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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19505397 | Imaging progression despite clinical remission in early rheumatoid arthritis patients afte | 2009 Apr | The aim of this preliminary study is to evaluate clinical and imaging response in twenty patients with early Rheumatoid Arthritits (eRA) treated with Etanercept (Etn) + Methotrexate (Mtx) and to investigate whether clinical and MRI remission may be maintained after biological therapy interruption. Assessment included: radiography, Visser score and anti-CCP antibodies at baseline; disease activity score in 44 joints (DAS44), rheumatoid factor (RF), Magnetic Resonance Imaging (MRI) of hands and wrists at baseline (T0), 12 (T1), and 24 months (T2). MRI was scored for synovitis, bone oedema and erosions (OMERACT study); patients who reached clinical and imaging remission at T1 were considered eligible for interrupting Etn. At T1 8/20 (40 percent) patients showed a total remission, DAS44 from 5 (T0) to 1.4 (T1); p<0.02, whereas the other 12/20 (60 percent) showed an improvement, without complete remission, DAS44 from 4.8 (T0) to 2.8 (T1); p<0.05. Etn was therefore interrupted in the first group of patients (group A), whereas it was continued in the other group (group B). At T2, group A maintained clinical remission and group B showed further not significant DAS44 reduction from T1. At T1, a significant reduction in synovitis, bone oedema and total score (p<0.01) was observed both in group A and in group B. At T2, group A showed an increase in all the MRI scores that was significant for the synovitis and total score, whereas group B exhibited a further not significant reduction. This preliminary study reports an excellent clinical and imaging response in eRA patients treated with Etn with total remission in 40 percent of them after a 1-year therapy period. However, it indicates that joint damage may progress, despite a sustained clinical remission, after Etn suspension. | |
21080350 | Abnormal bone geometry at the metacarpal bone shaft of rheumatoid arthritis patients with | 2011 Mar | OBJECTIVE: Metacarpal juxtaarticular bone is altered in rheumatoid arthritis (RA). However, a detailed analysis of disease-related geometric adaptations of the metacarpal shaft is missing. The aim of the present study was to assess the role of RA disease, forearm muscle cross-sectional area (CSA), age, and sex on bone geometry at the metacarpal shaft. METHODS: In 64 RA patients and 128 control subjects, geometric properties of the third metacarpal bone midshaft and forearm muscle CSA were measured by peripheral quantitative computed tomography (QCT). Linear models were performed for cortical CSA, total bone CSA, polar stress-strain index (SSI; a surrogate for a bone's resistance to bending and torsion), cortical thickness, and the metacarpal index (MI; cortical CSA/total CSA), with the explanatory variables muscle CSA, age, RA status, and sex. RESULTS: Forearm muscle CSA was associated with cortical and total metacarpal CSA and polar SSI. RA group status was associated with all bone parameters except cortical CSA. There was a significant interaction between RA status and age, indicating that the RA group had a greater age-related decrease in cortical CSA, cortical thickness, and the MI. CONCLUSION: Bone geometry of the metacarpal shaft is altered in RA patients compared to healthy controls. Whereas bone mass of the metacarpal shaft is adapted to forearm muscle mass, cortical thickness and the MI are reduced, but outer bone shaft circumference and the polar SSI increased in RA patients. These adaptations correspond to an enhanced aging pattern in RA patients. | |
19443940 | IL-1beta, IL-6, and TNF gene polymorphisms do not affect the treatment outcome of rheumato | 2009 Mar | Leflunomide is an isoxazole derivative that is structurally and functionally unrelated to other known immunomodulatory drugs. Previous studies have revealed that therapy with leflunomide causes decreased production of mediators such as IL-1beta, IL-6, and TNF-alpha, which are involved in inflammatory process. The aim of the present study was to examine whether the polymorphisms in genes IL1B, IL6, and TNF may affect treatment outcomes in RA patients treated with leflunomide. The study was carried out on 129 patients (106 women, 23 men, mean age 52.9 +/- 11.03) diagnosed with RA and treated with leflunomide 20 mg daily. Clinical improvement was evaluated according to the American College of Rheumatology (ACR) 20% and 50% response criteria. There were no statistically significant associations between the studied genotypes and improvement of disease activity parameters. The results of the present study suggest that IL1beta, IL6, and TNF gene polymorphisms are not significant factors influencing the therapy outcome of RA patients with leflunomide. | |
19847427 | Development of antisynthetase syndrome in a patient with rheumatoid arthritis. | 2011 Apr | Rheumatoid arthritis (RA) and antisynthetase syndrome (ASS) are distinct clinical syndromes, and their co-occurrence is rarely encountered. The authors report the case of a 56-year-old female patient with RA of 3 years duration who suddenly developed ASS, and include a review of the literature. The patient was diagnosed with ASS based on; positivity for anti-histidyl-tRNA synthetase (Jo-1) antibody, interstitial lung disease, polyarthritis, and mechanic's hands. High-dose corticosteroid and pulse intravenous cyclophosphamide were used to control the ASS. This case demonstrates that ASS should be considered during clinical presentations due to its potential overlap with RA. | |
19504146 | Persistent low grade synovitis without erosive progression in magnetic resonance imaging o | 2009 Oct | Disease remission is only reached by a minority of rheumatoid arthritis (RA) patients treated with infliximab. Radiological assessment reported in clinical trials support the view that even under persistent inflammatory activity there is no further structural damage. Magnetic resonance imaging (MRI) allows a highly accurate detection of synovitis, bone edema, and erosions, constituting the ideal instrument for the evaluation of treatment response. The goal of this study was to evaluate MRI changes over 1 year in RA patients treated with infliximab. Four RA patients refractory to methotrexate (MTX) therapy were treated with infliximab 3 mg/kg 8/8 weeks and followed up for 1 year. Disease Activity Score (DAS28) was measured in the day of each infliximab administration. MRI was performed at baseline, 3 months, and 1 year. A simplified OMERACT RA MRI scoring (RAMRIS) was applied to the dominant wrist: synovitis (0-3) was measured in the intercarpal-carpometacarpal joints (CMTJ); bone edema (0-39) and erosions (0-130) in the base of the metacarpal and wrist bones. Baseline DAS28 was superior to 3.2 in all patients (ranging from 4.8 up to 6.2). At 14 weeks, DAS28 was still superior to 3.2 (ranging from 3.5 up to 4.6) and at 46 weeks all patients have responded, however without having achieved clinical remission, as DAS28 was still above 2.6 (ranging from 2.6 up to 3.4). MRI showed that synovitis was reduced in all patients to a score of 1, bone edema was slightly reduced (10% reduction), and erosive score was unchanged (baseline values ranging from 2 up to 20). Despite persistent low disease activity, these four RA patients treated with infliximab had stable simplified RAMRIS erosive scores over 1 year. These results support the view that there might be an uncoupling process between inflammation and bone erosions when tumor necrosis factor alpha is targeted in RA. | |
19918035 | Agreement between Quantiferon-TB gold test and tuberculin skin test in the identification | 2009 Dec | OBJECTIVE: To compare the Quantiferon-TB Gold test (QTF-G) with the tuberculin skin test (TST) for the detection of latent tuberculosis infection (LTBI) among patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS), with reevaluation of the patients treated with tumor necrosis factor-alpha (TNF-alpha) antagonists in the followup. METHODS: The study involved 140 consecutive patients, 82 with RA and 58 with AS. Thirty patients were evaluated with QTF-G for detection of LTBI before and after 6 months of TNF-alpha antagonist treatment. QTF-G was also performed on 49 healthy controls. QTF-G results were recorded as positive, negative, or indeterminate. A positive TST was defined as >or= 5 mm for RA and AS. RESULTS: The percentages of positive QTF-G were comparable in RA and AS (37% vs 32%). The rate of positive QTF-G in healthy controls (29%) was also similar to RA and AS. In contrast to QTF-G results, a high rate of TST positivity was observed in AS compared to RA (82% vs 55%; p = 0.02). The total agreement between QTF-G and TST was observed to be 61% (kappa = 0.29) in the whole group, 70% (kappa = 0.42) in RA, and 49% (kappa = 0.14) in AS. After 6 months of treatment with TNF-alpha antagonists, a high rate of QTF-G change was observed in patients with indeterminate results (23% vs 3%; p = 0.03). CONCLUSION: The comparable prevalence of LTBI among the study groups according to QTF-G supports the view that QTF-G is less susceptible to external factors than TST. Sequential testing for QTF-G in patients with indeterminate or negative results may also be helpful in discriminating LTBI better. | |
19798028 | Promising bone-related therapeutic targets for rheumatoid arthritis. | 2009 Oct | Rheumatoid arthritis (RA) is a chronic, debilitating autoimmune disease that results in inflammation and structural destruction of the joints. A hallmark of RA pathogenesis is an imbalance of the osteoblast-osteoclast axis driven by inflammatory processes, resulting in elevated bone resorption by osteoclasts. Current therapies used to treat this disease have focused on inhibition of synovitis, but such treatments do not adequately repair damaged bone. A key pathway of osteoclast formation involves the receptor activator of nuclear factor kappaB ligand (RANKL) pathway acting on myeloid progenitor cells. The Wnt pathway has been shown to be important for the differentiation of osteoblasts from mesenchymal lineage precursors, and endogenous Wnt inhibitors, such as Dickkopf1 and sclerostin, might have important roles in osteoclast dysregulation in RA. Inhibition of the RANKL pathway, or blockade of Dickkopf1 and sclerostin, might serve to restore the osteoblast-osteoclast balance and repair bone erosion in RA joints. Such treatments, in combination with anti-inflammatory therapies, could stabilize and repair damaged joints and have the potential to be valuable additions to the armory of RA treatments. | |
20120782 | Role of omega-3 fatty acid supplementation with indomethacin in suppression of disease act | 2009 Aug | A study was conducted to see the disease activity suppression role of omega-3 fatty acids with indomethacin in patients with rheumatoid arthritis. One group received indomethacin (75 mg) only daily while another group received indomethacin (75 mg) along with omega-3 fatty acids (3 g) daily for 12 weeks. The main outcome measures were DAS 2-28 joints score, number of swollen joints, number of tender joints, duration of morning stiffness, grip strength, pain VAS, patients global VAS, erythrocyte sedimentation rate and C-reactive protein. In terms of outcome both the groups experienced a modest improvement in disease activity after 12 weeks of treatment. However, compared to indomethacin-treated group, omega-3 plus indomethacin-treated group achieved a better improvement in terms of reducing disease activity. Physical functioning, physical role, bodily pain, general health, vitality, social functioning, grip strength, duration of morning stiffness improved significantly better in the combination group compared to indomethacin only group. The safety measures included liver and kidney function tests done didn't differ between the study groups. This study suggests that omega-3 fatty acid supplementation with indomethacin might ameliorate disease activity and be non-steroidal anti-inflammatory drugs (NSAIDs) sparing in rheumatoid arthritis. | |
20173532 | Rheumatoid arthritis of the craniovertebral junction. | 2010 Mar | BACKGROUND: Rheumatoid arthritis (RA) is the most common inflammatory disease involving the spine. It has a predilection for involving the craniocervical spine. Despite widespread involvement of the cervical spine with RA, few patients need surgery. The 3 major spinal manifestations of RA in the cervical spine are basilar invagination, atlantoaxial instability, and subaxial subluxations. Surgical management of RA involving the craniovertebral junction remains a challenge despite a decline in severe cases and an improvement in surgical techniques. METHODS: We conducted an exhaustive review of English-language publications discussing RA involving the craniovertebral junction. We paid special attention to publications detailing modern surgical management of these conditions. In addition, we outline our own surgical experience with such patients. RESULTS: We discuss alternative surgical methods for treating basilar invagination, atlantoaxial instability, and concurrent subaxial subluxations. We detail our surgical technique for transoral odontoidectomy, occipital cervical fusion, and atlantoaxial fusion. We detail the use of spinal surgical navigation in both of these procedures. CONCLUSION: Surgical management of RA remains a challenging field. There clearly has been a decrease in cases of mutilating RA involving the craniovertebral junction. Surgical techniques for managing these conditions have steadily improved. | |
21190566 | Matrix metalloproteinase-8 deficiency increases joint inflammation and bone erosion in the | 2010 | INTRODUCTION: Rheumatoid arthritis is an autoimmune disease in which joint inflammation leads to progressive cartilage and bone erosion. Matrix metalloproteinases (MMPs) implicated in homeostasis of the extracellular matrix play a central role in cartilage degradation. However, the role of specific MMPs in arthritis pathogenesis is largely unknown. The aim of the present study was to investigate the role of Mmp-8 (collagenase-2) in an arthritis model. METHODS: Arthritis was induced in Mmp8-deficient and wildtype mice by K/BxN serum transfer. Arthritis severity was measured by a clinical index and ankle sections were scored for synovial inflammation, cartilage damage and bone erosion. cDNA microarray analysis, real-time PCR and western blot were performed to identify differential changes in gene expression between mice lacking Mmp8 and controls. RESULTS: Mmp8 deficiency increased the severity of arthritis, although the incidence of disease was similar in control and deficient mice. Increased clinical score was associated with exacerbated synovial inflammation and bone erosion. We also found that the absence of Mmp8 led to increased expression of IL-1β, pentraxin-3 (PTX3) and prokineticin receptor 2 (PROKR2) in arthritic mice joints. CONCLUSIONS: Lack of Mmp-8 is accompanied by exacerbated synovial inflammation and bone erosion in the K/BxN serum-transfer arthritis model, indicating that this Mmp has a protective role in arthritis. | |
19393212 | Autonomic dysfunction in autoimmune rheumatic disease. | 2009 Jun | Cardiovascular and neurological manifestations are known to occur in patients with autoimmune rheumatic disease (ARD), often in subclinical form. The term autonomic nervous system (ANS) describes nerves that are concerned predominantly with the regulation of bodily functions. It is comprised of sympathetic and parasympathetic nerves, and their function is complementary. ANS involvement has rarely been studied in patients with ARD, and studies have shown conflicting results. This may be because symptoms of autonomic dysfunction are nonspecific and extremely varied, and may pertain to several systems like the gastrointestinal, cardiovascular, and nervous. Moreover, tests to detect autonomic dysfunction are not routinely employed in clinical rheumatological practice. Another difficulty is to differentiate cardiovascular effects of drugs from ARD involvement. Previous studies on this topic found signs of parasympathetic and sympathetic dysfunction in variable proportions in patients with autoimmune diseases, between 24% and 100% in various tests depending on the methods used. Cardiovascular autonomic dysfunction is the most common type of ANS dysfunction, and was revealed in the majority of ARD patients. | |
19648126 | Prediction of radiographic progression in rheumatoid arthritis and the role of antibodies | 2010 Feb | OBJECTIVES: Anti-citrullinated peptide antibodies (ACPAs) are established as useful predictors of radiographic progression in rheumatoid arthritis (RA). The main objective of this study was to test the prognostic capacity of the recently developed test for anti-mutated citrullinated vimentin (anti-MCV). METHODS: A cohort of 238 patients with RA was followed longitudinally for 10 years; 125 patients with complete x ray sets were included in the main analyses. Radiographs were scored according to the van der Heijde modified Sharp score (SHS). Patients were analysed for anti-MCV and anti-cyclic citrullinated peptide (CCP), and were genotyped for human leukocyte antigen (HLA)-DRB1 "shared epitope" (SE) and protein tyrosine phosphatase, non-receptor type 22 (PTPN22) 1858T. RESULTS: Anti-MCV and anti-CCP were strongly associated with regard to status and level. Both antibodies were associated with SE, but only anti-MCV was significantly associated with PTPN22 1858T. A positive anti-MCV test increased the odds of radiographic progression by 7.3 (95% confidence interval (CI) 3.2 to 16.5) compared to 5.7 (95% CI 2.6 to 12.5) for a positive anti-CCP. Presence of MCV antibodies gave an average increase in the total SHS of 30 U compared to an average increase of 25 U for the presence of CCP antibodies. Anti-MCVs were more strongly associated to progression in erosions than joint space narrowing. Associations remained after adjustment for other predictors of radiographic progression. The odds of progression increased with increasing anti-MCV level. CONCLUSIONS: Presence of anti-MCV predicted joint damage, and the strength of this prediction was at least as strong as for anti-CCP. Antibody status showed a stronger association to bone than to cartilage destruction. This study also indicates that higher anti-MCV levels add prognostic information compared to their mere presence or absence. | |
20637236 | Sex hormones and autoimmunity. | 2010 Sep 6 | Autoimmune diseases occur more in women than in men, and this may be attributable to the role of estrogens. Androgens promote autoimmune diseases with a profile of type 1 cytokines, such as rheumatoid arthritis, whereas estrogens promote autoimmune diseases with a type 2 cytokine profile, like systemic lupus erythematosus. Both androgens and estrogens regulate the Th1/Th2 balance. Type 1 autoimmune diseases are improved when decrease type 1 cytokines (i.e. during fasting), or when there is a rise in type 2 cytokines (increased estrogens, as in pregnancy). Type 2 autoimmune diseases improve when type 2 cytokines are diminished (decreased estrogen, as in post-partum period) or when type 1 response is stimulated. | |
19160248 | Anakinra for rheumatoid arthritis. | 2009 Jan 21 | BACKGROUND: In the past decade, a novel class of therapies directed against specific cytokines implicated in the disease process of rheumatoid arthritis (RA), called the 'Biologics' have greatly improved and expanded treatment for RA. Anakinra is an interleukin-1 receptor antagonist that is currently FDA-approved for moderate-severe RA that has been unresponsive to initial disease-modifying anti-rheumatic drugs (DMARD) therapy. OBJECTIVES: To evaluate the clinical effectiveness and safety of anakinra in adult patients with rheumatoid arthritis. SEARCH STRATEGY: We searched the following electronic databases: the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 1, 2008), MEDLINE (1950 to Week 4 2008) , EMBASE (1980 to Week 5 2008), CINAHL (1982 to November 2007) and reference lists of articles. SELECTION CRITERIA: Randomized controlled trials comparing anakinra alone or in combination with DMARDs or biologics to placebo or other DMARDs or biologics in patients >18 years old with rheumatoid arthritis. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trial quality and extracted data. We contacted study authors for additional information. MAIN RESULTS: Five trials involving 2876 patients, 781 randomized to placebo and 2065 to anakinra, were included. There was a significant improvement in number of participants achieving ACR20 (38% versus 23%) who were treated with anakinra 50 to 150 mg daily versus placebo after 24 weeks. This 15% increase in patients achieving ACR20 with anakinra versus placebo is felt to be a clinically meaningful, though modest, outcome. Other efficacy data - including ACR50 (18% versus 7%), ACR70 (7% versus 2%), HAQ, visual analog score (VAS), Larsen radiographic scores, and change in erythrocyte sedimentation rate (ESR) - all demonstrated significant improvement with anakinra 50 to 150 mg daily versus placebo as well. There were no statistically significant differences noted in most safety outcomes with treatment with anakinra versus placebo - including number of withdrawals, deaths, adverse events (total and serious), and infections (total and serious). Injection site reactions were significantly increased, occurring in 1235/1729 (71%) versus 204/729 (28%) of patients treated with anakinra versus placebo, respectively. The incidence of serious infections was clinically higher, but not statistically different, in the anakinra (25/1366 patients, 1.8%) versus placebo group (3/534 patients, 0.6%). AUTHORS' CONCLUSIONS: Anakinra is a relatively safe and modestly efficacious biologic therapy for rheumatoid arthritis. Although head to head comparison trials have not been carried out, the amount of improvement is notably less when compared to studies using other biologic therapies. More studies are needed to evaluate safety and efficacy, especially in comparison to other therapies, and adverse event data for the long-term use of Anakinra has yet to be assessed. | |
20307272 | Interferon-gamma inhibits interleukin-1beta-induced matrix metalloproteinase production by | 2010 | INTRODUCTION: The first few months after symptom onset represents a pathologically distinct phase in rheumatoid arthritis (RA). We used relevant experimental models to define the pathological role of interferon-gamma (IFN-gamma) during early inflammatory arthritis. METHODS: We studied IFN-gamma's capacity to modulate interleukin-1beta (IL-1beta) induced degenerative responses using RA fibroblast-like synoviocytes (FLS), a bovine articular cartilage explant (BACE)/RA-FLS co-culture model and an experimental inflammatory arthritis model (murine antigen-induced arthritis (AIA)). RESULTS: IFN-gamma modulated IL-1beta driven matrix metalloproteinases (MMP) synthesis resulting in the down-regulation of MMP-1 and MMP-3 production in vitro. IFN-gamma did not affect IL-1beta induced tissue inhibitor of metalloproteinase-1 (TIMP-1) production by RA FLS but skewed the MMP/TIMP-1 balance sufficiently to attenuate glycosaminoglycan-depletion in our BACE model. IFN-gamma reduced IL-1beta expression in the arthritic joint and prevented cartilage degeneration on Day 3 of AIA. CONCLUSIONS: Early therapeutic intervention with IFN-gamma may be critical to orchestrate tissue-protective responses during inflammatory arthritis. | |
19393204 | B-cell depletion in autoimmune diseases. Advances in autoimmunity. | 2009 Jun | B cells play an important role in the pathogenesis of the autoimmune diseases. New advances in biological therapy provided a correct way in the management of these pathologies. Depletion of B cells with monoclonal antibodies reach an important place in the control of the diseases. I will present our experience with rituximab in the treatment of 131 patients with different autoimmune conditions, and conclude that this kind of therapy is safe, effective and constitutes a big step in the control of the majority of patients in which humoral response were aberrant. It is one of the many avenues that will allow to have a better future in the assessment and treatment of autoimmune diseases. | |
20132064 | Autologous stem cell transplantation in autoimmune and rheumatic diseases: from the molecu | 2010 | Autoimmune diseases have a multifactorial origin. Because of disturbances of the immune system, autoreactive T and B cells target self-antigens, leading to permanent organ damage. Despite novel therapeutic protocols, the disease course is chronic and in many instances the outcome is lethal. The efficacy of stem cell therapy has been observed in autoimmune animal models and in autoimmune diseases related to haematological abnormalities. Although the therapy is more than 30 years old, its broad spread has been delayed by the serious side-effects due to the conditioning treatments based on oncological protocols. Evaluation of the data of patients who have undergone autologous stem cell therapy reinforced the view that protocols used for conditioning treatments, mostly causing lymphoablation, and procedures carried out in specialist centres significantly reduced mortality, with an almost optimal therapeutical efficacy. New, multicentre investigations have been launched to compare the efficacy of various protocols. In this review, we summarize certain aspects of the molecular background of autologous stem cell transplantation and also depict the response to therapy in various autoimmune and rheumatic diseases. | |
19132793 | Rheumatoid atlantoaxial subluxation can be prevented by intensive use of traditional disea | 2009 Feb | OBJECTIVE: To evaluate the 5-year incidence of cervical spine disorders in patients with early rheumatoid arthritis (RA) treated by 2 different disease modifying antirheumatic drug (DMARD) strategies. METHODS: In a national, multicenter, prospective FIN-RACo-trial, a cohort of 199 patients with early, clinically active RA was randomly assigned to treatment with a combination of 3 DMARD and prednisolone (Combi group) or with a single DMARD (Single group) with or without prednisolone, aiming to induce remission. After 2 years, the DMARD therapy was unrestricted. Lateral view cervical spine radiographs during full flexion and extension were taken at the 5-year followup visits. The presence of anterior atlantoaxial subluxation (aAAS), atlantoaxial impaction (AAI), and subaxial subluxation (SAS) was assessed in the 149 patients with radiographs available (80 Single and 69 Combi). RESULTS: At the 5-year visits, aAAS, AAI, and SAS were found in 13 (9%), 6 (4%), and 9 (6%) patients, respectively. The corresponding Single/Combi group ratios were 11/2, 5/1, and 5/4. Of the baseline data, only poor physical function [Health Assessment Questionnaire (HAQ); p = 0.024] and Single treatment strategy (p = 0.019) were significantly associated with aAAS. Worse HAQ scores and Disease Activity Score 28 values were found in patients who developed aAAS during the 5-year followup. CONCLUSION: RA patients with sustained clinical disease activity and poor HAQ are at increased risk of developing aAAS. The development of aAAS during the first 5 years of RA was rare among the patients treated with a combination of DMARD for at least 2 years from the diagnosis. Intensive treatment with traditional DMARD prevents or retards the development of aAAS in patients with recent-onset RA. | |
19887889 | Group psychotherapy of dysfunctional fear of progression in patients with chronic arthriti | 2010 | BACKGROUND: This study investigated the effectiveness of brief psychotherapeutic group interventions in reducing dysfunctional fear of disease progression (FoP). The interventions comprised either cognitive-behavioral group therapy or supportive-experiential group therapy. We tested whether these generic interventions would prove effective in different illness types. METHODS: Chronic arthritis in- patients (n = 174) and cancer in-patients (n = 174), respectively, were randomized to receive one of the two interventions. The patients provided data before intervention, at discharge, and at 3 and 12 months of follow-up. FoP was the primary outcome, secondary outcomes were anxiety, depression and quality of life. A treatment-as-usual control group provided data on the primary outcome. RESULTS: Patients with chronic arthritis indicated higher levels of FoP than cancer patients. The results revealed that, compared with no specialized intervention, both group therapies were effective in reducing dysfunctional FoP, but only among cancer patients. The effect sizes were 0.54 (cognitive-behavioral therapy) and 0.50 (supportive experiential therapy). The interventions were not differently effective in reducing the secondary outcomes. CONCLUSIONS: Dysfunctional FoP can be effectively targeted with brief group interventions. Psychotherapeutic interventions for reducing FoP should focus on specific illness characteristics. | |
20969545 | T-cell agents in the treatment of rheumatoid arthritis. | 2010 | T cells play a prominent role in the pathogenesis of rheumatoid arthritis. Abatacept is the first FDA approved agent for rheumatoid arthritis that blocks the activation of T cells by interrupting the interaction between the CD28 ligand on the T cell and the CD80/86 ligand on the antigen presenting cell. Inhibition of T cell activation has pleotropic effects that lowers the downstream production of multiple cytokines. In clinical trials, abatacept is effective in treating the signs and symptoms of rheumatoid arthritis as well as in inhibiting structural damage. It has a favorable safety profile and can be used in patients who may have comorbidities that preclude the use of anti-TNF agents. While no direct head to head trials exist, a study in which both abatacept and infiximab were compared to an identical control population, suggested that the efficacy of the two drugs was similar but that there were fewer adverse effects with abatacept than with infiximab. Abatacept is an important addition to the therapeutic repertoire available to treat rheumatoid arthritis. Available data support its use as a first line agent to treat patients who have had and inadequate response to methotrexate. |