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Homeopathic dilutions of TNF-alfa in psoriasis and rheumatoid arthritis  [cached]
Adrian Alecu,Dumitru Gafitanu,Mariana Alecu,Diana Popa
International Journal of High Dilution Research , 2012,
Abstract: Aim: Clinical and biological studies in the past years underlined the proinflammatory action of the citokine Tumoral Necrosis Factor in the pathophysiolology of psoriasis, psoriatic arthritis, rheumatoid arthritis. Knowing that the high dilution of substances can have an inverted effect, our hypotesis was that dillution made of TNF-alfa can decrease the clinical manifestation of such diseases. Materials and method: We included as a pilot group 10 patients presented in Lotus Life Integrative Medicine Center or Profamilia Medical Center Iasi with psoriasis and rheumatoid arthritis previously diagnosed by specialists, under speciality treatment with insufficient results and patients who deliberately expressed their preference for alternative treatment. We decided to exclude the patients which during the study could present aggravation of symptoms. The treatment protocol consisted in the administration under the tongue of the dilution of TNF-alfa 9CH in liquid form, 12 drops twice a day for at least 3 months. This was prepared diluting from Guna TNF-alfa 4CH in distiled water, completing with 30% of alcohol in the last solution. Patients under other medications continued to take their previous treatment unchanged. We called the patients for follow-up after 3 months. We took the written consent from the patients and the approval of the Ethical Committee of the University of Medicine and Pharmacy "Gr. T. Popa" of Iasi. Results: To analize the results we followed the subjective evolution of the patients, the total surface and thickness of eruptions in psoriasis patients and the pain intensity and stiffness in arthritis patients. Under this conditions, all the patients showed amelioration, with 2 out of 6 psoriasis patients showing complete clearance of eruptions. No patient reported adverse reactions during the treatment Conclusions: Even though the group of patients was small and not appropriate for statistical data the presence of a clinical response in all the patients and the absence of adverse reactions sustains the opportunity to extend the research on this subject.
Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide The influence of -238 and -308 TNF alpha polymorphisms on the pathogenesis and response to treatment in rheumatoid arthritis  [cached]
Carolina Llanos M,Lilian Soto S,Francisca Sabugo S,M José Bastías Ch
Revista médica de Chile , 2005,
Abstract: Rheumatoid arthritis (RA) is a systemic autoimmune disease that affects 0.8% of the world population, it affects the synovial membrane of joints and the clinical presentation encompasses a wide spectrum, ranging from a mild to a severe and erosive disease that causes joint and cartilage destruction which finally provokes irreversible structural damage and patient disability. In the last years, there have been important advances in the pathogenesis of this disease, the efforts have been concentrated on pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha). This protein guides numerous events in the synovial and systemic inflammatory process and is encoded in the Major Histocompability Complex (MHC), one of the most polymorphic of the genome. Polymorphisms affecting the TNFalpha gene and its regulatory regions are associated with RA prevalence and course. There is a possible association between these polymorphisms and the clinical response to the use of monoclonal antibodies anti-TNFalpha. The possibility that the determination of genotypes -238 and -308 may have prognostic and therapeutic consequences is debated nowadays (Rev Méd Chile 2005; 133: 1089-95).
Tumor necrosis factor antagonists: structure, function and tuberculosis risks
Jacyr Pasternak
Einstein (S?o Paulo) , 2009,
Abstract: New therapeutic options bring new problems and also new knowledge about disease mechanisms. Ten years ago the first antagonist to tumor necrosis factor was first used to treat inflammatory diseases and the use of anti-cytokines has proved to be a revolution in therapeutics. The natural history of rheumatoid arthritis, psoriasis, ankilosing spondilitis and juvenile rheumatoid arthritis changed after those products were introduced in therapy. Today, there are three different antitumor necrosis factor antibodies and one antibody antitumor necrosis factor receptor. All of them increase the risk of tuberculosis, but there is a clear difference between them: the risk for inflaximab is 12 times the risk for etanercept. One of the receptors for tumor necrosis factor, TNFR1 is essential to activate macrophages, and probably this is the place in which antitumor necrosis factor monoclonal antibodies do interfere with defense against tuberculosis.
Influence of tumor necrosis factor α in rheumatoid arthritis  [cached]
Kulp, Werner,Corzillus, Michael,Greiner, Wolfgang,Pientka, Ludger
GMS Health Technology Assessment , 2005,
Abstract: Objective: Rheumatoid arthritis (RA) is the most prevalent inflammatory rheumatic disorder. It is a chronic and incurable disease that leads to painful inflammation, often irreversible joint damage, and eventually to functional loss. Conventional treatment is based on unspecific immunosuppressive agents, e.g. Methotrexate, Azathioprin or Gold. However, the longterm outcomes of these approaches have been poor with frequently ongoing inflammatory disease activity, functional decline, and temporary or permanent work disability. More recently, antagonists of the human cytokine Tumor Necrosis Factor α (TNF-α) have been introduced that are potent suppressors of inflammatory processes. Infliximab is a chimeric antibody against TNF-α. Etanercept is a soluble human TNF-α receptor. The report assesses the efficacy of TNF-α-antagonists to down-regulate inflammation, improve functional status and prevent joint damage in RA with particular regard to the following indications: Treatment of severe, refractory and ongoing disease activity despite adequate use of conventional antirheumatic agents; and treatment of early RA before conventional treatment failure has been demonstrated. Methods: A systematic review of the literature is been performed using established electronic databases. The literature search is supplemented by a hand search of journals and publications relevant to RA, reviews of websites of national and international rheumatologic expert societies, as well as contacts to manufacturers. A priori defined inclusion and exclusion criteria are used for literature selection. Analysis and evaluation of included publications are based on standardised criteria sets and checklists of the German Scientific Working Group for Technology Assessment in Health Care. Results: Health Technology Assessment reports and metaanalyses cannot be identified. A total of 12 clinical trials are analysed, as well as national and international expert recommendations and practice guidelines. Numerous non-systematic reviews are found and analysed for additional sources of information that is not identified through the systematic search. Case reports and safety assessements are considered as well. A total of 137 publications is included. The primary outcome measures in clinical trials are suppression of inflammatory disease activity and slowing of structural joint damage. Clinical response is usually measured by standardised response criteria that allow a semi-quantitative classification of improvement from baseline by 20%, 50%, or 70%. In patients with RA refractory to conventional trea
HBV Reactivation in Patients Treated with Antitumor Necrosis Factor-Alpha (TNF-α) Agents for Rheumatic and Dermatologic Conditions: A Systematic Review and Meta-Analysis  [PDF]
Fabrizio Cantini,Stefania Boccia,Delia Goletti,Florenzo Iannone,Emanuele Leoncini,Nikola Panic,Francesca Prignano,Giovanni Battista Gaeta
International Journal of Rheumatology , 2014, DOI: 10.1155/2014/926836
Abstract: Introduction. Antitumor necrosis factor-alpha (TNF-α) agents are widely used for treatment of rheumatic and dermatological diseases. We conducted the systematic review and meta-analysis to assess the prevalence of HBV reactivation among patients treated with anti-TNF-α. Methods and Findings. A comprehensive literature search of MEDLINE, Scopus, and ISI Web of Knowledge databases was conducted. From 21 studies included in the systematic review, 9 included patients with occult chronic HBV infection and 6 included patients with overt infection while 6 addressed both groups. Based on 10 studies eligible for meta-analysis we report pooled estimate of HBV reactivation of 4.2% (95% CI: 1.4–8.2%, : 74.7%). The pooled prevalence of reactivation was 3.0% (95% CI: 0.6–7.2, : 77.1%) for patients with occult infection, and 15.4% (95% CI: 1.2–41.2%, : 79.9%) for overt infection. The prevalence of reactivation was 3.9% (95% CI: 1.1–8.4%, : 51.1%) for treatment with etanercept and 4.6% (95% CI: 0.5–12.5%, : 28.7%) for adalimumab. For subgroup of patients without any antiviral prophylaxis the pooled reactivation was 4.0% (95% CI: 1.2–8.3%, : 75.6%). Conclusion. Although HBV reactivation rate is relatively low in patients treated with anti-TNF-α for rheumatic and dermatological conditions, the antiviral prophylaxis would be recommended in patients with overt chronic HBV infection. 1. Introduction Antitumor necrosis factor-alpha (TNF-α) agents are widely used for effective treatment of autoimmune rheumatic and dermatological diseases such as rheumatoid arthritis (RA), ankylosing spondylitis (SA), psoriasis (Ps), or psoriatic arthritis (PsA). Nevertheless, anti-TNF-α agents have been associated with growing number of adverse events, particularly infections [1, 2] of which some can be life threatening. TNF-α is an important proinflammatory cytokine in the host defense mechanism against many intracellular pathogens. It suppresses hepatitis B virus (HBV) replication and promotes HBV eradication by stimulating HBV-specific cytotoxic T-cell response [3–5]. It has been reported that reactivation of HBV infection may occur directly due to lack of TNF-α or indirectly via diminishing T-cell activation [6, 7]. TNF-α inhibitors are therefore likely to induce HBV replication and reactivation in cases when chronic infection is present. HBV is regarded as a leading cause of acute hepatitis, cirrhosis, and hepatocellular carcinoma [8], being responsible for about 600000 deaths every year [8]. Chronic HBV infection is defined as an overt when hepatitis B surface antigen (HBsAg) is
Upregulation of tumor necrosis factor receptor-associated factor 6 correlated with synovitis severity in rheumatoid arthritis
Lang-Jing Zhu, Lie Dai, Dong-Hui Zheng, Ying-Qian Mo, Xia Ou-Yang, Xiu-Ning Wei, Jun Shen, Bai-Yu Zhang
Arthritis Research & Therapy , 2012, DOI: 10.1186/ar3866
Abstract: Synovitis score was determined in needle biopsied synovium from 44 patients with active RA. Synovium from nine patients with osteoarthritis (OA) and seven with orthopedic arthropathies (Orth.A) were enrolled as "less inflamed" disease controls. Serial sections were stained immunohistochemically for TRAF6 as well as CD68 (macrophage), CD3 (T cell), CD20 (B cell), CD38 (plasmocyte), CD79a (B lineage cells from pre-B cell to plasmocyte stage), and CD34 (endothelial cell). Double immunofluorescence staining of TRAF6 and CD68 were tested. Densities of positive staining cells were determined and correlated with histological disease activity (synovitis score) and radiographic joint destruction (Sharp score).TRAF6 expression was found in the intimal and subintimal area of RA synovium, with intense staining found in the endochylema and nucleus of intimal synoviocytes and subintimal inflammatory cells. Double immunofluorescence staining showed TRAF6 was expressed in most of the intimal cells and obviously expressed in CD68+ cells and some other CD68- cells in subintimal area. Synovial TRAF6 was significantly over-expressed in the RA group compared with the OA and Orth.A group (2.53 ± 0.94 vs. 0.72 ± 0.44 and 0.71 ± 0.49, P < 0.0001). Synovial TRAF6 expression in RA correlated significantly with synovitis score (r = 0.412, P = 0.006), as well as the inflammatory cell infiltration (r = 0.367, P = 0.014). Significant correlation was detected between synovial TRAF6 expression and intimal CD68+ cells, as well as the cell density of subintimal CD68+ cells, CD3+ cells, CD20+ cells, CD38+ cells, and CD79a+ cells (all P < 0.05).Elevated synovial TRAF6 expression correlated with synovitis severity and CD68+ cell density in RA. It is, therefore, hypothesized that synovial TRAF6 is involved in the pathogenesis of synovial inflammation and osteoclast differentiation in RA.Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by chronic in?ammatory synovitis, leading to i
Total Knee Arthroplasty Considerations in Rheumatoid Arthritis  [PDF]
Jonathan R. Danoff,Garrett Moss,Barthelemy Liabaud,Jeffrey A. Geller
Autoimmune Diseases , 2013, DOI: 10.1155/2013/185340
Abstract: The definitive treatment for advanced joint destruction in the late stages of rheumatoid arthritis can be successfully treated with total joint arthroplasty. Total knee arthroplasty has been shown to be a well-proven modality that can provide pain relief and restoration of mobility for those with debilitating knee arthritis. It is important for rheumatologists and orthopedic surgeons alike to share an understanding of the special considerations that must be addressed in this unique population of patients to ensure success in the immediate perioperative and postoperative periods including specific modalities to maximize success. 1. Introduction Over the past thirty years, major advances have been realized in the understanding of the pathogenesis and treatment of rheumatoid arthritis (RA). As an immune mediated process, all joints are affected, as synovitis leads to destruction of cartilage, which may ultimately result in bone loss and joint deformity. Joint contractures, fixed flexion and valgus deformities, and ligamentous laxity are especially evident in large joints, complicating treatments. With the advent of highly effective biologic therapies, fewer individuals with rheumatoid arthritis suffer this end-stage joint destruction [1]. Despite this success, approximately 20–25% of afflicted individuals develop advanced arthritis in their joints, with the knee being one of the most commonly affected joints contributing to patient pain and overall disability [2, 3]. Total knee arthroplasty (TKA) has proven to be a highly successful treatment for advanced rheumatoid arthritis. The orthopedic surgeon must pay special attention to the unique challenges presented by this population of patients during preoperative, intraoperative, and postoperative planning in order to maximize successful outcome and quality of life for these patients. 2. Preoperative Considerations Rheumatoid arthritis is a systemic disease, which creates a unique set of challenges and considerations when treating patients afflicted with this disease. Care is often delivered by a variety of specialty physicians, including rheumatologists and orthopedic surgeons. Preoperative communication is vital among these providers to maximize outcomes. Surgeons and anesthesiologists alike must be aware of the increased risk to the cervical spine as 80% of patients have atlantoaxial instability [4]. The cervical spine also is at elevated risk of basilar invagination and subaxial instability, and thus preoperative radiographic investigation via flexion and extension images should be obtained, as intubation
Tumour necrosis factor-α, interleukin-2 soluble receptor and different inflammatory parameters in patients with rheumatoid arthritis  [PDF]
Tania Silvia Fr de,Patrícia Tenconi,Marilei Reynaud Debiasi,Yara Santos Medeiros
Mediators of Inflammation , 2002, DOI: 10.1080/0962935021000051539
Abstract: Background and aims: Although the participation of cytokines in the pathogenesis of rheumatoid arthritis (RA) seems to be unequivocal, their relationship with current serum markers of this disease is not clear. The present study analyses whether there is any correlation between the levels of tumour necrosis factor-α (TNF-α), interlukin-2 soluble receptor (sIL-2R) and the concentrations of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and β2-microglobulin in a group of 21 patients with RA, all rheumatoid factor positive.
Anti-tumour necrosis factor therapy and B cells in rheumatoid arthritis
Maria J Leandro
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2809
Abstract: Both blocking tumour necrosis factor (TNF) and depleting B cells are effective therapeutic strategies in rheumatoid arthritis (RA). Recently, some articles have focused on possible effects of anti-TNF agents on B cells, exploring whether this could contribute to the efficacy of these agents in the treatment of RA. In a study published in a recent issue of Arthritis Research & Therapy, Souto-Carneiro and colleagues [1] described a decrease in circulating pre-switch IgD+CD27+ memory B cells in patients with RA when compared with normal controls. Patients with longer disease duration had increased frequency of post-switch IgD-CD27+ memory B cells when compared with patients with shorter disease duration or normal controls. Treatment with infliximab was associated with an increase in the frequency of total and pre-switch memory B cells whereas no significant changes were seen in patients treated with only methotrexate.All B cells express CD19. Naive B cells exit the bone marrow at a transitional stage, already expressing both IgM and IgD but expressing higher levels of CD38 and CD24 than naive mature B cells and still expressing low levels of CD10 [2]. CD27 is a marker of somatic mutation and therefore of memory B cells [3]. Memory B cells are frequently subdivided into pre-switch memory B cells, expressing IgD and IgM, and post-switch memory B cells, no longer expressing IgD and expressing IgG or IgA.A few other studies have looked at circulating B-cell subsets in RA [2-4]. The results described are not consistent. This may be due to variability within the different RA cohorts (age, disease duration, disease activity and treatment with anti-TNF or other disease-modifying anti-rheumatic drugs) and differences between control groups. It may also be due to absence of a true pattern of changes in circulating B-cell subpopulations in patients with RA. Study of possible effects of anti-TNF therapy on circulating B-cell subsets has also shown variable results [1,4-6]. A cross
Endogenous endophthalmitis in a rheumatoid patient on tumor necrosis factor alpha blocker  [cached]
Agarwal Pankaj,Gallaghar Mick,Murphy Elizabeth,Virdi Meena
Indian Journal of Ophthalmology , 2007,
Abstract: The development of anti-tumor necrosis factor (TNF) therapies is a milestone in the therapy of rheumatic diseases. It is of concern whether all potential undesired complications of therapy have been evaluated within clinical trials which have led to treatment approval. Specialists prescribing TNF blockers should be aware of the unusual and severe complications that can occur. We describe a case of endogenous endophthalmitis in a rheumatoid patient on TNF alpha blocker.
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