Rheumatoid Arthritis: Sweden

Alenius GM. · Department of public Health and Clinical Medicine, Rheumatology, University Hospital, Umea, Sweden. · Curr Med Chem. · Pubmed #17305538 No free full text.

Abstract: Psoriatic arthritis (PsA), an inflammatory joint disease associated with psoriasis of the skin, has a heterogeneous pattern expressed by different manifestations, such as mild mono-oligoarthritis, a very severe, erosive and destructive polyarthritis indistinguishable from rheumatoid arthritis, and spondylarthropathy with axial involvement or enthesitis. The disease pattern often differs between patients as well as within the same patient over time. Measurable inflammatory activity is not always evident. Early detection of inflamed joints or axial involvement in patients with PsA is important in order to reduce the inflammation and prevent destruction, deformity and functional disability in the joints involved. Several factors, e.g., genetic, immunological, environmental and vascular, have been proposed to be of importance for the aetiology, the expression and prognosis of PsA. The basic treatment for PsA has been administration of non-steroid anti-inflammatory drugs (NSAIDs). Few disease modifying anti-rheumatic drugs (DMARDs) have been available due to a lack of efficacy of most of the DMARDs used for other rheumatic diseases. New insights into genetic, immunological and vascular factors in PsA are of interest as possible targets for future therapy and will be discussed in this review.

Strömbeck B, Jacobsson LT. · Department of Rheumatology, Malmö University Hospital, Malmö, Sweden. · Curr Opin Rheumatol. · Pubmed #17278938 No free full text.

Abstract: PURPOSE OF REVIEW: The purpose of this review is to present an update on the evidence-based effects of exercise in systemic lupus erythematosus and in primary Sjögren's syndrome. RECENT FINDINGS: Physical capacity is reduced in both systemic lupus erythematosus and primary Sjögren's syndrome and fatigue is a dominating and disabling symptom in both conditions. The documentation on the effect of exercise on the rehabilitation of patients with systemic lupus erythematosus and primary Sjögren's syndrome is sparse; the studies are few and the sample sizes often small. The available studies indicate that patients with systemic lupus erythematosus of mild to moderate disease activity as well as patients with primary Sjögren's syndrome benefit from exercise of moderate to high intensity. Positive effects can be expected with regard to aerobic capacity, fatigue, physical function and depression. SUMMARY: There is reason to believe that exercise should be included in the rehabilitation of patients with mild to moderate systemic lupus erythematosus and patients with primary Sjögren's syndrome. Further research is needed and should aim to evaluate the effect of exercise on groups with varying degree of disease severity and to document the long-term impact on the disease.

Turesson C, Matteson EL. · Department of Rheumatology, Malmö University Hospital, Malmö, Sweden. · Curr Opin Rheumatol. · Pubmed #17278937 No free full text.

Abstract: PURPOSE OF REVIEW: There is increased recognition of an excess risk of cardiovascular disease in patients with rheumatic disorders. Physical inactivity is a frequent complication of arthritis, and also common in the general population. In this review, we highlight recent findings on risk factors for cardiovascular disease in patients with rheumatic diseases, and explore the role of physical activity for the prevention of cardiovascular disease. RECENT FINDINGS: Inflammatory mechanisms are clearly involved in cardiovascular disease in patients with systemic lupus erythematosus and rheumatoid arthritis. In rheumatoid arthritis, disability is also a major predictor of cardiovascular disease. A sedentary lifestyle increases the risk of cardiovascular disease in the general population, and high physical activity prevents cardiovascular disease mortality and morbidity. Successful treatment of rheumatic disease with control of inflammation and improved functional capacity may also reduce the risk of cardiovascular disease. SUMMARY: As part of the effort to prevent vascular comorbidity, regular exercise should be encouraged in patients with rheumatic diseases, and structured interventions to reduce adverse lifestyle factors scientifically evaluated.

Nandakumar KS, Holmdahl R. · Medical Inflammation Research, Lund University, Lund 22184, Sweden. · Arthritis Res Ther. · Pubmed #17254316 links to  free full text

Abstract: During the development of rheumatoid arthritis (RA) autoantibodies to IgG-Fc, citrullinated proteins, collagen type II (CII), glucose 6 phosphoisomerase (G6PI) and some other self-antigens appear. Of these, a pathogenic effect of the anti-CII and anti-G6PI antibodies is well demonstrated using animal models. These new antibody mediated arthritis models have proven to be very useful for studies involved in understanding the molecular pathways of the induction of arthritis in joints. Both the complement and FcgammaR systems have been found to play essential roles. Neutrophils and macrophages are important inflammatory cells and the secretion of tumour necrosis factor-alpha and IL-1beta is pathogenic. The identification of the genetic polymorphisms predisposing to arthritis is important for understanding the complexity of arthritis. Disease mechanisms and gene regions studied using the two antibody-induced arthritis mouse models (collagen antibody-induced arthritis and serum transfer-induced arthritis) are compared and discussed for their relevance in RA pathogenesis.

Klareskog L, Padyukov L, Alfredsson L. · Rheumatology Unit, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Solna, Stockholm, Sweden. · Curr Opin Rheumatol. · Pubmed #17143096 No free full text.

Abstract: PURPOSE OF REVIEW: This review has two purposes: to describe the known effects of cigarette smoking on the development of inflammatory rheumatic diseases, in particular rheumatoid arthritis and systemic lupus erythematosus, and to review recent research aimed at understanding the mechanisms by which smoking may interact with genes and immunity in triggering these diseases. RECENT FINDINGS: Large case-control studies as well as cohort studies have demonstrated that cigarette smoking is a risk factor for RF positive and anti-citrulline antibody with rheumatoid arthritis and that the risk diminishes only several years after cessation of smoking. Evidence exists that smoking is a risk factor also for systemic lupus erythematosus, and that the risk may be related to the presence of anti-dsDNA antibodies. Mechanistic studies are reviewed that suggest that smoking can trigger specific and potentially disease-inducing immune reactions against citrullinated proteins in rheumatoid arthritis, and dsDNA in systemic lupus erythematosus, and it is suggested that the genetic context determines which immune reactions may be triggered by smoking. SUMMARY: Counselling against smoking should be mandatory in rheumatological practice both to patients and to their relatives. Studies on the mechanisms whereby smoking triggers rheumatoid arthritis and systemic lupus erythematosus may provide fundamental new knowledge about the cause and molecular pathogenesis of these diseases.

Tarkowski A. · Department of Rheumatology and Inflammation Research, Göteborg University and Sahlgrenska University Hospital, Guldhedsgatan 10, S-413 46 Göteborg, Sweden. · Best Pract Res Clin Rheumatol. · Pubmed #17127195 No free full text.

Abstract: In contrast to the outstanding achievements made in therapy for autoimmune arthritides, not least rheumatoid arthritis, the pace of progress in therapy for infectious arthritis remains slow. This has primarily to do with the complex task of, on the one hand, killing the invading microorganisms and, on the other, to down-regulate the exaggerated immune response which participates in the microbial clearance but at the same time contributes to the tissue destruction. The use of experimental models of microbial arthritides has clarified several bacterial virulence factors as well as many haematopoietic cell types and their products that are involved in the pathogenesis of joint infection. Recent studies have documented that T-cell-mediated responses are not only prominent but also decisive with respect to disease sequelae. This chapter also reviews the primarily protective non-antigen-specific immune responsiveness to microbial agents, including the impact of neutrophils, complement system, and nitric oxide. The knowledge gained regarding microbial virulence factors and the host immune responses has prompted researchers to develop new strategies on how to interact in vivo with the infectious process. Some of these approaches are commented upon in this review: e.g. vaccination procedures to prevent septic arthritis and sepsis, as well as therapeutic procedures to minimize joint damage during an ongoing infection.

Smedby KE, Baecklund E, Askling J. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, S-171 77 Stockholm, Sweden. · Cancer Epidemiol Biomarkers Prev. · Pubmed #17119030 links to  free full text

Abstract: Certain autoimmune and chronic inflammatory conditions, such as Sjögren's syndrome and rheumatoid arthritis (RA), have consistently been associated with an increased risk of malignant lymphomas, but it is unclear whether elevated lymphoma risk is a phenomenon that accompanies inflammatory conditions in general. Likewise, it is debated whether the increased risk identified in association with some disorders pertains equally to all individuals or whether it varies among groups of patients with different phenotypic or treatment-related characteristics. It is similarly unclear to what extent the increased lymphoma occurrence is mediated through specific lymphoma subtypes. This update reviews the many findings on risks, risk levels, and lymphoma characteristics that have been presented recently in relation to a broad range of chronic inflammatory, including autoimmune, conditions. Recent results clearly indicate an association between severity of chronic inflammation and lymphoma risk in RA and Sjögren's syndrome. Thus, the average risk of lymphoma in RA may be composed of a markedly increased risk in those with most severe disease and little or no increase in those with mild or moderate disease. The roles of immunosuppressive therapy and EBV infection seem to be limited. Furthermore, RA, Sjögren's syndrome, systemic lupus erythematosus, and possibly celiac disease may share an association with risk of diffuse large B-cell lymphoma, in addition to well-established links of Sjögren's syndrome with risk of mucosa-associated lymphoid tissue lymphoma and of celiac disease with risk of small intestinal lymphoma. However, there is also obvious heterogeneity in risk and risk mediators among different inflammatory diseases.

Klareskog L, Padyukov L, Rönnelid J, Alfredsson L. · Rheumatology Unit, Department of Medicine, Karolinska Institutet/Karolinska University Hospital, Stockholm, Sweden. · Curr Opin Immunol. · Pubmed #17010589 No free full text.

Abstract: The combined role of genes, environment and immunity in the development of rheumatoid arthritis (RA) has been the subject of recent investigations. New data support a gene-environment interaction between smoking and the MHC class II HLA-DRB1 shared epitope (SE) genes in anti-citrulline antibody (anti-CP(+)) RA but not in anti-CP(-) disease. These data from genetic epidemiology, together with information on citrullination in the lungs of smokers, have prompted the formulation of a new etiological hypothesis for anti-CP(+) RA, suggesting that smoking in the context of HLA-DR SE might trigger immunity to citrulline-modified proteins and that this immunity, after several years, might cause arthritis.

Klareskog L, Padyukov L, Lorentzen J, Alfredsson L. · Rheumatology Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. · Nat Clin Pract Rheumatol. · Pubmed #16932734 No free full text.

Abstract: Rheumatoid arthritis (RA) is a complex disease in which environmental agents are thought to interact with genetic factors that influence susceptibility. This interaction triggers immunologic events that eventually result in the clinical signs of arthritis. Knowledge of the chain of etiological events that lead to the development of RA is incomplete. In this review, we describe the experimental approaches that are used to address the issue of gene-environment interactions in the etiology of RA, and discuss relevant examples of such interactions. We focus on how smoking, the best-known environmental risk factor for RA, interacts with HLA-DR shared epitope genes, the main genetic risk factors for RA, and result in a high risk of RA in individuals exposed to both of these risk factors. From these and other related findings, we can begin to define the distinct environmental risk factors (such as smoking) that in certain genetic contexts (for example, the presence of HLA-DR shared epitope alleles) can trigger immune reactions (such as autoantibodies to citrullinated peptides) many years before onset of RA, and consider how these immune reactions might contribute to clinical symptoms in a subset of affected patients. Increased knowledge about these and other events involved in the development of RA should enable the design of new tools for suppressing RA pathogenesis before the onset of disease.

Nordmark G, Alm GV, Rönnblom L. · Uppsala University Hospital, Uppsala, Sweden. · Nat Clin Pract Rheumatol. · Pubmed #16932699 No free full text.

Abstract: Sjögren's syndrome is a chronic autoimmune disease of largely unknown etiology and pathogenesis. The salivary and lacrimal glands are the main target organs, and key cells and molecules involved in the autoimmune process have been detected in these glands. Chemokines, expressed by epithelial cells, can attract T cells and dendritic cells that produce proinflammatory cytokines, which stimulate the immune response and induce apoptosis in the acinar and ductal epithelial cells. The autoantigens SSA and SSB are translocated to the apoptotic blebs and trigger infiltrating B cells to produce autoantibodies against SSA and SSB. Germinal-center-like structures can form within glandular lymphocyte foci, facilitating the antigen-driven B-cell activation. Many of the autoimmune mechanisms described above can be induced by type I interferon (IFN), and activation of this system in patients with Sjögren's syndrome has been described. A possible scenario is that an initial viral infection induces type I IFN production in salivary glands with a subsequent activation of the adaptive immune system. Resultant autoantibodies form nucleic-acid-containing immune complexes that can trigger prolonged type I IFN production, leading to a self-perpetuating autoimmune reaction. Several potential therapeutic targets for Sjögren's syndrome exist within the type I IFN system.

Johannesson M, Hultqvist M, Holmdahl R. · Medical Inflammation Research, Lund University, Sweden. · Curr Top Microbiol Immunol. · Pubmed #16724810 No free full text.

Abstract: It has so far been difficult to identify genes behind polygenic autoimmune diseases such as rheumatoid arthritis (RA), multiple sclerosis (MS), and type I diabetes (T1D). With proper animal models, some of the complexity behind these diseases can be reduced. The use of linkage analysis and positional cloning of genes in animal models for RA resulted in the identification of one of the genes regulating severity of arthritis in rats and mice, the Ncf1 gene. The Ncf1 gene encodes for the Ncf1 protein that is involved in production of free oxygen radicals through the NADPH oxidase complex, which opens up a new pathway for therapeutic treatment of inflammatory diseases. In most cases, however, a quantitative trait locus (QTL) is the sum effect of several genes within and outside the QTL, which make positional cloning difficult. Here we will discuss the possibilities and difficulties of gene identification in animal models of autoimmune disorders.

Manthorpe R, Bredberg A, Henriksson G, Larsson A. · Outpatients Department, Sjögren's Syndrome Research Centre, Malmö, Sweden. · Scand J Rheumatol. · Pubmed #16467033 No free full text.

Abstract: The purpose of this review is to give a modern view and an update of important areas in primary Sjögren's syndrome (SS), which may be the most common of the autoimmune systemic rheumatic diseases. Interest in aspects of primary SS including clinical manifestations, pathogenesis, aetiology, treatment, prognosis, etc has increased during the past three decades, the volume of scientific papers and the number of theses being the indicators. However, only a fraction of the money that is used for research into rheumatoid arthritis (RA) is used for SS, and the statement that SS is under-diagnosed, under-treated and under-researched will still be valid for several years to come. The topics that are focused on in this review are: (a) clinical areas with subsections on signs and symptoms, terminology, predictors for development of non-Hodgkin malignant lymphoma (NHML) and prognosis, (b) treatment, (c) the Danger model (aetiopathogenesis) and (d) pathology, including immunoglobulin G4 (IgG4)-positive cells.

Askling J, Fored CM, Geborek P, Jacobsson LT, van Vollenhoven R, Feltelius N, Lindblad S, Klareskog L. · Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden. · Ann Rheum Dis. · Pubmed #16414975 links to  free full text

Abstract: Data from several different monitoring systems are examined. The potential for registers based on data obtained from clinical practice, and linkage of such data to national health and population registers, is discussed. The approach described is a possible prototype for long term surveillance systems needed for the safe introduction of new treatments.

Hillert J. · Department of Neurology,Karolinska University Hospital, Huddinge, SE 141 86 Stockholm, Sweden. · Clin Neurol Neurosurg. · Pubmed #16413964 No free full text.

Abstract: Because of the relative failure of linkage analysis in multiple sclerosis, despite the investigation of more than 700 affected relative pairs, we have applied four alternative strategies to identify genes that confer susceptibility to the disease. First, we have reported two clusters of MS patients from isolated populations where 19 and 13 patients, respectively, could be shown to have common ancestry tracing back several centuries. Three and five haplotypes, respectively, were shown to be shared by affected individuals, however, these haplotypes were extended and the statistical evidence modest. Second, we have recently reported the results of a two-stage candidate gene analysis of 66 selected genes, mostly of immune function. The IL-7 receptor alpha gene and LAG-3 both had three SNP markers associated with MS. Third, we recently identified the MHC class II transactivator gene in an animal model with inflammatory properties and later confirmed it to be of importance for MS, rheumatoid arthritis and acute myocardial infarction. Finally, in collaboration with the Serono Genetics Institute, we have completed a genome-wide screen with over 100,000 markers in three sets of 300 MS patients and 300 matched controls. Eighty genes showed evidence of importance in all three populations. These strategies appear to hold some promise of success where linkage analysis has proven less successful than anticipated.

Carlsten H. · Department of Rheumatology and Inflammation Research, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden. · Immunol Rev. · Pubmed #16313350 No free full text.

Abstract: In addition to its effects on sexual differentiation and reproduction, estrogen has important impact on the immune system and on bone. It has also been evident that the effects of estrogen on bone to a large extent are mediated via its action on immune cells. Estrogen has a dichotomous impact on the immune system by downregulation of inflammatory immune responses but simultaneous upregulation of immunoglobulin production. Consequently, immune-mediated diseases in humans and in animal models are modulated by estrogen. Estrogen deficiency after ovariectomy in mice and after menopause in women is associated with significant bone loss. In rheumatic diseases such as rheumatoid arthritis (RA), osteoporosis is frequent, and in patients with postmenopausal RA, the degree of bone loss is dramatically increased. Hormone replacement therapy (HRT) in murine and human arthritis has beneficial effects on bone loss, as expected, but it also ameliorates inflammation and inflammation-triggered joint destruction. Long-term use of HRT has been associated with increased risk of breast cancer, thrombosis, and possibly also stroke. Accordingly, there is great need for new activators of estrogen receptors (ERs) selectively reproducing only the beneficial effects of estrogen. To achieve this aim, better knowledge of the mechanisms of how activation of ER-alpha and ER-beta modulates the immune system and bone at the cellular and molecular levels is necessary.

Adolfsson L. · Department of Orthopaedic Surgery, University Hospital 581, 85 Linkoping, Sweden. · Hand Clin. · Pubmed #16274861 No free full text.

Abstract: Arthroscopic synovectomy is a safe outpatient procedure with minimal postoperative morbidity.In patients who have rheumatoid arthritis and possibly also in patients who have JRA, SLE, and postinfectious arthritis, a long period of increased comfort and improved function can be anticipated. The procedure may be considered in post-traumatic cases with joint contracture and as an adjunct to other measures for certain osteoarthritic disorders. In patients who have septic arthritis with insufficient clinical improvement after systemic antibiotics and lavage, arthroscopic synovectomy seems advantageous.

Grimby G, Harms-Ringdahl K, Morgell R, Nordenskiöld U, Sunnerhagen KS. · Institutionen för klinisk neurovetenskap, Rehabiliteringsmedicin, Sahlgrenska akademin vid Göteborgs universitet, Sahlgrenska Universitetssjukhuset, Göteborg. · Lakartidningen. · Pubmed #16200901 No free full text.

This publication has no abstract.

Rantapää-Dahlqvist S. · Department of Rheumatology, University Hospital, Umeå, Sweden. · Scand J Rheumatol. · Pubmed #16095003 No free full text.

Abstract: A positive rheumatoid factor (RF) test has been included as one of the criteria for the diagnosis of rheumatoid arthritis (RA) according to the 1987 classification criteria of the American College of Rheumatology (ACR). During the past 20-30 years many different autoantibodies have been described in patients with RA. The presence of some of the autoantibodies in RA directed against various autoantigens, such as anti-neutrophil cytoplasmic antibodies, anti-nuclear antibodies, antibodies against interleukin-1 (IL-1), anti-cardiolipin antibodies, and antibodies against oxidized low density lipoprotein, is not specific for RA and these are not discussed here. This review summarizes the most relevant autoantibodies, and discusses their sensitivity, specificity, and possible diagnostic and prognostic significance in early RA. The antibodies are presented with the two clinically most relevant antibody tests first, followed by others in alphabetic order.

Kimby E. · Center of Hematology, Karolinska University Hospital, Stockholm, Sweden. · Cancer Treat Rev. · Pubmed #16054760 No free full text.

Abstract: Rituximab, a human/mouse chimeric anti-CD20 antibody, has become part of standard therapy for patients with CD20-expressing B-cell lymphoma, and is currently under investigation for other indications including autoimmune diseases, in particular rheumatoid arthritis (RA). Its characteristic tolerability profile was established soon after clinical testing began and compares favourably with chemotherapy. The majority of patients experience mild to moderate infusion-related reactions (IRRs) during the first administration of rituximab, but the incidence decreases markedly with subsequent infusions. Current data suggest that the type of adverse events in patients with RA are similar to those in lymphoma, but that adverse events related to the rituximab infusions are less severe and less frequent. Rituximab induces a rapid depletion of normal CD20-expressing B-cells in the peripheral blood, and levels remain low or undetectable for 2-6 months before returning to pretreatment levels, generally within 12 months. Serum immunoglobulin levels remain largely stable, although a reduction in IgM has been described. T-cells are unaffected by rituximab and consequently opportunistic infections rarely occur in association with rituximab therapy. When used in combination with a variety of chemotherapeutic regimens, rituximab does not add to the toxicity of chemotherapy, with the exception of a higher rate of neutropenia. However, this does not translate into a higher infection rate. Over 540,000 patients worldwide have now received rituximab and serious adverse reactions have occurred in a small minority of patients, but for the great majority of patients, rituximab is safe and well tolerated.

Frostegård J. · Department of Medicine, Karolinska University Hospital, Huddinge, 141 86 Stockholm, Sweden. · Arterioscler Thromb Vasc Biol. · Pubmed #15976324 links to  free full text

Abstract: Recent findings indicate that presence of activated immune competent cells and inflammation are typical of atherosclerosis, the main cause of cardiovascular disease (CVD). The risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE), and is also raised in other autoimmune diseases such as rheumatoid arthritis. Autoimmunity-related CVD and atherosclerosis are important clinical problems. They may also shed light on interactions between immune reactions and atherosclerosis development and manifestations, not least in women, who have a much higher risk of autoimmune disease than men. In general, a combination of traditional and nontraditional risk factors, including dyslipidemia (and to a varying degree, hypertension, diabetes, and smoking), inflammation, antiphospholipid antibodies (aPLs), and lipid oxidation, contribute to CVD in autoimmune diseases. Premature atherosclerosis is likely to be a major underlying mechanism, although distinctive features, if any, of autoimmunity-related atherosclerosis compared with "normal" atherosclerosis are not clear. One interesting possibility is that factors such as inflammation, neoepitopes on endothelial cells, or aPLs make atherosclerotic lesions in autoimmune disease more prone to rupture than in "normal" atherosclerosis. Some cases of autoimmunity-related CVD may be more related to thrombosis than atherosclerosis. Whether premature atherosclerosis is a general feature of autoimmune diseases such as SLE or only affects a subgroup of patients whereas others do not have an increased risk remains to be demonstrated. Treatment of patients with autoimmune disease should also include CVD aspects and be focused on traditional risk factors as well as on disease-related factors. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation present in atherosclerotic lesions.

Hultqvist M, Holmdahl R. · Section for Medical Inflammation Research, Lund University, Lund, Sweden. · Cell Immunol. · Pubmed #15936744 No free full text.

Abstract: Identifying genes that regulate polygenic diseases influenced by the environment such as rheumatoid arthritis (RA), has so far proven to be difficult. By using an alternative approach, i.e., linkage analysis using relevant animal models we succeeded in finding the Ncf1 gene residing in the Pia4 quantitative trait locus to be responsible for the severity of pristane induced arthritis in rats. The influence of another mutation in the mouse Ncf1 gene showed the same association between decreased oxidative burst and enhanced arthritis. In this case the mutation affected a splice site giving a non-detectable oxidative burst response and enhanced collagen induced arthritis as well as myelin oligodendrocyte protein induced experimental autoimmune encephalomyelitis. These findings open up new possibilities for new treatments for autoimmune diseases, i.e., RA, targeting the NADPH oxidase pathway.

Ekbom A. · Karolinska Institute, Unit of Clinical Epidemiology, Department of Medicine, Stockholm, Sweden. · Semin Arthritis Rheum. · Pubmed #15852252 No free full text.

This publication has no abstract.

Bredberg A, Henriksson G, Larsson A, Manthorpe R, Sallmyr A. · Department of Medical Microbiology, University Hospital, S-20502 Malmo, Sweden. · Rheumatology (Oxford). · Pubmed #15840601 links to  free full text

This publication has no abstract.

Malmström V, Trollmo C, Klareskog L. · Department of Medicine, Karolinska Institutet, Stockholm, Sweden. · Arthritis Res Ther. · Pubmed #15833144 No free full text.

Abstract: Rheumatoid arthritis (RA) is a common destructive inflammatory disease that affects 0.5-1% of the population in many countries. Even though several new treatments have been introduced for patients with RA, a considerable proportion of patients do not benefit from these, and the need for alternative treatment strategies is clear. This review explores the potential for a therapy targeting the adaptive immune system by modulating co-stimulation of T cells with a CTLA4-Ig fusion protein (abatacept).

Rönnelid J, Klareskog L, Skogh T, Svensson B. · Enheten för klinisk immunologi, klinisk immunologi och transfusionsmedicin, Uppsala universitet/Akademiska sjukhuset. · Lakartidningen. · Pubmed #15631262 No free full text.

Abstract: Antibodies directed against citrullinated proteins (anti-CP) constitute a newly defined group of autoantibodies with very high diagnostic specificity for rheumatoid arthritis (RA). The most recently developed assays have a sensitivity comparable to that of traditional tests for Rheumatoid Factor (RF). Due to its considerably higher specificity, the authors recommend that anti-CP antibody analysis should replace the RF test in primary healthcare when investigating cases of clinically suspect RA.