morning (0200 h) low-dose corticosteroids, the significant correlation between total body 11β-HSD1 activity and erythrocyte sedimentation rate, and the effectiveness of 11β-HSD inhibition in both the prevention and treatment of adjuvant arthritis in rat models of rheumatoid arthritis. It could also explain why anti-TNF therapy benefit can be predicted on the basis of the pretreatment plasma cortisol and the subsequent cortisol rise. In contrast, this mechanism is likely to be beneficial in the body's response to chronic infections such as tuberculosis and could explain why anti-TNF treatment markedly increases the risk of reactivation of the disease.
22751605 Interleukin 6 blockade: tocilizumab in psoriatic arthritis. 2012 Jul Psoriatic arthritis (PsA) is a chronic inflammatory arthropathy of unknown etiology that is associated with psoriasis. Joint destruction is often progressive: almost half of the patients attending an early arthritis clinic showed radiological damage 2 years after diagnosis. Proinflammatory cytokines are major mediators of systemic and local inflammation, and high levels of interleukin 1 (IL-1), IL-6, and tumor necrosis factor have been found in psoriatic skin lesions and the synovial tissue of patients with rheumatoid arthritis and PsA. IL-6 is a pleiotropic cytokine that mainly signals by membrane (neutrophil and lymphocyte) or soluble (endothelial cell) IL-6 receptors. IL-6 was originally identified as a factor in B cell differentiation, but is now known to influence T cell development: in the presence of IL-6 and transforming growth factor-ß (TGF-ß), naive T cells develop into Th17 cells, which are important mediators in PsA. IL-6 may also directly contribute to the epidermal hyperplasia seen in psoriatic epithelium and affect the function of dermal inflammatory cells. However, there are no data concerning the use of tocilizumab in patients with PsA, although a pilot study is currently being carried out because the role of IL-6 in the pathogenesis of PsA supports the idea that targeted treatments against IL-6 might be effective.
22641127 Amelioration by the natural polyamine spermine of cartilage and bone destruction in rats w 2012 We investigated pharmacological properties of naturally occurring polyamines on cartilage and bone destruction seen in joints of rats with collagen-induced arthritis (CIA). Daily supplementation of spermine (SPM), but not spermidine, significantly inhibited increases in the hind paw volume and arthritis score in CIA rats, in addition to the increased mRNA expression of receptor activator of nuclear factor-κB ligand in both cartilage and synovial tissues. Histological analysis clearly revealed a drastic prevention by SPM of the cartilage and bone destruction in synovial joints of CIA rats. Particular natural polyamines would be beneficial for the prophylaxis of synovial joint destruction in rheumatoid arthritis.
21339224 The early phase of psoriatic arthritis. 2011 Mar Evaluation of the preclinical phases of the classic autoimmune diseases including rheumatoid arthritis has been facilitated by the availability of autoantibody and genetic markers that point firmly towards the early dysregulation of the adaptive immune responses. The association of psoriatic disease with the human leucocyte antigen-Cw0602 (HLA-Cw0602) gene has likewise led to the perception that autoimmunity has a pivotal role in early psoriatic arthritis (PsA). However, this HLA-Cw0602 genetic association does not appear to hold for PsA or associated nail, scalp and intergluteal skin involvement. Of note, these three sites of psoriasis are predictive of PsA evolution. For initiation of both skin and nail disease there is a link with Koebnerisation, or site-specific trauma. Nail disease is most common in the dominant hand thumbnail, pointing towards local tissue factors as disease initiators Likewise, for PsA, there is also good evidence for a history of previous joint trauma and histological studies showing microdamage in normal entheses which are typical locations where PsA frequently occurs. Furthermore, subclinical enthesopathy including osteitis is common in subjects with psoriasis but without arthritis. Collectively, these findings indicate that the classic model of adaptive immune dysregulation does not generally hold for the early stages of PsA. The way in which knowledge pertaining to tissue-specific factors in PsA, combined with the emerging data relating to monogenic disorders and animal models, points towards perturbation in the healing response and dysregulation of innate immune responses in early PsA is discussed. The way in which this model explains the clinical disconnect between skin and joint disease and the emerging human data that support it are demonstrated.
21229360 Schistosoma mansoni infection: an immune complex disease presenting with polyarthritis. 2013 May Schistosomiasis or bilharzia is a parasitic disease found in tropical countries. Most infections are subclinical but may progress to chronic form characterized most frequently by the presence of liver involvement and portal hypertension. We report a patient that presented chronic polyarthritis with positive rheumatoid factor. During investigation, increased liver enzymes, negative hepatitis serologies and signs of portal hypertension on an ultrasound examination raised suspicion of S. mansoni infection. We will discuss pathophysiology and clinical manifestations of S. mansoni infection with special attention to articular involvement.
21123320 Disease activity, smoking, and reproductive-related predictors of poor prognosis in patien 2011 Mar OBJECTIVE: To identify disease activity, smoking, and reproductive-related predictors of a poor prognosis in patients with very early inflammatory polyarthritis (IP). METHODS: Patients with very early IP (symptom duration 4-11 weeks) included in our study were participants in the STIVEA (Steroids In Very Early Arthritis) randomized placebo-controlled trial. At baseline, disease-related variables were measured and patients were asked to complete a questionnaire covering smoking status and reproductive questions. Baseline predictors of poor prognosis [i.e., the need to start disease-modifying antirheumatic drug (DMARD) therapy by 6 months or the clinical diagnosis of rheumatoid arthritis (RA) at 12 months] were identified, applying logistic regression analyses adjusted for treatment group. RESULTS: Rheumatoid factor (RF) positivity was one of the strongest clinical predictors of a poor prognosis: OR for DMARD therapy at 6 months, 4.00 (95% CI 2.00-8.00) and OR for a diagnosis of RA at 12 months, 9.48 (95% CI 4.48-20.07). There was a significant association between current smoking at baseline compared to never smoking and a diagnosis of RA at 12 months (OR 3.15, 95% CI 1.16-8.56). CONCLUSION: About 6 in 7 patients with very early RF-positive IP were diagnosed with RA 1 year later. In addition, 1 in 4 IP patients who smoke will develop RA later. It is recommended to treat RF-positive patients who have IP with DMARD at presentation and to advise patients to stop smoking.
22220307 Pharmacodynamics of bisphosphonates in arthritis. 2011 Sep Inflammatory arthritis is a group of autoimmune diseases characterized by chronic inflammation of the joints. Rheumatoid arthritis, the most common form of arthritis, is associated with local joint destruction and systemic bone loss. Osteoclasts, the only cells of the body able to resorbe bone, are key players in these two types of bone loss. Bisphosphonates are analogs of pyrophosphate that inhibit osteoclast action and bone resorption. They are indicated in pathology associated with excess resorption. Besides their effect on bone they also exhibit extra-osseous properties, acting on tumor cells, inflammation and angiogenesis. As a result, they have been trialed in the context of arthritis. It is now clear that they do not have any significant direct effect on disease activity or pain. If their indication in the prevention of glucocorticoid-induced osteoporosis is clear, any beneficial effects on bone erosions are still controversial but interesting preliminary results warrant further investigations.
21871883 Inhibiting effects of Leflunomide metabolite on overexpression of CD147, MMP-2 and MMP-9 i 2011 Nov 16 Recent studies have reported elevated expression of cluster of differentiation (CD) 147 on CD14(+) monocytes of the peripheral blood of patients with active rheumatoid arthritis and a correlation of CD147 expression with Disease Activity Score. Thus, CD147 may be a new target for treatment of rheumatoid arthritis. Leflunomide is a disease-modifying antirheumatic drug that is commonly used to treat rheumatoid arthritis. The effect of leflunomide in blocking the up-regulation of CD147 and in blocking the down-regulation of metalloproteinases (MMP)-2 and MMP-9 in active macrophages has not yet been established. In this study we investigated the effect of A771726, the active metabolite of leflunomide, on expression of CD147 and on the gelatinolytic activity of MMP-2 and MMP-9 in phorbol myristate acetate (PMA) differentiated THP-1 cells. The expression of CD147, MMP-2, and MMP-9 mRNAs were determined by real-time quantitative reverse transcription PCR, the levels of cellular surface expression of CD147 were determined by flow cytometry, and the gelatinolytic activity of MMP-2 and MMP-9 were determined by zymography. Our results showed that A771726 significantly inhibited the expression of CD147 on the cell surface of activated THP-1 cells in a dose-dependent manner (P<0.01), inhibited the expression of MMP-2 and MMP-9 mRNAs in a dose-dependent manner (P<0.01), and inhibited the gelatinolytic activity of MMP-2 and MMP-9 at concentration of 15 μg/ml and 45 μg/ml (P<0.01). Our results indicate that A771726, the active metabolite of leflunomide, inhibited CD147 expression at the protein level and inhibited gelatinolytic activity of MMP-2 and MMP-9 in PMA-differentiated THP-1 cells.
21220091 Role of diet in rheumatic disease. 2011 Feb Millions of people suffer from rheumatic diseases such as gout, fibromyalgia, osteoarthritis, and rheumatoid arthritis. These can be incapacitating and detrimental to quality of life. Diet, nutrition, and weight loss have shown promise in alleviating some of this disease burden. These lifestyle changes may give patients a feeling of control and ownership over their disease as well as a nonpharmacologic means of treatment. This article reviews the available research on the effects of diet and nutrition on rheumatoid disease.
21681567 Protective effect of soy protein on collagen-induced arthritis in rat. 2012 Aug To evaluate preventive and therapeutic effects of soy protein on collagen-induced arthritis rats. Sprague-Dawley rats immunized with bovine type II collagen emulsified in adjuvant and treated with soy protein (7 g/kg), dexamethasone (1 mg/kg), and casein (in control groups) by daily gavages feedings for 30 days. Score of arthritis recorded every day for each paws of animal. Tumor necrosis factor-alpha, interleukin6, leptin, and adiponectin were measured in serums. Treatment with soy protein resulted in significant delay in time to onset of arthritis as well as significantly decreased arthritis incidence, clinical arthritis severity score, histopathological arthritis severity score, and in vivo cell-mediated immunity to collagen (P < 0.05). Administration of soy protein significantly suppressed the progression of collagen II-induced arthritis and inhibited the production of tumor necrosis factor-alpha, interleukin6, leptin, and adiponectin. Soy protein appeared to be a potent immunomodulatory inhibitor of collagen II-induced arthritis in rats. It could delay onset of RA and reduced cartilage erosion and synovitis inflammation. Therefore, it may be a useful protein in the prevention and treatment of rheumatoid arthritis patient.
21570969 Arthritis in space and time--to boldly go! 2011 Dec 1 Despite the profound impact of biologics on the treatment of rheumatoid arthritis (RA), long lasting disease remission remains elusive. We propose that this is a consequence of failing to target the right molecular pathway in the most relevant patient group at the appropriate time and place in disease progression. A limitation to testing this approach is the availability of disease models representing the discrete steps in autoimmune pathogenesis. A particular example is the paucity of models to dissect the conditions permissive for the breach of self-tolerance, which would subsequently allow identification and testing of therapeutics for re-establishment of self-tolerance. We conclude that a detailed understanding of the location and timing of events leading to the systemic breach of self-tolerance and subsequent progression to tissue specific pathology are required if rational application of existing drugs and identification of novel targets is to be achieved. This will take the personalised medicine revolution into the realms of contextualised medicine, whereby the right drug is targeted to the right tissue, in the right patient, at the right time.
22545055 The Th17/IL-23 Axis and Natural Immunity in Psoriatic Arthritis. 2012 Psoriatic arthritis (PsA) is a chronic inflammatory skin disease that causes enthesitis and destructive arthritis and significantly lowers patient quality of life. Recognition of the two target organs (the skin and joints) involved in the immunopathophysiology of PsA helped in elucidating the pathology of various systemic autoimmune diseases targeting multiple organs. Recent advances in immunology and genetics have made it clear that acquired immunity, especially that mediated by the Th17/IL-23 axis, plays an important role in the inflammatory pathology observed in psoriasis and PsA. Additionally, involvement of natural immunity has also been suggested. Microbial infection has been known to trigger psoriasis and PsA. Recent clinical studies using biopharmaceuticals, such as tumor-necrosis-factor- (TNF-) α inhibitors and IL-12/23 p40 antibodies, indicate that studies need not be based only on the immunological phenomena observed in PsA pathology since disease pathology can now be verified using human-based science. Considering this aspect, this paper discusses the immunopathology of PsA compared to psoriasis (cutaneous) and rheumatoid arthritis in humans and immunopathology of PsA with respect to the Th17/IL-23 axis and microbial infection.
22533153 [Toxic epidermal necrolysis during therapy with sulphasalazine in a patient with arthritis 2011 Toxic epidermal necrolysis (TEN) is a severe, life-threatening disease appearing after certain drugs, characterized by keratinocyte necrosis, which shows with painful cutaneous and mucosal exfoliation and systemic involvement. TEN mortality rate is between 30% to 70%, so patients need early administration of medical care. We report a case of a 40-year old woman with TEN-like symptoms, who received treatment with sulphasalazine for 3 weeks because of arthritis. Various diagnostic procedures were performed which caused many doubts about diagnosis. In differential diagnosis we thought about: firstly TEN after treatment with sulphasalazine--patient with systemic lupus erythematosus, secondly toxic epidermal necrolisis like lupus erythematosus, finally TEN and LE after treatment with sulpasalazine--patient with rheumatoid arthritis. Final diagnosis needs more investigation and further diagnostic procedures. The patient stays under our control.
21725847 Induction of toll-like receptor 2 positive antigen-presenting cells in spleen of pristane- 2012 Apr Toll-like receptors (TLRs) have been found to contribute to the pathogenesis of rheumatoid arthritis (RA). The aim of this study is to investigate the regulation and potential role of TLR2 in spleen of pristane-induced arthritis (PIA) rat, which can be used to further understand the mechanisms of RA. Arthritis in DA rats was induced by pristane. TLR2 expression in spleen was detected by real-time quantitative PCR and western blotting, and TLR2 expression at both mRNA and protein levels was upregulated in PIA rats. Peptidoglycan (PGN) was systemically administrated to PIA rats, and arthritis severity was evaluated macroscopically and microscopically. Results showed that systemic administration of PGN to PIA rats obviously deteriorated arthritis severity. TLR2 expression on splenocytes and different types of immune cells was measured by flow cytometry. And it was found that TLR2 was mainly expressed on antigen-presenting cells (APCs) of spleen, and the proportion of TLR2(+) dendritic cells and macrophages in spleen of PIA rats was increased remarkably. Thus, we conclude that the induction of TLR2(+) APCs in spleen may participate in the maintenance of PIA.
21721805 Chemical changes demonstrated in cartilage by synchrotron infrared microspectroscopy in an 2011 Jun Collagen antibody-induced arthritis develops in mice following passive transfer of monoclonal antibodies (mAbs) to type II collagen (CII) and is attributed to effects of proinflammatory immune complexes, but transferred mAbs may react directly and damagingly with CII. To determine whether such mAbs cause cartilage damage in vivo in the absence of inflammation, mice lacking complement factor 5 that do not develop joint inflammation were injected intravenously with two arthritogenic mAbs to CII, M2139 and CIIC1. Paws were collected at day 3, decalcified, paraffin embedded, and 5-μm sections were examined using standard histology and synchrotron Fourier-transform infrared microspectroscopy (FTIRM). None of the mice injected with mAb showed visual or histological evidence of inflammation but there were histological changes in the articular cartilage including loss of proteoglycan and altered chondrocyte morphology. Findings using FTIRM at high lateral resolution revealed loss of collagen and the appearance of a new peak at 1635 cm(-1) at the surface of the cartilage interpreted as cellular activation. Thus, we demonstrate the utility of synchrotron FTIRM for examining chemical changes in diseased cartilage at the microscopic level and establish that arthritogenic mAbs to CII do cause cartilage damage in vivo in the absence of inflammation.
31644093 Gold Preparations. 2012 Gold salts, including auranofin and gold sodium thiomalate, have been used for the therapy of rheumatoid arthritis for many decades, but have recently been replaced by more modern disease-modifying antirheumatic drugs. Parenteral gold therapy (chrysotherapy) can cause acute, clinically apparent hepatitis that is usually cholestatic and self-limited in nature, but can be severe and even fatal. In contrast, oral gold preparations (such as auranofin) are associated with a low rate of serum enzyme elevations during treatment, but have not been convincingly linked to clinically apparent liver injury.
23285506 Medicines for Rheumatoid Arthritis: A Review of the Research for Adults. 2005 This summary will tell you about two types of medicine to treat RA: DMARDs and corticosteroids. It will explain what research has found about how well DMARDs work when taken alone or with corticosteroids to treat RA. It will also tell you what research says about the side effects of these medicines. You can use this summary to talk with your doctor about whether one of these medicines may be right for you.
28925305 Pneumocystis jirovecii pneumonia associated with etanercept treatment in patients with rhe 2012 Nov Objectives The association of anti-tumor necrosis factor therapy with opportunistic infections in rheumatoid arthritis (RA) patients has been reported. The goal of this study was to clarify the clinical characteristics and the risk factors of RA patients who developed Pneumocystis jirovecii pneumonia (PCP) during etanercept therapy. Methods We conducted a multicenter, case-control study in which 15 RA patients who developed PCP were compared with 74 RA patients who did not develop PCP during etanercept therapy. Results PCP developed within 26 weeks following the first injection of etanercept in 86.7% of the patients. All PCP patients presented with a rapid and severe clinical course and the overall mortality was 6.7%. Independent risk factors were identified using multivariate analysis and included age ≥ 65 years [hazard ratio (HR) 3.35, p = 0.037], coexisting lung disease (HR 4.48, p = 0.009), and concomitant methotrexate treatment (HR 4.68, p = 0.005). In patients having a larger number of risk factors, the cumulative probability of developing PCP was significantly higher (p < 0.001 for patients with two or more risk factors vs. those with no risk factor, and p = 0.001 for patients with one risk factor vs. those with no risk factor). Conclusion Physicians must consider the possibility of PCP developing during etanercept therapy in RA patients, particularly if one or more risk factors are present.