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  • 251.
    Eneslätt, Kjell
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Uddhammar, Agneta
    Sundqvist, Karl-Gösta
    The regulation of FasL expression: a distinguishing feature between monocytes and T lymphocytes/NK cells with possible implications for SLE2001Inngår i: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 21, nr 3, s. 183-192Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Monocytes and lymphocytes from patients with systemic lupus erythematosus (SLE) had a higher cell surface expression of Fast than the corresponding cells from healthy individuals. Inhibitors of metalloproteases upregulated the surface expression of Fast in peripheral blood lymphocytes (PBL), indicating that a metalloprotease is responsible for the cleavage of FasL. The level of sFasL in serum was slightly increased in the patient group compared to the controls. Therefore, the possible contribution of various mononuclear cell types to the release of Fast was analyzed. Isolated NK cells and T lymphocytes released Fast into the medium and the release was prevented by inhibitors of metalloproteases. In contrast, isolated monocytes did not release Fast. FasR expression was elevated in patients with inverted CD4/CD8 ratio, while Fast expression showed no relationship to CD4/CD8 ratio. The absence of Fast release by isolated cells and a high level of surface expression of Fast distinguish monocytes and T lymphocytes/NK cells.

  • 252. Engdahl, C.
    et al.
    Raufer, J.
    Harre, U.
    Bondt, A.
    Pfeifle, R.
    Kroenke, G.
    Scherer, H. U.
    Forsblad, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi. Department of Rhemtology and Inflammation reserch, CBAR, Institue of Medicine, Gothenburg, Sweden.
    Schett, G.
    Estrogen influences the sialylation profile and inflammatory properties of antibodies – a potential explanation for the sex differences and increased risk for ra in postmenopausal women2017Inngår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 76, s. 775-775Artikkel i tidsskrift (Annet vitenskapelig)
  • 253. Engdahl, Cecilia
    et al.
    Bondt, Albert
    Harre, Ulrike
    Raufer, Jasmin
    Pfeifle, René
    Camponeschi, Alessandro
    Wuhrer, Manfred
    Seeling, Michaela
    Mårtensson, Inga-Lill
    Nimmerjahn, Falk
    Krönke, Gerhard
    Scherer, Hans U.
    Forsblad-d'Elia, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Schett, Georg
    Estrogen induces St6gal1 expression and increases IgG sialylation in mice and patients with rheumatoid arthritis: a potential explanation for the increased risk of rheumatoid arthritis in postmenopausal women2018Inngår i: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 20, artikkel-id 84Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Rheumatoid arthritis (RA) preferentially affects women, with the peak incidence coinciding with estrogen decrease in menopause. Estrogen (E2) may therefore have intrinsic immune-regulatory properties that vanish with menopause. Fc sialylation is a crucial factor determining the inflammatory effector function of antibodies. We therefore analyzed whether E2 affects immunoglobulin G (IgG) sialylation.

    Methods: Postmenopausal (ovariectomized) mice were immunized with ovalbumin and treated with E2 or vehicle. Total and ovalbumin-specific IgG concentrations, sialylation, and Fc. receptor expression were analyzed. Postmenopausal women with RA receiving hormone replacement therapy, including E2, or no treatment were analyzed for IgG sialylation. Furthermore, effects of E2 on the expression of the sialylation enzyme beta-galactoside a2,6-sialyltransferase 1 (St6Gal1) were studied in mouse and human antibody-producing cells.

    Results: E2 treatment significantly increased Fc sialylation of total and ovalbumin-specific IgG in postmenopausal mice. Furthermore, E2 led to increased expression of inhibitory Fc. receptor IIb on bone marrow leukocytes. Treatment with E2 also increased St6Gal1 expression in mouse and human antibody-producing cells, providing a mechanistic explanation for the increase in IgG-Fc sialylation. In postmenopausal women with RA, treatment with E2 significantly increased the Fc sialylation of IgG.

    Conclusions: E2 induces anti-inflammatory effector functions in IgG by inducing St6Gal1 expression in antibodyproducing cells and by increasing Fc sialylation. These observations provide a mechanistic explanation for the increased risk of RA in conditions with low estrogen levels such as menopause.

  • 254.
    Englund, Martin
    et al.
    Lund University, Sweden; Boston University, MA 02215 USA.
    Merkel, Peter A.
    University of Penn, PA 19104 USA.
    Tomasson, Gunnar
    University of Iceland, Iceland.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    Mohammad, Aladdin J.
    Lund University, Sweden; Addenbrookes Hospital, England.
    Comorbidities in Patients with Antineutrophil Cytoplasmic Antibody-associated Vasculitis versus the General Population2016Inngår i: Journal of Rheumatology, ISSN 0315-162X, E-ISSN 1499-2752, Vol. 43, nr 8, s. 1553-1558Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective. To evaluate the consultation rates of selected comorbidities in patients with antineutrophil cytoplasmic antibody-associated vasculitis (AAV) compared with the general population in southern Sweden. Methods. We used data from a population-based cohort of patients with AAV diagnosed between 1998 and 2010 in Southern Sweden (701,000 inhabitants). For each patient we identified 4 reference subjects randomly sampled from the general population and matched for year of birth, sex, area of residence, and index year. Using the population-based Skane Healthcare Register, we identified relevant diagnostic codes, registered between 1998 and 2011, for selected comorbidities assigned after the date of diagnosis of AAV or the index date for the reference subjects. We calculated rate ratios for comorbidities (AAV: reference subjects). Results. There were 186 patients with AAV (95 women, mean age 64.5 yrs) and 744 reference persons included in the analysis. The highest rate ratios (AAV: reference) were obtained for osteoporosis (4.6, 95% CI 3.0-7.0), followed by venous thromboembolism (4.0, 95% CI 1.9-8.3), thyroid diseases (2.1, 95% CI 1.3-3.3), and diabetes mellitus (2.0, 95% CI 1.3-2.9). For ischemic heart disease, the rate ratio of 1.5 (95% CI 1.0-2.3) did not reach statistical significance. No statistically significant differences were found for cerebrovascular accidents. Conclusion. AAV is associated with increased consultation rates of several comorbidities including osteoporosis and thromboembolic and endocrine disorders. Comorbid conditions should be taken into consideration when planning and providing care for patients with AAV.

  • 255. Engvall, Inga-Lill
    et al.
    Svensson, Björn
    Boonen, Annelies
    van der Heijde, Désirée
    Lerner, Ulf H
    Umeå universitet, Medicinska fakulteten, Institutionen för odontologi.
    Hafström, Ingiäld
    Low-dose prednisolone in early rheumatoid arthritis inhibits collagen type I degradation by matrix metalloproteinases as assessed by serum 1CTP--a possible mechanism for specific inhibition of radiological destruction2013Inngår i: Rheumatology, ISSN 1462-0324, E-ISSN 1462-0332, Vol. 52, nr 4, s. 733-742Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To study the effects of low-dose prednisolone on the osteoclast-regulating proteins osteoprotegerin (OPG) and RANK ligand (RANKL) and on markers of bone resorption, 1CTP generated by MMPs and CTX-1 generated by cathepsin K, in patients with early RA in relation to inflammation and joint destruction.

    METHODS: In 225 patients, who at the start of the first DMARD had been randomized to 7.5 mg prednisolone daily for 2 years, the P-group, or no prednisolone, the NoP-group, OPG and RANKL were analysed at 0-24 months and 1CTP and CTX-1 at 0-12 months. Radiographs of hands and feet were assessed at 0, 1 and 2 years using the modified Sharp-van der Heijde score and radiological progression defined as increase in total Sharp score above 5.8. Data were analysed with a mixed linear model and by the GENMOD procedure.

    RESULTS: In the P-group, RANKL and the ratio OPG/RANKL were stable between baseline and 24 months, whereas in the NoP-group, RANKL increased and the ratio OPG/RANKL decreased. CTX-1 decreased significantly more in the P-group. 1CTP decreased over time in both groups, but more in the P-group, P < 0.001, a difference also present in the subgroups of patients in remission. The decrease in 1CTP was associated with less radiological progression after 2 years and displayed a significant interaction with treatment. CONCLUSION: Low-dose prednisolone may inhibit progression of joint destruction by interfering with MMP activity, seen as a marked decrease in 1CTP, as well as by impairing osteoclast activation, shown by a stable OPG/RANKL ratio.

  • 256. Enocsson, Helena
    et al.
    Sjowall, Christopher
    Wirestam, Lina
    Dahle, Charlotte
    Kastbom, Alf
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Wettero, Jonas
    Skogh, Thomas
    Four Anti-dsDNA Antibody Assays in Relation to Systemic Lupus Erythematosus Disease Specificity and Activity2015Inngår i: Journal of Rheumatology, ISSN 0315-162X, E-ISSN 1499-2752, Vol. 42, nr 5, s. 817-825Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective. Analysis of antibodies against dsDNA is an important diagnostic tool for systemic lupus erythematosus (SLE), and changes in anti-dsDNA antibody levels are also used to assess disease activity. Herein, 4 assays were compared with regard to SLE specificity, sensitivity, and association with disease activity variables. Methods. Cross-sectional sera from 178 patients with SLE, of which 11 were followed consecutively, from a regional Swedish SLE register were analyzed for immunoglobulin G (IgG) anti-dsDNA by bead-based multiplex assay (FIDIS; Theradig), fluoroenzyme-immunoassay (EliA; Phadia/Thermo Fisher Scientific), Crithidia luciliae immunofluorescence test (CLIFT; ImmunoConcepts), and line blot (EUROLINE; Euroimmun). All patients with SLE fulfilled the 1982 American College of Rheumatology and/or the 2012 Systemic Lupus International Collaborating Clinics (SLICC-12) classification criteria. Healthy individuals (n = 100), patients with rheumatoid arthritis (n = 95), and patients with primary Sjogren syndrome (n = 54) served as controls. Results. CLIFT had the highest SLE specificity (98%) whereas EliA had the highest sensitivity (35%). When cutoff levels for FIDIS, EliA, and EUROLINE were adjusted according to SLICC-12 (i.e., double the reference limit when using ELISA), the specificity and sensitivity of FIDIS was comparable to CLIFT. FIDIS and CLIFT also showed the highest concordance (84%). FIDIS performed best regarding association with disease activity in cross-sectional and consecutive samples. Fisher's exact test revealed striking differences between methods regarding associations with certain disease phenotypes. Conclusion. CLIFT remains a good choice for diagnostic purposes, but FIDIS performs equally well when the cutoff is adjusted according to SLICC-12. Based on results from cross-sectional and consecutive analyses, FIDIS can also be recommended to monitor disease activity.

  • 257.
    Enocsson, Helena
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Sjöwall, Christoffer
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Wetterö, Jonas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten.
    Soluble urokinase plasminogen activator receptor: A valuable biomarker in systemic lupus erythematosus?2015Inngår i: Clinica Chimica Acta, ISSN 0009-8981, E-ISSN 1873-3492, Vol. 444, s. 234-241Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Systemic lupus erythematosus (SLE) is a potentially severe autoimmune condition with an unpredictable disease course, often with fluctuations in disease activity over time. Long term inflammation and drug-related side-effects may subsequently lead to permanent organ damage, a consequence which is intimately connected to decreased quality of life and mortality. New lupus biomarkers that convey information regarding inflammation and/or organ damage are thus warranted. Today, there is no clinical biomarker that indicates the risk of damage accrual. Herein we highlight the urokinase plasminogen activator receptor (uPAR) and especially its soluble form (suPAR) that besides having biological functions in e.g. proteolysis, cell migration and tissue homeostasis, recently has emerged as a promising biomarker of inflammation and prognosis of several disorders. A strong association between suPAR and organ damage in SLE was recently demonstrated, and preliminary data (presented in this review) suggests the possibility of a predictive value of suPAR blood levels. The involvement of suPAR in the pathogenesis of SLE remains obscure, but its effects in leukocyte recruitment, phagocytic uptake of dying cells (efferocytosis) and complement regulation suggests that the central parts of the SLE pathogenesis could be regulated by suPAR, and vice versa.

  • 258. Enocsson, Helena
    et al.
    Sjöwall, Christopher
    Kastbom, Alf
    Skogh, Thomas
    Eloranta, Maija-Leena
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi.
    Rönnblom, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi.
    Wetterö, Jonas
    Serum C-reactive protein (CRP) associates with lupus disease activity in the absence of measurable interferon alpha and a CRP gene variant2014Inngår i: Arthritis & rheumatology, ISSN 2326-5205, Vol. 66, nr 6, s. 1568-1573Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: The type I interferon (IFN) system is important in the pathogenesis of systemic lupus erythematosus (SLE). We previously demonstrated an inhibitory effect of IFNα on interleukin 6 (IL-6) induced C-reactive protein (CRP) in vitro, hypothetically explaining the poor correlation between disease activity and CRP levels in SLE. Herein we investigated disease activity, IL-6 and CRP in relation to a CRP gene polymorphism and IFNα

    Methods: Sera from 155 SLE patients and 100 controls were analyzed for CRP. Patients were genotyped for a CRP single nucleotide polymorphism (rs1205) associated with low CRP levels. Serum IFNα and IL-6 was quantified by immunoassays. Clinical disease activity was assessed by SLE disease activity index 2000 (SLEDAI-2K).

    Results: CRP levels were increased in SLE patients compared to controls, but were not associated with SLEDAI-2K or IL-6 levels. However, exclusion of patients carrying at least one rs1205 minor allele revealed an association between disease activity and CRP levels (p=0.005). We found a strong association between disease activity and CRP levels (p<0.0005) when patients with measurable IFNα as well as the minor allele of rs1205 where excluded from the analysis. Similarly, when patients with raised IFNα and/or the rs1205 polymorphism were excluded, IL-6 associated with CRP levels.

    Conclusions: The present study demonstrates that serum IFNα as well as CRP genotype affects the CRP response in SLE patients. Lack of correlation between serum levels of CRP and disease activity could therefore be explained by activation of the type I IFN system and polymorphisms in the CRP gene.

  • 259. Enocsson, Helena
    et al.
    Sjöwall, Christopher
    Skogh, Thomas
    Eloranta, Maija-Leena
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Rönnblom, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Wetterö, Jonas
    Interferon-alpha Mediates Suppression of C-Reactive Protein Explanation for Muted C-Reactive Protein Response in Lupus Flares?2009Inngår i: Arthritis and Rheumatism, ISSN 0004-3591, E-ISSN 1529-0131, Vol. 60, nr 12, s. 3755-3760Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective. C-reactive protein (CRP) is synthesized by hepatocytes in response to interleukin-6 (IL-6) during inflammation. Despite raised IL-6 levels and extensive systemic inflammation, serum CRP levels remain low during most viral infections and disease flares of systemic lupus erythematosus (SLE). Because both viral infections and SLE are characterized by high levels of interferon-alpha (IFN alpha), the aim of this study was to determine whether this cytokine can inhibit the induction of CRP. Methods. The interference of all 12 IFN alpha subtypes with CRP promoter activity induced by IL-6 and IL-1 beta was studied in a CRP promoter- and luciferase reporter-transfected human hepatoma cell line, Hep-G2. CRIP secretion by primary human hepatocytes was analyzed by enzyme-linked immunosorbent assay. Results. CRP promoter activity was inhibited by all single IFN alpha subtypes, as well as by 2 different mixtures of biologically relevant IFN alpha subtypes. The most prominent effect was seen using a leukocyte-produced mixture of IFN alpha (56% inhibition at 1,000 IU/ml). The inhibitory effect of IFN alpha was confirmed in primary human hepatocytes. CRP promoter inhibition was dose dependent and mediated via the type I IFN receptor. Transferrin production and Hep-G2 proliferation/viability were not affected by IFN alpha. Conclusion. The current study demonstrates that IFN alpha is an inhibitor of CRP promoter activity and CRP secretion. This finding concords with previous observations of up-regulated IFN alpha and a muted CRP response during SLE disease flares. Given the fundamental role of both IFN alpha and CRP in the immune response, our results are of importance for understanding the pathogenesis of SLE and may also contribute to understanding the differences in the CRP response between viral and bacterial infections.

  • 260.
    Ericson, Lisa
    et al.
    Nordic Health Economics AB.
    Ambring, Anneli
    Björholt, Ingela
    Dahm, Peter
    Opioid rotation in patients initiated on oxycodone or morphine: a register study.2013Inngår i: Journal of Pain Research, ISSN 1178-7090, E-ISSN 1178-7090, Vol. 6, s. 379-86Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    PURPOSE: Strong opioids are recommended for the treatment of moderate to severe pain. However, some patients do not achieve a successful treatment outcome due to intolerable adverse events and/or inadequate analgesia, thus may benefit from switching to another opioid, a procedure known as "opioid rotation." The type of opioid at treatment initiation may influence the risk of opioid rotation and the objective of this study was to assess such rotation after treatment initiation with two alternative treatments, controlled-release (CR) oxycodone versus CR morphine in patients suffering from non-cancer pain.

    METHOD: The study reported here was a real-life study based on Swedish register data: the Prescribed Drug, National Patient, and Cause of Death registers. The captured data cover the entire Swedish population treated in specialist care. A statistical analysis plan was agreed and signed before data were accessed.

    RESULTS: Data from 50,223 cases were included in the analyses. The risk of rotation was 19% higher in patients initiating treatment with morphine compared with oxycodone (hazard ratio 1.19; 95% confidence interval 1.11-1.27; P < 0.001), after adjusting for such baseline variables that were both significantly correlated with the outcome variable (time to rotation) and significantly different between the groups; age at index date, osteoarthritis and number of pain-related drugs.

    CONCLUSION: Patients with non-cancer pain who initiated treatment with CR morphine had a higher risk of opioid rotation than patients initiated with CR oxycodone.

  • 261.
    Eriksson, Catharina
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi. Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Immunological mechanisms in systemic autoimmunity: autoantibodies and chemokines in systemic lupus erythematosus and during treatment with TNF inhibitors in rheumatoid arthritis2011Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Background. Rheumatoid Arthritis (RA) is an autoimmune inflammatory disease that, without powerful treatment, may lead to irreversible joint damage. During the past decade, anti-cytokine therapy has become available, e.g., infliximab, a chimeric antibody targeting the pro-inflammatory cytokine TNF that has a central role in the inflammatory process in RA patients. Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease that may affect all organs and is characterized by a massive antibody production. Chemokines, chemokine receptors and lipoprotein receptor-related protein 1(CD91) are regulators of inflammation in autoimmune diseases and T-cell migration.

    Objectives. The aim of this study was to get a deeper understanding how TNF blocking treatment influences inflammatory mechanisms and autoantibody formation in RA with special reference to similarities and differences with SLE.

    Methods. In patients with RA treated with anti-TNF, and in SLE patients (ACR criteria) clinical evaluation was performed and blood samples analyzed. Autoantibodies were analyzed using indirect immunofluorescence, ELISA and multiplex flow cytometry in samples from anti-TNF treated RA patients (n=59) followed longitudinally for 54 weeks, in pre-diseased samples from SLE patients (n=38) and matched population-based controls (n=152). T-cell expression of chemokine receptors and CD91 was analyzed by flow cytometry, whilst serum levels of chemokines were determined using ELISA in anti-TNF treated RA-patients (n=24) followed longitudinally (30 weeks), and cross-sectionally in SLE-patients (n=23). Expression of mRNA for chemokines was analyzed in T-cells from SLE-patients (n=10) using PCR.

    Results. After treatment with infliximab, RA patients produced ANA, anti-dsDNA and anti-nucleosome antibodies, but not anti-ENA antibodies. Although these antibodies are considered typical for SLE only one patient developed a transient lupus-syndrome. Antibodies against cell nuclear antigens, including ENA, were detected several years before the first clinical symptom of SLE; anti-SSA was the earliest detectable antibody.

    In RA-patients before infliximab treatment, the T-cell expression of several chemokine receptors was elevated compared with healthy controls. In contrast, only one soluble chemokine, IP-10 was elevated. After treatment the levels of soluble MIP-1β, MCP-1 and IP-10, and the T-cell expression of CCR2 were decreased. In SLE-patients MIP-1β, MCP-1, SDF-1, IP-10 and RANTES in blood were elevated, whilst expression of CXCR5 and CCR6 on T-cells was lower than in healthy controls. T-cell expression of CXCR2 and CCR1 was elevated in active disease (measured as SLEDAI index), whereas the CXCR5 and CCR2 expression was lower in inactive SLE. In SLE patients with nephritis IP-10 was lower and T-cell expression of CXCR3 and CCR3 elevated compared with patients without nephritis. The expression of CD91 was higher on T-cells from patients not responsive to infliximab treatment compared with responders.

    Conclusion. These findings indicate that anti-TNF (infliximab) treatment in RA-patients has a major impact on the production of autoantibodies and chemokines. The autoantibody profile in infliximab-treated patients was similar to that predating disease onset in SLE patients with the exception of anti-ENA being detectable in SLE, but the development of lupus-syndromes was rare. The expression of CD91 on T-cells may predict responsiveness to infliximab. The expression of chemokine receptors in SLE- patients seemed to be related to disease activity. Anti-nuclear antibodies were detectable years before clinical disease onset in patients who developed SLE suggesting a gradual pathogenic process.

  • 262.
    Eriksson, Catharina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Dahlqvist, Solbritt Rantapää
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Cytokines and Their Relation to Autoantibodies Before Disease Onset in Systemic Lupus Erythematosus2012Inngår i: Arthritis and Rheumatism, ISSN 0004-3591, E-ISSN 1529-0131, Vol. 64, nr 10, s. S286-S287Artikkel i tidsskrift (Annet vitenskapelig)
  • 263.
    Eriksson, Catharina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Eneslätt, Kjell
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Ivanoff, J
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Sundqvist, Karl-Gösta
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Abnormal expression of chemokine receptors on T-cells from patients with systemic lupus erythematosus2003Inngår i: Lupus, ISSN 0961-2033, E-ISSN 1477-0962, Vol. 12, nr 10, s. 766-774Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The expression of chemokine receptors on T-cells and chemokine levels in the blood was studied in 23 patients with SLE (ACR criteria), seven patients with rheumatoid arthritis (RA) and in 15 healthy controls using flow cytometry, RT-PCR and ELISA. The cell surface expression of the chemokine receptors CXCR5 and CCR6 was decreased in SLE patients compared with controls (P = 0.051 and P = 0.002, respectively). The decrease of CXCR5 was confined to SLE patients with inactive disease (SLEDAI < 6) compared with active disease (SLEDAI &GE; 6) and controls. CXCR2 and CCR1 were increased in patients with active SLE compared with patients with inactive disease (P = 0.001 and P = 0.01, respectively) and with controls ( P = 0.02 and P = 0.053, respectively). The levels of the chemokines MIP-1β MCP-1, SDF-1α, IP-10 and RANTES were significantly elevated in SLE patients compared with controls. Patients with renal involvement had increased surface expression of CXCR3 and CCR3 (P = 0.04 in both) and a lower level of soluble IP-10 compared with patients without renal disease (P = 0.025) and compared with controls (P = 0.001). The ratio between CCR5 and CCR3 was significantly increased in RA patients compared with SLE patients and controls supporting a Th1 overweight in RA. In conclusion, patients with SLE showed abnormal T-cell expression of several chemokine receptors and levels of soluble chemokines in their plasma/ serum.

  • 264.
    Eriksson, Catharina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Engstrand, S
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Sundqvist, K-G
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Autoantibody formation in patients with rheumatoid arthritis treated with anti-TNF alpha2005Inngår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 64, nr 3, s. 403-407Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Research on autoantibody formation in patients treated with TNFα inhibitors has produced contradictory results.

    Objective: To study the prevalence of autoantibodies in patients with rheumatoid arthritis treated with the TNFα inhibitor infliximab.

    Methods: 53 patients (48 female, 11 male) treated with infliximab for rheumatoid arthritis were followed for autoantibody production before treatment and after 14, 30, and 54 weeks. Six patients treated with etanercept were studied for comparison. The analyses included antibodies against nuclear antigens (ANA), extractable nuclear antigens, double stranded (ds)DNA (by ELISA, IIF on Crithidia luciliae for IgM and IgG, and Farr assay), nucleosomes, cardiolipin, smooth muscle, mitochondria, proteinase 3, and myeloperoxidase antigens.

    Results: The number of patients treated with infliximab who developed antibodies against dsDNA of both IgG and IgM class (tested by IIF) increased significantly. The prevalence of patients positive for IgG class increased to 66% at 30 weeks and 45% at 54 weeks, and of IgM class to 85% and 70%, respectively. The titre and number of patients expressing antibodies against nucleosomes and ANA also increased significantly. The number of rheumatoid factor or anticardiolipin positive patients was stable and there was no increase in antibodies against the other antigens. A lupus-like syndrome was seen in one patient. No patient treated with etanercept developed any of these autoantibodies.

    Conclusions: Patients treated with infliximab may develop anti-dsDNA antibodies of both IgM and IgG class, anti-nucleosome antibodies, and ANA, with a gradual increase until 30 weeks.

  • 265.
    Eriksson, Catharina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Kokkonen, Heidi
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Johansson, Martin
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Wadell, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Autoantibodies predate the onset of Systemic Lupus Erythematosus in northern Sweden2011Inngår i: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 13, nr 1, s. R30-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    INTRODUCTION: Autoantibodies have a central role in systemic lupus erythematosus (SLE). The presence of autoantibodies preceding disease onset by years has been reported both in patients with SLE and those with rheumatoid arthritis, suggesting a gradual development of these diseases. To identify autoantibodies in a Northern European population predating the onset of symptoms of SLE and their relationship to presenting symptoms.

    METHODS: The register of patients fulfilling the American College of Rheumatology (ACR) criteria for SLE and with a given date for the onset of symptoms was co-analysed with the register of the Medical Biobank, Umea, Sweden. Thirty-eight patients were identified as having donated blood samples prior to symptom onset. A nested case-control study (1:4) was performed with 152 age- and sex-matched controls identified from within the Biobank register. Antibodies against anti- Sjogren's syndrome antigen A (Ro/SSA) (60 and 52 kDa), anti- Sjogren's syndrome antigen B (La/SSB), anti-Smith antibody (Sm), ribonucleoprotein (RNP), scleroderma-70 (Scl-70), anti- histidyl-tRNA synthetase antibody (Jo-1), double-stranded DNA (dsDNA); Centromere protein B and histones were analysed using the anti-nuclear antibody test II (ANA-II) Plus Test System (Athena Multi-Lyte(R)) on a Bio-Plex Array Reader (Luminex200). ANA were analysed using indirect immunofluorescence on Human Epidermal cells-2 (HEp2-cells) at a sample dilution of 1:100.

    RESULTS: Autoantibodies against nuclear antigens were detected 5.6 (+/- 4.7; mean +/- SD) years before the onset of symptoms and 8.7 (+/- 5.6) years before diagnosis in 63% of the individuals who subsequently developed SLE. The sensitivity (45.7%) was highest for ANA with a specificity of 95%, followed by anti-dsDNA and anti-Ro/SSA antibodies both with sensitivities of 20.0% at specificities of 98.7% and 97.4%, respectively. The odds ratio (OR) for anti-dsDNA predicting disease was 18.13 (CI 95%; 3.58-91.84), and for ANA 11.5 (CI 95%; 4.54-28.87). Anti-Ro/SSA antibodies appeared first, 6.6 (+/- 2.5) years prior to symptom onset. The mean number of autoantibodies in pre-diseased individuals was 1.4 and after disease onset 3.1 (P< 0.0005). The time predating disease was shorter, and the number of autoantibodies greater, in those individuals with serositis as a presenting symptom in comparison to those with arthritis and skin manifestations.

    CONCLUSIONS: Autoantibodies against nuclear antigens were detected in individuals developing SLE several years before the onset of symptoms and diagnosis. The most sensitive autoantibodies were ANA, Ro/SSA and dsDNA, with the highest predictive OR for anti-dsDNA antibodies. The first autoantibodies detected were anti-Ro/SSA.

  • 266.
    Eriksson, Catharina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Rantapää Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Cytokines in relation to autoantibodies before onset of symptoms for systemic lupus erythematosus2014Inngår i: Lupus, ISSN 0961-2033, E-ISSN 1477-0962, Vol. 23, nr 7, s. 691-696Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: A number of cytokines and chemokines were analysed and related to autoantibodies in blood samples pre-dating the onset of symptoms of systemic lupus erythematosus. Methods: Thirty-five patients with systemic lupus erythematosus (American College of Rheumatology criteria) were identified as having donated blood samples, prior to symptom onset, to the Biobank of northern Sweden. Altogether, 140 age-and sex-matched controls were also identified. The concentrations of interferon-a, interleukin-4, interleukin-9, interleukin-10, interferon inducible protein-10 and monocyte chemotactic protein-1 were analysed using multiplex technology and related to autoantibodies (ANA, ENA, anti-dsDNA and anti-histone antibodies) analysed from the same blood sample. Results: The interferon-g inducible protein-10 levels were higher in the pre-symptomatic individuals than in controls (p < 0.05) and correlated with interferon-a (p < 0.01). The interferon-g inducible protein-10 and interferon-a concentrations were significantly increased in individuals positive for autoantibodies: interferon-g inducible protein-10 for ANA; anti-SSA/Ro and anti-Jo-1 antibodies; interferon-a with anti-SSB/La antibodies. The levels of interleukin-10, interferon-g inducible protein-10 and monocyte chemotactic protein-1 increased significantly from the pre-symptomatic individuals to after onset of systemic lupus erythematosus. Conclusions: An increased concentration of interferon-gamma inducible protein-10 pre-dated the onset of systemic lupus erythematosus and was related to autoantibodies before the onset of disease. The levels of interferon-gamma inducible protein-10 and interferon-alpha were correlated. These findings support the proposal that the interferon system is important early in the pathogenesis of systemic lupus erythematosus and autoantibody formation.

  • 267.
    Eriksson, Catharina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Sundqvist, Karl-Gösta
    Department of Laboratory Medicine, Division of Clinical Immunology, Karolinska Institute at Karolinska University Hospital, Huddinge, Stockholm, Sweden.
    T-cell expression of CD91: a marker of unresponsiveness to anti-TNF therapy in rheumatoid arthritis2010Inngår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 118, nr 11, s. 837-845Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to investigate the expression of thrombospondin-1 (TSP-1) and its receptors, lipoprotein receptor-related protein/cluster of differentiation (CD)91, calreticulin (CRT), and CD47, on T cells and monocytes from patients with rheumatoid arthritis (RA) treated with anti-tumor necrosis factor (TNF) therapy. The surface expression of CD91 and associated components on CD3- and CD14-positive cells was examined using flow cytometry in 12 patients with established RA before and after beginning therapy and compared with that of 9 healthy controls and 12 patients with early RA treated with conventional therapies. CD3-positive cells from anti-TNF non-responders showed significantly greater expression of CD91 expression than those from responders (p<0.05) after 6 weeks and when all measurements were pooled (p<0.001). CD91 expression on CD3-positive cells from non-responders to other therapies was at the same level as in healthy controls. In contrast, CD14-positive cells showed no differences in CD91 expression between patients and controls or between responders and non-responders to anti-TNF therapy. The expression of TSP-1, CRT, and CD47 showed no differences between responders and non-responders. The results suggest T-lymphocyte expression of CD91 to be a biomarker that signifies unresponsiveness to anti-TNF therapy in patients with RA and may be used to identify potential responders and non-responders.

  • 268.
    Eriksson, Catharina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Klinisk immunologi.
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Sundqvist, KG
    Changes in chemokines and their receptors in blood during treatment with the TNF inhibitor infliximab in patients with rheumatoid arthritis2013Inngår i: Scandinavian Journal of Rheumatology, ISSN 0300-9742, E-ISSN 1502-7732, Vol. 42, nr 4, s. 260-265Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background. Chemokines are involved in leucocyte recruitment into inflammatory sites, such as the synovial tissue of patients with rheumatoid arthritis (RA). The release of certain chemokines is augmented by pro-inflammatory cytokines, such as tumor necrosis factor (TNF). Infliximab, a monoclonal antibody against TNF that blocks the biological effects of TNF, is used in the treatment of chronic inflammatory diseases. The effect of blocking TNF activity on chemokines is not fully understood.

    Aim. The aim of this study was to analyse the effects on chemokines and their receptors on peripheral mononuclear cells of anti-TNF treatment in RA-patients.

    Material and methods. Twelve patients with established RA who began treatment with infliximab, and nine patients with early RA treated with traditional disease-modifying anti-rheumatic drugs, were followed clinically for 30 weeks and chemokine levels in blood samples and chemokine receptor expression on the surface of T-cells and monocytes analysed. Three SLE-patients, as a small control group of another inflammatory disease, and nine healthy subjects were also included in the study.

    Result. CXCL10/IP-10 was significantly higher in RA-patients compared with healthy controls and decreased significantly two weeks after infliximab infusion. CCL2/MCP-1 and CCL4/MIP-1β decreased significantly after infliximab treatment although the concentrations were not significantly elevated at baseline compared with controls. There was an inverse correlation between the chemokine cleaving molecule dipeptidyl peptidase-IV/CD26 and CCL5/RANTES. Several chemokine receptors on T-cells were elevated in RA patients at inclusion into the study. The CCR2 expression on T-cells decreased significantly after infliximab treatment.

    Conclusion. The chemokines CXCL10/IP-10, CCL2/MCP-1 and CCL4/MIP-1β, mainly targeting the Th1 immune response, decreased after treatment with anti-TNF suggesting a more pronounced effect onTh1 activity than on the Th2 mediated response. Several chemokine receptors on blood T-cells were elevated in RA-patients, suggesting that they may be involved in the recruitment of T-lymphocytes from the blood to affected tissues.

  • 269.
    Eriksson, D.
    et al.
    Karolinska Institute, Sweden; Metab and Diabet Karolinska University Hospital, Sweden.
    Bianchi, M.
    Uppsala University, Sweden.
    Landegren, N.
    Karolinska Institute, Sweden; Uppsala University, Sweden.
    Nordin, J.
    Uppsala University, Sweden.
    Dalin, F.
    Karolinska Institute, Sweden; Uppsala University, Sweden.
    Mathioudaki, A.
    Uppsala University, Sweden.
    Eriksson, G. N.
    Karolinska Institute, Sweden.
    Hultin-Rosenberg, L.
    Uppsala University, Sweden.
    Dahlqvist, J.
    Uppsala University, Sweden.
    Zetterqvist, H.
    Uppsala University, Sweden; Uppsala University, Sweden.
    Karlsson, A.
    Uppsala University, Sweden.
    Hallgren, A.
    Karolinska Institute, Sweden; Uppsala University, Sweden.
    Farias, F. H. G.
    Uppsala University, Sweden.
    Muren, E.
    Uppsala University, Sweden.
    Ahlgren, K. M.
    Uppsala University, Sweden.
    Lobell, A.
    Uppsala University, Sweden.
    Andersson, G.
    Swedish University of Agriculture Science, Sweden.
    Tandre, K.
    Uppsala University, Sweden.
    Dahlqvist, S. R.
    Umeå University, Sweden.
    Söderkvist, Peter
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk patologi och klinisk genetik.
    Rönnblom, L.
    Uppsala University, Sweden.
    Hulting, A. -L.
    Karolinska Institute, Sweden.
    Wahlberg Topp, Jeanette
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Endokrinmedicinska kliniken.
    Ekwall, O.
    University of Gothenburg, Sweden.
    Dahlqvist, P.
    Umeå University, Sweden.
    Meadows, J. R. S.
    Uppsala University, Sweden.
    Bensing, S.
    Metab and Diabet Karolinska University Hospital, Sweden; Karolinska Institute, Sweden.
    Lindblad-Toh, K.
    Uppsala University, Sweden; Broad Institute MIT and Harvard, MA USA.
    Kampe, O.
    Karolinska Institute, Sweden; Metab and Diabet Karolinska University Hospital, Sweden; Uppsala University, Sweden.
    Pielberg, G. R.
    Uppsala University, Sweden.
    Extended exome sequencing identifies BACH2 as a novel major risk locus for Addisons disease2016Inngår i: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 286, nr 6, s. 595-608Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BackgroundAutoimmune disease is one of the leading causes of morbidity and mortality worldwide. In Addisons disease, the adrenal glands are targeted by destructive autoimmunity. Despite being the most common cause of primary adrenal failure, little is known about its aetiology. MethodsTo understand the genetic background of Addisons disease, we utilized the extensively characterized patients of the Swedish Addison Registry. We developed an extended exome capture array comprising a selected set of 1853 genes and their potential regulatory elements, for the purpose of sequencing 479 patients with Addisons disease and 1394 controls. ResultsWe identified BACH2 (rs62408233-A, OR = 2.01 (1.71-2.37), P = 1.66 x 10(-15), MAF 0.46/0.29 in cases/controls) as a novel gene associated with Addisons disease development. We also confirmed the previously known associations with the HLA complex. ConclusionWhilst BACH2 has been previously reported to associate with organ-specific autoimmune diseases co-inherited with Addisons disease, we have identified BACH2 as a major risk locus in Addisons disease, independent of concomitant autoimmune diseases. Our results may enable future research towards preventive disease treatment.

  • 270. Eriksson, Daniel
    et al.
    Bianchi, Matteo
    Landegren, Nils
    Dalin, Frida
    Skov, Jakob
    Hultin-Rosenberg, Lina
    Mathioudaki, Argyri
    Nordin, Jessika
    Hallgren, Åsa
    Andersson, Göran
    Tandre, Karolina
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Söderkvist, Peter
    Rönnblom, Lars
    Hulting, Anna-Lena
    Wahlberg, Jeanette
    Dahlqvist, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Ekwall, Olov
    Meadows, Jennifer R. S.
    Lindblad-Toh, Kerstin
    Bensing, Sophie
    Pielberg, Gerli Rosengren
    Kämpe, Olle
    Common genetic variation in the autoimmune regulator (AIRE) locus is associated with autoimmune Addison's disease in Sweden2018Inngår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, artikkel-id 8395Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Autoimmune Addison's disease (AAD) is the predominating cause of primary adrenal failure. Despite its high heritability, the rarity of disease has long made candidate-gene studies the only feasible methodology for genetic studies. Here we conducted a comprehensive reinvestigation of suggested AAD risk loci and more than 1800 candidate genes with associated regulatory elements in 479 patients with AAD and 2394 controls. Our analysis enabled us to replicate many risk variants, but several other previously suggested risk variants failed confirmation. By exploring the full set of 1800 candidate genes, we further identified common variation in the autoimmune regulator (AIRE) as a novel risk locus associated to sporadic AAD in our study. Our findings not only confirm that multiple loci are associated with disease risk, but also show to what extent the multiple risk loci jointly associate to AAD. In total, risk loci discovered to date only explain about 7% of variance in liability to AAD in our study population.

  • 271.
    Eriksson, Daniel
    et al.
    Karolinska Inst, Dept Med Solna, Ctr Mol Med, Stockholm, Sweden; Karolinska Univ Hosp, Dept Endocrinol Metab & Diabet, Stockholm, Sweden.
    Dalin, Frida
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Med Solna, Ctr Mol Med, Stockholm, Sweden.
    Eriksson, Gabriel Nordling
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.
    Landegren, Nils
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Med Solna, Ctr Mol Med, Stockholm, Sweden.
    Bianchi, Matteo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Hallgren, Åsa
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Med Solna, Ctr Mol Med, Stockholm, Sweden.
    Dahlqvist, Per
    Umeå Univ, Dept Publ Hlth & Clin Med, Umeå, Sweden.
    Wahlberg, Jeanette
    Linköping Univ, Dept Endocrinol, Linköping, Sweden; Linköping Univ, Dept Med & Hlth Sci, Linköping, Sweden; Linköping Univ, Dept Clin & Expt Med, Linköping, Sweden.
    Ekwall, Olov
    Univ Gothenburg, Dept Pediat, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden; Univ Gothenburg, Dept Rheumatol & Inflammat Res, Inst Med, Sahlgrenska Acad, Gothenburg, Sweden.
    Winqvist, Ola
    Karolinska Inst, Dept Med Solna, Stockholm, Sweden.
    Catrina, Sergiu-Bogdan
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Hulting, Anna-Lena
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.
    Lindblad-Toh, Kerstin
    Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Alimohammad, Mohammad
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Dermatologi och venereologi.
    Husebye, Eystein S
    Karolinska Inst, Dept Med Solna, Ctr Mol Med, Stockholm, Sweden; Univ Bergen, Dept Clin Sci, Bergen, Norway; Univ Bergen, Dept Med, Bergen, Norway; KG Jebsen Ctr Autoimmune Disorders, Bergen, Norway.
    Knappskog, Per Morten
    Univ Bergen, Dept Clin Sci, Bergen, Norway; Haukeland Hosp, Ctr Med Genet & Mol Med, Bergen, Norway.
    Pielberg, Gerli Rosengren
    Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Bensing, Sophie
    Karolinska Univ Hosp, Dept Endocrinol Metab & Diabet, Stockholm, Sweden; Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden .
    Kämpe, Olle
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Med Solna, Ctr Mol Med, Stockholm, Sweden; Karolinska Univ Hosp, Dept Endocrinol Metab & Diabet, Stockholm, Sweden; KG Jebsen Ctr Autoimmune Disorders, Bergen, Norway.
    Cytokine Autoantibody Screening in the Swedish Addison Registry Identifies Patients With Undiagnosed APS12018Inngår i: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 103, nr 1, s. 179-186Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Context: Autoimmune polyendocrine syndrome type 1 (APS1) is a monogenic disorder that features autoimmune Addison disease as a major component. Although APS1 accounts for only a small fraction of all patients with Addison disease, early identification of these individuals is vital to prevent the potentially lethal complications of APS1.

    Objective: To determine whether available serological and genetic markers are valuable screening tools for the identification of APS1 among patients diagnosed with Addison disease.

    Design: We systematically screened 677 patients with Addison disease enrolled in the Swedish Addison Registry for autoantibodies against interleukin-22 and interferon-α4. Autoantibody-positive patients were investigated for clinical manifestations of APS1, additional APS1-specific autoantibodies, and DNA sequence and copy number variations of AIRE.

    Results: In total, 17 patients (2.5%) displayed autoantibodies against interleukin-22 and/or interferon-α4, of which nine were known APS1 cases. Four patients previously undiagnosed with APS1 fulfilled clinical, genetic, and serological criteria. Hence, we identified four patients with undiagnosed APS1 with this screening procedure.

    Conclusion: We propose that patients with Addison disease should be routinely screened for cytokine autoantibodies. Clinical or serological support for APS1 should warrant DNA sequencing and copy number analysis of AIRE to enable early diagnosis and prevention of lethal complications.

  • 272.
    Eriksson, Karin G.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Zickert, Agneta
    Sandling, Johanna K.
    Jonsen, Andreas
    Rönnblom, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Behrens, Timothy W.
    Graham, Robert R.
    Ortmann, Ward
    Syvänen, Ann-Christine
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär medicin.
    Gunnarsson, Iva
    Nordmark, Gunnel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Association of STAT4, IRF5 and BLK polymorphisms with severity and outcome in lupus nephritis2012Inngår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 71, s. A55-A55Artikkel i tidsskrift (Annet vitenskapelig)
  • 273.
    Eriksson, Per
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    Hallböök, Olof
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    Frequency, Diagnosis, Treatment, and Outcome of Gastrointestinal Disease in Granulomatosis with Polyangiitis and Microscopic Polyangiitis2018Inngår i: Journal of Rheumatology, ISSN 0315-162X, E-ISSN 1499-2752, Vol. 45, nr 4, s. 529-537Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective. Involvement of the gastrointestinal (GI) tract is a rare complication of granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA). The aim was to describe frequency, diagnosis, treatment, and outcome of GI disease in a large series of patients in a single center. Methods. A database that includes all patients with GPA and MPA diagnosed since 1997 in a defined area of southeastern Sweden as well as prevalent older cases and tertiary referral patients was screened for patients with GI disease. Data were retrieved from the patients medical records, and GI manifestations of vasculitis were defined as proposed by Pagnoux, et al in 2005. Results. Fourteen (6.5%) of 216 consecutive patients with GPA/MPA had GI manifestations. Abdominal pain and GI bleeding were the most common symptoms. Radiology was important for detection of GI disease, while endoscopy failed to support the diagnosis in many patients. Because of perforation, 5 patients underwent hemicolectomy or small intestine resection. Primary anastomosis was created in 2/5 and enterostomy in 3/5 patients. One patient had a hemicolectomy because of lower GI bleeding. One sigmoid abscess was treated with drainage, and 1 intraabdominal bleeding condition with arterial coiling. Two patients died from GI disease. GPA and MPA patients with and without GI disease exhibited a similar overall survival. Conclusion. GI disease was found in 6.5% among 216 patients with GPA or MPA. Surgery was judged necessary only in cases with GI perforation or severe bleeding. Multidisciplinary engagement is strongly recommended.

  • 274. Erlandsson, Malin C.
    et al.
    Turkkila, Minna
    Siljehult, Filip
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Pullerits, Rille
    Eriksson, Catharina
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi. Laboratory of Clinical Immunology University Hospital of Umeå , Umeå, Sweden.
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Bokarewa, Maria I.
    Survivin improves the early recognition of rheumatoid arthritis among patients with arthralgia: A population-based study within two university cities of Sweden2018Inngår i: Seminars in Arthritis & Rheumatism, ISSN 0049-0172, E-ISSN 1532-866X, Vol. 47, nr 6, s. 778-785Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Objectives: The aim of this study was to validate the use of survivin for preclinical recognition of rheumatoid arthritis (RA) among patients with unexplained arthralgia.

    Methods: Serum levels of survivin and the arthritis-specific autoantibodies RF and ACPA were measured in total of 5046 patients with musculoskeletal complains during 12 consecutive months in Gothenburg and in Umea. Among them, 303 arthralgia patients were identified and prospectively followed.

    Results: After 48 months, 12.2% of the arthralgia patients developed RA. Most of RA cases had high serum survivin, which increased the relative risk for RA (RR = 5.90,p = 3 x 10(-7)). Combination of survivin with autoantibodies was present in only 4.6% of the arthralgia patients and increased further the risk of RA and shortened time to RA development. Presence of any single autoantibody in the survivin-negative patients was associated with a minor risk for RA and had RA-free survival similar to the reference group.

    Conclusion: This study shows that measurement of survivin in serum improves estimation of RA risk and prospectively predicts RA development in patients with arthralgia. Survivin may indicate a phase preceding autoantibody production. 

  • 275.
    Ernberg, M.
    et al.
    Karolinska Inst, Sweden; SCON, Sweden.
    Christidis, N.
    Karolinska Inst, Sweden; SCON, Sweden.
    Ghafouri, Bijar
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Smärt och rehabiliteringscentrum.
    Bileviciute-Ljungar, I.
    Karolinska Inst, Sweden; Danderyd Hosp, Sweden.
    Lofgren, M.
    Karolinska Inst, Sweden; Danderyd Hosp, Sweden.
    Bjersing, J.
    Univ Gothenburg, Sweden.
    Palstam, A.
    Univ Gothenburg, Sweden.
    Larsson, A.
    Univ Gothenburg, Sweden.
    Mannerkorpi, K.
    Univ Gothenburg, Sweden.
    Gerdle, Björn
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Smärt och rehabiliteringscentrum.
    Kosek, E.
    Karolinska Inst, Sweden; Stockholm Spine Ctr, Sweden.
    Plasma Cytokine Levels in Fibromyalgia and Their Response to 15 Weeks of Progressive Resistance Exercise or Relaxation Therapy2018Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, artikkel-id 3985154Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aims of this study were to compare circulating cytokines between FM and healthy controls and to investigate the effect on cytokine levels by 15 weeks of progressive resistance exercise or relaxation therapy in FM. Baseline plasma cytokine levels and clinical data were analyzed in 125 women with FM and 130 age-matched healthy women. The FM women were then randomized to progressive resistance exercise (n = 49) or relaxation (n = 43). Baseline IL-2, IL-6, TNF-alpha, IP-10, and eotaxin were higher in FM than in healthy controls (P amp;lt; 0.041), whereas IL-beta was lower (P amp;lt; 0.001). There were weak correlations between cytokine levels and clinical variables. After both interventions, IL-1ra had increased (P=0.004), while IL-1 beta had increased in the relaxation group (P = 0.002). Changes of IFN-gamma, IL-2, IL-4, IL-6, IL-8, and IL-17A were weakly correlated with changes of PPT, but there were no significant correlations between changes of cytokine and changes in other clinical variables. The elevated plasma levels of several cytokines supports the hypothesis that chronic systemic inflammation may underlie the pathophysiology of FM even if the relation to clinical variables was weak. However, 15 weeks of resistance exercise, as performed in this study, did not show any anti-inflammatory effect on neither FM symptoms nor clinical and functional variables.

  • 276.
    Ernberg, Malin
    et al.
    Karolinska Institute, Sweden; SCON, Sweden.
    Christidis, Nikolaos
    Karolinska Institute, Sweden; SCON, Sweden.
    Ghafouri, Bijar
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Smärt och rehabiliteringscentrum.
    Bileviciute-Ljungar, Indre
    Karolinska Institute, Sweden; Danderyd Hospital, Sweden.
    Löfgren, Monika
    Karolinska Institute, Sweden; Danderyd Hospital, Sweden.
    Larsson, Anette
    University of Gothenburg, Sweden; University of Gothenburg, Sweden.
    Palstam, Annie
    University of Gothenburg, Sweden.
    Bjersing, Jan
    University of Gothenburg, Sweden.
    Mannerkorpi, Kaisa
    University of Gothenburg, Sweden; University of Gothenburg, Sweden.
    Kosek, Eva
    Karolinska Institute, Sweden; Stockholm Spine Centre, Sweden.
    Gerdle, Björn
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Smärt och rehabiliteringscentrum.
    Effects of 15 weeks of resistance exercise on pro-inflammatory cytokine levels in the vastus lateralis muscle of patients with fibromyalgia2016Inngår i: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 18, nr 137Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: This study aimed at investigating the effect of a resistance exercise intervention on the interstitial muscle levels of pro-inflammatory cytokines in fibromyalgia (FMS) and healthy controls (CON). Methods: Twenty-four female patients with FMS (54 +/- 8 years) and 27 female CON (54 +/- 9 years) were subjected to intramuscular microdialysis of the most painful vastus lateralis muscle before and after 15 weeks of progressive resistance exercise twice per week. Baseline dialysates were sampled in the resting muscle 140 min after insertion of the microdialysis catheter. The participants then performed repetitive dynamic contractions (knee extension) for 20 min, followed by 60 min rest. Pain intensity was assessed with a 0-100 mm visual analogue scale (VAS), and fatigue was assessed with Borgs RPE throughout microdialysis. Dialysates were sampled every 20 min and analyzed with Luminex for interleukin (IL)-1 beta, tumor necrosis factor (TNF) alpha, IL-6, and IL-8. Results: At both sessions and for both groups the dynamic contractions increased pain (P amp;lt; 0.012) and fatigue (P amp;lt; 0.001). The levels of TNF were lower in the FMS group than the CON group at both sessions (P amp;lt; 0.05), but none of the other cytokines differed between the groups. IL-6 and IL-8 increased after the dynamic contractions in both groups (P amp;lt; 0.010), while TNF increased only in CON (P amp;lt; 0.05) and IL-1 beta did not change. Overall pain intensity was reduced after the 15 weeks of resistance exercise in FMS (P amp;lt; 0.05), but there was no changes in fatigue or cytokine levels. Conclusion: Progressive resistance exercise for 15 weeks did not affect the interstitial levels of IL-1 beta, TNF, IL-6, and IL-8 in the vastus lateralis muscle of FMS patients or CON.

  • 277.
    Ertzgaard, Per
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Rehabiliteringsmedicinska kliniken.
    Alwin, Jenny
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för hälso- och sjukvårdsanalys. Linköpings universitet, Medicinska fakulteten.
    Sorbo, Ann
    Sahlgrens Acad, Sweden; Sodra Alvsborg Hosp, Sweden.
    Lindgren, Marie
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Rehabiliteringsmedicinska kliniken.
    Sandsjo, Leif
    Univ Boras, Sweden.
    Evaluation of a self-administered transcutaneous electrical stimulation concept for the treatment of spasticity: a randomized placebo-controlled trial2018Inngår i: European Journal of Physical and Rehabilitation Medicine, ISSN 1973-9087, E-ISSN 1973-9095, Vol. 54, nr 4, s. 507-517Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Spasticity is a common consequence of injury to the central nervous system negatively affecting patients everyday activities. Treatment mainly consists of training and different drugs, often with side effects. There is a need for treatment options that can be performed by the patient in their home environment. AIM: The objective of this study was to assess the effectiveness of an assistive technology (AT), Mono, a garment with integrated electrodes for multifocal transcutaneous electrical stimulation intended for self-treatment of spasticity, in study participants with spasticity due to stroke or CP. DESIGN: The study was a randomized, controlled, double-blind study with a cross-over design. SETTING: Participants were recruited from two rehabilitation clinics. Treatments were performed in participants homes and all follow-ups were performed in the two rehabilitation clinics. POPULATION: Thirty-one participants were included in the study and 27 completed the study. Four participants discontinued the study. Two declined participation before baseline and two withdrew due to problems handling the garment. METHODS: Participants used the AT with and without electrical stimulation (active/non-active period) for six weeks each. followed by six weeks without treatment. Goal Attainment Scaling (GAS), change in mobility, arm-hand ability, spasticity and pain were measured at baseline and after 6, 12 and 18 weeks. RESULTS: Fifteen of the 27 participants fulfilled the treatment protocol in terms of recommended use. Deviations were frequent. No statistically significant differences in outcome were found between the active and the non-active treatment periods. During the active period, an improvement was seen in the 10-meter comfortable gait test, time and steps. An improvement was seen in both the active and non-active periods for the GAS. CONCLUSIONS: Compliance was low, partly due to deviations related to the garment, complicating the interpretation of the results. Further research should focus on identifying the target population and concomitant rehabilitation strategies. CLINICAL REHABILITATION IMPACT: The evaluated concept of multifocal transcutaneous electrical stimulation (TES) represents an interesting addition to the existing repertoire of treatments to alleviate muscle spasticity. The evaluated concept allows TES to be self-administered by the patient in the home environment. A more elaborate design of training activities directly related to patients own rehabilitation goals is recommended and may increase the value of the evaluated concept.

  • 278. Esbjornsson, A-C
    et al.
    Aalto, K.
    Univ Helsinki, Childrens Hosp, Dept Paediat, FIN-00014 Helsinki, Finland.;Univ Helsinki, Cent Hosp, FIN-00014 Helsinki, Finland..
    Brostrom, E. W.
    Karolinska Inst, Dept Womens & Children Hlth, Stockholm, Sweden..
    Fasth, A.
    Univ Gothenburg, Dept Pediat, Gothenburg, Sweden..
    Herlin, T.
    Aarhus Univ Hosp, Dept Paediat, DK-8000 Aarhus, Denmark..
    Nielsen, S.
    Copenhagen Univ Hosp, Rigshosp, Dept Pediat Rheumatol, Copenhagen, Denmark..
    Nordal, E.
    Univ Hosp North Norway, Dept Paediat, Tromso, Norway.;Arctic Univ Norway, UIT, Inst Clin Med, Tromso, Norway..
    Peltoniemi, S.
    Univ Helsinki, Childrens Hosp, Dept Paediat, FIN-00014 Helsinki, Finland.;Univ Helsinki, Cent Hosp, FIN-00014 Helsinki, Finland..
    Rygg, M.
    Norwegian Univ Sci & Technol, Dept Lab Med Childrens & Womens Hlth, N-7034 Trondheim, Norway.;St Olavs Hosp, Dept Paediat, Trondheim, Norway..
    Zak, M.
    Copenhagen Univ Hosp, Rigshosp, Dept Pediat Rheumatol, Copenhagen, Denmark..
    Berntson, Lillemor
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Pediatrik.
    Ankle arthritis predicts polyarticular disease course and unfavourable outcome in children with juvenile idiopathic arthritis2015Inngår i: Clinical and Experimental Rheumatology, ISSN 0392-856X, E-ISSN 1593-098X, Vol. 33, nr 5, s. 751-757Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective To evaluate the occurrence, clinical characteristics and prognostic factors associated with ankle arthritis in children with juvenile idiopathic arthritis (JIA). Methods 440 children with JIA were followed for eight years in a prospective Nordic population-based cohort study. Data on remission was available for 427 of these children. Occurrence of clinically assessed ankle arthritis was analysed in relation to JIA category, clinical characteristics and remission data eight years after disease onset. Results In 440 children with JIA, 251 (57%) experienced ankle arthritis during the first eight years of disease. Ankle arthritis was least common in the persistent oligoarticular category (25%) and most common in children with extended oligoarticular (83%) and polyarticular RF-negative (85%) JIA. Children who developed ankle arthritis during the first year of disease were younger at disease onset (median age 4.9 (IQR 2.1-8.8) vs. 6.6 (IQR 2.8-10.1) years, p<0.003) and had more cumulative affected joints at 8-year follow-up (median involved joints 10 (IQR 6-16) vs. 3 (IQR 2-9), p<0.001). The odds ratio for not achieving remission eight years after disease onset, if the ankle joint was involved during the first year of disease was 2.0 (95 %.0, p<0.001). Hind-, mid- and forefoot involvements were more common compared to patients without ankle arthritis. Conclusion In this Nordic population-based 8-year follow-up study, occurrence of ankle arthritis during the first year was associated with an unfavourable disease outcome. We suggest that ankle arthritis should be recognised in the assessment of prognosis and choice of treatment strategy in JIA.

  • 279.
    Esbjörnsson, A-C
    et al.
    Department of Women's and Children's Health, Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden.
    Rozumalski, A
    Gillette Children's Specialty Healthcare, St Paul MN, United States; Department of Biomedical Engineering, University of Minnesota, Minneapolis MN, United States.
    Iversen, M D
    Department of Physical Therapy, Bouve College of Health Sciences, Northeastern University, Boston MA, United States; Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States.
    Schwartz, M H
    Gillette Children's Specialty Healthcare, St Paul MN, United States; Department of Biomedical Engineering, University of Minnesota, Minneapolis MN, United States; Department of Orthopaedic Surgery, University of Minnesota, Minneapolis MN, United States.
    Wretenberg, Per
    Region Örebro län. Department of Molecular Medicine, Section of Orthopaedics, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden.
    Broström, E W
    Department of Women's and Children's Health, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden.
    Quantifying gait deviations in individuals with rheumatoid arthritis using the Gait Deviation Index2014Inngår i: Scandinavian Journal of Rheumatology, ISSN 0300-9742, E-ISSN 1502-7732, Vol. 43, nr 2, s. 124-131Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVES: In this study we evaluated the usability of the Gait Deviation Index (GDI), an index that summarizes the amount of deviation in movement from a standard norm, in adults with rheumatoid arthritis (RA). The aims of the study were to evaluate the ability of the GDI to identify gait deviations, assess inter-trial repeatability, and examine the relationship between the GDI and walking speed, physical disability, and pain.

    METHOD: Sixty-three adults with RA and 59 adults with typical gait patterns were included in this retrospective case-control study. Following a three-dimensional gait analysis (3DGA), representative gait cycles were selected and GDI scores calculated. To evaluate the effect of walking speed, GDI scores were calculated using both a free-speed and a speed-matched reference set. Physical disability was assessed using the Health Assessment Questionnaire (HAQ) and subjects rated their pain during walking.

    RESULTS: Adults with RA had significantly increased gait deviations compared to healthy individuals, as shown by lower GDI scores [87.9 (SD = 8.7) vs. 99.4 (SD = 8.3), p < 0.001]. This difference was also seen when adjusting for walking speed [91.7 (SD = 9.0) vs. 99.9 (SD = 8.6), p < 0.001]. It was estimated that a change of ≥ 5 GDI units was required to account for natural variation in gait. There was no evident relationship between GDI and low/high RA-related physical disability and pain.

    CONCLUSIONS: The GDI seems to useful for identifying and summarizing gait deviations in individuals with RA. Thus, we consider that the GDI provides an overall measure of gait deviation that may reflect lower extremity pathology and may help clinicians to understand the impact of RA on gait dynamics.

  • 280.
    Espinosa-Ortega, Fabricio
    et al.
    Karolinska Inst, Dept Med, Div Rheumatol, Stockholm, Sweden.
    Holmqvist, Marie
    Karolinska Inst, Dept Med Solna, Clin Epidemiol Unit, Stockholm, Sweden.
    Alexanderson, Helene
    Karolinska Inst, Dept Med, Div Rheumatol, Stockholm, Sweden;Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Physiotherapy, Stockholm, Sweden.
    Storfors, Helena
    Uppsala Univ Hosp, Dept Clin Immunol & Transfus Med, Uppsala, Sweden.
    Mimori, Tsuneyo
    Kyoto Univ, Grad Sch Med, Dept Rheumatol & Clin Immunol, Kyoto, Japan.
    Lundberg, Ingrid E.
    Karolinska Inst, Dept Med, Div Rheumatol, Stockholm, Sweden.
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Comparison of autoantibody specificities tested by a line blot assay and immunoprecipitation-based algorithm in patients with idiopathic inflammatory myopathies2019Inngår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 78, nr 6, s. 858-860Artikkel i tidsskrift (Fagfellevurdert)
  • 281. Exarchou, S.
    et al.
    Lindström, U.
    Sigurdardottir, V
    Sundström, Björn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Askling, J.
    Eriksson, J. K.
    Forsblad d'Elia, H.
    Turesson, C.
    Kristensen, L. E.
    Jacobsson, L.
    Validity of ankylosing spondylitis and spondyloarthritis diagnoses in the swedish national patient register2014Inngår i: Clinical and Experimental Rheumatology, ISSN 0392-856X, E-ISSN 1593-098X, Vol. 32, nr 5, s. 802-802Artikkel i tidsskrift (Annet vitenskapelig)
  • 282. Exarchou, Sofia
    et al.
    Lie, Elisabeth
    Lindström, Ulf
    Askling, Johan
    Forsblad-d'Elia, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Turesson, Carl
    Kristensen, Lars Erik
    Jacobsson, Lennart Th
    Mortality in ankylosing spondylitis: results from a nationwide population-based study2016Inngår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 75, nr 8, s. 1466-1472Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: Information on mortality in ankylosing spondylitis (AS) is scarce. Our study therefore aimed to assess: (1) mortality in AS versus the general population, and (2) predictors of death in the AS population. Methods: Nationwide cohorts of patients with AS diagnosed at rheumatology or internal medicine outpatient clinics (n=8600) and age-matched, sex-matched and county-matched general population comparators (n=40 460) were identified from the National Patient Register and the census register, respectively. The follow-up period began on 1 January 2006 or at the first date of registered diagnosis thereafter and extended until death, emigration or 31 December 2012, whichever occurred first. Socioeconomic variables, AS-related clinical manifestations, joint surgery, comorbidities and medication were identified from other national registers. Cox regression models were used to determine mortality and predictors for death in the AS cohort. Results: There were 496 deaths in the AS cohort and 1533 deaths in the control cohort resulting in an age-adjusted and sex-adjusted HR of 1.60 (95% CI 1.44 to 1.77), with increased mortality for men (age-adjusted HR=1.53, 95% CI 1.36 to 1.72) and women (ageadjusted HR=1.83, 95% CI 1.50 to 2.22). Within the AS cohort, statistically significant predictors for death were a lower level of education, general comorbidities (diabetes, infections, cardiovascular, pulmonary and malignant diseases) and previous hip replacement surgery. Conclusions: Mortality was increased for male and female patients with AS. Predictors of death within the AS cohort included socioeconomic status, general comorbidities and hip replacement surgery.

  • 283. Exarchou, Sofia
    et al.
    Lindström, Ulf
    Askling, Johan
    Eriksson, Jonas K
    Forsblad-d'Elia, Helena
    Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at University of Gothenburg.
    Neovius, Martin
    Turesson, Carl
    Kristensen, Lars Erik
    Jacobsson, Lennart Th
    The prevalence of clinically diagnosed ankylosing spondylitis and its clinical manifestations: a nationwide register study2015Inngår i: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 17, nr 1, artikkel-id 118Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    INTRODUCTION: Prevalence estimates of ankylosing spondylitis vary considerably, and there are few nationwide estimates. The present study aimed to describe the national prevalence of clinically diagnosed ankylosing spondylitis in Sweden, stratified according to age, sex, geographical, and socio-economic factors, and according to subgroups with ankylosing spondylitis-related clinical manifestations and pharmacological treatment.

    METHODS: All individuals diagnosed with ankylosing spondylitis according to the World Health Organization International Classification of Disease codes, between 1967 and 2009, were identified from the National Patient Register. Data regarding disease manifestations, patient demographics, level of education, pharmacological treatment, and geographical region were retrieved from the National Patient Register and other national registers.

    RESULTS: A total of 11,030 cases with an ankylosing spondylitis diagnosis (alive, living in Sweden, and 16 to 64 years old in December 2009) were identified in the National Patient Register, giving a point prevalence of 0.18% in 2009. The prevalence was higher in northern Sweden, and lower in those with a higher level of education. Men had a higher prevalence of ankylosing spondylitis (0.23% versus 0.14%, P < 0.001), a higher frequency of anterior uveitis (25.5% versus 20.0%, P < 0.001) and were more likely to receive tumor necrosis factor inhibitors than women (15.6% versus 11.8% in 2009, P < 0.001). Women were more likely than men to have peripheral arthritis (21.7% versus 15.3%, P < 0.001), psoriasis (8.0% versus 6.9%, P = 0.03), and treatment with oral corticosteroids (14.0% versus 10.4% in 2009, P < 0.001).

    CONCLUSION: This nationwide, register-based study demonstrated a prevalence of clinically diagnosed ankylosing spondylitis of 0.18%. It revealed phenotypical and treatment differences between the sexes, as well as geographical and socio-economic differences in disease prevalence.

  • 284. Eyre, Steve
    et al.
    Bowes, John
    Barton, Anne
    Amos, Chris
    Diogo, Dorothee
    Lee, Annette
    Padyukov, Leonid
    Stahl, Eli A.
    Martin, Javier
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi. Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Raychaudhuri, Soumya
    Plenge, Robert
    Klareskog, Lars
    Gregersen, Peter
    Worthington, Jane
    Fine mapping in over 14,000 rheumatoid arthritis cases and 18,500 controls refines associations to known loci, indicates multiple independent affects and reveals novel associations2012Inngår i: Rheumatology, ISSN 1462-0324, E-ISSN 1462-0332, Vol. 51, s. 50-50Artikkel i tidsskrift (Annet vitenskapelig)
  • 285. Eyre, Steve
    et al.
    Bowes, John
    Diogo, Dorothee
    Lee, Annette
    Barton, Anne
    Martin, Paul
    Zhernakova, Alexandra
    Stahl, Eli
    Viatte, Sebastien
    McAllister, Kate
    Amos, Christopher I.
    Padyukov, Leonid
    Toes, Rene E. M.
    Huizinga, Tom W. J.
    Wijmenga, Cisca
    Trynka, Gosia
    Franke, Lude
    Westra, Harm-Jan
    Alfredsson, Lars
    Hu, Xinli
    Sandor, Cynthia
    de Bakker, Paul I. W.
    Davila, Sonia
    Khor, Chiea Chuen
    Heng, Khai Koon
    Andrews, Robert
    Edkins, Sarah
    Hunt, Sarah E.
    Langford, Cordelia
    Symmons, Deborah
    Concannon, Pat
    Onengut-Gumuscu, Suna
    Rich, Stephen S.
    Deloukas, Panos
    Gonzalez-Gay, Miguel A.
    Rodriguez-Rodriguez, Luis
    Ärlestig, Lisbeth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Martin, Javier
    Rantapää-Dahlqvist, Solbritt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Plenge, Robert M.
    Raychaudhuri, Soumya
    Klareskog, Lars
    Gregersen, Peter K.
    Worthington, Jane
    High-density genetic mapping identifies new susceptibility loci for rheumatoid arthritis2012Inngår i: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 44, nr 12, s. 1336-1340Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Using the Immunochip custom SNP array, which was designed for dense genotyping of 186 loci identified through genome-wide association studies (GWAS), we analyzed 11,475 individuals with rheumatoid arthritis (cases) of European ancestry and 15,870 controls for 129,464 markers. We combined these data in a meta-analysis with GWAS data from additional independent cases (n = 2,363) and controls (n = 17,872). We identified 14 new susceptibility loci, 9 of which were associated with rheumatoid arthritis overall and five of which were specifically associated with disease that was positive for anticitrullinated peptide antibodies, bringing the number of confirmed rheumatoid arthritis risk loci in individuals of European ancestry to 46. We refined the peak of association to a single gene for 19 loci, identified secondary independent effects at 6 loci and identified association to low-frequency variants at 4 loci. Bioinformatic analyses generated strong hypotheses for the causal SNP at seven loci. This study illustrates the advantages of dense SNP mapping analysis to inform subsequent functional investigations.

  • 286.
    Falahee, Marie
    et al.
    Univ Birmingham, Birmingham, W Midlands, England..
    Simons, Gwenda
    Univ Birmingham, Birmingham, W Midlands, England..
    Buckley, Christopher D.
    Univ Birmingham, Birmingham, W Midlands, England.;Sandwell & West Birmingham Hosp NHS Trust, Birmingham, W Midlands, England..
    Hansson, M G
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Centrum för forsknings- och bioetik.
    Stack, Rebecca J.
    Univ Birmingham, Birmingham, W Midlands, England.;Trent Univ, Nottingham, England..
    Raza, Karim
    Sandwell & West Birmingham Hosp NHS Trust, Birmingham, W Midlands, England..
    Patients' Perceptions of Their Relatives' Risk of Developing Rheumatoid Arthritis and of the Potential for Risk Communication, Prediction, and Modulation2017Inngår i: Arthritis care & research, ISSN 2151-464X, E-ISSN 2151-4658, Vol. 69, nr 10, s. 1558-1565Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: To understand the perspectives of patients with rheumatoid arthritis (RA) about the risk of their relatives developing RA in the future, and about communicating with their relatives concerning risk and its modulation.

    Methods: Twenty-one RA patients took part in semistructured interviews.

    Results: Participants reported willingness to communicate with relatives about their risk of developing RA, but described choosing which relatives to communicate with, on the basis of the relatives' perceived receptivity to such risk information. Participants described the potential for risk information to cause negative emotions. Some participants did not consider RA to be hereditable, and few reported smoking as a risk factor. Patients described a lack of public awareness about the causes of RA and the negative impact that RA has on the quality of life. Awareness of this negative impact was identified as an important driver for predictive and preventive strategies. Participants held positive perceptions of predictive testing for RA, though the results of predictive tests were conceptualized as having a high degree of accuracy. Negative views of predictive testing were associated with an appreciation of the probabilistic nature of risk information. Participants felt that their relatives would prefer lifestyle modification over medication as a risk reduction strategy.

    Conclusion: Information about risk factors for RA, and the potential impact of RA on the quality of life, is needed to support family communication about RA risk. Management of expectations is needed in relation to the probabilistic nature of risk information, and appropriate support should be provided for negative psychological outcomes.

  • 287. Falkenburg, W.
    et al.
    Bos, W. H.
    Sohrabian, Azita
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Wolbink, G.
    van Schaardenburg, D.
    Igg ACPA Level Increase Drives Rheumatoid Factor Response Maturation in Patients before Onset of Clinically Apparent Rheumatoid Arthritis2014Inngår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 73, nr S2, s. 359-360Artikkel i tidsskrift (Annet vitenskapelig)
  • 288.
    Farias, Fabiana
    et al.
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Wilbe, Maria
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Medicinsk genetik och genomik.
    Dahlqvist, Johanna
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Leonard, Dag
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi.
    Kozyrev, Sergey
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Pielberg, Gerli
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Eloranta, Maija-Leena
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi.
    Rönnblom, Lars
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi.
    Lindblad-Toh, Kerstin
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    High-Throughput Sequencing of 219 Candidate Genes for Identification of SLE-Associated Risk Variants2014Inngår i: Arthritis & Rheumatology, ISSN 2326-5191, Vol. 66, nr S10, s. S1170-S1170, artikkel-id 2673Artikkel i tidsskrift (Annet vitenskapelig)
  • 289.
    Feldhusen, Caroline
    et al.
    Sahlgrenska akademin, Göteborgs universitet.
    Björk, Mathilda
    Avd. för rehabilitering, HHJ, Hälsohögskolan, Högskolan i Jönköping.
    Forsblad d'Elia, Helena
    Sahlgrenska akademin, Göteborgs universitet.
    Mannerkorpi, Kaisa
    Sahlgrenska akademin, Göteborgs universitet.
    I am so tired of being tired: – a focus group study of fatigue in RA2011Konferansepaper (Annet vitenskapelig)
    Abstract [en]

    BakgrundFatigue is a prominent symptom in persons with Rheumatoid Arthritis (RA)and has great impact of daily life. The knowledge about how persons with RA in working age are affected by fatigue is limited. The aim of this study was to describe how persons with RA in working age experience and handle their fatigue in everyday life.MetodSix focus group discussions were conducted in 25 persons with RA (19 women/ 6 men) age 20-60 years. The discussions were recorded, transcribed verbatim and analyzed according to qualitative content analysis which resulted in four categories: The nature of fatigue in RA, limitations due to the fatigue, communicating the fatigue and strategies to handle the fatigue.ResultatThe participants experienced their fatigue as a major symptom. Because of its persistence and unpredictable nature it caused feelings of frustration, helplessness and anger. The increased need for rest and sleep caused an imbalance in daily life when valued life activities were forced to be omitted in favor of work. They were feeling limited in everyday life when the fatigue made it impossible to fulfill their roles as expected by themselves and by others. The participants expressed difficulties in communicating about the fatigue and to gain acceptance from the social environment including family, friends and health professionals. They adjusted to whom they were talking to about their fatigue to avoid being seen as lazy, boring or whining. To handle the fatigue in everyday life, planning and prioritizing to find balance was essential. The respondents also used mental strategies to handle the fatigue such as accepting the fatigue and focusing on the possibilities.SammanfattningFatigue causes considerable consequences in persons with RA in working age, living an active life and rating a low general disability. The responsibility for managing fatigue and the struggle of finding balance between important parts in life was taken by the participants themselves because fatigue was not perceived to be a factor given much consideration during medical consultation. This draws attention to the importance for health professionals to address the fatigue and its complexity and unpredictability, even in working persons with low disability.

  • 290.
    Feldhusen, Caroline
    et al.
    Sahlgrenska akademin.
    Björk, Mathilda
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Avd. för rehabilitering. Högskolan i Jönköping, Hälsohögskolan, HHJ. ADULT.
    Forsblad d'Elia, Helena
    Sahlgrenska akademin.
    Mannerkorpi, Kaisa
    Sahlgrenska akademin.
    I am so tired of being tired: – a focus group study of fatigue in RA2011Konferansepaper (Fagfellevurdert)
    Abstract [en]

    BakgrundFatigue is a prominent symptom in persons with Rheumatoid Arthritis (RA)and has great impact of daily life. The knowledge about how persons with RA in working age are affected by fatigue is limited. The aim of this study was to describe how persons with RA in working age experience and handle their fatigue in everyday life.MetodSix focus group discussions were conducted in 25 persons with RA (19 women/ 6 men) age 20-60 years. The discussions were recorded, transcribed verbatim and analyzed according to qualitative content analysis which resulted in four categories: The nature of fatigue in RA, limitations due to the fatigue, communicating the fatigue and strategies to handle the fatigue.ResultatThe participants experienced their fatigue as a major symptom. Because of its persistence and unpredictable nature it caused feelings of frustration, helplessness and anger. The increased need for rest and sleep caused an imbalance in daily life when valued life activities were forced to be omitted in favor of work. They were feeling limited in everyday life when the fatigue made it impossible to fulfill their roles as expected by themselves and by others. The participants expressed difficulties in communicating about the fatigue and to gain acceptance from the social environment including family, friends and health professionals. They adjusted to whom they were talking to about their fatigue to avoid being seen as lazy, boring or whining. To handle the fatigue in everyday life, planning and prioritizing to find balance was essential. The respondents also used mental strategies to handle the fatigue such as accepting the fatigue and focusing on the possibilities.SammanfattningFatigue causes considerable consequences in persons with RA in working age, living an active life and rating a low general disability. The responsibility for managing fatigue and the struggle of finding balance between important parts in life was taken by the participants themselves because fatigue was not perceived to be a factor given much consideration during medical consultation. This draws attention to the importance for health professionals to address the fatigue and its complexity and unpredictability, even in working persons with low disability.

  • 291.
    Feldthusen, Caroline
    et al.
    Sahlgrenska akademin, Göteborgs universitet.
    Björk, Mathilda
    Avd. för rehabilitering, HHJ, Hälsohögskolan, Högskolan i Jönköping.
    Forsblad-d'Elia, Helena
    Sahlgrenska akademin, Göteborgs universitet.
    Mannerkorpi, Kaisa
    Sahlgrenska akademin, Göteborgs universitet.
    I am so tired of being tired: – a focus group study of fatigue in RA2011Konferansepaper (Fagfellevurdert)
    Abstract [en]

    Background: Fatigue is a prominent symptom in RA and most negative impact from fatigue seems to be experienced by younger persons. Even in individuals with RA who are able to successfully participate in a wide spectrum of demanding daily activities, fatigue has been shown to be significant. The knowledge about how younger persons with RA experience and handle their fatigue is limited.Objectives: The aims were to explore, by means of qualitative interviews, how fatigue is experienced by persons with RA in working age and to identify when fatigue is experienced as a limitation and how it is handled in everyday life.Methods: Six focus group interviews were conducted with 25 (19 women, 6 men) persons. Inclusion criteria: >30 mm fatigue on a 100 mm visual analogue scale, age between 20-60 years and fulfill classification criteria of rheumatoid arthritis. The persons were asked to discuss their fatigue related to RA as well as how fatigue affected everyday life and how fatigue was handled. Transcripts were systematically analyzed by content analysis identifying units, codes, sub categories, categories and a theme (1). The categories and theme were validated by an expert in the field and by a research partner with RA.Results: Fatigue was experienced by the respondents as a significant symptom. Because of its persistence and unpredictable nature it caused feelings of frustration, helplessness and anger. The respondents expressed difficulties in communicating about the fatigue and to get understanding from the social environment including family, friends and healthcare. They were feeling limited in everyday life when the fatigue made it impossible to fulfill the roles as expected by themselves and by others. Feelings of shame, being lazy and boring were common. Finding balance between important parts of life such as work, family, leisure time, social activities and rest was mentioned as difficult. To handle the fatigue in everyday life planning and prioritizing among activities was essential. The respondents also used mental strategies to handle the fatigue including trying to accept the fatigue and focus on the possibilities.Conclusions: The result showed that fatigue in persons with RA in working age was a symptom of great importance that needs to be more highlighted in the clinical care. Even if the patients did not report extremely high levels of fatigue the consequences were extensive. An understanding of the complexity of fatigue in RA could help the persons to find a better balance between important parts in life.

  • 292.
    Feldthusen, Caroline
    et al.
    Sahlgrenska akademin.
    Björk, Mathilda
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Avd. för rehabilitering. Högskolan i Jönköping, Hälsohögskolan, HHJ. ADULT.
    Forsblad-d'Elia, Helena
    Sahlgrenska akademin.
    Mannerkorpi, Kaisa
    Sahlgrenska akademin.
    I am so tired of being tired: – a focus group study of fatigue in RA2011Konferansepaper (Fagfellevurdert)
    Abstract [en]

    Background: Fatigue is a prominent symptom in RA and most negative impact from fatigue seems to be experienced by younger persons. Even in individuals with RA who are able to successfully participate in a wide spectrum of demanding daily activities, fatigue has been shown to be significant. The knowledge about how younger persons with RA experience and handle their fatigue is limited.Objectives: The aims were to explore, by means of qualitative interviews, how fatigue is experienced by persons with RA in working age and to identify when fatigue is experienced as a limitation and how it is handled in everyday life.Methods: Six focus group interviews were conducted with 25 (19 women, 6 men) persons. Inclusion criteria: >30 mm fatigue on a 100 mm visual analogue scale, age between 20-60 years and fulfill classification criteria of rheumatoid arthritis. The persons were asked to discuss their fatigue related to RA as well as how fatigue affected everyday life and how fatigue was handled. Transcripts were systematically analyzed by content analysis identifying units, codes, sub categories, categories and a theme (1). The categories and theme were validated by an expert in the field and by a research partner with RA.Results: Fatigue was experienced by the respondents as a significant symptom. Because of its persistence and unpredictable nature it caused feelings of frustration, helplessness and anger. The respondents expressed difficulties in communicating about the fatigue and to get understanding from the social environment including family, friends and healthcare. They were feeling limited in everyday life when the fatigue made it impossible to fulfill the roles as expected by themselves and by others. Feelings of shame, being lazy and boring were common. Finding balance between important parts of life such as work, family, leisure time, social activities and rest was mentioned as difficult. To handle the fatigue in everyday life planning and prioritizing among activities was essential. The respondents also used mental strategies to handle the fatigue including trying to accept the fatigue and focus on the possibilities.Conclusions: The result showed that fatigue in persons with RA in working age was a symptom of great importance that needs to be more highlighted in the clinical care. Even if the patients did not report extremely high levels of fatigue the consequences were extensive. An understanding of the complexity of fatigue in RA could help the persons to find a better balance between important parts in life.

  • 293.
    Feldthusen, Caroline
    et al.
    Department of Rheumatology and Inflammation research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden .
    Björk, Mathilda
    Department of Rheumatology and Inflammation research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden .
    Forsblad-d'Elia, Helena
    Department of Rheumatology and Inflammation research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden .
    Mannerkorpi, Kaisa
    Department of Rheumatology and Inflammation research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden .
    Perception, consequences, communication, and strategies for handling fatigue in persons with rheumatoid arthritis of working age-a focus group study2013Inngår i: Clinical Rheumatology, ISSN 0770-3198, E-ISSN 1434-9949, Vol. 32, nr 5, s. 557-566Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to describe how persons with rheumatoid arthritis (RA) of working age experience and handle their fatigue in everyday life. Six focus group discussions were conducted focusing on experiences of fatigue in 25 persons with RA (19 women, 6 men), aged 20–60 years. The discussions were recorded, transcribed verbatim, and analyzed according to qualitative content analysis. The analyses resulted in four categories. (1) Perception of fatigue: Fatigue was experienced different from normal tiredness, unpredictable, and overwhelming. It was associated with negative emotions, changed self-image, and fears. Feelings of frustration and shame were central when the persons were forced to omit valued life activities. (2) Consequences due to fatigue: The fatigue caused changes in cognitive ability, ability to act, and overall activity pattern where the increased need for rest and sleep caused an imbalance in daily life. The participants struggled not to let the fatigue interfere with work. The fatigue also brought negative consequences for their significant others. (3) Communicating fatigue: Fatigue was difficult to gain understanding for, and the participants adjusted their communication accordingly; it was important to keep up appearances. During medical consultation, fatigue was perceived as a factor not given much consideration, and the participants expressed taking responsibility for managing their fatigue symptoms themselves. (4) Strategies to handle fatigue: Strategies comprised conscious self-care, mental strategies, planning, and prioritizing. Fatigue caused considerable health problems for persons with RA of working age: negative emotions, imbalance in daily life due to increased need for rest, and difficulties gaining understanding. This draws attention to the importance of developing new modes of care to address fatigue in RA. Person-centered care to improve balance in life may be one approach needing further investigations.

  • 294.
    Feldthusen, Caroline
    et al.
    Department of Physical and Occupational Therapy, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Björk, Mathilda
    Högskolan i Jönköping, Hälsohögskolan, HHJ, Avd. för rehabilitering. Högskolan i Jönköping, Hälsohögskolan, HHJ. ADULT.
    Forsblad-d'Elia, Helena
    Department of Physical and Occupational Therapy, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Mannerkorpi, Kaisa
    Department of Physical and Occupational Therapy, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Perception, consequences, communication, and strategies for handling fatigue in persons with rheumatoid arthritis of working age-a focus group study2013Inngår i: Clinical Rheumatology, ISSN 0770-3198, E-ISSN 1434-9949, Vol. 32, nr 5, s. 557-566Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to describe how persons with rheumatoid arthritis (RA) of working age experience and handle their fatigue in everyday life. Six focus group discussions were conducted focusing on experiences of fatigue in 25 persons with RA (19 women, 6 men), aged 20–60 years. The discussions were recorded, transcribed verbatim, and analyzed according to qualitative content analysis. The analyses resulted in four categories. (1) Perception of fatigue: Fatigue was experienced different from normal tiredness, unpredictable, and overwhelming. It was associated with negative emotions, changed self-image, and fears. Feelings of frustration and shame were central when the persons were forced to omit valued life activities. (2) Consequences due to fatigue: The fatigue caused changes in cognitive ability, ability to act, and overall activity pattern where the increased need for rest and sleep caused an imbalance in daily life. The participants struggled not to let the fatigue interfere with work. The fatigue also brought negative consequences for their significant others. (3) Communicating fatigue: Fatigue was difficult to gain understanding for, and the participants adjusted their communication accordingly; it was important to keep up appearances. During medical consultation, fatigue was perceived as a factor not given much consideration, and the participants expressed taking responsibility for managing their fatigue symptoms themselves. (4) Strategies to handle fatigue: Strategies comprised conscious self-care, mental strategies, planning, and prioritizing. Fatigue caused considerable health problems for persons with RA of working age: negative emotions, imbalance in daily life due to increased need for rest, and difficulties gaining understanding. This draws attention to the importance of developing new modes of care to address fatigue in RA. Person-centered care to improve balance in life may be one approach needing further investigations.

  • 295. Feldthusen, Caroline
    et al.
    Björk, Mathilda
    Forsblad-d'Elia, Helena
    Dept of Rheumatology and Inflammation Research, Sahlgrenska Academy, Göteborgs universitet.
    Mannerkorpi, Kaisa
    Perception, consequences, communication, and strategies for handling fatigue in persons with rheumatoid arthritis of working age--a focus group study.2013Inngår i: Clinical Rheumatology, ISSN 0770-3198, E-ISSN 1434-9949, Vol. 32, nr 5, s. 557-66Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to describe how persons with rheumatoid arthritis (RA) of working age experience and handle their fatigue in everyday life. Six focus group discussions were conducted focusing on experiences of fatigue in 25 persons with RA (19 women, 6 men), aged 20-60 years. The discussions were recorded, transcribed verbatim, and analyzed according to qualitative content analysis. The analyses resulted in four categories. (1) Perception of fatigue: Fatigue was experienced different from normal tiredness, unpredictable, and overwhelming. It was associated with negative emotions, changed self-image, and fears. Feelings of frustration and shame were central when the persons were forced to omit valued life activities. (2) Consequences due to fatigue: The fatigue caused changes in cognitive ability, ability to act, and overall activity pattern where the increased need for rest and sleep caused an imbalance in daily life. The participants struggled not to let the fatigue interfere with work. The fatigue also brought negative consequences for their significant others. (3) Communicating fatigue: Fatigue was difficult to gain understanding for, and the participants adjusted their communication accordingly; it was important to keep up appearances. During medical consultation, fatigue was perceived as a factor not given much consideration, and the participants expressed taking responsibility for managing their fatigue symptoms themselves. (4) Strategies to handle fatigue: Strategies comprised conscious self-care, mental strategies, planning, and prioritizing. Fatigue caused considerable health problems for persons with RA of working age: negative emotions, imbalance in daily life due to increased need for rest, and difficulties gaining understanding. This draws attention to the importance of developing new modes of care to address fatigue in RA. Person-centered care to improve balance in life may be one approach needing further investigations.

  • 296. Feldthusen, Caroline
    et al.
    Dean, Elizabeth
    Forsblad-d'Elia, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Mannerkorpi, Kaisa
    Effects of Person-Centered Physical Therapy on Fatigue-Related Variables in Persons With Rheumatoid Arthritis: A Randomized Controlled Trial2016Inngår i: Archives of Physical Medicine and Rehabilitation, ISSN 0003-9993, E-ISSN 1532-821X, Vol. 97, nr 1, s. 26-36Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To examine effects of person-centered physical therapy on fatigue and related variables in persons with rheumatoid arthritis (RA).

    DESIGN: Randomized controlled trial.

    SETTING: Hospital outpatient rheumatology clinic.

    PARTICIPANTS: Persons with RA aged 20-65y (n=70); intervention-group (n=36) and reference-group (n=34).

    INTERVENTION: The 12-week intervention, with 6-month follow-up, focused on partnership between participant and physical therapist, and tailored health-enhancing physical activity and balancing life activities. The reference-group continued with regular activities; both groups received usual healthcare.

    MAIN OUTCOME MEASURES: Primary outcome was general fatigue (Visual Analogue Scale, VAS). Secondary outcomes included multidimensional fatigue (Bristol Rheumatoid Arthritis Fatigue - Multi-Dimensional Questionnaire, BRAF-MDQ), and fatigue-related variables, i.e., disease, health and function.

    RESULTS: At posttest, general fatigue improved more in the intervention-group than reference-group (p=0.042). Improvement in median general fatigue reached minimal clinically important difference between and within groups at posttest and follow-up. Improvement was also observed for anxiety (p=0.0099) and trends toward improvements was observed for most multidimensional aspects of fatigue (p=0.023-p=0.048), leg strength/endurance (p=0.024) and physical activity (p=0.023). Compared with the reference-group at follow-up, intervention-group improvement was observed for leg strength/endurance (p=0.001) and the trends toward improvements persisted for physical (p=0.041) and living-related (p=0.031) aspects of fatigue, physical activity (p=0.019) and anxiety (p=0.015) and self-rated health (p=0.010) and self-efficacy (p=0.046).

    CONCLUSIONS: Person-centered physical therapy focused on health-enhancing physical activity and balancing life activities, showed significant benefits on fatigue in persons with RA.

  • 297. Feldthusen, Caroline
    et al.
    Grimby-Ekman, Anna
    Forsblad-d'Elia, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Jacobsson, Lennart
    Mannerkorpi, Kaisa
    Explanatory factors and predictors of fatigue in persons with rheumatoid arthritis: a longitudinal study2016Inngår i: Journal of Rehabilitation Medicine, ISSN 1650-1977, E-ISSN 1651-2081, Vol. 48, nr 5, s. 469-476Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To investigate the impact of disease-related aspects on long-term variations in fatigue in persons with rheumatoid arthritis.

    DESIGN: Observational longitudinal study.

    METHODS: Sixty-five persons with rheumatoid arthritis, age range 20-65 years, were invited to a clinical examination at 4 time-points during the 4 seasons. Outcome measures were: general fatigue rated on visual analogue scale (0-100) and aspects of fatigue assessed by the Bristol Rheumatoid Arthritis Fatigue Multidimensional Questionnaire. Disease-related variables were: disease activity (erythrocyte sedimentation rate), pain threshold (pressure algometer), physical capacity (six-minute walk test), pain (visual analogue scale (0-100)), depressive mood (Hospital Anxiety and Depression scale, depression subscale), personal factors (age, sex, body mass index) and season. Multivariable regression analysis, linear mixed effects models were applied.

    RESULTS: The strongest explanatory factors for all fatigue outcomes, when recorded at the same time-point as fatigue, were pain threshold and depressive mood. Self-reported pain was an explanatory factor for physical aspects of fatigue and body mass index contributed to explaining the consequences of fatigue on everyday living. For predicting later fatigue pain threshold and depressive mood were the strongest predictors.

    CONCLUSION: Pain threshold and depressive mood were the most important factors for fatigue in persons with rheumatoid arthritis.

  • 298. Feldthusen, Caroline
    et al.
    Grimby-Ekman, Anna
    Forsblad-d'Elia, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Jacobsson, Lennart
    Mannerkorpi, Kaisa
    Seasonal variations in fatigue in persons with rheumatoid arthritis: a longitudinal study2016Inngår i: BMC Musculoskeletal Disorders, ISSN 1471-2474, E-ISSN 1471-2474, Vol. 17, artikkel-id 59Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Fatigue is a prominent symptom in persons with rheumatoid arthritis (RA). Although this symptom has been described to vary in duration and frequency little is known about fluctuations in fatigue over time and season. The aim of this study was to describe monthly and seasonal variations in fatigue, in persons with RA of working age.

    Methods: Sixty-five participants diagnosed with RA and aged 20-65 years were recruited from a rheumatology clinic in Sweden. The participants provided self-assessments of their fatigue at seven time points during the four seasons using a 0-100 mm visual analogue scale (VAS) and the Bristol Rheumatoid Arthritis Fatigue Multidimensional Questionnaire (BRAF-MDQ). Multiple regression analysis using mixed models was used to analyze changes in fatigue over time.

    Results: The mean +/- SD of fatigue rated on the VAS was 51 +/- 13, indicating substantial fatigue. Analysis of monthly variation showed statistically significant variation in fatigue ratings concerning VAS fatigue score (p < 0.01) as well as the BRAF-MDQ total score and Living, Cognition (p < 0.001), and Physical (p < 0.05) sub-scores, but not the BRAF-MDQ Emotional sub-score. The greatest variations were seen from January to September, with higher fatigue ratings in January. The changes in VAS fatigue scores over time were considered to be of clinical importance. Analysis of seasonal variation revealed a statistically significant seasonal variation in fatigue levels, with higher fatigue values during the winter as measured by VAS fatigue score (p < 0.01) as well as BRAF-MDQ total score (p < 0.01) and Physical and Living sub-scores (both p < 0.01). The greatest variation was seen between winter and autumn for VAS fatigue and between winter and summer for BRAF-MDQ total score and Physical and Living sub-scores. There were no statistical differences in fatigue levels, monthly or seasonal, between sexes or age groups.

    Conclusions: The majority of rating scales used in this study showed fluctuations in fatigue, general and physical fatigue being significantly greater during the winter. As fatigue is a substantial symptom in many persons with RA, this information is important for rheumatology professionals when dealing with persons with RA in routine care.

  • 299. Fernandes-Cerqueira, Catia
    et al.
    Ossipova, Elena
    Gunasekera, Sunithi
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för läkemedelskemi, Avdelningen för farmakognosi.
    Hansson, Monika
    Mathsson, Linda
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Catrina, Anca I.
    Sommarin, Yngve
    Klareskog, Lars
    Lundberg, Karin
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Göransson, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för läkemedelskemi, Avdelningen för farmakognosi.
    Jakobsson, Per-Johan
    Targeting of anti-citrullinated protein/peptide antibodies in rheumatoid arthritis using peptides mimicking endogenously citrullinated fibrinogen antigens2015Inngår i: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 17, artikkel-id 155Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Introduction: We have previously identified endogenously citrullinated peptides derived from fibrinogen in rheumatoid arthritis (RA) synovial tissues. In this study, we have investigated the auto-antigenicity of four of those citrullinated peptides, and explored their feasibility to target anti-citrullinated protein/peptide antibodies (ACPA). Methods: The autoantigenic potential of the fibrinogen peptides was investigated by screening 927 serum samples from the Epidemiological Investigation of RA (EIRA) cohort on a peptide microarray based on the ImmunoCAP ISAC (R) system. In order to assay for ACPA blocking, two independent pools of purified ACPA were incubated with the respective targeting peptide prior to binding to cyclic citrullinated peptide (CCP) 2 using the CCPlus (R) ELISA kit. Results: Two peptides derived from the fibrinogen a chain, Arg573Cit (563-583) and Arg591Cit (580-600), referred to as Cit573 and Cit591, and two peptides from the fibrinogen beta chain, Arg72Cit (62-81) and Arg74Cit (62-81) (Cit72 and Cit74), displayed 65 %, 15 %, 35 %, and 53 % of immune reactivity among CCP2-positive RA sera, respectively. In CCP2-negative RA sera, a positive reactivity was detected in 5 % (Cit573), 6 % (Cit591), 8 % (Cit72), and 4 % (Cit74). In the competition assay, Cit573 and Cit591 peptides reduced ACPA binding to CCP2 by a maximum of 84 % and 63 % respectively. An additive effect was observed when these peptides were combined. In contrast, Cit74 and Cit72 were less effective. Cyclization of the peptide structure containing Cit573 significantly increased the blocking efficiency. Conclusions: Here we demonstrate extensive autoantibody reactivity against in vivo citrullinated fibrinogen epitopes, and further show the potential use of these peptides for antagonizing ACPA.

  • 300. Fisher, Benjamin A.
    et al.
    Plant, Darren
    Brode, Monica
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    van Vollenhoven, Ronald F.
    Mathsson, Linda
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Symmons, Deborah
    Lundberg, Karin
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Venables, Patrick J.
    Antibodies to citrullinated α-enolase peptide 1 and clinical and radiological outcomes in rheumatoid arthritis2011Inngår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 70, nr 6, s. 1095-1098Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    INTRODUCTION:

    The anticyclic citrullinated peptide 2 (anti-CCP2) assay is a generic test for antibodies to citrullinated proteins, among which there is a subset of about 50% with antibodies to citrullinated enolase peptide 1 (CEP-1). The anti-CEP-1 positive subset is strongly associated with the HLA-DRB1 shared epitope and its interaction with smoking.

    OBJECTIVE:

    To investigate whether anti-CEP-1 antibodies may be helpful in predicting outcome.

    METHODS:

     Anti-CEP-1 and anti-CCP2 antibodies were measured in two prospective cohorts of patients (Karolinska n=272, Norfolk Arthritis Register (NOAR) n=408) with early rheumatoid arthritis (RA). Outcomes measured were C-reactive protein, erythrocyte sedimentation rate, visual analogue scales for pain and global assessment of disease activity, Health Assessment Questionnaire, physician's assessment, swollen and tender joint counts and radiological progression.

    RESULTS:

     Anti-CCP2 antibodies were present in 57% and 50%, and anti-CEP-1 in 27% and 24% of the Karolinska and NOAR cohorts, respectively. Importantly, no statistically significant differences in clinical outcomes were demonstrated between the anti-CEP-1-/CCP2+ and the anti-CEP-1+/CCP2+ subsets in either cohort, or in radiological outcomes in the Karolinska cohort.

    CONCLUSION:

     Although antibodies to specific citrullinated proteins may have distinct genetic and environmental risk factors, the similarity in clinical phenotype suggests that they share common pathways in the pathogenesis of joint disease in RA.

     

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