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61. SAT0204 COMPARING OCCURRENCE AND CLINICAL SIGNIFICANCE OF ANTI-PHOSPHOLIPID AUTOANTIBODIES AMONG SUDANESE AND SWEDISH SLE PATIENTS USING CONVENTIONAL AND NATION-BASED CUTOFFS

Author

Elbagir, S., primary, Elshafie, A., additional, Elagib, E. M., additional, Mohammed, N. A., additional, Manivel, V. A., additional, Pertsinidou, E., additional, Nur, M. A. M., additional, Gunnarsson, I., additional, Svenungsson, E., additional, and Rönnelid, J., additional

Published
2020
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63. Elevated IgA antiphospholipid antibodies in healthy pregnant women in Sudan but not Sweden, without corresponding increase in IgA anti-β2 glycoprotein I domain 1 antibodies

Author

Elbagir, S, primary, Mohammed, N A, additional, Kaihola, H, additional, Svenungsson, E, additional, Gunnarsson, I, additional, Manivel, V A, additional, Pertsinidou, E, additional, Elagib, EM, additional, Nur, M A M, additional, Elussein, E A, additional, Elshafie, A, additional, Åkerud, H, additional, and Rönnelid, J, additional

Published
2020
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66. Genome-wide association study of eosinophilic granulomatosis with polyangiitis reveals genomic loci stratified by ANCA status

Author

Lyons, P.A., Peters, J.E., Alberici, F., Liley, J., Coulson, R.M.R., Astle, W., Baldini, C., Bonatti, F., Cid, M.C., Elding, H., Emmi, G., Epplen, J., Guillevin, L., Jayne, D.R.W., Jiang, T., Gunnarsson, I., Lamprecht, P., Leslie, S., Little, M.A., Martorana, D., Moosig, F., Neumann, T., Ohlsson, S., Quickert, S., Ramirez, G.A., Rewerska, B., Schett, G., Sinico, R.A., Szczeklik, W., Tesar, V., Vukcevic, D., Akil, M., Barratt, J., Basu, N., Butterworth, A.S., Bruce, I., Clarkson, M., Conlon, N., DasGupta, B., Doulton, T.W.R., Espígol-Frigolé, Georgina, Flossmann, O., Gabrielli, A., Gasior, J., Gregorini, G., Guida, G., Hernández Rodríguez, José, Hruskova, Z., Hudson, A., Knight, A., Lanyon, P., Luqmani, R., Magliano, M., Manfredi, A.A., Marguerie, C., Maritati, F., Marvisi, C., McHugh, N.J., Molloy, E., Motyer, A., Mukhtyar, C., Padyukov, L., Pesci, A., Prieto-Gonzalez, S., Ramentol-Sintas, Marc, Reis, P., Roccatello, D., Rovere-Querini, P., Salvarani, C., Santarsia, F., Solans-Laque, R., Soranzo, N., Taylor, J., Wessels, J., Zwerina, J., Terrier, B., Watts, R.A., Vaglio, A., Holle, J.U., Wallace, C., Smith, K.G.C., and Universitat Autònoma de Barcelona

Subjects
Eosinophils, Genetic Loci, Granulomatosis with Polyangiitis, Humans, Genetic Predisposition to Disease, Mendelian Randomization Analysis, Genetic Association Studies, Antibodies, Antineutrophil Cytoplasmic, Genome-Wide Association Study
Abstract

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare inflammatory disease of unknown cause. 30% of patients have anti-neutrophil cytoplasmic antibodies (ANCA) specific for myeloperoxidase (MPO). Here, we describe a genome-wide association study in 676 EGPA cases and 6809 controls, that identifies 4 EGPA-associated loci through conventional case-control analysis, and 4 additional associations through a conditional false discovery rate approach. Many variants are also associated with asthma and six are associated with eosinophil count in the general population. Through Mendelian randomisation, we show that a primary tendency to eosinophilia contributes to EGPA susceptibility. Stratification by ANCA reveals that EGPA comprises two genetically and clinically distinct syndromes. MPO+ ANCA EGPA is an eosinophilic autoimmune disease sharing certain clinical features and an HLA-DQ association with MPO+ ANCA-associated vasculitis, while ANCA-negative EGPA may instead have a mucosal/barrier dysfunction origin. Four candidate genes are targets of therapies in development, supporting their exploration in EGPA.

Published
2019

67. Targeted next-generation sequencing suggests novel risk loci in juvenile onset systemic lupus erythematosus

Author

Sandling, JK., Rosenberg, L. Hultin, Farias, FHG., Alexsson, A., Leonard, D., Kozyrev, S., Murén, E., Karlsson, Å., Mathioudaki, A., Pucholt, P., Eriksson, D., Pielberg, G., Meadows, J., Nordin, J., Dahlqvist, J., Bianchi, M., Jonsson, R., Omdal, R., Lerang, K., Molberg, Ø., Lie, BA., Massarenti, L., Jacobsen, S., Voss, A., Jakobsen, MA., Lillevang, ST., Troldborg, AM., Steffensen, Rudi, Bengtsson, C., Jönsen, A., Padyukov, L., Eloranta, M-L., Sjöwall, C., Gunnarsson, I., Svenungsson, E., Rantapää-Dahlqvist, S., Bengtsson, AA., Syvänen, A-C., Lindblad-Toh, K., and Rönnblom, L.

Published
2019

73. Targeted next-generation sequencing suggests novel risk loci in juvenile onset systemic lupus erythematosus

Author

Sandling, J. K., Rosenberg, L. Hultin, Farias, F. H. G., Alexsson, A., Leonard, D., Kozyrev, S., Muren, E., Karlsson, A., Mathioudaki, A., Pucholt, P., Eriksson, D., Pielberg, G., Meadows, J., Nordin, J., Dahlqvist, J., Bianchi, M., Bengtsson, Christine, Jonsen, A., Padyukov, L., Eloranta, M. L., Sjowall, C., Gunnarsson, I., Svenungsson, E., Rantapää-Dahlqvist, Solbritt, Bengtsson, A. A., Syvanen, A. C., Lindblad-Toh, K., Ronnblom, L., Sandling, J. K., Rosenberg, L. Hultin, Farias, F. H. G., Alexsson, A., Leonard, D., Kozyrev, S., Muren, E., Karlsson, A., Mathioudaki, A., Pucholt, P., Eriksson, D., Pielberg, G., Meadows, J., Nordin, J., Dahlqvist, J., Bianchi, M., Bengtsson, Christine, Jonsen, A., Padyukov, L., Eloranta, M. L., Sjowall, C., Gunnarsson, I., Svenungsson, E., Rantapää-Dahlqvist, Solbritt, Bengtsson, A. A., Syvanen, A. C., Lindblad-Toh, K., and Ronnblom, L.

Published
2019

74. Genome-wide association study of eosinophilic granulomatosis with polyangiitis reveals genomic loci stratified by ANCA status

Author

Lyons, P, Peters, J, Alberici, F, Liley, J, Coulson, R, Astle, W, Baldini, C, Bonatti, F, Cid, M, Elding, H, Emmi, G, Epplen, J, Guillevin, L, Jayne, D, Jiang, T, Gunnarsson, I, Lamprecht, P, Leslie, S, Little, M, Martorana, D, Moosig, F, Neumann, T, Ohlsson, S, Quickert, S, Ramierez, G, Rewerska, B, Schett, G, Sinico, R, Szczeklik, W, Tesar, V, Vukcevic, D, Akil, M, Barratt, J, Basu, N, Butterworth, A, Bruce, I, Clarkson, M, Conlon, N, Dasgupta, B, Doulton, T, Espigol-Frigole, G, Flossmann, O, Gabrielli, A, Gasior, J, Gregorini, G, Guida, G, Hernandez-Rodriguez, J, Hruskova, Z, Hudson, A, Knight, A, Lanyon, P, Luqmani, R, Magliano, M, Manfredi, A, Marguerie, C, Maritati, F, Marvisi, C, Mchugh, N, Molloy, E, Motyer, A, Mukhtyar, C, Padyukov, L, Pesci, A, Prieto-Gonzalez, S, Ramentol-Sintas, M, Reis, P, Roccatello, D, Rovere-Querini, P, Salvarani, C, Santarsia, F, Solans-Laque, R, Soranzo, N, Taylor, J, Wessels, J, Zwerina, J, Terrier, B, Watts, R, Vaglio, A, Holle, J, Wallace, C, Smith, K, Lyons, PA, Peters, JE, Cid, MC, Little, MA, Ramierez, GA, Butterworth, AS, DasGupta, B, Doulton, TWR, Manfredi, AA, McHugh, NJ, Watts, RA, Holle, JU, Smith, KGC, Lyons, P, Peters, J, Alberici, F, Liley, J, Coulson, R, Astle, W, Baldini, C, Bonatti, F, Cid, M, Elding, H, Emmi, G, Epplen, J, Guillevin, L, Jayne, D, Jiang, T, Gunnarsson, I, Lamprecht, P, Leslie, S, Little, M, Martorana, D, Moosig, F, Neumann, T, Ohlsson, S, Quickert, S, Ramierez, G, Rewerska, B, Schett, G, Sinico, R, Szczeklik, W, Tesar, V, Vukcevic, D, Akil, M, Barratt, J, Basu, N, Butterworth, A, Bruce, I, Clarkson, M, Conlon, N, Dasgupta, B, Doulton, T, Espigol-Frigole, G, Flossmann, O, Gabrielli, A, Gasior, J, Gregorini, G, Guida, G, Hernandez-Rodriguez, J, Hruskova, Z, Hudson, A, Knight, A, Lanyon, P, Luqmani, R, Magliano, M, Manfredi, A, Marguerie, C, Maritati, F, Marvisi, C, Mchugh, N, Molloy, E, Motyer, A, Mukhtyar, C, Padyukov, L, Pesci, A, Prieto-Gonzalez, S, Ramentol-Sintas, M, Reis, P, Roccatello, D, Rovere-Querini, P, Salvarani, C, Santarsia, F, Solans-Laque, R, Soranzo, N, Taylor, J, Wessels, J, Zwerina, J, Terrier, B, Watts, R, Vaglio, A, Holle, J, Wallace, C, Smith, K, Lyons, PA, Peters, JE, Cid, MC, Little, MA, Ramierez, GA, Butterworth, AS, DasGupta, B, Doulton, TWR, Manfredi, AA, McHugh, NJ, Watts, RA, Holle, JU, and Smith, KGC

Abstract

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare inflammatory disease of unknown cause. 30% of patients have anti-neutrophil cytoplasmic antibodies (ANCA) specific for myeloperoxidase (MPO). Here, we describe a genome-wide association study in 676 EGPA cases and 6809 controls, that identifies 4 EGPA-associated loci through conventional case-control analysis, and 4 additional associations through a conditional false discovery rate approach. Many variants are also associated with asthma and six are associated with eosinophil count in the general population. Through Mendelian randomisation, we show that a primary tendency to eosinophilia contributes to EGPA susceptibility. Stratification by ANCA reveals that EGPA comprises two genetically and clinically distinct syndromes. MPO+ ANCA EGPA is an eosinophilic autoimmune disease sharing certain clinical features and an HLA-DQ association with MPO+ ANCA-associated vasculitis, while ANCA-negative EGPA may instead have a mucosal/barrier dysfunction origin. Four candidate genes are targets of therapies in development, supporting their exploration in EGPA.

Published
2019

75. Genome-wide association study of eosinophilic granulomatosis with polyangiitis reveals genomic loci stratified by ANCA status

Author

Lyons, PA, Peters, JE, Alberici, F, Liley, J, Coulson, RMR, Astle, W, Baldini, C, Bonatti, F, Cid, MC, Elding, H, Emmi, G, Epplen, J, Guillevin, L, Jayne, DRW, Jiang, T, Gunnarsson, I, Lamprecht, P, Leslie, S, Little, MA, Martorana, D, Moosig, F, Neumann, T, Ohlsson, S, Quickert, S, Ramirez, GA, Rewerska, B, Schett, G, Sinico, RA, Szczeklik, W, Tesar, V, Vukcevic, D, Akil, M, Barratt, J, Basu, N, Butterworth, AS, Bruce, I, Clarkson, M, Conlon, N, DasGupta, B, Doulton, TWR, Espigol-Frigole, G, Flossmann, O, Gabrielli, A, Gasior, J, Gregorini, G, Guida, G, Hernandez-Rodriguez, J, Hruskova, Z, Hudson, A, Knight, A, Lanyon, P, Luqmani, R, Magliano, M, Manfredi, AA, Marguerie, C, Maritati, F, Marvisi, C, McHugh, NJ, Molloy, E, Motyer, A, Mukhtyar, C, Padyukov, L, Pesci, A, Prieto-Gonzalez, S, Ramentol-Sintas, M, Reis, P, Roccatello, D, Rovere-Querini, P, Salvarani, C, Santarsia, F, Solans-Laque, R, Soranzo, N, Taylor, J, Wessels, J, Zwerina, J, Terrier, B, Watts, RA, Vaglio, A, Holle, JU, Wallace, C, Smith, KGC, Lyons, PA, Peters, JE, Alberici, F, Liley, J, Coulson, RMR, Astle, W, Baldini, C, Bonatti, F, Cid, MC, Elding, H, Emmi, G, Epplen, J, Guillevin, L, Jayne, DRW, Jiang, T, Gunnarsson, I, Lamprecht, P, Leslie, S, Little, MA, Martorana, D, Moosig, F, Neumann, T, Ohlsson, S, Quickert, S, Ramirez, GA, Rewerska, B, Schett, G, Sinico, RA, Szczeklik, W, Tesar, V, Vukcevic, D, Akil, M, Barratt, J, Basu, N, Butterworth, AS, Bruce, I, Clarkson, M, Conlon, N, DasGupta, B, Doulton, TWR, Espigol-Frigole, G, Flossmann, O, Gabrielli, A, Gasior, J, Gregorini, G, Guida, G, Hernandez-Rodriguez, J, Hruskova, Z, Hudson, A, Knight, A, Lanyon, P, Luqmani, R, Magliano, M, Manfredi, AA, Marguerie, C, Maritati, F, Marvisi, C, McHugh, NJ, Molloy, E, Motyer, A, Mukhtyar, C, Padyukov, L, Pesci, A, Prieto-Gonzalez, S, Ramentol-Sintas, M, Reis, P, Roccatello, D, Rovere-Querini, P, Salvarani, C, Santarsia, F, Solans-Laque, R, Soranzo, N, Taylor, J, Wessels, J, Zwerina, J, Terrier, B, Watts, RA, Vaglio, A, Holle, JU, Wallace, C, and Smith, KGC

Abstract

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare inflammatory disease of unknown cause. 30% of patients have anti-neutrophil cytoplasmic antibodies (ANCA) specific for myeloperoxidase (MPO). Here, we describe a genome-wide association study in 676 EGPA cases and 6809 controls, that identifies 4 EGPA-associated loci through conventional case-control analysis, and 4 additional associations through a conditional false discovery rate approach. Many variants are also associated with asthma and six are associated with eosinophil count in the general population. Through Mendelian randomisation, we show that a primary tendency to eosinophilia contributes to EGPA susceptibility. Stratification by ANCA reveals that EGPA comprises two genetically and clinically distinct syndromes. MPO+ ANCA EGPA is an eosinophilic autoimmune disease sharing certain clinical features and an HLA-DQ association with MPO+ ANCA-associated vasculitis, while ANCA-negative EGPA may instead have a mucosal/barrier dysfunction origin. Four candidate genes are targets of therapies in development, supporting their exploration in EGPA.

Published
2019

81. 1 Using stable Mg isotope signatures to assess the fate of magnesium during the in situ mineralisation of CO2 and H2S at the CarbFix site in SW-Iceland

Author

Oelkers, E., Butcher, R., Pogge von Strandmann, Philip A.E., Schuessler, J., von Blankenburg, F., Snaebjornsdottir, S., Mesfin, K., Aradottir, E., Gunnarsson, I., Sigfusson, B., Gunnlaugsson, E., Matter, J., Stute, M., and Gislason, S.

Subjects
es
Abstract

The in-situ carbonation of basaltic rocks could provide a long-term carbon storage solution. To investigate the viability of this carbon storage solution, 175 tonnes of pure CO2 and 73 tonnes of a 75% CO2-24% H2S-1% H2-gas mixture were sequentially injected into basaltic rocks as a dissolved aqueous fluid at the CarbFix site at Hellisheidi, SW-Iceland. This paper reports the Mg stable isotope compositions of sub-surface fluids sampled prior to, during, and after the CO2 injections. These Mg isotopic compositions are used to trace the fate of this element during the subsurface carbonation of basalts. The measured Mg isotopic compositions of the monitoring well fluids are isotopically lighter than the dissolving basalts and continue to become increasingly lighter for at least two years after the gas-charged water injection was stopped. The results indicate that the formation of isotopically heavy Mg-clays rather than Mg-carbonates are the predominant Mg secondary phases precipitating from the sampled fluids. Isotope mass balance calculations suggest that more than 70% of the Mg liberated from the basalt by the injected gas charged water was precipitated as Mg-clays, with this percentage increasing with time after the injection, consistent with the continued precipitation of Mg clays over the whole of the study period. The formation of Mg clays in response to the injection of CO2 into basalts, as indicated in this study, could be detrimental to carbon storage efforts because the formation of these minerals consume divalent Mg that could otherwise be used for the formation of carbonate minerals and because such clays could decrease host rock permeability.

Published
2018

82. Glomerular membrane attack complex is not a reliable marker of ongoing C5 activation in lupus nephritis

Author

Wilson, H, Medjeral-Thomas, NR, Gilmore, AC, Trivedi, P, Seyb, K, Farzaneh-Far, R, Gunnarsson, I, Zickert, A, Cairns, TD, Lightstone, L, Cook, HT, and Pickering, MC

Subjects
Adult, Male, Adolescent, Biopsy, Kidney Glomerulus, chemical and pharmacologic phenomena, Complement Membrane Attack Complex, Article, Young Adult, systemic lupus erythematosus, renal pathology, parasitic diseases, Humans, complement, Complement Activation, Aged, Retrospective Studies, Patient Selection, Complement C5, Reproducibility of Results, 1103 Clinical Sciences, Middle Aged, Urology & Nephrology, Lupus Nephritis, female genital diseases and pregnancy complications, Female, Biomarkers, Immunosuppressive Agents, glomerulonephritis
Abstract

Complement plays an important role in the pathogenesis of lupus nephritis (LN). With the emergence of therapeutic complement inhibition, there is a need to identify patients in whom complement-driven inflammation is a major cause of kidney injury in LN. Clinical and histopathological data were obtained retrospectively from 57 biopsies with class III, IV, and V LN. Biopsies were stained for complement components C9, C5b-9, C3c, and C3d and for the macrophage marker CD68. C9 and C5b-9 staining were highly correlated (r = 0.92 in the capillary wall). C5b-9 staining was detected in the mesangium and/or capillary wall of both active and chronic proliferative LN in all but one biopsy and in the capillary wall of class V LN in all biopsies. C5b-9 staining intensity in the tubular basement membrane correlated with markers of tubulointerstitial damage, and more intense capillary wall C5b-9 staining was significantly associated with nonresponse to conventional treatment. Glomerular C5b-9 staining intensity did not differ between active and chronic disease; in contrast, C3c and CD68 staining were associated with active disease. Evaluation of serial biopsies and comparison of staining in active and chronic LN demonstrated that C5b-9 staining persisted for months to years. These results suggest that C5b-9 staining is almost always present in LN, resolves slowly, and is not a reliable marker of ongoing glomerular C5 activation. This limits the utility of C5b-9 staining to identify patients who are most likely to benefit from C5 inhibition., Graphical abstract

Published
2018

84. Systemic lupus erythematosus subgroups, with features of antiphospholipid or Sjogren's syndrome, differ in molecular signatures and treatment perspectives

Author

Idborg, H., Zandian, A., Sandberg, A., Truedsson, L., Nilsson, Berith, Elvin, K., Mo, J., Gustafsson, J., Gunnarsson, I., Lehtio, J., Nilsson, P., Svenungsson, E., Jakobsson, P., Idborg, H., Zandian, A., Sandberg, A., Truedsson, L., Nilsson, Berith, Elvin, K., Mo, J., Gustafsson, J., Gunnarsson, I., Lehtio, J., Nilsson, P., Svenungsson, E., and Jakobsson, P.

Published
2018

85. Shared and unique patterns of DNA methylation in primary Sjogren's syndrome and systemic lupus erythematosus

Author

Imgenberg-Kreuz, Juliana, Leonard, Dag, Carlsson Almlöf, Jonas, Rantapaa-Dahlqvist, S., Bengtsson, A., Jonsen, A., Padyukov, L., Gunnarsson, I., Svenungsson, E., Sjowall, C., Syvänen, Ann-Christine, Rönnblom, Lars, Nordmark, Gunnel, Sandling, Johanna K., Imgenberg-Kreuz, Juliana, Leonard, Dag, Carlsson Almlöf, Jonas, Rantapaa-Dahlqvist, S., Bengtsson, A., Jonsen, A., Padyukov, L., Gunnarsson, I., Svenungsson, E., Sjowall, C., Syvänen, Ann-Christine, Rönnblom, Lars, Nordmark, Gunnel, and Sandling, Johanna K.

Published
2018

86. Immunoglobulin A anti-phospholipid antibodies in Swedish cases of systemic lupus erythematosus : associations with disease phenotypes, vascular events and damage accrual

Author

Frodlund, M., Vikerfors, A., Grosso, G., Skogh, T., Wetterö, J., Elvin, K., Gunnarsson, I., Kastbom, A., Dahlström, Ö., Rönnelid, Johan, Svenungsson, E., Sjöwall, C., Frodlund, M., Vikerfors, A., Grosso, G., Skogh, T., Wetterö, J., Elvin, K., Gunnarsson, I., Kastbom, A., Dahlström, Ö., Rönnelid, Johan, Svenungsson, E., and Sjöwall, C.

Abstract

Immunoglobulin (Ig) G- and IgM-class anti-cardiolipin antibodies (aCL) and lupus anti-coagulant (LA) are included in the 1997 update of the American College of Rheumatology (ACR-97) systemic lupus erythematosus (SLE) criteria. Despite limited evidence, IgA-aCL and IgA anti-(2)-glycoprotein-I (anti-(2)GPI) were included in the 2012 Systemic Lupus International Collaborating Clinics criteria. The present study aimed to evaluate IgG-/IgA-/IgM-aCL and anti-(2)GPI occurrence in relation to disease phenotype, smoking habits, pharmacotherapy, anti-phospholipid syndrome (APS) and organ damage among 526 Swedish SLE patients meeting ACR-97. Patients with rheumatoid arthritis (n=100), primary Sjogren's syndrome (n=50) and blood donors (n=507) served as controls. Anti-phospholipid antibodies (aPL) were analysed by fluoroenzyme-immunoassays detecting aCL/anti-(2)GPI. Seventy-six (14%) SLE cases fulfilled the Sydney APS-criteria, and 1 aCL/anti-(2)GPI isotype (IgG/IgA/IgM) occurred in 138 SLE patients (26%). Forty-five (9%) of the SLE cases had IgA-aCL, 20 of whom (4%) lacked IgG-/IgM-aCL. Seventy-four (14%) tested positive for IgA anti-(2)GPI, 34 (6%) being seronegative regarding IgG/IgM anti-(2)GPI. Six (1%) had APS manifestations but were seropositive regarding IgA-aCL and/or IgA anti-(2)GPI in the absence of IgG/IgM-aPL and LA. Positive LA and IgG-aPL tests were associated with most APS-related events and organ damage. Exclusive IgA anti-(2)GPI occurrence associated inversely with Caucasian ethnicity [odds ratio (OR)=021, 95% confidence interval (CI)=006-072) and photosensitivity (OR=019, 95% CI=005-072). Nephritis, smoking, LA-positivity and statin/corticosteroid-medication associated strongly with organ damage, whereas hydroxychloroquine-medication was protective. In conclusion, IgA-aPL is not rare in SLE (16%) and IgA-aPL analysis may have additional value among SLE cases with suspected APS testing negative for other isotypes of aPL and LA.

Published
2018
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87. Novel gene variants associated with cardiovascular disease in systemic lupus erythematosus and rheumatoid arthritis

Author

Leonard, D., Svenungsson, E., Dahlqvist, J., Alexsson, A., Ärlestig, L., Taylor, K. E., Sandling, J. K., Bengtsson, C., Frodlund, M., Jönsen, A., Eketjäll, S., Jensen-Urstad, K., Gunnarsson, I., Sjöwall, C., Bengtsson, A. A., Eloranta, M. -L, Syvänen, A. -C, Rantapää-Dahlqvist, Solbritt, Criswell, L. A., Rönnblom, L., Leonard, D., Svenungsson, E., Dahlqvist, J., Alexsson, A., Ärlestig, L., Taylor, K. E., Sandling, J. K., Bengtsson, C., Frodlund, M., Jönsen, A., Eketjäll, S., Jensen-Urstad, K., Gunnarsson, I., Sjöwall, C., Bengtsson, A. A., Eloranta, M. -L, Syvänen, A. -C, Rantapää-Dahlqvist, Solbritt, Criswell, L. A., and Rönnblom, L.

Abstract

Supplement: 2Meeting Abstract: OP0362

Published
2018

88. Shared and unique patterns of DNA methylation in primary Sjogren's syndrome and systemic lupus erythematosus

Author

Imgenberg-Kreuz, J., Leonard, D., Almlof, J. Carlsson, Rantapää-Dahlqvist, Solbritt, Bengtsson, A., Jonsen, A., Padyukov, L., Gunnarsson, I., Svenungsson, E., Sjowall, C., Syvanen, A., Ronnblom, L., Nordmark, G., Sandling, J., Imgenberg-Kreuz, J., Leonard, D., Almlof, J. Carlsson, Rantapää-Dahlqvist, Solbritt, Bengtsson, A., Jonsen, A., Padyukov, L., Gunnarsson, I., Svenungsson, E., Sjowall, C., Syvanen, A., Ronnblom, L., Nordmark, G., and Sandling, J.

Abstract

Supplement: 129Meeting Abstract: OP04

Published
2018

89. Elevated IgA antiphospholipid antibodies in healthy pregnant women in Sudan but not Sweden, without corresponding increase in IgA anti-β2 glycoprotein I domain 1 antibodies.

Author

Elbagir, S, Mohammed, N A, Kaihola, H, Svenungsson, E, Gunnarsson, I, Manivel, V A, Pertsinidou, E, Elagib, EM, Nur, M A M, Elussein, E A, Elshafie, A, Åkerud, H, and Rönnelid, J

Subjects
PHOSPHOLIPID antibodies, PREGNANT women, RHEUMATOID factor, IMMUNOGLOBULINS, AUTOANTIBODIES
Abstract

Objective: The role of antiphospholipid antibodies (aPL) during apparently normal pregnancy is still unclear. IgA aPL are prevalent in populations of African origin. Our aim was to measure all isotypes of anticardiolipin (anti-CL) and anti–β2 glycoprotein I (anti-β2GPI) in healthy pregnant and non-pregnant women of different ethnicities. Methods: Healthy Sudanese pregnant women (n = 165; 53 sampled shortly after delivery), 96 age-matched Sudanese female controls and 42 healthy pregnant and 249 non-pregnant Swedish women were included. IgA/G/M anti-CL and anti-β2GPI were tested at one time point only with two independent assays in Sudanese and serially in pregnant Swedes. IgA anti-β2GPI domain 1 and as controls IgA/G/M rheumatoid factor (RF), IgG anti–cyclic citrullinated peptide 2 (anti-CCP2) and anti–thyroid peroxidase (anti-TPO) were investigated in Sudanese females. Results: Pregnant Sudanese women had significantly higher median levels of IgA anti-CL, IgA anti-β2GPI (p < 0.0001 for both antibodies using two assays) and IgM anti-β2GPI (both assays; p < 0.0001 and 0.008) compared with non-pregnant Sudanese. IgA anti-CL and anti-β2GPI occurrence was increased among Sudanese pregnant women compared with national controls. No corresponding increase during pregnancy was found for IgA anti-β2GPI domain 1 antibodies. Both IgG anti-CL and IgG control autoantibodies decreased during and directly after pregnancy among Sudanese. Serially followed Swedish women showed no changes in IgA aPL, whereas IgG/M anti-CL decreased. Conclusions: IgA aPL are increased in Sudanese but not in Swedish women, without corresponding increase in IgA domain 1. Whether due to ethnicity and/or environmental influences the occurrence of IgA aPL during Sudanese pregnancies, and its clinical significance, is yet to be determined. [ABSTRACT FROM AUTHOR]

Published
2020
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90. Immunoglobulin A anti-phospholipid antibodies in Swedish cases of systemic lupus erythematosus: associations with disease phenotypes, vascular events and damage accrual

Author

Frodlund, M, primary, Vikerfors, A, additional, Grosso, G, additional, Skogh, T, additional, Wetterö, J, additional, Elvin, K, additional, Gunnarsson, I, additional, Kastbom, A, additional, Dahlström, Ö, additional, Rönnelid, J, additional, Svenungsson, E, additional, and Sjöwall, C, additional

Published
2018
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94. OP0362 Novel gene variants associated with cardiovascular disease in systemic lupus erythematosus and rheumatoid arthritis

Author

Leonard, D., primary, Svenungsson, E., additional, Dahlqvist, J., additional, Alexsson, A., additional, Ärlestig, L., additional, Taylor, K.E., additional, Sandling, J.K., additional, Bengtsson, C., additional, Frodlund, M., additional, Jönsen, A., additional, Eketjäll, S., additional, Jensen-Urstad, K., additional, Gunnarsson, I., additional, Sjöwall, C., additional, Bengtsson, A.A., additional, Eloranta, M.-L., additional, Syvänen, A.-C., additional, Rantapää-Dahlqvist, S., additional, Criswell, L.A., additional, and Rönnblom, L., additional

Published
2018
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100. S4D:6 Sle comprises four immune-phenotypes, which differ regarding hla-drb1 and clinical associations

Author

Diaz Gallo, LM, primary, Lundström, E, additional, Oke, V, additional, Elvin, K, additional, Wu, YL, additional, Gustafsson, J, additional, Jönsen, A, additional, Leonard, D, additional, Zickert, A, additional, Nordmark, G, additional, Bengtsson, AA, additional, Sandling, J, additional, Rönnblom, L, additional, Gunnarsson, I, additional, Yu, CY, additional, Padyukov, L, additional, and Svenungsson, E, additional

Published
2018
Full Text
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