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  • 1.
    Ambrosi, Aurelie
    et al.
    Karolinska Institutet, Stockholm.
    Salomonsson, Stina
    Karolinska Institutet, Stockholm.
    Eliasson, Håkan
    Karolinska Institutet, Stockholm.
    Zeffer, Elisabeth
    Karolinska Institutet, Stockholm.
    Skog, Amanda
    Karolinska Institutet, Stockholm.
    Dzikaite, Vijole
    Karolinska Institutet, Stockholm.
    Bergman, Gunnar
    Karolinska Institutet, Stockholm.
    Fernlund, Eva
    Skåne University Hospital, Lund.
    Tingström, Joanna
    Skåne University Hospital, Lund.
    Theander, Elke
    Skåne University Hospital, Malmö.
    Rydberg, Annika
    Umeå University Hospital.
    Skogh, Thomas
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Rheumatology in Östergötland.
    Öhman, Annika
    Uppsala University.
    Lundström, Ulla
    Sahlgrenska University Hospital.
    Mellander, Mats
    Sahlgrenska University Hospital.
    Winqvist, Ola
    Karolinska Institutet, Stockholm.
    Fored, Michael
    Karolinska Institutet, Stockholm.
    Ekbom, Anders
    Karolinska Institutet, Stockholm.
    Alfredsson, Lars
    Institute of Environmental Medicine, Stockholm.
    Källberg, Henrik
    Institute of Environmental Medicine, Stockholm.
    Olsson, Tomas
    Karolinska Institutet, Stockholm.
    Gadler, Fredrik
    Karolinska Institutet, Stockholm.
    Jonzon, Anders
    Sahlgrenska University Hospital, Göteborg.
    Kockum, Ingrid
    Karolinska Institutet, Stockholm.
    Sonesson, Sven-Erik
    Karolinska Institutet, Stockholm.
    Wahren-Herlenius, Marie
    Karolinska Institutet, Stockholm.
    Development of heart block in children of SSA/SSB-autoantibody-positive women is associated with maternal age and displays a season-of-birth pattern2012In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 71, no 3, p. 334-340Article in journal (Refereed)
    Abstract [en]

    Objective Congenital heart block may develop in the fetuses of Ro/SSA-positive and La/SSB-positive mothers. Recurrence rates of only 10-20% despite persisting maternal antibodies indicate that additional factors are critical for the establishment of heart block. The authors investigated the influence of other maternal and fetal factors on heart block development in a Swedish population-based cohort. less thanbrgreater than less thanbrgreater thanMethods The influence of fetal gender, maternal age, parity and time of birth on heart block development was analysed in 145 families, including Ro/La-positive (n=190) and Ro/La-negative (n=165) pregnancies. less thanbrgreater than less thanbrgreater thanResults There was a recurrence rate of 12.1% in Ro/La-positive women, and no recurrence in Ro/La-negative women. Fetal gender and parity did not influence the development of heart block in either group. Maternal age in Ro/La-positive pregnancies with a child affected by heart block was, however, significantly higher than in pregnancies resulting in babies without heart block (pandlt;0.05). Seasonal timing of pregnancy influenced the outcome. Gestational susceptibility weeks 18-24 occurring during January-March correlated with a higher proportion of children with heart block and lower vitamin D levels during the same period in a representative sample of Swedish women and a corresponding higher proportion of children with heart block born in the summer (pandlt;0.02). Maternal age or seasonal timing of pregnancy did not affect the outcome in Ro/La-negative pregnancies. less thanbrgreater than less thanbrgreater thanConclusion This study identifies maternal age and seasonal timing of pregnancy as novel risk factors for heart block development in children of Ro/La-positive women. These observations may be useful for counselling when pregnancy is considered.

  • 2.
    Arkema, Elizabeth V
    et al.
    Clinical Epidemiology Unit, Karolinska Institutet, Stockholm.
    Rossides, Marios
    Clinical Epidemiology Unit, Karolinska Institutet, Stockholm.
    Von Euler, Mia
    Karolinska Institutet, Stockholm, Sweden.
    Svenungsson, Elisabet
    Rheumatology Unit, Karolinska Institutet, Stockholm.
    Sjöwall, Christopher
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Rheumatology.
    Simard, Julia F
    Karolinska Institutet, Stockholm, Sweden, Stanford School of Medicine, Stanford, California, USA.
    Response to: 'Increased stroke incidence in systemic lupus erythematosus patients2017In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, article id annrheumdis-2017-212604Article in journal (Refereed)
  • 3.
    Arkema, Elizabeth V.
    et al.
    Karolinska Institute, Sweden.
    Svenungsson, Elisabet
    Karolinska Institute, Sweden.
    Von Euler, Mia
    Karolinska Institute, Sweden.
    Sjöwall, Christopher
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Rheumatology.
    Simard, Julia F.
    Karolinska Institute, Sweden; Stanford School Med, CA USA; Stanford School Med, CA USA.
    Stroke in systemic lupus erythematosus: a Swedish population-based cohort study2017In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 76, no 9, p. 1544-1549Article in journal (Refereed)
    Abstract [en]

    Objective To study the occurrence of ischaemic and haemorrhagic stroke in systemic lupus erythematosus (SLE) compared with the general population by age, sex and time since SLE diagnosis Methods Adults with incident SLE were identified from the Swedish National Patient Register (NPR, n=3390) and general population comparators from the Total Population Register were matched on age, sex and county (n=16730). Individuals were followed prospectively until first of death, December 2013, emigration or incident stroke (identified from the NPR, Cause of Death Register and the Stroke Register). Incidence rates, rate differences and HR were estimated comparing SLE with non-SLE. Estimates were stratified by sex, age and time since diagnosis. Results We observed 126 strokes in SLE and 304 in the general population. Individuals with SLE had a twofold increased rate of ischaemic stroke compared with the general population (HR 2.2; 95% CI 1.7 to 2.8). The HR for intracerebral haemorrhage was 1.4 (95% CI 0.7 to 2.8). There was effect modification by sex and age, with the highest HRs for females and individuals amp;lt;50 years old. The HR for ischaemic stroke was highest in the first year of follow-up (3.7; 95% CI 2.1 to 6.5). Conclusions The relative risk of ischaemic stroke in SLE was more than doubled compared with the general population, and importantly, the highest relative risks were observed within the first year after SLE diagnosis. Thus, the first encounter with patients presents an opportunity for rheumatologists to screen for risk factors and intervene.

  • 4.
    Askling, J
    et al.
    Karolinska University Hospital, Stockholm, Sweden.
    Baecklund, E
    Uppsala University Hospital, Uppsala, Sweden.
    Granath, F
    Karolinska University Hospital, Stockholm, Sweden.
    Geborek, P
    Lund University Hospital, Lund, Sweden.
    Fored, M
    Karolinska University Hospital, Stockholm, Sweden.
    Backlin, C
    Uppsala University, Uppsala, Sweden.
    Bertilsson, L
    Sahlgrens University Hospital, Gothenburg, Sweden.
    Cöster, Lars
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Jacobsson, L T
    Malmö University Hospital, Malmö, Sweden.
    Lindblad, S
    Karolinska University Hospital, Stockholm, Sweden.
    Lysholm, J
    Falu County Hospital, Falun, Sweden.
    Rantapaa-Dahlqvist, S
    Umeå University Hospital, Umeå, Sweden.
    Saxne, T
    University of Lund Hospital, Lund, Sweden.
    van Vollenhoven, R
    Karolinska University Hospital, Stockholm, Sweden.
    Klareskog, L
    Karolinska University Hospital, Stockholm, Sweden.
    Feltelius, N
    Medical Products Agency, Uppsala, Sweden.
    Anti-tumour necrosis factor therapy in rheumatoid arthritis and risk of malignant lymphomas: relative risks and time trends in the Swedish Biologics Register2009In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 68, no 5, p. 648-653Article in journal (Refereed)
    Abstract [en]

    Background: Tumour necrosis factor (TNF) antagonists have proved effective as treatment against rheumatoid arthritis ( RA), but the unresolved issue of whether the use of anti-TNF therapy increases the already elevated risk of lymphoma in RA remains a concern.

    Methods: Using the Swedish Biologics Register (ARTIS), the Swedish Cancer Register, pre-existing RA cohorts and cross-linkage with other national health and census registers, a national RA cohort (n = 67 743) was assembled and patients who started anti-TNF therapy between 1998 and July 2006 ( n = 6604) were identified. A general population comparator ( n = 471 024) was also assembled and the incidence of lymphomas from 1999 to 31 December 2006 was assessed and compared in these individuals.

    Results: Among the 6604 anti-TNF-treated RA patients, 26 malignant lymphomas were observed during 26 981 person-years of follow-up, which corresponded to a relative risk (RR) of 1.35 (95% CI 0.82 to 2.11) versus anti-TNF-naive RA patients ( 336 lymphomas during 365 026 person-years) and 2.72 ( 95% CI 1.82 to 4.08) versus the general population comparator ( 1568 lymphomas during 3 355 849 person-years). RA patients starting anti-TNF therapy in 1998-2001 accounted for the entire increase in lymphoma risk versus the two comparators. By contrast, RR did not vary significantly by time since start of first treatment or with the accumulated duration of treatment, nor with the type of anti-TNF agent.

    Conclusion: Overall and as used in routine care against RA, TNF antagonists are not associated with any major further increase in the already elevated lymphoma occurrence in RA. Changes in the selection of patients for treatment may influence the observed risk.

  • 5. Askling, J
    et al.
    Fored, CM
    Baecklund, E
    Brandt, L
    Backlin, C
    Ekbom, A
    Sundström, C
    Bertilsson, L
    Cöster, Lars
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Geborek, P
    Jacobsson, Lt
    Lindblad, S
    Lysholm, J
    Rantapää-Dahlqvist, S
    Saxne, T
    Klareskog, L
    Feltelius, N
    Haematopoietic malignancies in rheumatoid arthritis: Lymphoma risk and characteristics after exposure to tumour necrosis factor antagonists2005In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 64, no 10, p. 1414-1420Article in journal (Refereed)
    Abstract [en]

    Background: Patients with rheumatoid arthritis (RA) are at increased risk of malignant lymphomas, and maybe also of leukaemia and multiple myeloma. The effect of tumour necrosis factor (TNF) antagonists on lymphoma risk and characteristics is unclear. Objective: To assess expected rates and relative risks of haematopoietic malignancies, especially those associated with TNF antagonists, in large population based cohorts of patients with RA. Methods: A population based cohort study was performed of patients with RA (one prevalent cohort (n = 53 067), one incident cohort (n = 3703), and one TNF antagonist treated cohort 1999 through 2003 (n = 4160)), who were linked with the Swedish Cancer Register. Additionally, the lymphoma specimens for the 12 lymphomas occurring in patients with RA exposed to TNF antagonists in Sweden 1999 through 2004 were reviewed. Results: Study of almost 500 observed haematopoietic malignancies showed that prevalent and incident patients with RA were at increased risk of lymphoma (SIR =1.9 and 2.0, respectively) and leukaemia (SIR = 2.1 and 2.2, respectively) but not of myeloma. Patients with RA treated with TNF antagonists had a tripled lymphoma risk (SIR = 2.9) compared with the general population. After adjustment for sex, age, and disease duration, the lymphoma risk after exposure to TNF antagonists was no higher than in the other RA cohorts. Lymphomas associated with TNF antagonists had characteristics similar to those of other RA lymphomas. Conclusion: Overall, patients with RA are at equally increased risks for lymphomas and leukaemias. Patients with RA treated with TNF antagonists did not have higher lymphoma risks than other patients with RA. Prolonged observation is needed to determine the long term effects of TNF antagonists on lymphoma risk.

  • 6. Askling, J
    et al.
    Fored, CM
    Brandt, L
    Baecklund, E
    Bertilsson, L
    Feltelius, N
    Cöster, Lars
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Geborek, P
    Jacobsson, LT
    Lindblad, S
    Lysholm, J
    Rantapää-Dahlqvist, S
    Saxne, T
    Klareskog, L
    Risks of solid cancers in patients with rheumatoid arthritis and after treatment with tumour necrosis factor antagonists2005In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 64, no 10, p. 1421-1426Article in journal (Refereed)
    Abstract [en]

    Background: Existing studies of solid cancers in rheumatoid arthritis (RA) reflect cancer morbidity up until the early 1990s in prevalent cohorts admitted to hospital during the 1980s. Objective: To depict the cancer pattern of contemporary patients with RA, from updated risk data from prevalent and incident RA populations. To understand the risk of solid cancer after tumour necrosis factor (TNF) treatment by obtaining cancer data from cohorts treated in routine care rather than trials. Methods: A population based study of three RA cohorts (one prevalent, admitted to hospital 1990-2003 (n = 53 067), one incident, diagnosed 1995-2003 (n = 3703), and one treated with TNF antagonists 1999-2003 (n = 4160)), which were linked with Swedish nationwide cancer and census registers and followed up for cancer occurrence through 2003. Results: With 3379 observed cancers, the prevalent RA cohort was at marginally increased overall risk of solid cancer, with 20-50% increased risks for smoke related cancers and +70% increased risk for non-melanoma skin cancer, but decreased risk for breast (-20%) and colorectal cancer (-25%). With 138 cancers, the incident RA cohort displayed a similar cancer pattern apart from non-decreased risks for colorectal cancer. TNF antagonist treated patients displayed solid cancer (n = 67) risks largely similar to those of other patients with RA. Conclusion: The cancer pattern in patients treated with TNF antagonists mirrors those of other contemporary as well as historic RA cohorts. The consistent increase in smoking associated cancers in patients with RA emphasises the potential for smoking cessation as a cancer preventive measure in RA.

  • 7. Askling, J
    et al.
    Fored, CM
    Brandt, L
    Baecklund, E
    Bertilsson, L
    Feltelius, N
    Cöster, Lars
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Geborek, P
    Jacobsson, LT
    Lindblad, S
    Lysholm, J
    Rantapää-Dahlqvist, S
    Saxne, T
    van Vollenhoven, RF
    Klareskog, L
    Time-dependent increase in risk of hospitalisation with infection among Swedish RA patients treated with TNF antagonists2007In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 66, no 10, p. 1339-1344Article in journal (Refereed)
    Abstract [en]

    Objectives: The degree to which treatment with tumour necrosis factor (TNF) antagonists may be associated with increased risks for serious infections is unclear. An observational cohort study was performed using prospectively collected data from the Swedish Biologics Register (ARTIS) and other national Swedish registers. Methods: First, in the ARTIS, all 4167 rheumatoid arthritis (RA) patients starting TNF antagonist treatment between 1999 and 2003 were identified. Secondly, in the Swedish Inpatient Register, all individuals hospitalised for any reason and who also carried a diagnosis of RA, between 1964 and 2003 (n = 44 946 of whom 2692 also occurred in ARTIS), were identified. Thirdly, in the Swedish Inpatient Register, all hospitalisations listing an infection between 1999 and 2003 were identified. By cross-referencing these three data sets, RRs for hospitalisation with infection associated with TNF antagonist treatment were calculated within the cohort of 44 946 RA patients, using Cox regression taking sex, age, geography, co-morbidity and use of inpatient care into account. Results: Among the 4167 patients treated with TNF antagonists, 367 hospitalisations with infections occurred during 7776 person-years. Within the cohort of 44 496 RA patients, the RR for infection associated with TNF antagonists was 1.43 (95% Cl 1.18 to 1.73) during the first year of treatment, 1.15 (95% Cl 0.88 to 1.51) during the second year of treatment, and 0.82 (95% Cl 0.62 to 1.08) for subjects remaining on their first TNF antagonist treatment after 2 years. Conclusion: Treatment with TNF antagonists may be associated with a small to moderate increase in risk of hospitalisation with infection, which disappears with increasing treatment duration.

  • 8.
    Basu, Neil
    et al.
    University of Aberdeen, Aberdeen, UK.
    Watts, Richard
    University of East Anglia, School of Medicine, Norwich, Norfolk, UK.
    Bajema, Ingeborg
    Leiden University Medical Center, Leiden, The Netherlands.
    Baslund, Bo
    Rigshospitalet, Copenhagen, Denmark .
    Bley, Thorsten
    University Hospital Freiburg, Freiburg, Germany .
    Boers, Maarten
    VU University Medical Center, Amsterdam, The Netherlands.
    Brogan, Paul
    Institute of Child Health, London, UK.
    Calabrese, Len
    Cleveland Clinic Foundation, Cleveland, Ohio, USA .
    Cid, Maria C
    Hospital Clinic, University of Barcelona IDIBAPS, Barcelona, Spain.
    Cohen-Tervaert, Jan Willem
    Maastricht UMC, Maastricht, The Netherlands.
    Flores-Suarez, Luis Felipe
    National Institute of Respiratory Disease, Mexico City, Mexico.
    Fujimoto, Shouichi
    Miyazaki University, Miyazaki, Japan.
    de Groot, Kirsten
    Klinikum Offenbach, Offenbach, Germany.
    Guillevin, Loic
    University of Paris Descartes, Paris, France.
    Hatemi, Gulen
    University of Istanbul, Istanbul, Turkey.
    Hauser, Thomas
    Immunologie-Zentrum Zürich, Zurich, Switzerland .
    Jayne, David
    Addenbrooke's Hospital, Cambridge, UK .
    Jennette, Charles
    University of North Carolina, Chapel Hill, North Carolina, USA .
    Kallenberg, Cees G M
    University Hospital Groningen, Groningen, The Netherlands.
    Kobayashi, Shigeto
    Juntendo Koshigaya Hospital, Saitama, Japan.
    Little, Mark A
    Renal Institute of Birmingham, University of Birmingham, Birmingham, UK.
    Mahr, Alfred
    University of Paris Descartes, Paris, France.
    McLaren, John
    Whytemans Brae Hospital, Kirkcaldy, Fife, UK.
    Merkel, Peter A
    Boston University School of Medicine, Boston, Massachusetts, USA .
    Ozen, Seza
    Hacettepe University, Ankara, Turkey .
    Puechal, Xavier
    Centre Hospitalier Le Mans, Le Mans, France .
    Rasmussen, Niels
    Rigshospitalet, Copenhagen, Denmark.
    Salama, Alan
    Imperial College London, London, UK.
    Salvarani, Carlo
    Arcispedale S Maria Nuova, Reggio Emilia, Italy.
    Savage, Caroline
    Renal Institute of Birmingham, University of Birmingham, Birmingham, UK .
    Scott, David G I
    Norfolk and Norwich University Hospital Trust, Norwich, Norfolk, UK .
    Segelmark, Mårten
    Lund University, Lund, Sweden.
    Specks, Ulrich
    Mayo Clinc, Minnesota, Minneapolis, USA.
    Sunderköetter, Cord
    Universitätsklinikum Münster, Münich, Germany.
    Suzuki, Kazuo
    Chiba University Graduate School of Medicine, Chiba, Japan .
    Tesar, Vladimir
    Charles University, Prague, Czech Republic.
    Wiik, Allan
    Statens Serum Institut, Copenhagen, Denmark .
    Yazici, Hasan
    University of Istanbul, Istanbul, Turkey .
    Luqmani, Raashid
    University of Oxford, Oxford, UK.
    EULAR points to consider in the development of classification and diagnostic criteria in systemic vasculitis2010In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 69, no 10, p. 1744-1750Article in journal (Refereed)
    Abstract [en]

    Objectives The systemic vasculitides are multiorgan diseases where early diagnosis and treatment can significantly improve outcomes. Robust nomenclature reduces diagnostic delay. However, key aspects of current nomenclature are widely perceived to be out of date, these include disease definitions, classification and diagnostic criteria. Therefore, the aim of the present work was to identify deficiencies and provide contemporary points to consider for the development of future definitions and criteria in systemic vasculitis.

    Methods The expert panel identified areas of concern within existing definitions/criteria. Consequently, a systematic literature review was undertaken looking to address these deficiencies and produce ‘points to consider’ in accordance with standardised European League Against Rheumatism (EULAR) operating procedures. In the absence of evidence, expert consensus was used.

    Results There was unanimous consensus for re-evaluating existing definitions and developing new criteria. A total of 17 points to consider were proposed, covering 6 main areas: biopsy, laboratory testing, diagnostic radiology, nosology, definitions and research agenda. Suggestions to improve and expand current definitions were described including the incorporation of anti-neutrophil cytoplasm antibody and aetiological factors, where known. The importance of biopsy in diagnosis and exclusion of mimics was highlighted, while equally emphasising its problems. Thus, the role of alternative diagnostic tools such as MRI, ultrasound and surrogate markers were also discussed. Finally, structures to develop future criteria were considered.

    Conclusions Limitations in current classification criteria and definitions for vasculitis have been identified and suggestions provided for improvement. Additionally it is proposed that, in combination with the updated evidence, these should form the basis of future attempts to develop and validate revised criteria and definitions of vasculitis.

  • 9. Carville, S F
    et al.
    Arendt-Nielsen, S
    Bliddal, H
    Blotman, F
    Branco, J C
    Buskila, D
    Da Silva, J. A.
    Danneskiold-Samsøe, B
    Dincer, F
    Henriksson, Chris
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Social and Welfare Studies.
    Henriksson, Karl-Gösta
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Rehabilitation Medicine . Östergötlands Läns Landsting, Centre for Medicine, Pain and Rehabilitation Centre.
    Kosek, E
    Longley, K
    McCarthy, G M
    Perrot, S
    Puszczewicz, M
    Sarzi-Puttini, P
    Silman, A
    Späth, M
    Choy, E H
    EULAR evidence-based recommendations for the management of fibromyalgia syndrome2008In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 67, no 4, p. 536-541Article in journal (Refereed)
    Abstract [en]

    Objective: To develop evidence-based recommendations for the management of fibromyalgia syndrome. Methods: A multidisciplinary task force was formed representing 11 European countries. The design of the study, including search strategy, participants, interventions, outcome measures, data collection and analytical method, was defined at the outset. A systematic review was undertaken with the keywords "fibromyalgia", "treatment or management" and "trial". Studies were excluded if they did not utilise the American College of Rheumatology classification criteria, were not clinical trials, or included patients with chronic fatigue syndrome or myalgic encephalomyelitis. Primary outcome measures were change in pain assessed by visual analogue scale and fibromyalgia impact questionnaire. The quality of the studies was categorised based on randomisation, blinding and allocation concealment. Only the highest quality studies were used to base recommendations on. When there was insufficient evidence from the literature, a Delphi process was used to provide basis for recommendation. Results: 146 studies were eligible for the review. 39 pharmacological intervention studies and 59 non-pharmacological were included in the final recommendation summary tables once those of a lower quality or with insufficient data were separated. The categories of treatment identified were antidepressants, analgesics, and "other pharmacological" and exercise, cognitive behavioural therapy, education, dietary interventions and "other non-pharmacological". In many studies sample size was small and the quality of the study was insufficient for strong recommendations to be made. Conclusions: Nine recommendations for the management of fibromyalgia syndrome were developed using a systematic review and expert consensus.

  • 10.
    Helmers, S.B.
    et al.
    Karolinska University Hospital, Rheumatology Unit, CMM L8:04, SE-171 76 Stockholm, Sweden, Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Sweden, Karolinska Institutet, Stockholm, Sweden.
    Dastmalchi, M.
    Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Sweden, Karolinska Institutet, Stockholm, Sweden.
    Alexanderson, H.
    Karolinska Institutet, Stockholm, Sweden, Rheumatology Unit, Department of Physical Therapy, Karolinska University Hospital, Solna, Sweden.
    Nennesmo, I.
    Karolinska Institutet, Stockholm, Sweden, Department of Pathology, Karolinska University Hospital, Huddinge, Sweden.
    Esbjornsson, M.
    Esbjörnsson, M., Karolinska Institutet, Stockholm, Sweden, Division of Clinical Physiology, Department of Medical Laboratory Medicine, Karolinska University Hospital, Huddinge, Sweden.
    Lindvall, Björn
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Neurology . Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Neurology.
    Lundberg, I.E.
    Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Sweden, Karolinska Institutet, Stockholm, Sweden.
    Limited effects of high-dose intravenous immunoglobulin (IVIG) treatment on molecular expression in muscle tissue of patients with inflammatory myopathies2007In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 66, no 10, p. 1276-1283Article in journal (Refereed)
    Abstract [en]

    Objectives: The study was conducted with the aim of achieving an improved understanding of the molecular mechanisms of high-dose intravenous immunoglobulin (IVIG) in inflammatory myopathies by investigating the effects on muscle function and immunological molecules in skeletal muscle of polymyositis (PM), dermatomyositis (DM) and inclusion body myositis (IBM) patients. Methods: Thirteen treatment-resistant patients, 6 PM, 4 DM, 2 IBM and 1 juvenile DM, were treated with 2 g/kg of IVIG, three times at monthly intervals. Functional Index in Myositis and serum creatinine kinase (CK) levels were determined, and muscle biopsies were performed before treatment and after the third IVIG infusion. Immunological molecules were also studied in biopsies taken 24-48 h after the first infusion. Results: Improved muscle function was observed in three patients (1 PM, 1 DM and 1 IBM) and CK levels decreased in five. T cells, macrophages, major histocompatibility complex (MHC) class I antigen on muscle fibres, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression and membranolytic attack complex (MAC) deposits on capillaries were present to an equal degree in biopsies before and after MG treatment. No correlation between the clinical response and molecular changes was found. Conclusions: The clinical effects of high-dose IVIG on muscle function in patients with refractory inflammatory active myositis did not correspond to effects on any of the investigated molecules in our study. T cells, macrophages, phenotypical changes in muscle fibres and endothelial cell activation were still present after treatment. These observations question a role for IVIG as an immune-modulating therapy in patients with inflammatory myopathies.

  • 11.
    Imgenberg-Kreuz, Juliana
    et al.
    Uppsala Univ, Sweden.
    Carlsson Almlöf, Jonas
    Uppsala Univ, Sweden.
    Leonard, Dag
    Uppsala Univ, Sweden.
    Alexsson, Andrei
    Uppsala Univ, Sweden.
    Nordmark, Gunnel
    Uppsala Univ, Sweden.
    Eloranta, Maija-Leena
    Uppsala Univ, Sweden.
    Rantapaa-Dahlqvist, Solbritt
    Umea Univ, Sweden.
    Bengtsson, Anders A.
    Lund Univ, Sweden.
    Jonsen, Andreas
    Lund Univ, Sweden.
    Padyukov, Leonid
    Karolinska Inst, Sweden.
    Gunnarsson, Iva
    Karolinska Inst, Sweden.
    Svenungsson, Elisabet
    Karolinska Inst, Sweden.
    Sjöwall, Christopher
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Rheumatology.
    Ronnblom, Lars
    Uppsala Univ, Sweden.
    Syvanen, Ann-Christine
    Uppsala Univ, Sweden.
    Sandling, Johanna K.
    Uppsala Univ, Sweden; Uppsala Univ, Sweden.
    DNA methylation mapping identifies gene regulatory effects in patients with systemic lupus erythematosus2018In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 77, no 5, p. 736-743Article in journal (Refereed)
    Abstract [en]

    Objectives Systemic lupus erythematosus (SLE) is a chronic autoimmune condition with heterogeneous presentation and complex aetiology where DNA methylation changes are emerging as a contributing factor. In order to discover novel epigenetic associations and investigate their relationship to genetic risk for SLE, we analysed DNA methylation profiles in a large collection of patients with SLE and healthy individuals. Methods DNA extracted from blood from 548 patients with SLE and 587 healthy controls were analysed on the Illumina HumanMethylation 450 k BeadChip, which targets 485 000 CpG sites across the genome. Single nucleotide polymorphism (SNP) genotype data for 196 524 SNPs on the Illumina ImmunoChip from the same individuals were utilised for methylation quantitative trait loci (cis-meQTLs) analyses. Results We identified and replicated differentially methylated CpGs (DMCs) in SLE at 7245 CpG sites in the genome. The largest methylation differences were observed at type I interferon-regulated genes which exhibited decreased methylation in SLE. We mapped cis-meQTLs and identified genetic regulation of methylation levels at 466 of the DMCs in SLE. The meQTLs for DMCs in SLE were enriched for genetic association to SLE, and included seven SLE genome-wide association study (GWAS) loci: PTPRC (CD45), MHC-class III, UHRF1BP1, IRF5, IRF7, IKZF3 and UBE2L3. In addition, we observed association between genotype and variance of methylation at 20 DMCs in SLE, including at the HLADQB2 locus. Conclusions Our results suggest that several of the genetic risk variants for SLE may exert their influence on the phenotype through alteration of DNA methylation levels at regulatory regions of target genes.

  • 12.
    Isine Bolstad, Anne
    et al.
    University of Bergen.
    Le Hellard, Stephanie
    University of Bergen.
    Kristjansdottir, Gudlaug
    Uppsala University.
    Vasaitis, Lilian
    Uppsala University.
    Kvarnstrom, Marika
    Karolinska Institute.
    Sjöwall, Christoffer
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Rheumatology in Östergötland.
    Joar Auglaend Johnsen, Svein
    Stavanger University Hospital.
    Eriksson, Per
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Nephrology UHL.
    Omdal, Roald
    Stavanger University Hospital.
    Brun, Johan G
    University of Bergen.
    Wahren-Herlenius, Marie
    Karolinska Institute.
    Theander, Elke
    Lund University.
    Syvanen, Ann-Christine
    Uppsala University.
    Ronnblom, Lars
    Uppsala University.
    Nordmark, Gunnel
    Uppsala University.
    Jonsson, Roland
    University of Bergen.
    Association between genetic variants in the tumour necrosis factor/lymphotoxin alpha/lymphotoxin beta locus and primary Sjogrens syndrome in Scandinavian samples2012In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 71, no 6, p. 981-988Article in journal (Refereed)
    Abstract [en]

    Objectives Lymphotoxin beta (LTB) has been found to be upregulated in salivary glands of patients with primary Sjogrens syndrome (pSS). An animal model of pSS also showed ablation of the lymphoid organisation and a marked improvement in salivary gland function on blocking the LTB receptor pathway. This study aimed to investigate whether single-nucleotide polymorphisms (SNP) in the lymphotoxin alpha (LTA)/LTB/tumour necrosis factor (TNF) gene clusters are associated with pSS. less thanbrgreater than less thanbrgreater thanMethods 527 pSS patients and 532 controls participated in the study, all of Caucasian origin from Sweden and Norway. 14 SNP markers were genotyped and after quality control filtering, 12 SNP were analysed for their association with pSS using single marker and haplotype tests, and corrected by permutation testing. less thanbrgreater than less thanbrgreater thanResults Nine markers showed significant association with pSS at the p=0.05 level. Markers rs1800629 and rs909253 showed the strongest genotype association (p=1.64E-11 and p=4.42E-08, respectively, after correcting for sex and country of origin). When the analysis was conditioned for the effect of rs1800629, only the association with rs909253 remained nominally significant (p=0.027). In haplotype analyses the strongest effect was observed for the haplotype rs909253G_rs1800629A (p=9.14E-17). The associations were mainly due to anti-Ro/SSA and anti-La/SSB antibody-positive pSS. less thanbrgreater than less thanbrgreater thanConclusions A strong association was found between several SNP in the LTA/LTB/TNF alpha locus and pSS, some of which led to amino acid changes. These data suggest a role for this locus in the development of pSS. Further studies are needed to examine if the genetic effect described here is independent of the known genetic association between HLA and pSS.

  • 13.
    Jones, Rachel B.
    et al.
    Addenbrookes Hospital, England.
    Furuta, Shunsuke
    Addenbrookes Hospital, England.
    Cohen Tervaert, Jan Willem
    Maastricht University, Netherlands.
    Hauser, Thomas
    IZZ Immunol Zentrum, Switzerland.
    Luqmani, Raashid
    Nuffield Orthopaed Centre, England.
    Morgan, Matthew D.
    University of Birmingham, England.
    Au Peh, Chen
    Royal Adelaide Hospital, Australia; University of Adelaide, Australia.
    Savage, Caroline O.
    University of Birmingham, England.
    Segelmark, Mårten
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Nephrology.
    Tesar, Vladimir
    Charles University of Prague, Czech Republic.
    van Paassen, Pieter
    Maastricht University, Netherlands.
    Walsh, Michael
    McMaster University, Canada; McMaster University, Canada.
    Westman, Kerstin
    University Hospital Skåne, Sweden; Lund University, Sweden.
    Jayne, David R. W.
    Addenbrookes Hospital, England.
    Rituximab versus cyclophosphamide in ANCA-associated renal vasculitis: 2-year results of a randomised trial2015In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 74, no 6, p. 1178-1182Article in journal (Refereed)
    Abstract [en]

    Objectives The RITUXVAS trial reported similar remission induction rates and safety between rituximab and cyclophosphamide based regimens for antineutrophil cytoplasm antibody (ANCA)-associated vasculitis at 12months; however, immunosuppression maintenance requirements and longer-term outcomes after rituximab in ANCA-associated renal vasculitis are unknown. Methods Forty-four patients with newly diagnosed ANCA-associated vasculitis and renal involvement were randomised, 3:1, to glucocorticoids plus either rituximab (375mg/m(2)/weekx4) with two intravenous cyclophosphamide pulses (n=33, rituximab group), or intravenous cyclophosphamide for 3-6months followed by azathioprine (n=11, control group). Results The primary end point at 24months was a composite of death, end-stage renal disease and relapse, which occurred in 14/33 in the rituximab group (42%) and 4/11 in the control group (36%) (p=1.00). After remission induction treatment all patients in the rituximab group achieved complete B cell depletion and during subsequent follow-up, 23/33 (70%) had B cell return. Relapses occurred in seven in the rituximab group (21%) and two in the control group (18%) (p=1.00). All relapses in the rituximab group occurred after B cell return. Conclusions At 24months, rates of the composite outcome of death, end-stage renal disease and relapse did not differ between groups. In the rituximab group, B cell return was associated with relapse. Trial registration number ISRCTN28528813.

  • 14.
    Karras, Alexandre
    et al.
    Hop Europeen Georges Pompidou, France; University of Paris 05, France.
    Pagnoux, Christian
    Mt Sinai Hospital, Canada.
    Haubitz, Marion
    Klinikum Fulda, Germany; Klinikum Fulda, Germany.
    de Groot, Kirsten
    Klinikum Offenbach, Germany.
    Puechal, Xavier
    Hop Cochin, France.
    Cohen Tervaert, Jan Willem
    Maastricht University, Netherlands.
    Segelmark, Mårten
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Nephrology.
    Guillevin, Loic
    University of Paris 05, France; Hop Cochin, France.
    Jayne, David
    University of Cambridge, England.
    Randomised controlled trial of prolonged treatment in the remission phase of ANCA-associated vasculitis2017In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 76, no 10, p. 1662-1668Article in journal (Refereed)
    Abstract [en]

    Objectives A prospective randomised trial to compare two different durations of maintenance immunosuppressive therapy for the prevention of relapse in anti-neutrophil cytoplasmic antibodies (ANCA)associated vasculitis (AAV). Methods Patients with AAV were recruited 18-24 months after diagnosis if they were in stable remission after cyclophosphamide/prednisolone-based induction followed by azathioprine/prednisolone maintenance therapy. They were randomised (1: 1) to receive continued azathioprine/prednisolone to 48 months from diagnosis (continuation group) or to withdraw azathioprine/prednisolone by 24 months (withdrawal group). The primary endpoint was the relapse risk, from randomisation to 48 months from diagnosis. Results One hundred and seventeen patients were randomised and 110 remained to the trial end. At entry, median serum creatinine was 116 mu mol/L (range 58-372), 53% were ANCA positive. The percentage of patients presenting with relapse was higher in the withdrawal than in the continuation treatment group (63% vs 22%, pamp;lt;0.0001, OR 5.96, 95% CI 2.58 to 13.77). ANCA positivity at randomisation was associated with relapse risk (51% vs 29%, p=0.017, OR 2.57, 95% CI 1.16 to 5.68). Renal function, ANCA specificity, vasculitis type and age were not predictive of relapse. Severe adverse events were more frequent in the continuation than withdrawal groups (nine vs three events), but the continuation group had better renal outcome (0 vs 4 cases of end-stage renal disease), with no difference in patient survival. Conclusions Prolonged remission maintenance therapy with azathioprine/prednisolone, beyond 24 months after diagnosis reduces relapse risk out to 48 months and improves renal survival in AAV.

  • 15.
    Kastbom, Alf
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Region Östergötland, Heart and Medicine Center, Department of Rheumatology. Linköping University, Faculty of Medicine and Health Sciences. Karolinska Institute, Sweden.
    Forslind, Kristina
    Helsingborgs Lasarett, Sweden; Skåne University Hospital, Sweden.
    Ernestam, Sofia
    Karolinska Institute, Sweden.
    Geborek, Pierre
    Skåne University Hospital, Sweden.
    Karlsson, Johan A.
    Skåne University Hospital, Sweden.
    Petersson, Ingemar F.
    Lund University, Sweden.
    Saevarsdottir, Saedis
    Karolinska Institute, Sweden.
    Klareskog, Lars
    Karolinska Institute, Sweden.
    van Vollenhoven, Ronald F.
    Karolinska Institute, Sweden.
    Lundberg, Karin
    Karolinska Institute, Sweden.
    Changes in the anticitrullinated peptide antibody response in relation to therapeutic outcome in early rheumatoid arthritis: results from the SWEFOT trial2016In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 75, no 2, p. 356-361Article in journal (Refereed)
    Abstract [en]

    Objective To determine the relationship between changes in antibody levels towards citrullinated peptides derived from different candidate autoantigens and therapeutic outcome in early rheumatoid arthritis (RA). Methods Baseline and 3-month serum samples from 316 patients with early RA enrolled in the Swedish Farmacotherapy (SWEFOT) trial were analysed for antibodies against cyclic citrullinated peptides (CCP) and citrullinated peptides derived from vimentin (cVim), fibrinogen (cFib) and a-enolase (CEP-1). At 3-month follow-up, methotrexate monotherapy-inadequate responders were randomised to add-on therapy with sulfasalazine and hydroxychloroquine or infliximab. In these patients, anticitrullinated peptide antibodies (ACPA) were also assessed at 12 and 24 months. The proportion of antibody-positive patients and relative changes in antibody levels were compared across ACPA specificities and related to therapeutic response and radiographic progression. Results During the 2-year follow-up, the proportion of patients testing positive declined significantly regarding antibodies to cVim, cFib and CEP-1, while anti-CCP antibody occurrence remained stable over time. Turning anti-cVim antibody negative was most common, and anti-cVim antibody seroreversion during the first three months associated with significantly less 2-year radiographic progression compared with patients who remained positive. Median antibody levels of all tested ACPAs declined uniformly during initial methotrexate therapy and following response to add-on therapy, with no significant relation to treatment regimen or radiographic progression. Conclusions The influence of early antirheumatic therapy on ACPA seroreversions was markedly different across specificities, and early disappearance of anti-cVim antibodies associated with better radiological outcome. Thus, these data suggest that the disappearance of particular ACPA reactivities may be beneficial in early RA.

  • 16.
    Lindström, FD
    et al.
    Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Linköping University, Faculty of Health Sciences.
    Skogh, Thomas
    Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Lundström, Inger
    Linköping University, Department of Neuroscience and Locomotion, Dental Surgery. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Reconstruction Centre, Department of Oral Surgery UHL.
    α1 Antitrypsin deficiency in a patient with systemic vasculitis and primary Sjögren's syndrome2002In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 61, no 10, p. 945-946Article in journal (Other academic)
    Abstract [en]

    [No abstract available]

  • 17. Locht, H
    et al.
    Skogh, Thomas
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Wiik, A
    Characterisation of autoantibodies to neutrophil granule constituents among patients with reactive arthritis, rheumatoid arthritis, and ulcerative colitis.2000In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 59, p. 898-903Article in journal (Refereed)
  • 18.
    Nissinen, R
    et al.
    Dept of Molecular Medicine Helsinki, Finland.
    Leirisalo-Repo, M
    Dept of Medicine Helsinki, Finland.
    Halme, L
    Dept of Surgery Helsinki, Finland.
    Färkkilä, M
    Dept of Medicine Helsinki, Finland.
    Vaarala, Outi
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
    Immune activation in the small intestine in patients with rheumatoid arthritis2004In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 63, no 10, p. 1327-1330Article in journal (Refereed)
    Abstract [en]

    Objectives: To determine whether inflammation in the gut associated immune system is activated in rheumatoid arthritis (RA). The expression of chemokine receptor- (CCR4, CCR5) and cytokine- (interleukin (IL)2, IL10, interferon γ (IFNγ), tumour necrosis factor α (TNFα), and transforming growth factor β (TGFβ)) specific mRNA in intestinal biopsy samples from patients with RA was examined. Methods: Duodenal biopsy samples from 13 patients with RA and 15 control subjects were studied. The mRNA expression of CCR4, CCR5, IL2, IL10, IFNγ, TNFα, and TGFβ in intestinal biopsy samples was demonstrated by real time quantitative reverse transcriptase-polymerase chain reaction. Results: The mRNA expression of CCR4, CCR5, and IL10 in intestinal biopsy samples was increased in patients with RA in comparison with control subjects (p = 0.001, p = 0.046, p = 0.019). No difference in the expression levels of IL2, IFNγ, TNFα, or TGFβ was seen between patients with RA and controls. Conclusions: The increased intestinal mRNA expression of IL10, CCR5, and CCR4 suggests that gut associated immune cells are activated in patients with RA.

  • 19.
    Nissinen, R
    et al.
    Dept of Mol Med National Publ Health, Helsingfors, Finland.
    Leirisalo-Repo, M
    Dept of Medicine, Div of Rheumatol Central Hospital, Helsingfors, Finland.
    Peltomaa, R
    Dept of MEdicine, Div of Rheumatol Central Hospital, Helsingfors, Finland.
    Palosuo, T
    Dept of Health and Functional Capacity National Public Health Inst, Helsingfors, Finland.
    Vaarala, Outi
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
    Cytokine and chemokine receptor profile of peripheral blood mononuclear cells during treatment with infliximab in patients with active rheumatoid arthritis2004In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 63, no 6, p. 681-687Article in journal (Refereed)
    Abstract [en]

    Objectives: To analyse immunological changes during treatment with a monoclonal anti-tumour necrosis factor α (TNFα) antibody, infliximab, in patients with rheumatoid arthritis (RA). Methods: 25 patients with RA and 5 patients with other arthritides were studied during the first 6 weeks of treatment with infliximab. At the start of treatment and after 2 and 6 weeks, spontaneous expression of CCR3 and CCR5 on peripheral blood T cells and monocytes was studied by flow cytometry. The secretion and mRNA expression of interferon γ (IFNγ), interleukin (IL)4, IL5, and TNFα from phytohaemagglutinin (PHA) stimulated peripheral blood mononuclear cells was measured with an ELISA and RT-PCR. Plasma levels of C reactive protein, serum amyloid protein A, rheumatoid factor, and antibodies to filaggrin and citrullinated cyclic peptide were measured with an ELISA. Results: The number of CD4 T cells and CD14 monocytes expressing CCR3 (p = 0.013, p = 0.009, respectively) and CD8 T cells expressing CCR5 (p = 0.040) as well as PHA stimulated secretion of IL4 and IFNγ (p<0.05) increased during treatment in patients with RA. 15 (60%) patients with RA achieved clinical response (at least ACR20) during the first 2 weeks. The number of T cells expressing CCR3 and CCR5 was higher before treatment in non-responders than in responders (p<0.05). The number of T cells increased in responders. Conclusion: Increase in secretion of Th1 and Th2 cytokines together with induced expression of chemokine receptors on T cells and monocytes suggest restoration of peripheral cell mediated immunity and blockade of the accumulation of inflammatory cells in joints as response to treatment.

  • 20.
    Olsson, Lina M
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Johansson, Åsa C
    Lund University, Lund, Sweden.
    Gullstrand, Birgitta
    Lund University, Lund, Sweden.
    Jönsen, Andreas
    Lund University, Lund, Sweden.
    Saevarsdottir, Saedis
    Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Rönnblom, Lars
    Uppsala University, Uppsala, Sweden.
    Leonard, Dag
    Uppsala University, Uppsala, Sweden.
    Wetterö, Jonas
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Sjöwall, Christopher
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Rheumatology.
    Svenungsson, Elisabet
    Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Gunnarsson, Iva
    Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Bengtsson, Anders A
    Lund University, Lund, Sweden.
    Holmdahl, Rikard
    Karolinska Institutet, Stockholm, Sweden.
    A single nucleotide polymorphism in the NCF1 gene leading to reduced oxidative burst is associated with systemic lupus erythematosus2017In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 76, no 9, p. 1607-1613Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Ncf1 polymorphisms leading to low production of reactive oxygen species (ROS) are strongly associated with autoimmune diseases in animal models. The human NCF1 gene is very complex with both functional and non-functional gene copies and genotyping requires assays specific for functional NCF1 genes. We aimed at investigating association and function of the missense single nucleotide polymorphism (SNP), rs201802880 (here denoted NCF1-339) in NCF1 with systemic lupus erythematosus (SLE).

    METHODS: We genotyped the NCF1-339 SNP in 973 Swedish patients with SLE and 1301 controls, using nested PCR and pyrosequencing. ROS production and gene expression of type 1 interferon-regulated genes were measured in isolated cells from subjects with different NCF1-339 genotypes.

    RESULTS: We found an increased frequency of the NCF1-339 T allele in patients with SLE, 11% compared with 4% in controls, OR 3.0, 95% CI 2.4 to 3.9, p=7.0×10(-20). The NCF1-339 T allele reduced extracellular ROS production in neutrophils (p=0.004) and led to an increase expression of type 1 interferon-regulated genes. In addition, the NCF1-339 T allele was associated with a younger age at diagnosis of SLE; mean age 30.3 compared with 35.9, p=2.0×1(-6).

    CONCLUSIONS: These results clearly demonstrate that a genetically controlled reduced production of ROS increases the risk of developing SLE and confirm the hypothesis that ROS regulate chronic autoimmune inflammatory diseases.

  • 21.
    Reckner Olsson, Åsa
    et al.
    Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine. Linköping University, Faculty of Health Sciences.
    Skogh, Thomas
    Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Linköping University, Faculty of Health Sciences.
    Wingren, Gun
    Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine. Linköping University, Faculty of Health Sciences.
    Comorbidity and lifestyle, reproductive factors, and environmental exposures associated with rheumatoid arthritis2001In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 60, no 10, p. 934-939Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE To evaluate the influence of lifestyle, reproduction, and some external factors on the development of rheumatoid arthritis (RA) and to describe its comorbidity.

    METHODS Cases were identified retrospectively from 1980 to 1995 at the University Hospital in Linköping, Sweden. The study comprised 422 cases and 859 randomly selected population referents. Data on possible aetiological factors and comorbidity were collected by postal questionnaire.

    RESULTS The response rates were 67% among cases and 59% among referents. A decrease in the occurrence of atopic allergy was seen in the cases (odds ratio (OR) 0.6, 95% confidence interval (CI) 0.4 to 1.0). There was a positive association between RA and insulin treatment (OR 10.2, 95% CI 1.7 to 60.8) in women, and women with a short fertile period had an increased risk of RA (OR 2.5, 95% CI 1.1 to 5.4). Current and previous smoking were associated with increased risks for RA in both sexes, and in men a dose-response relationship was found with number of tobacco pack years (p for trend <0.005). The risk for RA decreased with increasing level of education in both men and women. Increased risks were seen in men born into households with private wells (OR 2.8, 95% CI 1.5 to 5.2), residentially exposed to mould (OR 4.6, 95% CI 1.1 to 20.2), or exposed to farm animals (OR 3.3, 95% CI 0.7 to 16.6). In women there were positive associations between RA and reporting a previous joint injury (OR 2.5, 95% CI 1.0 to 6.6) and prolonged exposure to hair dyes (OR 1.9, 95% CI 0.8 to 4.5).

    CONCLUSIONS RA, a disease with features of T helper 1 (Th1) dominated immune response, was inversely associated with atopic allergy, a Th2 dominated condition, while there were indications of a strong positive association with Th1 related diabetes mellitus. The results support a causal relationship between smoking and RA. The level of education was inversely associated with RA, while there was a positive association between RA and certain residential factors in men and a short fertile period in women.

  • 22.
    Reksten, Tove Ragna
    et al.
    University of Bergen, Norway / Uppsala University, Sweden .
    Johnsen, Svein Joar Auglænd
    Stavanger University Hospital, Norway.
    Jonsson, Malin Viktoria
    University of Bergen, Norway .
    Omdal, Roald
    Stavanger University Hospital, Norway.
    Brun, Johan G
    University of Bergen, Norway .
    Theander, Elke
    Skåne University Hospital, Lund University, Malmö, Sweden .
    Eriksson, Per
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Rheumatology.
    Wahren-Herlenius, Marie
    Karolinska Institutet, Stockholm, Sweden .
    Jonsson, Roland
    University of Bergen, Norway / Haukeland University Hospital, Bergen, Norway .
    Nordmark, Gunnel
    Uppsala University, Sweden.
    Genetic associations to germinal centre formation in primary Sjogren's syndrome2014In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 73, no 6, p. 1253-1258Article in journal (Refereed)
    Abstract [en]

    Background Primary Sjögren's syndrome (pSS) is an autoimmune rheumatic disease mainly characterised by focal mononuclear cell infiltration in the salivary and lacrimal glands, and by the symptoms xerostomia and keratoconjunctivitis sicca. Germinal centre-like structures (GC) are found in the minor salivary glands of approximately 25% of patients. In this study, we aimed to assess genetic variations in pSS patients with GC-like formations (GC+) compared with patients without such formations (GC−).                                

    Methods Minor salivary gland biopsies from Swedish and Norwegian pSS patients (n=320) were evaluated for GC-like formations, identifying 76 GC+ and 244 GC− patients. A panel of 1536 single-nucleotide polymorphisms (SNPs) in 107 genes was genotyped. Minor allele frequencies in GC+ and GC− patients were compared using Fisher's exact test, and associations were considered significant when p<4.7×10−4 and suggestive when p<0.01.                                

    Results In this case-only analysis, we identified two SNPs in CCL11 (eotaxin) associated with GC-like structures (p<4.7×10−4, OR 0.45 and 0.41, respectively). A haplotype of the two minor alleles was associated with GC status with p=2.6×10−4, OR 0.40. Suggestive associations (p<0.01) were found in SNPs in the B cell activation and/or GC-formation related genes AICDA, BANK1 and BCL2. Furthermore, SNPs in IL17A, ICA1, PKN1 and SNPs in the NF-κB pathway genes CARD8, IKBKE and TANK were found suggestively associated with GC-like structures.                                

    Conclusions Our findings suggest that genetic variations may explain why ectopic GC-like structures are present in some pSS patients, and support the hypothesis that GC+ and GC− patients represent distinct disease phenotypes.

  • 23. Sharp, CA
    et al.
    Brown, SJ
    Davie, MWJ
    Magnusson, Per
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of clinical chemistry. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Chemistry.
    Mohan, S
    Increased matrix concentrations of IGFBP-5 in cancellous bone in osteoarthritis2004In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 63, no 9, p. 1162-1165Article in journal (Refereed)
    Abstract [en]

    Background: In osteoarthritis cancellous bone adapts to meet altered mechanical loading. These changes may be mediated by insulin-like growth factors (IGF-I and IGF-II), but the matrix bound binding protein, IGFBP-5 has not been investigated. Objectives: To measure IGF-I, IGF-II, and IGFBP-5 in femoral head bone from non-OA controls and patients with OA, and to relate these to apparent density (PA) and elastic modulus (Ec). Methods: ρA, Ec, and IGF system components were measured in cancellous bone from superior and inferior regions of femoral heads from 31 patients with OA and 11 age selected controls. Results: Ec and ρA were greater (p<0.05) in the superior region of all femoral heads. In primary OA, ρA was increased in the inferior region (p<0.05). IGFBP-5 was increased, about twofold, at superior and inferior regions in primary OA (1.60 and 1.54 ng/mg bone, respectively, both p<0.05) and in Paget's disease (2.44 and 1.75 ng/mg bone, both p<0.05) compared with controls (0.73 and 0.95 ng/mg bone). In controls, inverse correlations between IGFBP-5 and both ρA and Ec at superior (rs = -0.64 and -0.73, both p<0.05) and inferior regions (rs = -0.72, p<0.05 and -0.24 (NS)) were seen, but these were lost in OA. Conclusions: IGFBP-5 may modulate cancellous bone formation by negative feedback. In end stage OA this is disrupted, but has little influence on material properties.

  • 24.
    Skogh, Thomas
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Gustafsson, D
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology.
    Kjellberg, M
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology.
    Husberg, M
    Twenty eight joint count disease activity score in recent onset rheumatoid arthritis using C reactive protein instead of erythrocyte sedimentation rate [2]2003In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 62, no 7, p. 681-682Article in journal (Refereed)
    Abstract [en]

    [No abstract available]

  • 25.
    Svärd, Anna
    et al.
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Kastbom, Alf
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Rheumatology in Östergötland.
    Sommarin, Yngve
    EuroDiagnostica AB, Malmö.
    Skogh, Thomas
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Rheumatology in Östergötland.
    A disease-modifying role for mucosal IgA antibodies to citrullinated antigens?2012In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 71, no Issue suppl. 1, p. A38-A39Article in journal (Refereed)
    Abstract [en]

    Objective

    The aim of this study was to investigate whether immunoglobulin A (IgA) antibodies to cyclic citrullinated peptides CCP) can be detected in saliva of patients with established heumatoid arthritis (RA) and if it relates to clinical manifestations.

    Methods

    Salivary samples were collected (by ‘passive drooling’) from 63 consecutive patients with established RA at a visit to the rheumatology outpatient clinic (Falun, Sweden), and from 20 healthy persons (hospital staff). The samples were centrifuged and kept frozen at −70°C until analysis. IgA-class anti-CCP antibodies in saliva were analysed by adaptation of commercial ELISA (Immunoscan RA, Euro-Diagnostica AB, Malmo, Sweden) using polyclonal rabbit antihuman α-chain specific antibodies conjugated with horseradish peroxidase(DakoCytomation, Glostrup, Denmark) as secondary antibody. To ensure specificity of the reaction, a corresponding ELISA was set up to analyse IgA antibodies to control antigen(cyclic arginine peptide, CAP), and anti-CCP/anti-CAP ratios were calculated. Also, inhibition studies were performed by preincubation of sera with soluble CCP or CAP. Clinical and laboratory data on disease activity, that is, C reactive protein (CRP), erythrocyte sedimentation rate (ESR), and 28-joint count disease activity score (DAS28) as well as radiological outcome (occurrence or absence of erosions as judged by a radiologist in diagnostic routine) were achieved retrospectively via the patients’ medical records.

    Results

    Background reactivity against CCP was found in virtually all patients and healthy subjects, whereas a positive anti-CCP/anti-CAP ratio (≥1.5) was found in 14 out of 63 RA patients (22%) and in one healthy subject (5%). Salivary IgA-reactivity with CCP was dose-dependently inhibited by soluble CCP (but not with CAP) in sera with anti-CCP/anti- CAP ratios ≥1.5. No IgG-reactivity to CCP was found in saliva, although all patients with salivary IgA anti-CCP tested IgG anti-CCP-positive in serum. Furthermore, less than half of those testing IgA-positive in saliva were IgA anti-CCP positive in serum, strongly arguing against passive leakage of anti-CCP antibodies from blood to saliva. The patients testing positive for salivary IgA antibodies had lower average disease activity measures (CRP, ESR, DAS28) at presentation and fewer developed bony erosions within 6 years after presentation (p=0.043, Fisher’s exact test).

    Conclusion

    Salivary IgA antibodies to citrullinated proteins were found in a subset of IgG anti-CCP positive RA patients. In contrast to their serum counterparts, salivary IgA antibodies may associate with a milder/less destructive disease course. This accords with the notion that secretory IgA antibodies exert anti-inflammatory actions, and that they may be associated with induction of systemic tolerance (oral tolerance). The possible disease-modifying role of mucosal immunity to citrullinated proteins needs further investigation!

                    

                                                                    

  • 26.
    Wevers-de Boer, K. V. C.
    et al.
    LUMC, Netherlands.
    Heimans, L.
    LUMC, Netherlands.
    Visser, K.
    LUMC, Netherlands.
    Kälvesten, Johan
    Linköping University, Center for Medical Image Science and Visualization (CMIV). Sectra, Linkoping, Sweden.
    Goekoop, R. J.
    Haga Hospital, Netherlands.
    van Oosterhout, M.
    Groene Hart Hospital, Netherlands.
    Harbers, J. B.
    Franciscus Hospital, Netherlands.
    Bijkerk, C.
    Reinier Graaf Gasthuis, Netherlands.
    Steup-Beekman, M.
    Bronovo Hospital, Netherlands.
    de Buck, M. P. D. M.
    MCH, Netherlands.
    de Sonnaville, P. B. J.
    Oosterschelde Hospital, Netherlands.
    Huizinga, T. W. J.
    LUMC, Netherlands.
    Allaart, C. F.
    LUMC, Netherlands.
    Four-month metacarpal bone mineral density loss predicts radiological joint damage progression after 1 year in patients with early rheumatoid arthritis: exploratory analyses from the IMPROVED study2015In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 74, no 2, p. 341-346Article in journal (Refereed)
    Abstract [en]

    Aim To assess whether in early (rheumatoid) arthritis (RA) patients, metacarpal bone mineral density (BMD) loss after 4 months predicts radiological progression after 1 year of antirheumatic treatment. Methods Metacarpal BMD was measured 4 monthly during the first year by digital X-ray radiogrammetry (DXR-BMD) in patients participating in the IMPROVED study, a clinical trial in 610 patients with recent onset RA (2010 criteria) or undifferentiated arthritis, treated according to a remission (disease activity scoreless than1.6) steered strategy. With Sharp/van der Heijde progression greater than= 0.5 points after 1 year (yes/no) as dependent variable, univariate and multivariate logistic regression analyses were performed. Results Of 428 patients with DXR-BMD results and progression scores available, 28 (7%) had radiological progression after 1 year. Independent predictors for radiological progression were presence of baseline erosions (OR (95% CI) 6.5 (1.7 to 25)) and early DXR-BMD loss (OR (95% CI) 1.5 (1.1 to 2.0)). In 366 (86%) patients without baseline erosions, early DXR-BMD loss was the only independent predictor of progression (OR (95% CI) 2.0 (1.4 to 2.9)). Conclusions In early RA patients, metacarpal BMD loss after 4 months of treatment is an independent predictor of radiological progression after 1 year. In patients without baseline erosions, early metacarpal BMD loss is the main predictor of radiological progression.

  • 27.
    Yates, M.
    et al.
    Norfolk and Norwich University Hospital, England; University of East Anglia, England.
    Watts, R. A.
    University of East Anglia, England; Ipswich Hospital NHS Trust, England.
    Bajema, I. M.
    Leiden University, Netherlands.
    Cid, M. C.
    University of Barcelona, Spain.
    Crestani, B.
    Bichat Claude Bernard University Hospital, France.
    Hauser, T.
    Immunol Zentrum Zurich, Switzerland.
    Hellmich, B.
    Kreiskliniken Esslingen, Germany.
    Holle, J. U.
    Rheumazentrum Schleswig Holstein Mitte, Germany.
    Laudien, M.
    University of Kiel, Germany.
    Little, M. A.
    Tallaght Hospital, Ireland.
    Luqmani, R. A.
    University of Oxford, England.
    Mahr, A.
    University of Paris 07, France.
    Merkel, P. A.
    University of Penn, PA 19104 USA; University of Penn, PA 19104 USA.
    Mills, J.
    Vasculitis UK, England.
    Mooney, J.
    Norfolk and Norwich University Hospital, England.
    Segelmark, Mårten
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Nephrology.
    Tesar, V.
    Charles University of Prague, Czech Republic.
    Westman, K.
    Lund University, Sweden.
    Vaglio, A.
    University Hospital Parma, Italy.
    Yalcindag, N.
    Ankara University, Turkey.
    Jayne, D. R.
    Addenbrookes Hospital, England.
    Mukhtyar, C.
    Norfolk and Norwich University Hospital, England.
    EULAR/ERA-EDTA recommendations for the management of ANCA-associated vasculitis2016In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 75, no 9, p. 1583-1594Article in journal (Refereed)
    Abstract [en]

    In this article, the 2009 European League Against Rheumatism (EULAR) recommendations for the management of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) have been updated. The 2009 recommendations were on the management of primary small and medium vessel vasculitis. The 2015 update has been developed by an international task force representing EULAR, the European Renal Association and the European Vasculitis Society (EUVAS). The recommendations are based upon evidence from systematic literature reviews, as well as expert opinion where appropriate. The evidence presented was discussed and summarised by the experts in the course of a consensus-finding and voting process. Levels of evidence and grades of recommendations were derived and levels of agreement (strengths of recommendations) determined. In addition to the voting by the task force members, the relevance of the recommendations was assessed by an online voting survey among members of EUVAS. Fifteen recommendations were developed, covering general aspects, such as attaining remission and the need for shared decision making between clinicians and patients. More specific items relate to starting immunosuppressive therapy in combination with glucocorticoids to induce remission, followed by a period of remission maintenance; for remission induction in life-threatening or organ-threatening AAV, cyclophosphamide and rituximab are considered to have similar efficacy; plasma exchange which is recommended, where licensed, in the setting of rapidly progressive renal failure or severe diffuse pulmonary haemorrhage. These recommendations are intended for use by healthcare professionals, doctors in specialist training, medical students, pharmaceutical industries and drug regulatory organisations.

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