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• Garen, Torhild Oddveig; Lerang, Karoline; Hoffmann-Vold, Anna-Maria; Andersson, Anna Helena; Midtvedt, Øyvind; Brunborg, Cathrine; Kilian, Karin Renate; Gudbrandsson, Birgir Mar; Gunnarsson, Ragnar; Norby, Gudrun; Chaudhary, Asad; Thoen, Jørn; Forseth, Karin Maria Øien; Fresjar, Kari; Førre, Øystein Thorleiv; Haugen, Margaretha; Haga, Hans-Jacob; Gran, Jan Tore; Gilboe, Inge-Margrethe; Molberg, Øyvind & Palm, Øyvind (2019). Mortality and causes of death across the systemic connective tissue diseases and the primary systemic vasculitides. Rheumatology.  ISSN 1462-0324.  58(2), s 313- 320 . doi: 10.1093/rheumatology/key285
• Hokstad, Ingrid; Deyab, Gia; Fagerland, Morten; Lyberg, Torstein; Hjeltnes, Gunnbjørg; Førre, Øystein Thorleiv; Agewall, Stefan; Mollnes, Tom Eirik & Hollan, Ivana (2019). Tumor necrosis factor inhibitors are associated with reduced complement activation in spondylarthropathies: An observational study. PLOS ONE.  ISSN 1932-6203.  14(7), s 1- 16 . doi: 10.1371/journal.pone.0220079 Full text in Research Archive. Show summary

  Background The complement system is involved in pathogenesis of cardiovascular disease, and might play a role in accelerated atherogenesis in spondylarthropathies (SpA). Hence, we examined complement activation in SpA, and its relationship to antirheumatic treatment, inflammatory and cardiovascular markers. Methods From PSARA, a prospective observational study, we examined 51 SpA patients (31 psoriatic arthritis (PsA), and 20 ankylosing spondylitis (AS)), starting tumor necrosis factor (TNF) inhibitor alone (n = 25), combined with methotrexate (MTX) (n = 10), or MTX monotherapy (n = 16). Complement activation was determined by the soluble terminal complement complex (sC5b-9), inflammation by erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and endothelial function by finger plethysmography (Endopat) at baseline, after 6 weeks and 6 months of treatment. Results SpA patients had sC5b-9 levels at (PsA) or above (AS) the upper limit of the estimated reference range. Median sC5b-9 levels decreased significantly from baseline to 6 weeks, with no significant difference between the AS and PsA group. Notably, a significant reduction in sC5b-9 was observed after administration of TNF inhibitor ± MTX, whereas no significant changes were observed in patients treated with MTX alone. Between 6 weeks and 6 months, sC5b-9 remained stable across all subgroups. Reduction in sC5b-9 was independently related to decreased ESR and CRP, and to increased high density cholesterol and total cholesterol. Reduction in sC5b-9 from baseline to 6 weeks was associated with improved EF in age and gender adjusted analyses. Conclusion TNF-inhibition, but not MTX monotherapy, led to rapid and sustained reduction of complement activation in SpA. Thus, the observed decrease in cardiovascular morbidity in patients treated with TNF-inhibitors might be partly due to its beneficial effect on complement. Trial registration Clinical Trials (NCT00902005), retrospectively registered on the 14th of May 2009.

• Finkel, Terri H.; Li, Jin; Wei, Zhi; Wang, Wei; Zhang, Haitao; Behrens, Edward M.; Reuschel, Emma L.; Limou, Sophie; Wise, Carol; Punaro, Marilynn; Becker, Mara L.; Munro, Jane E.; Flatø, Berit; Førre, Øystein Thorleiv; Thompson, Susan D.; Langefeld, Carl D.; Glass, David N.; Glessner, Joseph T.; Kim, Cecilia E.; Frackelton, Edward; Shivers, Debra K.; Thomas, Kelly A.; Chiavacci, Rosetta M.; Hou, Cuiping; Xu, Kexiang; Snyder, James; Qiu, Haijun; Mentch, Frank; Wang, Kai; Winkler, Cheryl A.; Lie, Benedicte Alexandra; Ellis, Justine A. & Hakonarson, Hakon (2016). Variants in CXCR4 associate with juvenile idiopathic arthritis susceptibility. BMC Medical Genetics.  ISSN 1471-2350.  17(1) . doi: 10.1186/s12881-016-0285-3
• Chiaroni-Clarke, Rachel C.; Li, Yun R.; Munro, Jane E.; Chavez, Raul A.; Scurrah, Katrina J.; Pezic, Angela; Akikusa, Jonathan D.; Allen, Roger C.; Piper, Susan E.; Becker, Mara L.; Thompson, Susan D.; Lie, Benedicte Alexandra; Flatø, Berit; Førre, Øystein Thorleiv; Punaro, Marilynn; Wise, Carol; Saffery, Richard; Finkel, Terri H.; Hakonarson, Hakon; Ponsonby, Anne-Louise & Ellis, Justine A. (2015). The association of PTPN22 rs2476601 with juvenile idiopathic arthritis is specific to females. Genes and Immunity.  ISSN 1466-4879.  16(7), s 495- 498 . doi: 10.1038/gene.2015.32
• Cortes, Adrian; Pulit, Sara L.; Leo, Paul J.; Pointon, Jenny J.; Robinson, Philip C.; Weisman, Michael H.; Ward, Michael; Gensler, Lianne S.; Zhou, Xiaodong; Garchon, Henri-Jean; Chiocchia, Gilles; Nossent, Johannes; Lie, Benedicte Alexandra; Førre, Øystein Thorleiv; Tuomilehto, Jaakko; Laiho, Kari; Bradbury, Linda A.; Elewaut, Dirk; Burgos-Vargas, Ruben; Stebbings, Simon; Appleton, Louise; Farrah, Claire; Lau, Jonathan; Haroon, Nigil; Mulero, Juan; Blanco, Francisco J.; González-Gay, Miguel A.; López-Larrea, Carlos; Bowness, Paul; Gaffney, Karl; Gaston, Hill; Gladman, Dafna D.; Rahman, Proton; Maksymowych, Walter P.; Crusius, J. Bart A.; van der Horst-Bruinsma, Irene E.; Valle-Oñate, Raphael; Romero-Sánchez, Consuelo; Myrnes, Inger; Pimentel-Santos, Fernando M.; Inman, Robert D.; Martin, Javier; Breban, Maxime; Wordsworth, Bryan Paul; Reveille, John D.; Evans, David M.; de Bakker, Paul I.W. & Brown, Matthew A. (2015). Major histocompatibility complex associations of ankylosing spondylitis are complex and involve further epistasis with ERAP1. Nature Communications.  ISSN 2041-1723.  6 . doi: 10.1038/ncomms8146
• Ellis, Justine A.; Scurrah, Katrina J.; Li, Yun R.; Ponsonby, Anne-Louise; Chavez, Raul A.; Pezic, Angela; Dwyer, Terence; Akikusa, Jonathan D.; Allen, Roger C.; Becker, Mara L.; Thompson, Susan D.; Lie, Benedicte Alexandra; Flatø, Berit; Førre, Øystein Thorleiv; Punaro, Marilynn; Wise, Carol; Finkel, Terri H.; Hakonarson, Hakon & Munro, Jane E. (2015). Epistasis amongst PTPN2 and genes of the vitamin D pathway contributes to risk of juvenile idiopathic arthritis. Journal of Steroid Biochemistry and Molecular Biology.  ISSN 0960-0760.  145, s 113- 120 . doi: 10.1016/j.jsbmb.2014.10.012
• Kåss, Anita Anjali Suri; Hollan, Ivana; Fagerland, Morten; Gulseth, Hans-Christian; Torjesen, Peter A & Førre, Øystein Thorleiv (2015). Rapid anti-inflammatory effects of gonadotropin-releasing hormone antagonism in rheumatoid arthritis patients with high gonadotropin levels in the Agra trial. PLOS ONE.  ISSN 1932-6203.  10:e013439(10) . doi: 10.1371/journal.pone.0139439 Show summary

  Abstract Objectives Gonadotropin-releasing hormone (GnRH) and pituitary gonadotropins, which appear to be proinflammatory, undergo profound secretory changes during events associated with rheumatoid arthritis (RA) onset, flares, or improvement e.g. menopausal transition, postpartum, or pregnancy. Potential anti-inflammatory effects of GnRH-antagonists may be most pronounced in patients with high GnRH and gonadotropin levels. Therefore, we investigated the efficacy and safety of a GnRH-antagonist, cetrorelix, in RA patients with high gonadotropin levels. Methods We report intention-to-treat post hoc analyses among patients with high gonadotropin levels (N = 53), i.e. gonadotropin levels>median, from our proof-of-concept, double-blind AGRA-study (N = 99). Patients with active longstanding RA, randomized to subcutaneous cetrorelix (5mg days1–2; 3mg days 3–5) or placebo, were followed through day 15. Only predefined primary and secondary endpoints were analyzed. Results The primary endpoint, Disease Activity Score of 28-joint counts with C-reactive protein (DAS28-CRP), improved with cetrorelix compared with placebo by day 5 (-1.0 vs. -0.4, P = 0∙010). By day 5, more patients on cetrorelix achieved at least a 20% improvement in the American College of Rheumatology scale (44% vs. 19%, P = 0.049), DAS28-CRP≤3.2 (24% vs. 0%, P = 0.012), and European League against Rheumatism ‘Good-responses’ (19% vs. 0%, P = 0.026). Tumor necrosis factor-α, interleukin-1β, interleukin-10, and CRP decreased with cetrorelix (P = 0.045, P = 0.034, P = 0.020 and P = 0.042 respectively) compared with placebo by day 15. Adverse event rates were similar between groups. Conclusions GnRH-antagonism produced rapid anti-inflammatory effects in RA patients with high gonadotropin levels. GnRH should be investigated further in RA. Trial Registration ClinicalTrials.gov NCT00667758

• Li, Yun R.; Li, Jin; Zhao, Sihai D.; Bradfield, Jonathan P.; Mentch, Frank D.; Maggadóttir, Sólrún Melkorka; Hou, Cuiping; Abrams, Debra J.; Chang, Diana; Gao, Feng; Guo, Yiran; Wei, Zhi; Connolly, John J.; Cardinale, Christopher J.; Bakay, Marina; Glessner, Joseph T.; Li, Dong; Kao, Charlly; Thomas, Kelly A.; Qiu, Haijun; Chiavacci, Rosetta M.; Kim, Cecilia E.; Wang, Fengxiang; Snyder, James; Richie, Marylyn D.; Flatø, Berit; Førre, Øystein Thorleiv; Denson, Lee A.; Thompson, Susan D.; Becker, Mara L.; Guthery, Stephen L; Latiano, Anna; Perez, Elena; Resnick, Elena; Russell, Richard K.; Wilson, David C.; Silverberg, Mark S.; Annese, Vito; Lie, Benedicte Alexandra; Punaro, Marilynn; Dubinsky, Marla C.; Monos, Dimitri S.; Strisciuglio, Caterina; Staiano, Annamaria; Miele, Erasmo; Kugathasan, Subra; Ellis, Justine A.; Munro, Jane E.; Sullivan, Kathleen E.; Wise, Carol A.; Chapel, Helen; Cunningham-Rundles, Charlotte; Grant, Struan F.A.; Orange, Jordan S.; Sleiman, Patrick M.A.; Behrens, Edward M.; Griffiths, Anne M.; Satsangi, Jack; Finkel, Terri H.; Keinan, Alon; Prak, Eline T. Luning; Polychronakos, Constantin; Baldassano, Robert N.; Li, Hongzhe; Keating, Brendan J. & Hakonarson, Hakon (2015). Meta-analysis of shared genetic architecture across ten pediatric autoimmune diseases. Nature Medicine.  ISSN 1078-8956.  21(9), s 1018- 1027 . doi: 10.1038/nm.3933
• Li, Yun R.; Zhao, Sihai D.; Li, Jin; Bradfield, Jonathan P.; Mohebnasab, Maede; Steel, Laura; Kobie, Julie; Abrams, Debra J.; Mentch, Frank D.; Glessner, Joseph T.; Guo, Yiran; Wei, Zhi; Connolly, John J.; Cardinale, Christopher J.; Bakay, Marina; Li, Dong; Maggadóttir, Sólrún Melkorka; Thomas, Kelly A.; Qui, Haijun; Chiavacci, Rosetta M.; Kim, Cecilia E.; Wang, Fengxiang; Snyder, James; Flatø, Berit; Førre, Øystein Thorleiv; Denson, Lee A.; Thompson, Susan D.; Becker, Mara L.; Guthery, Stephen L.; Latiano, Anna; Perez, Elena; Resnick, Elena; Strisciuglio, Caterina; Staiano, Annamaria; Miele, Erasmo; Silverberg, Mark S.; Lie, Benedicte Alexandra; Punaro, Marilynn; Russell, Richard K.; Wilson, David C.; Dubinsky, Marla C.; Monos, Dimitri S.; Annese, Vito; Munro, Jane E.; Wise, Carol; Chapel, Helen; Cunningham-Rundles, Charlotte; Orange, Jordan S.; Behrens, Edward M.; Sullivan, Kathleen E.; Kugathasan, Subra; Griffiths, Anne M.; Satsangi, Jack; Grant, Struan F.A.; Sleiman, Patrick M.A.; Finkel, Terri H.; Polychronakos, Constantin; Baldassano, Robert N.; Luning Prak, Eline T.; Ellis, Justine A.; Li, Hongzhe; Keating, Brendan J. & Hakonarson, Hakon (2015). Genetic sharing and heritability of paediatric age of onset autoimmune diseases. Nature Communications.  ISSN 2041-1723.  6:8442 . doi: 10.1038/ncomms9442
• Curran, Samuel A.; Hollan, Ivana; Erridge, Clett; Lappin, David F.; Murray, Colin A.; Sturfelt, Gunnar; Mikkelsen, Knut; Førre, Øystein Thorleiv; Almdahl, Sven Martin; Fagerhol, Magne Kristoffer; Goodyear, Carl S & Riggio, Marcello P. (2014). Bacteria in the adventitia of cardiovascular disease patients with and without rheumatoid arthritis. PLOS ONE.  ISSN 1932-6203.  9(5:e98627) . doi: 10.1371/journal.pone.0098627
• Haugeberg, Glenn; Helgetveit, Knut; Førre, Øystein Thorleiv; Garen, Torhild Oddveig; Sommerseth, Hege & Prøven, Anne (2014). Generalized bone loss in early rheumatoid arthritis patients followed for ten years in the biologic treatment era. BMC Musculoskeletal Disorders.  ISSN 1471-2474.  15(1) . doi: 10.1186/1471-2474-15-289 Full text in Research Archive.
• Kåss, Anita Anjali Suri; Førre, Øystein Thorleiv; Fagerland, Morten; Gulseth, Hans-Christian; Torjesen, Peter A & Hollan, Ivana (2014). Short-term treatment with a gonadotropin-releasing hormone antagonist, cetrorelix, in rheumatoid arthritis (AGRA): a randomized, double-blind, placebo-controlled study. Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  43(1), s 22- 27 . doi: 10.3109/03009742.2013.825007 Show summary

  Objectives: Gonadotropin-releasing hormone (GnRH) stimulates immune responses; therefore, antagonizing GnRH with cetrorelix may have anti-inflammatory effects. The aim of this study was to assess short-term cetrorelix therapy in rheumatoid arthritis (RA) patients. Method: In this proof-of-concept, randomized, double-blind study involving 99 patients with active, long-standing RA, 48 patients received subcutaneous cetrorelix (5 mg/day on days 1 and 2; 3 mg/day on days 3–5) and 51 received placebo. The primary end-point was the change in the 28-joint Disease Activity Score based on C-reactive protein (DAS28-CRP) by day 5, when the greatest GnRH suppression was anticipated. Secondary end-points included the change in tumour necrosis factor (TNF)-α, and achievement of American College of Rheumatology (ACR) responses and DAS28-CRP < 2.6 by day 5. Patients were followed up on days 10 and 15. Results: By day 5, DAS28-CRP was non-significantly reduced by 0.82 in the cetrorelix group compared to a 0.57 reduction in the placebo group (p = 0.091), TNF-α (log pg/mL) was significantly reduced in the cetrorelix group compared with the placebo group [0.55, 95% confidence interval (CI) 0.08–1.01, p = 0.023], and more patients on cetrorelix achieved ACR20 responses (40% vs. 18%, p = 0.015) and DAS28-CRP < 2.6 (13% vs. 0%, p = 0.009). Inflammatory markers increased towards baseline levels after withdrawal of treatment. Rates of adverse events were similar in both groups. Conclusions: Although there was no significant difference in the primary end-point between groups, antagonizing GnRH led to significant improvements in key secondary end-points. Thus, GnRH antagonists may have rapid anti-inflammatory effects in RA, already occurring within 5 days. The data suggest a novel mode of action for TNF-α inhibition in RA, and potentially in other autoimmune diseases.

• Cortes, Adrian; Hadler, Johanna; Pointon, JP; Robinson, Philip; Karaderi, Kudce; Leo, Paul; Cremin, Katie; Pryce, Karena; Harris, Jessica; Lee, Seunghun; Joo, Kyung Bin; Shim, Seung-Cheol; Weisman, Michael; Ward, Michael; Xiaodong, Zhou; Garchon, Henri-Jean; Karaderi, T; Nossent, Johannes C; Lie, Benedicte Alexandra; Førre, Øystein Thorleiv; Tuomilehto, Jaako; Laiho, Kari; Jiang, Lei; Liu, Yu; Wu, Xin; Bradbury, Linda A; Elewaut, Dirk; Bourgos-Vargas, Ruben; Stebbings, Simon; Appleton, Louise; Farrah, Claire; Lau, Jonathan; Kenna, Tony J; Haroon, Nigel; Ferreira, Manuel A.; Yang, J; Mulero, Juan; Fernandez-Sueiro, Jose Luis; Gonzalez-Gay, Miguel A.; Lopez-Larrea, Carlos; Deloukas, Panos; Donelly, Peter; Bowness, Paul; Gafney, Karl; Gaston, Hill; Gladman, Dafna D.; Rahman, Proton; Maksymowych, Walter P.; Xu, Huji; Crusius, J Bart A; Horst-Bruinsma, Irene E van der; Chou, CT; Valle-Onate, R; Romero-Sanchez, C; Hansen, Inger Myrnes; Pimentel-Santos, FM; Inman, Robert D; Videm, Vibeke; Martin, J; Breban, Maxime; Reveille, John D; Evans, DM; Kim, Tae-Hwan; Wordsworth, Bryan Paul; Brown, Matthew & Chiocchia, Gilles (2013). Identification of multiple risk variants for ankylosing spondylitis through high-density genotyping of immune-related loci. Nature Genetics.  ISSN 1061-4036.  45(7), s 730- 738 . doi: 10.1038/ng.2667
• Hjeltnes, Gunnbjørg; Hollan, Ivana; Førre, Øystein Thorleiv; Wiik, A; Lyberg, Torstein; Mikkelsen, Knut & Agewall, Stefan (2013). Serum levels of lipoprotein(a) and E-selectin are reduced in rheumatoid arthritis patients treated with methotrexate or methotrexate in combination with TNF-alpha-inhibitor. Clinical and Experimental Rheumatology.  ISSN 0392-856X.  31(3), s 415- 421
• Hollan, Ivana; Nebuloni, Manuela; Bottazzi, Barbara; Mikkelsen, Knut; Førre, Øystein Thorleiv; Almdahl, Sven Martin; Mantovani, Alberto; Fagerland, Morten; Aukrust, Pål & Meroni, Pier Luigi (2013). Pentraxin 3, a novel cardiovascular biomarker, is expressed in aortic specimens of patients with coronary artery disease with and without rheumatoid arthritis. Cardiovascular pathology.  ISSN 1054-8807.  22(5), s 324- 331 . doi: 10.1016/j.carpath.2013.01.007
• Eike, Morten Christoph; Skinningsrud, Beate; Ronninger, Marcus; Stormyr, Alice; Kvien, Tore Kristian; Joner, Geir; Njølstad, Pål Rasmus; Førre, Øystein Thorleiv; Flatø, Berit; Alfredsson, Lars; Padyukov, Leonid; Undlien, Dag Erik & Lie, Benedicte Alexandra (2012). CIITA gene variants are associated with rheumatoid arthritis in Scandinavian populations. Genes and Immunity.  ISSN 1466-4879.  13(5), s 431- 436 . doi: 10.1038/gene.2012.11 Show summary

  Expression of the major autoimmune risk loci DRB1 and DQB1 is regulated by the class II MHC (major histocompatibility complex) transactivator (CIITA), making the CIITA gene a strong autoimmune risk locus candidate. A CIITA promoter single-nucleotide polymorphism (SNP), rs3087456 (-168 A/G), has indeed been associated with several autoimmune diseases, including rheumatoid arthritis (RA). Recently, an intronic SNP rs8048002 has been suggested as a better susceptibility marker in Addison's disease. Therefore, we tested both SNPs in a panel of autoimmune diseases, consisting of Norwegian patients with RA (n=819), juvenile idiopathic arthritis (JIA; n=524), or type 1 diabetes (T1D; n=1211), and 2149 controls. We also included an independent Swedish RA cohort (n=2503) and controls (n=1416). Both rs3087456 and rs8048002 were significantly associated with RA (combined Norwegian and Swedish patients P(corrected)=0.012 and P(corrected)=0.0016, respectively), but not with JIA or T1D. Meta-analysis of 16 RA cohorts confirmed rs3087456 with only marginal significance (P=0.016). However, results were stronger in the Scandinavian subgroup (4 cohorts, P=3.8 × 10(-4)), indicating a population-dependent effect. A similar pattern was observed in a meta-analysis of rs8048002. Our results support involvement of CIITA in RA, but imply that this is population dependent and that the aetiological variant is yet to be discovered.

• Grub, Carola; Brunborg, Cathrine; Hasseltvedt, Viggo H; Aukrust, Pål; Førre, Øystein Thorleiv; Almdahl, Sven Martin & Hollan, Ivana (2012). Antibodies to common infectious agents in coronary artery disease patients with and without rheumatic conditions. Rheumatology.  ISSN 1462-0324.  51(4), s 679- 685 . doi: 10.1093/rheumatology/ker251
• Hjeltnes, Gunnbjørg; Hollan, Ivana; Førre, Øystein Thorleiv; Wiik, Allan; Lyberg, Torstein; Mikkelsen, Knut & Agewall, Stefan (2012). Relations of Serum COMP to Cardiovascular Risk Factors and Endothelial Function in Patients with Rheumatoid Arthritis Treated with Methotrexate and TNF-alpha Inhibitors. Journal of Rheumatology.  ISSN 0315-162X.  39(7), s 1341- 1347 . doi: 10.3899/jrheum.111401
• Nordang, Gry Beate Namløs; Viken, Marte K; Amundsen, Svanstrøm Silja; Sanchez, Elena S.; Flatø, Berit; Førre, Øystein Thorleiv; Martin, Javier; Kvien, Tore Kristian & Lie, Benedicte Alexandra (2012). Interferon regulatory factor 5 gene polymorphism confers risk to several rheumatic diseases and correlates with expression of alternative thymic transcripts. Rheumatology.  ISSN 1462-0324.  51(4), s 619- 626 . doi: 10.1093/rheumatology/ker364
• Rasmussen, Lars Bjørn; Mikkelsen, Knut; Haugen, Margaretha; Pripp, Are Hugo; Fields, Jeremy Z. & Førre, Øystein Thorleiv (2012). Treatment of fibromyalgia at the Maharishi Ayurveda Health Centre in Norway II-a 24-month follow-up pilot study. Clinical Rheumatology.  ISSN 0770-3198.  31(5), s 821- 827 . doi: 10.1007/s10067-011-1907-y
• Hjeltnes, Gunnbjørg; Hollan, Ivana; Førre, Øystein Thorleiv; Wiik, A; Mikkelsen, Knut & Agewall, Stefan (2011). Anti-CCP and RF IgM: predictors of impaired endothelial function in rheumatoid arthritis patients. Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  40(6), s 422- 427 . doi: 10.3109/03009742.2011.585350
• Breland, Unni Mathilde; Hollan, Ivana; Saatvedt, Kjell; Almdahl, Sven Martin; Damås, Jan Kristian; Yndestad, Arne; Mikkelsen, Knut; Førre, Øystein Thorleiv; Aukrust, Pål & Ueland, Thor (2010). Inflammatory markers in patients with coronary artery disease with and without inflammatory rheumatic disease. Rheumatology.  ISSN 1462-0324.  49(6), s 1118- 1127 . doi: 10.1093/rheumatology/keq005
• Grundtman, Cecilia; Hollan, Ivana; Førre, Øystein Thorleiv; Saatvedt, Kjell; Mikkelsen, Knut & Lundberg, Ingrid (2010). Cardiovascular Disease in Patients With Inflammatory Rheumatic Disease Is Associated With Up-Regulation of Markers of Inflammation in Cardiac Microvessels and Cardiomyocytes. Arthritis and Rheumatism.  ISSN 0004-3591.  62(3), s 667- 673 . doi: 10.1002/art.27264
• Hollan, Ivana; Bottazzi, B; Cuccovillo, I; Førre, Øystein Thorleiv; Mikkelsen, Knut; Saatvedt, Kjell; Almdahl, Sven Martin; Mantovani, A & Meroni, PL (2010). Increased Levels of Serum Pentraxin 3, a Novel Cardiovascular Biomarker, in Patients With Inflammatory Rheumatic Disease. Arthritis Care and Research.  ISSN 0893-7524.  62(3), s 378- 385 . doi: 10.1002/acr.20094
• Kåss, Anita Anjali Suri; Lea, Tor; Torjesen, Peter A; Gulseth, Hans-Christian & Førre, Øystein Thorleiv (2010). The association of luteinizing hormone and follicle-stimulating hormone with cytokines and markers of disease activity in rheumatoid arthritis: a case-control study. Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  39(2), s 109- 117 . doi: 10.3109/03009740903270607 Show summary

  Conclusions: The significant associations between percentage changes in LH and FSH and percentage changes in key cytokines and several cross-sectional markers of disease activity may indicate that LH and FSH influence crucial points of the cytokine cascade in RA. This may help to explain, partially, why disease activity initiates or worsens during periods of increased LH and FSH, such as the postpartum period and the menopause.

• Lien, Gunhild; Ueland, Thor; Godang, Kristin; Selvaag, Anne Marit G; Førre, Øystein Thorleiv & Flatø, Berit (2010). Serum levels of osteoprotegerin and receptor activator of nuclear factor -kappa B ligand in children with early juvenile idiopathic arthritis: a 2-year prospective controlled study. Pediatric Rheumatology.  ISSN 1546-0096.  8 . doi: 10.1186/1546-0096-8-30
• Skinningsrud, Beate; Lie, Benedicte; Husebye, Eystein S; Kvien, Tore K; Førre, Øystein; Flatø, Berit; Stormyr, Alice; Joner, Geir; Njølstad, Pål R; Egeland, Thore & Undlien, Dag E. (2010). A CLEC16A variant confers risk for juvenile idiopathic arthritis and anti-cyclic citrullinated peptide antibody negative rheumatoid arthritis. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  69(8), s 1471- 1474 . doi: 10.1136/ard.2009.114934
• Skinningsrud, Beate; Lie, Benedicte Alexandra; Husebye, Eystein; Kvien, TK; Førre, Øystein Thorleiv; Flatø, Berit; Stormyr, Alice; Joner, Geir; Njølstad, Pål R.; Egeland, Thore & Undlien, Dag Erik (2009). A CLEC16A variant confers risk for juvenile idiopathic arthritis and anti-CCP negative rheumatoid arthritis. Annals of the Rheumatic Diseases.  ISSN 0003-4967. . doi: 10.1136/ard.2009.114934
• Aaløkken, Trond Mogens; Lilleby, Vibke; Søyseth, Vidar; Mynarek, Georg; Pripp, Are Hugo; Johansen, Bjørn; Førre, Øystein Thorleiv & Kolbenstvedt, Alf (2009). Chest Abnormalities in Juvenile-Onset Mixed Connective Tissue Disease: Assessment with High-Resolution Computed Tomography and Pulmonary Function Tests. Acta Radiologica.  ISSN 0284-1851.  50(4), s 430- 436 . doi: 10.1080/02841850902787677
• Magitta, Ng'weina Francis; Wolff, Anette Susanne Bøe; Johansson, Stefan; Skinningsrud, Beate; Lie, Benedicte A; Myhr, Kjell-Morten; Undlien, Dag Erik; Joner, Geir; Njølstad, Pål Rasmus; Kvien, Tore K.; Førre, Øystein; Knappskog, Per Morten & Husebye, Eystein Sverre (2009). A coding polymorphism in NALP1 confers risk for autoimmune Addison's disease and type 1 diabetes. Genes and Immunity.  ISSN 1466-4879.  10(2), s 120- 124 . doi: 10.1038/gene.2008.85
• Nordang, GB; Viken, Marte K; Hollis-Moffatt, JE; Merriman, TR; Førre, Øystein Thorleiv; helgetveit, Knut; Kvien, Tore Kristian & Lie, Benedicte Alexandra (2009). Association analysis of the interleukin 17A gene in Caucasian rheumatoid arthritis patients from Norway and New Zealand. Rheumatology.  ISSN 1462-0324.  48(4), s 367- 370 . doi: 10.1093/rheumatology/ken512
• Eike, MC; Namløs, Gry Beate; Nordang, GBN; Karlsen, TH; Boberg, KM; Vatn, MH; Dahl-Jørgensen, Knut; Rønningen, Kjersti Skjold; Joner, Geir; Flatø, B.; Bergquist, A; Thorsby, E; Førre, Øystein Thorleiv; Kvien, TK; Undlien, DE & Lie, BA (2008). The FCRL3 -169T>C polymorphism is associated with rheumatoid arthritis and shows suggestive evidence of involvement with juvenile idiopathic arthritis in a Scandinavian panel of autoimmune diseases. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  67(9), s 1287- 1291 . doi: 10.1136/ard.2007.077826
• Hollan, Ivana; Prayson, R; Saatvedt, Kjell; Almdahl, Sven M; Nossent, Johannes C; Mikkelsen, Knut; Liang, Matthew; Kvelstad, Ingjerd Lien; Aamodt, Geir & Førre, Øystein Thorleiv (2008). Inflammatory cell infiltrates in vessels with different susceptibility to atherosclerosis in rheumatic and non-rheumatic patients. Circulation Journal.  ISSN 1346-9843.  72(12), s 1986- 1992
• Bruyn, GAW; Tate, G; Caeiro, F; Maldonado-Cocco, J; Westhovens, R; Tannenbaum, H; Bell, M; Førre, Øystein Thorleiv; Bjørneboe, Olav; Tak, PP; Abeywickrama, KH; Bernhardt, P & van Riel, PLC (2008). Everolimus in patients with rheumatoid arthritis receiving concomitant methotrexate: a 3-month, double-blind, randomised, placebo-controlled, parallel-group, proof-of-concept study. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  67, s 1090- 1095 . doi: 10.1136/ard.2007.078808
• Magitta, Ng’weina Francis; Bøe, AS; Johansson, S; Skinningsrud, Beate; Lie, Benedicte Alexandra; Myhr, KM; Undlien, Dag Erik; Joner, Geir; Njølstad, Pål R.; Kvien, Tore Kristian; Førre, Øystein Thorleiv; Knappskog, P.M. & Husebye, Eystein (2008). A coding polymorphism in NALP1 confers risk for autoimmune Addison's disease and type 1 diabetes. Genes and Immunity.  ISSN 1466-4879. . doi: 10.1038/gene.2008.85
• Hollan, Ivana; Scott, Helge; Saatvedt, Kjell; Prayson, R; Mikkelsen, Knut; Nossent, Hans C; Kvelstad, L.I; Liang, M.H. & Førre, Øystein Thorleiv (2007). Inflammatory rheumatic disease and smoking are predictors of aortic inflammation. Arthritis and Rheumatism.  ISSN 0004-3591.  56(6), s 2072- 2079
• Viken, Marte K; Olsson, M; Tennebø flåm, ST; Førre, Øystein Thorleiv; Kvien, Tore Kristian; Thorsby, Erik & Lie, A B (2007). The PTPN22 promoter polymorphism - 1123G &gt; C association cannot be distinguished from the 1858C &gt; T association in a Norwegian rheumatoid arthritis material. Tissue Antigens.  ISSN 0001-2815.  70(3), s 190- 197 . doi: 10.1111/j.1399-0039.2007.00871.x
• Lilleby, Vibke; Aaløkken, Trond Mogens; Johansen, Bjørn & Førre, Øystein Thorleiv (2006). Pulmonay involvement in patients with childhood-onset systemic lupus erythematosus. Clinical and Experimental Rheumatology.  ISSN 0392-856X.  24(2), s 203
• Lilleby, Vibke; Flato, B & Førre, Øystein Thorleiv (2005). Disease duration, hypertension and medication requirements are associated with organ damage in childhood-onset systemic lupus erythematosus. Clinical and Experimental Rheumatology.  ISSN 0392-856X.  23
• Lilleby, Vibke; Lien, Gunhild; Froslie, KF; Haugen, M; Flato, B & Førre, Øystein Thorleiv (2005). Frequency of osteopenia in children and young adults with childhood-onset systemic lupus erythematosus. Arthritis and Rheumatism.  ISSN 0004-3591.  52, s 2051- 2059
• Rødevand, E; Nordvåg, B-Y; Mikkelsen, K; Haga, H-J; Førre, Øystein Thorleiv; Johnsen, V & Kvien, Tore Kristian (2005). Medikamentell profylakse og behandling av steroidindusert osteoporose. Tidsskrift for Den norske legeforening.  ISSN 0029-2001.  s 1643- 1645
• Smerdel, Anna; Finholt, Camilla; Lilleby, Vibke; Gilboe, Inger-Margrethe; Harbo, Hanne Flinstad; Maslinski, S; Førre, Øystein Thorleiv; Thorsby, Erik & Lie, Benedicte Alexandra (2005). Systemic lupus erythematosus and the extended major histocompatibility complex—evidence for several predisposing loci. Rheumatology (Sveits).  ISSN 0080-2727.  44, s 1368- 1373 . doi: 10.1093/rheumatology/kei015
• Viken, Marte K; Amundsen, Svanstrøm Silja; Kvien, Tore Kristian; Boberg, Kirsten Muri; Gilboe, Inger-Margrethe; Lilleby, Vibke; Sollid, Ludvig Magne; Førre, Øystein Thorleiv; Thorsby, Erik; Smerdel, Anna & Lie, Benedicte Alexandra (2005). Association analysis of the 1858C > T polymorphism in the PTPN22 gene in juvenile idiopathic arthritis and other autoimmune diseases. Genes and Immunity.  ISSN 1466-4879.  6
• Værøy, Henning; Tanum, Lars; Bruaset, Helga; Mørkrid, Lars & Førre, Øystein Thorleiv (2005). Symptoms of depression and anxiety in functionally disabled rheumatic pain patients. Nordic Journal of Psychiatry.  ISSN 0803-9488.  59
• Flatø, Berit; Sørensen, R & Førre, Øystein Thorleiv (2004). Spinal problems in children, In D.A. Isenberg (ed.),  Oxford textbook of rheumatology. 3rd edition.  Oxford University Press.  ISBN 0-19-850948-0.  1.2.1.2.
• Smerdel, Anna; Dai, Kezheng; Lorentzen, Åslaug Rudjord; Flatø, Berit; Maslinski, S; Thorsby, Erik; Førre, Øystein Thorleiv & Spurkland, Anne (2004). Genetic association between juvenile rheumatoid arthritis and polymorphism in the SH2D2A gene. Genes and Immunity.  ISSN 1466-4879.  5(4), s 310- 312 Show summary

  T-cell-specific adapter protein (TSAd) involved in the negative control of T-cell activation is encoded by the SH2D2A gene. Our recent studies indicate that homozygosity for short (ie GA(13) and GA(16)) alleles of the SH2D2A gene promoter is associated with development of multiple sclerosis. To study whether the same SH2D2A promoter polymorphism also contributes to the genetic susceptibility to develop juvenile rheumatoid arthritis (JRA), we examined 210 JRA patients and 558 healthy unrelated controls from Norway. The frequency of the short allele GA(13) was increased among the JRA patients compared to control (0.098 vs 0.05; P(n=8)=0.042). There was a significant increased frequency of HLA-DRB1(*)08-positive patients carrying two copies of 'short' alleles GA(13) and/or GA(16) compared to healthy controls (16% vs 6%; P(n=4)=0.016). Our data indicate that the 'short' alleles of the SH2D2A promoter could contribute to the genetic susceptibility to JRA.

• Flatø, Berit; Lien, Gunhild; Smerdel, Anna; Vinje, Odd; Dale, Knut; Johnston, Virginia; Sørskaar, Dag; Moum, Torbjørn; Ploski, Rafal & Førre, Øystein Thorleiv (2003). Prognostic factors in juvenile rheumatoid arthritis: a case-control study revealing early predictors and outcome after 14.9 years. Journal of Rheumatology.  ISSN 0315-162X.  30(2), s 386- 393
• Hollan, I.; Mikkelsen, K. V.; Nossent, H.; Saatvedt, Kjell; Aamodt, Geir; Wiik, A; Liang, M.H. & Førre, Øystein Thorleiv (2003). Mononuclear Cell Infiltrates in the Aorta, not in the Intramural Vessels of the Cardiac Atrium, in Patients with Systemic Rheumatic Diseases. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  1
• Johnson, V; Førre, Øystein Thorleiv; Haga, Hans-Jacob; Kvien, Tore Kristian; Mikkelsen, K. V.; Nordvag, Bjørn-Yngvar & Rodevand, E (2003). Kombinasjonsbehandling ved revmatoid artritt. Tidsskrift for Den norske legeforening.  ISSN 0029-2001.  123(11), s 1511- 1513
• Lien, Gunhild; Flatø, Berit; Haugen, Margaretha; Vinje, Odd; Sørskaar, Dag; Dale, Knut; Johnston, Virginia; Egeland, Thore & Førre, Øystein Thorleiv (2003). Frequency of osteopenia in adolescents with early-onset juvenile idiopa arthritis: a long-term outcome study of one hundred five patients. Arthritis and Rheumatism.  ISSN 0004-3591.  48(8), s 2214- 2223
• Selvaag, Anne Marit; Flatø, Berit; Lien, Gunhild; Sørskaar, Dag; Vinje, Odd & Førre, Øystein Thorleiv (2003). Measuring health status in early juvenile idiopathic arthritis: determination and responsiveness of the child health questionnaire. Journal of Rheumatology.  ISSN 0315-162X.  30(7), s 1602- 1610
• Smerdel, Anna; Lie, Benedicte Alexandra; Finholt, C.; Ploski, Rafal; Førre, Øystein Thorleiv; Undlien, Dag Erik & Thorsby, Erik (2003). An additional susceptibility gene for juvenile idiopathic arthritis in the HLA class I region on several DR-DQ haplotypes. Tissue Antigens.  ISSN 0001-2815.  61, s 80- 84
• Haugen, Margaretha; Lien, Gunhild; Flatø, Berit; Kvammen, J.A.; Vinje, Odd; Sørskaar, Dag & Førre, Øystein Thorleiv (2002). Minor impact of juvenile arthritis on nutritional status in young adult patients. Arthritis and Rheumatism.  ISSN 0004-3591.  47, s 623- 629
• Hollan, I.; Mikkelsen, K. V.; Scott, Helge; Nossent, H.; Saatvedt, Kjell; Sturfelt, G. & Førre, Øystein Thorleiv (2002). High prevalence of polymyalgia rheumatica and giant cell arteritis in subjects undergoing coronary artery bypass grafting in Feiringklinikken, Norway. Arthritis and Rheumatism.  ISSN 0004-3591.  46(9), s 72
• Hollan, I.; Nossent, H.; Saatvedt, Kjell; Mikkelsen, K. V.; Scott, Helge & Førre, Øystein Thorleiv (2002). Mononuclear infiltration of vessel walls in subjects undergoing coronary artery bypass grafting (CABG). Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  31, s 24
• Hollan, I.; Saatvedt, Kjell; Nossent, H.; Mikkelsen, K. V.; Scott, Helge; Liang, M.H.; Aukrust, Pål; Sturfelt, G. & Førre, Øystein Thorleiv (2002). Enhanced infiltration of mononuclear cells in the aorta in patients with polyarthritis and systemic lupus erythematosus undergoing coronary artery bypass grafting. Arthritis and Rheumatism.  ISSN 0004-3591.  46
• Hollan, I.; Scott, Helge; Saatvedt, Kjell; Mikkelsen, K. V.; Førre, Øystein Thorleiv; Myrmel, T & Nossent, H. (2002). Aortic inflammation in patients wit systemic inflammatory diseases. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  61(1), s 324
• Lien, Gunhild; Flatø, Berit; Haugen, Margaretha; Vinje, Odd; Sørskaar, Dag & Førre, Øystein Thorleiv (2002). Total body bone mineral content in adolescents with early onset juvenile idiopathic arthritis. Calcified Tissue International.  ISSN 0171-967X.  70(5)
• Flatø, Berit; Smerdel, Anna; Johnston, Virginia; Lien, Gunhild; Dale, Knut; Vinje, Odd; Egeland, Thore; Sørskaar, Dag & Førre, Øystein Thorleiv (2002). The influence of patient characteristics, disease variables, and HLA alleles on the development of radiographically evident sacroiliitis in juvenile idiopathic arthritis. Arthritis and Rheumatism.  ISSN 0004-3591.  46, s 986- 994
• Førre, Øystein Thorleiv & Smerdel, Anna (2002). Genetic epidemiology of juvenile idiopathic arthritis. Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  31(3), s 123- 128
• Kvien, Tore Kristian; Zeidler, H.K.; Hannonen, P.; Wollheim, F.A.; Førre, Øystein Thorleiv; Hafstrøm, I.; Kaltwasser, J.P.; Leirisalo-Repo, M.; Manger, B.; Laasonen, L.; Prestele, H. & Kurki, P. (2002). Long term efficacy and safety of cyclosporin versus parenteral gold in early rheumatoid arthritis: a three year study of radiographic progression, renal function, and arterial hypertension. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  61, s 511- 516
• Kvien, Tore Kristian; Zeidler, H.K.; Hannonen, P.; Wollheim, F.A.; Førre, Øystein Thorleiv; Hafstrøm, I.; Kaltwasser, J.P.; Leirisalo-Repo, M.; Manger, B.; Laasonen, L.; Prestele, H. & Kurki, P. (2002). Long-term efficacy and safety of cyclosporine versus parenteral gold in early rheumatoid arthritis. A 3-year study of radiographic progression, renal function and arterial hypertension. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  61, s 511- 516
• Smerdel, Anna; Lie, Benedicte Alexandra; Ploski, Rafal; Koeleman, B.P.C.; Førre, Øystein Thorleiv; Thorsby, Erik & Undlien, E. (2002). A gene in the telomeric HLA complex distinct from HLA-A is involved in predisposition to juvenile idiopathic arthritis (JIA) (22nd EWRR). Arthritis Research.  ISSN 1465-9905.  4
• Smerdel, Anna; Lie, Benedicte Alexandra; Ploski, Rafal; Koelman, Bobby; Førre, Øystein Thorleiv; Thorsby, Erik & Undlien, Dag Erik (2002). A gene in the telomeric HLA complex distinct from HLA-A is involved in predisposition to juvenile idiopathic arthritis. Arthritis and Rheumatism.  ISSN 0004-3591.  46(6), s 1614- 1619 Show summary

  Institute of Immunology and Center for Rheumatic Diseases, Rikshospitalet University Hospital, N-0027 Oslo, Norway. anna.smerdel@klinmed.uio.no OBJECTIVE: Juvenile idiopathic arthritis (JIA) is associated with particular alleles at 3 different HLA loci: HLA-A, HLA-DR/DQ, and HLA-DP. These associations are independent of each other (i.e., they cannot be explained by the known linkage disequilibrium between alleles at these loci). The purpose of this study was to look for additional JIA susceptibility genes in the HLA complex. METHODS: One hundred two Norwegian JIA patients and 270 healthy individuals, all carrying the DQ4;DR8 haplotype, were investigated by scanning approximately 10 megabases of DNA covering the HLA complex with microsatellite polymorphisms. An expectation-maximization algorithm was used to estimate haplotype frequencies, and the distribution of microsatellite alleles on the high-risk DQ4;DR8 haplotype was compared between patients and controls, to exclude effects secondary to linkage disequilibrium with these susceptibility genes. RESULTS: Allele 5 at the microsatellite locus D6S265 (D6S265* 5), 100 kb centromeric of HLA-A, showed a strong positive association with the disease (odds ratio 4.7, corrected P < 10(-6)). Haplotype analysis demonstrated that the D6S265*5 association was not caused by linkage disequilibrium to the gene encoding HLA-A*02, which has previously been reported to be associated with JIA. Instead, our data suggested that a gene in linkage disequilibrium with D6S265*5, but distinct from HLA-A*02, is involved in the predisposition to JIA. CONCLUSION: We found that D6S265*5 could be a marker for an additional susceptibility gene in JIA which is distinct from A*02, adding to the risk conferred by DQ4;DR8. PMID: 12115193 [PubMed - indexed for MEDLINE]

• Smerdel, Anna; Ploski, Rafal; Flatø, Berit; Musiej-Nowakowska, E.; Thorsby, Erik & Førre, Øystein Thorleiv (2002). Juvenile idiopathic arthritis (JIA) is primarily associated with HLA-DR8 but not DQ4 on the DR8-DQ4 haplotype. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  61(4), s 354- 357 Show summary

  Institute of Immunology, Rikshospitalet University Hospital, Oslo, Norway. asmerdel@klinmed.uio.no BACKGROUND: Juvenile idiopathic arthritis (JIA) is strongly associated with the DR8-DQ4 haplotype. The genes encoding DR8 and DQ4 are in strong linkage disequilibrium (LD) and occur together on the same HLA haplotype in almost all patients and controls. Because of the strong LD it is not clear whether DR8, DQ4, or both, are primarily associated with JIA. OBJECTIVE: To unveil the primary association of JIA--that is, with DR8 or DQ4. METHODS: DRB1, DQA1, and DQB1 alleles of 585 Norwegian and 47 Polish unrelated patients with JIA (categorised as pauciarticular and rheumatoid factor negative polyarticular JIA), and of 3155 Norwegian and 158 Polish unrelated controls, were typed using a polymerase chain reaction or oligonucleotide hybridisation and sequence-specific primers method. RESULTS: Several haplotypes which encoded DR8 (that is, carried DRB1*08) and which did not encode DQ4 (that is, did not carry DQA1*0401) were found. Such haplotypes were found in three Norwegian patients and two controls (p=0.029). In the Polish population such haplotypes were found among four patients with JIA and two controls (p=0.025). No haplotypes which carried DQA1*0401 and DQB1*0402 in the absence of DRB1*08 were found, either among patients with JIA (Polish and Norwegian) or among the controls (Polish). CONCLUSION: On the DR8-DQ4 haplotype the DRB1*08 allele is primarily associated with JIA. PMID: 11874841 [PubMed - indexed for MEDLINE]

• Omtvedt, Lone Aanerud; Kolset, Svein Olav; Thoen, J. E.; Førre, Øystein Thorleiv & Gill, Mark R. (2001). Serglycin expression in CD2+ and CD14+ cells from patients with various rheumatic diseases. Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  30, s 164- 166
• Selvaag, Anne Marit; Ruperto, N.; Asplin, L.; Rygg, Marianne; Landgraf, J.M.; Førre, Øystein Thorleiv & Flatø, Berit (2001). The Norwegian version of the Childhood Health Assessment Questionnaire (CHAQ) and the Child Health Questionnaire (CHQ). Clinical and Experimental Rheumatology.  ISSN 0392-856X.  4, Suppl. 23, s 116- 120
• Fraser, D. A.; Thoen, J. E.; Bondhus, S.; Haugen, Margaretha; Reseland, Janne Elin; Djøseland, J.E.; Førre, Øystein Thorleiv & Kjeldsen-Kragh, Jens (2000). Reduction in serum leptin and IGF-1 but preserved T-lymphocyte numbers and activation after a ketogenic diet in rheumatoid arthritis patients. Clinical and Experimental Rheumatology.  ISSN 0392-856X.  18, s 209- 214
• Førre, Øystein Thorleiv; Haugen, Margaretha & Hassfeld, W. G. (2000). New treatment for rheumatic patients. Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  29, s 73- 84
• Haugen, Margaretha; Lien, Gunhild; Kvamme, Odd Jarle; Vinje, Odd; Sørskaar, Dag & Førre, Øystein Thorleiv (2000). Young adults with juvenile arthritis in remission attain normal peak bone mass at the lumbar spine and forearm. Arthritis and Rheumatism.  ISSN 0004-3591.  43, s 1504- 1510
• Hansen, M.H.; Dybwad, Anne; Førre, Øystein Thorleiv & Sioud, Mouldy (2000). Probing antinuclear antibody specificities by peptide phage display libraries. Clinical and Experimental Rheumatology.  ISSN 0392-856X.  18, s 465- 472
• Vinje, Odd; Flatø, Berit & Førre, Øystein Thorleiv (2000). Klassifisering av idiopatiske juvenile artritter. Tidsskrift for Den norske legeforening.  ISSN 0029-2001.  120, s 459- 465

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• Hansen, Inger Myrnes; Bakland, Gunnstein & Førre, Øystein Thorleiv (2016). PLASMA CALPROTECTIN IN SPA-PATIENTS, A BIOMARKER FOR PERIPHERAL ARTHRITIS. Scandinavian Journal of Rheumatology.  ISSN 0300-9742.  45(Supplement 128) . doi: 10.1080/03009742.2016.1207299 Show summary

  Background: Spondyloarthritis (SpA) comprises a group of rheumatic diseases involving axial and peripheral inflammatory arthritis. Inflammatory biomarkers such as ESR and CRP are weakly correlated with disease activity. Calprotectin, mainly secreted by neutrophils, is elevated in sites of active inflammation. Plasma calprotectin (p-calprotectin) is elevated in RA, SLE, and IBD. Objectives: To investigate p-calprotectin in SpA patients from Rana, Norway: to determine whether p-calprotectin is elevated in SpA patients, whether calprotectin differs with age and gender, and whether calprotectin is correlated to BMI, inflammatory markers, or disease manifestations. Method: SpA patients were recruited from hospital registers, family doctors, and by local newspaper advertisement. We collected clinical data and blood samples. Patients fulfilling the European Spondyloarthropathy Study Group (ESSG) criteria were included. First-degree relatives were asked about symptoms of synovitis or inflammatory back pain by questionnaire. Symptomatic relatives were investigated, and included if they fulfilled the ESSG criteria. A total of 387 SpA patients were included. Of these, 273 patients with inflammatory back pain had X-ray and MRI of SI joints. Tests for p-calprotectin were carried out in 235 patients, 51 symptomatic relatives, and 74 healthy relatives. Statistical tests were carried out with SPSS. Results: Calprotectin levels are not significantly different in men and women, in SpA patients, relatives with symptoms, and healthy relatives of SpA patients. In SpA patients there was no difference in calprotectin levels with regard to inflammatory back pain, radiological sacroiliitis, MRI sacroiliitis, psoriasis, IBD, acute uveitis, reactive arthritis, and HLA-B27 positivity. Calprotectin levels were correlated to other inflammatory markers: ESR, CRP, Hb, and TRC; the best correlation was with CRP. Calprotectin was correlated to BMI and swollen joint count but not to BASDAI, BASFI, or MHAQ scores. Conclusions: Plasma calprotectin could be a valuable biomarker in SpA with polyarthritis.

• Hansen, Inger Myrnes; Bakland, Gunnstein & Førre, Øystein Thorleiv (2016). PLASMA CALPROTECTIN IN SPA-PATIENTS, A BIOMARKER FOR PERIPHERAL ARTHRITIS. Clinical and Experimental Rheumatology.  ISSN 0392-856X.  34, s 737- 737 Show summary

  P15 PLASMA CALPROTECTIN IN SPA-PATIENTS, A BIOMARKER FOR PERIPHERAL ARTHRITIS Hansen I.M., Førre O.T., Bakland G. 1Medical Dept. Helgelandssykehuset Mo i Rana; 2University of Oslo, Oslo; 3University Hospital of Northern Norway, Tromsø, Norway Introduction. Spondyloarthritis (SpA) is a rheumatic disease with axial and peripheral inflammatory arthritis. Inflammatory biomarkers as SR and CRP are weakly correlated with disease activity. Calprotectin, mainly secreted by neutrophilic granulocytes is elevated in sites of active inflammation. P-Calprotectin is elevated in RA, SLE and IBD. Aims: To investigate Plasma-Calprotectin in SpA patients from Rana, Norway. Is P-Calprotectin elevated in Spa compared to healthy relatives and relatives with symptoms of Spa? Materials and Methods. SpA-patients were recruited from hospital registers, family doctors and local newspaper-advertisement. Patients fulfilling ESSGcriteria were included. First-degree relatives were asked for symptoms of synovitis or inflammatory back pain by questionnaire. Symptomatic relatives were investigated, and included if they fulfilled the ESSG-criteria. 387 SpA-patients were included. 273 patients with inflammatory back-pain had x-ray and MRI of SI-joints. 235 patients, 51 symptomatic relatives and 74 healthy relatives were tested for Plasma- Calprotectin. Statistic testing with SPSS Chi square test or Students t-test. Results. Calprotectin levels are not significantly different in men, women, SpApatients, relatives with symptoms and healthy relatives. In SpA-patients there is no difference in Calprotectin-levels in inflammatory back-pain, radiological sacroiliitis, sacroiliitis on MRI, psoriasis, IBD, uveitis, reactive arthritis and HLA B27 positivity. Calprotectin levels are correlated to inflammatory markers. Calprotectin is correlated to BMI and swollen joint count but not to BASDAI, BASFI or MHAQ.

• Hansen, Inger Myrnes; Bakland, Gunnstein & Førre, Øystein Thorleiv (2016). PLASMA CALPROTECTIN IN SPA-PATIENTS, A BIOMARKER FOR PERIPHERAL ARTHRITIS. Annals of the Rheumatic Diseases.  ISSN 0003-4967.  75(supplement 2), s 587- 587 . doi: 10.1136/annrheumdis-2016-eular.6088 Show summary

  FRI0420 (2016) PLASMA CALPROTECTIN IN SPA-PATIENTS, A BIOMARKER FOR PERIPHERAL ARTHRITIS I.M. Hansen1, G. Bakland2, Ø. Førre3 1Medical departement, Helgelandssykehuset, Mo i Rana 2Rheumatology, University Hospital of Northern Norway, Tromsø 3Rheumatology, University of Oslo, Oslo, Norway Background: Spondyloarthritis (Spa) is a rheumatic disease with axial and peripheral inflammatory arthritis. The disease is associated with psoriasis, inflammatory bowel disease and uveitis. Inflammatory biomarkers as Sedimentation rate (SR) and CRP ar not as well correlated with disease activity in Spa as it is in Rheumatoid arthritis. Calprotectin, mainly secreted by neutrophilic granulocytes is elevated in sites of active inflammation Serum or plasma Calprotectin is elevated in rheumatoid arthritis, SLE and in IBD Objectives: To investigate Plasma Calprotectin in Spa patients from Rana, Norway. Is Calprotectin elevated in Spa compared to healthy relatives, and relatives with symptoms of Spa? Is Calprotectin associated to age and gender? Is Calprotectin correlated to body mass index, other markers of inflammation, disease manifestations? Methods: Patients with spondyloarthritis, were recruited from hospital registers, family doctors and by advertisement in local newspaper. Clinical data, Crp and HLAB27 were collected, x-ray and mri of SI-joint was performed if the patient had inflammatory backpain. If they fulfilled the ESSG-critera for Spondylarthritis they were included. The first degree relatives of the included patients were contacted and asked for symptoms of synovitis or inflammatory backpain by questionnaire. Symptomatic relatives were investigated, and included if they fulfilled the ESSG-critera. 387 spondylarthrits patients were included. 273 patients had mri of SI-joints235 patients, 51 symptomatic relatives and 74 healthy relatives were tested for Plasma Calprotectin, by Statistic testing with SPSS Chi square test or Students T-test Results: Calprotectin levels are not significantly different in men and women, in Spa-patients, relatives with symptoms and healthy relatives of Spa patients. In Spa-patients there is no difference in Calprotectin-levels in inflammatory back-pain, radiological sacroiliitis, sacroiliitis on mri, psoriasis, inflammatory bowel disease, acute uveitis, reactive arthritis and HLA B27 positivity. Calprotectin levels are correlated to other inflammatory markers: SR, Crp, Hb and Trc, The best correlation is with Crp. Calprotectin is correlated to swollen joint count but not to BASDAI, BASFI or MHAQ Calprotectin N Calprotectin (nG/mL), T-test mean Healthy relatives/Spa-patients 74/235 460/719 0.308 Symptomatic relatives/ Spa-patients 61/235 520/719 0.515 Male 158 812 0.097 Female 202 501 Correlations with Calprotectin in Spa-patients 235 Spearmans rho Chi-square test Body mass index 0.164 0.013 Age −0.105 0.111 Disease duration 0.050 0.480 SR 0.421 0.000 Crp 0.725 0.000 Hb −0.249 0.000 Trc 0.545 0.000 Lkc 0.050 0.457 Tender joint count 0.057 0.437 Swollen joint count 0.250 0.002 Basdai −0.044 0.504 Basfi 0.003 0.962 MHAQ 0.024 0.745 Conclusions: Se-Calprotectin could be a valuable biomarker I Spa, especially in peripheral Spa with polyarthritis References: 1. Hansson C, Eriksson C, Alenius G-M. S-Calprotectin (S100A8/S100A9): A Potential Marker of Inflammation in Patients with Psoriatic Arthritis. Journal of Immunology Research. 2014;2014:696415. doi:10.1155/2014/696415. Acknowledgement: CALPRO AS, Arnstein Arnebergsvei 30 1366 Lysaker, Norway for analysing Plasma Calprotectin Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2016-eular.6088 Citation: Annals of the Rheumatic Diseases, volume 75, supplement 2, year 2016, page 587 Session: Spondyloarthritis - clinical aspects (other than treatment) (Poster Presentations )

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