Skip to main content
Erschienen in: Current Rheumatology Reports 7/2017

01.07.2017 | Antiphospholipid Syndrome (S Zuily, Section Editor)

Antibodies Against Complement Components: Relevance for the Antiphospholipid Syndrome—Biomarkers of the Disease and Biopharmaceuticals

verfasst von: Mirjana Bećarević

Erschienen in: Current Rheumatology Reports | Ausgabe 7/2017

Einloggen, um Zugang zu erhalten

Abstract

Purpose of Review

Laboratory criterion for the diagnosis of antiphospholipid syndrome (APS) is the presence of antiphospholipid antibodies (aPL Abs). Complement system has a role in mediating aPL Abs-induced thrombosis in animal models. The importance of antibodies against complement components (potential biomarkers of APS) and the importance of antibodies with beneficial anti-complement effects in APS (as biopharmaceuticals) are reviewed.

Recent Findings

Antibodies against complement components described in APS patients, so far, are anti-C1q and anti-factor H Abs, although anti-factor B Abs and anti-C5a Abs were described in animal models of APS. Clinical studies in APS patients are limited to a small number of case reports.

Summary

Studies that would confirm potential role of Abs against complement components (as potential biomarkers of APS) are lacking. Lack of randomized clinical trials (that would provide complete data for confirmation of beneficial effects of biopharmaceuticals in complement inhibition) in APS is alarming.
Literatur
1.
Zurück zum Zitat Bertolaccini ML, Ammengual O, Andreolii L, et al. 14th International Congress on Antiphospholipid Antibodies Task Force. Report on antiphospholipid syndrome laboratory diagnostics and trends. Autoimmun Rev. 2014;13:917–30.CrossRefPubMed Bertolaccini ML, Ammengual O, Andreolii L, et al. 14th International Congress on Antiphospholipid Antibodies Task Force. Report on antiphospholipid syndrome laboratory diagnostics and trends. Autoimmun Rev. 2014;13:917–30.CrossRefPubMed
2.
Zurück zum Zitat Miyakis S, Lockshin MD, Atsumi T, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006;4:295–306.CrossRefPubMed Miyakis S, Lockshin MD, Atsumi T, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006;4:295–306.CrossRefPubMed
3.
Zurück zum Zitat van den Hoogen LL, van Roon JAG, Radstake TRDJ, et al. Delineating the deranged immune system in the antiphospholipid syndrome. Autoimmun Rev. 2016;15:50–60.CrossRefPubMed van den Hoogen LL, van Roon JAG, Radstake TRDJ, et al. Delineating the deranged immune system in the antiphospholipid syndrome. Autoimmun Rev. 2016;15:50–60.CrossRefPubMed
4.
Zurück zum Zitat Rodríguez-Pintó I, Moitinho M, Santacreu I, Shoenfeld Y, Erkan D, Espinosa G, et al. Catastrophic antiphospholipid syndrome (CAPS): descriptive analysis of 500 patients from the International CAPS Registry. Autoimmun Rev. 2016;15:1120–4.CrossRefPubMed Rodríguez-Pintó I, Moitinho M, Santacreu I, Shoenfeld Y, Erkan D, Espinosa G, et al. Catastrophic antiphospholipid syndrome (CAPS): descriptive analysis of 500 patients from the International CAPS Registry. Autoimmun Rev. 2016;15:1120–4.CrossRefPubMed
5.
Zurück zum Zitat Rodriguez-Pinto I, Espinosa G, Cervera R. Catastrophic antiphospholipid syndrome: the current management approach. Best Pract Res Clin Rheum. 2016;30:239–49.CrossRef Rodriguez-Pinto I, Espinosa G, Cervera R. Catastrophic antiphospholipid syndrome: the current management approach. Best Pract Res Clin Rheum. 2016;30:239–49.CrossRef
6.
Zurück zum Zitat Shapira I, Andrade D, Allen SL, Salmon JE. Induction of sustained remission in recurrent catastrophic antiphospholipid syndrome via inhibition of terminal complement with eculizumab. Arthrithis Rheum. 2012;64(8):2719–23.CrossRef Shapira I, Andrade D, Allen SL, Salmon JE. Induction of sustained remission in recurrent catastrophic antiphospholipid syndrome via inhibition of terminal complement with eculizumab. Arthrithis Rheum. 2012;64(8):2719–23.CrossRef
7.
Zurück zum Zitat Espinosa G, Berman H, Cervera R. Management of refractory cases of catastrophic antiphospholipid syndrome. Autoimmun Rev. 2011;10:664–8.CrossRefPubMed Espinosa G, Berman H, Cervera R. Management of refractory cases of catastrophic antiphospholipid syndrome. Autoimmun Rev. 2011;10:664–8.CrossRefPubMed
8.
Zurück zum Zitat D’Ippolito S, Meroni PL, Koike T, Veglia M, Scambia G, Di Simone N. Obstetric antiphospholipid syndrome: a recent classification for an old defined disorder. Autoimmun Rev. 2014;13:901–8.CrossRefPubMed D’Ippolito S, Meroni PL, Koike T, Veglia M, Scambia G, Di Simone N. Obstetric antiphospholipid syndrome: a recent classification for an old defined disorder. Autoimmun Rev. 2014;13:901–8.CrossRefPubMed
9.
Zurück zum Zitat Galarza-Maldonado C, Kourilovitch MR, Perez-Fernandez OM, Gaybor M, Cordero C, Cabrera C, et al. Obstetric antiphospholipid syndrome. Autoimmun Rev. 2012;11:288–95.CrossRefPubMed Galarza-Maldonado C, Kourilovitch MR, Perez-Fernandez OM, Gaybor M, Cordero C, Cabrera C, et al. Obstetric antiphospholipid syndrome. Autoimmun Rev. 2012;11:288–95.CrossRefPubMed
10.
Zurück zum Zitat Meroni PL, Raschi E, Grossi E, Pregnolato F, Traspidi L, Acaia B, et al. Obstetric and vascular APS: same autoantibodies but different diseases? Lupus. 2012;21:708–10.CrossRefPubMed Meroni PL, Raschi E, Grossi E, Pregnolato F, Traspidi L, Acaia B, et al. Obstetric and vascular APS: same autoantibodies but different diseases? Lupus. 2012;21:708–10.CrossRefPubMed
11.
Zurück zum Zitat Cavazzana I, Manuela N, Irene C, Barbara A, Sara S, Orietta BM, et al. Complement activation in anti-phospholipid syndrome: a clue for an inflammatory process? J Autoimmun. 2007;28:160–4.CrossRefPubMed Cavazzana I, Manuela N, Irene C, Barbara A, Sara S, Orietta BM, et al. Complement activation in anti-phospholipid syndrome: a clue for an inflammatory process? J Autoimmun. 2007;28:160–4.CrossRefPubMed
12.
Zurück zum Zitat •• Melis JPM, Strumane K, Ruuls SR, Beurskens FJ, Schuurman J, Parren PWHI. Complement in therapy and disease regulating the complement system with antibody-based therapeutics. Mol Immunol. 2015;67:117–30. Showed the importance of Ab-based drugs that increase or decrease the complement system CrossRefPubMed •• Melis JPM, Strumane K, Ruuls SR, Beurskens FJ, Schuurman J, Parren PWHI. Complement in therapy and disease regulating the complement system with antibody-based therapeutics. Mol Immunol. 2015;67:117–30. Showed the importance of Ab-based drugs that increase or decrease the complement system CrossRefPubMed
13.
Zurück zum Zitat Mollnes TE, Kirschfink M. Strategies of therapeutic complement inhibition. Mol Immunol. 2006;43:107–21.CrossRefPubMed Mollnes TE, Kirschfink M. Strategies of therapeutic complement inhibition. Mol Immunol. 2006;43:107–21.CrossRefPubMed
15.
Zurück zum Zitat Abbas AK, Lichtmann AH, Pober JC. Cellular and molecular immunology. Philadelphia: WB Saunders Company; 2015. Abbas AK, Lichtmann AH, Pober JC. Cellular and molecular immunology. Philadelphia: WB Saunders Company; 2015.
17.
Zurück zum Zitat Truedsson L, Bengtsson AA, Sturfelt G. Complement deficiencies and systemic lupus erythematosus. Autoimmunity. 2007;40:560–6.CrossRefPubMed Truedsson L, Bengtsson AA, Sturfelt G. Complement deficiencies and systemic lupus erythematosus. Autoimmunity. 2007;40:560–6.CrossRefPubMed
18.
Zurück zum Zitat Sevciovic Grumach A, Kirschfink M. Are complement deficiencies really rare? Overview on prevalence, clinical importance and modern diagnostic approach. Mol Immunol. 2014;61:110–7.CrossRef Sevciovic Grumach A, Kirschfink M. Are complement deficiencies really rare? Overview on prevalence, clinical importance and modern diagnostic approach. Mol Immunol. 2014;61:110–7.CrossRef
19.
Zurück zum Zitat Peerschke EIB, Yin W, Alpert DR, Roubey RAS, Salmon JE, Ghebrehiwet B. Serum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodies. Lupus. 2009;18:530–8.CrossRefPubMedPubMedCentral Peerschke EIB, Yin W, Alpert DR, Roubey RAS, Salmon JE, Ghebrehiwet B. Serum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodies. Lupus. 2009;18:530–8.CrossRefPubMedPubMedCentral
20.
Zurück zum Zitat Peerschke EI, Yin W, Ghebrehiwet B. Complement activation on platelets: implications for vascular inflammation and thrombosis. Mol Immunol. 2010;47:2170–5.CrossRefPubMedPubMedCentral Peerschke EI, Yin W, Ghebrehiwet B. Complement activation on platelets: implications for vascular inflammation and thrombosis. Mol Immunol. 2010;47:2170–5.CrossRefPubMedPubMedCentral
21.
Zurück zum Zitat Thurman J, Kraus D, Girardi G, et al. A novel inhibitor of the alternative complement pathway prevents antiphospholipid antibody-induced pregnancy loss in mice. Mol Immunol. 2005;42:87–97.CrossRefPubMed Thurman J, Kraus D, Girardi G, et al. A novel inhibitor of the alternative complement pathway prevents antiphospholipid antibody-induced pregnancy loss in mice. Mol Immunol. 2005;42:87–97.CrossRefPubMed
22.
Zurück zum Zitat Carrera-Marın AL, Romay-Penabad Z, Papalardo E, Reyes-Maldonado E, Garcıa-Latorrem E, Vargas G, et al. C6 knock-out mice are protected from thrombophilia mediated by antiphospholipid antibodies. Lupus. 2012;21:1497–505.CrossRefPubMed Carrera-Marın AL, Romay-Penabad Z, Papalardo E, Reyes-Maldonado E, Garcıa-Latorrem E, Vargas G, et al. C6 knock-out mice are protected from thrombophilia mediated by antiphospholipid antibodies. Lupus. 2012;21:1497–505.CrossRefPubMed
23.
Zurück zum Zitat Holers M, Girardi G, Mo L, et al. Complement C3 activation is required for antiphospholipid antibody-induced fetal loss. J Exp Med. 2002;195:211–20.CrossRefPubMedPubMedCentral Holers M, Girardi G, Mo L, et al. Complement C3 activation is required for antiphospholipid antibody-induced fetal loss. J Exp Med. 2002;195:211–20.CrossRefPubMedPubMedCentral
24.
Zurück zum Zitat Salmon JE, Girardi G, Holers VM. Activation of complement mediates antiphospholipid antibody-induced pregnancy loss. Lupus. 2003;12:535–8.CrossRefPubMed Salmon JE, Girardi G, Holers VM. Activation of complement mediates antiphospholipid antibody-induced pregnancy loss. Lupus. 2003;12:535–8.CrossRefPubMed
25.
Zurück zum Zitat •• Salmon JE, Girardi G, Holers VM. Complement activation as a mediator of antiphospholipid antibody induced pregnancy loss and thrombosis. Ann Rheum Dis. 2002;61:46–50. One of the earliest reports that showed that complement activation is a mediator of aPL Abs-induced pregnancy losses and thrombosis CrossRef •• Salmon JE, Girardi G, Holers VM. Complement activation as a mediator of antiphospholipid antibody induced pregnancy loss and thrombosis. Ann Rheum Dis. 2002;61:46–50. One of the earliest reports that showed that complement activation is a mediator of aPL Abs-induced pregnancy losses and thrombosis CrossRef
26.
Zurück zum Zitat Pierangeli S, Vega-Ostertag M, Liu X, Girardi G. Complement activation: a novel mechanism in the antiphospholipid syndrome. Ann N Y Acad Sci. 2005;1051:413–20.CrossRefPubMed Pierangeli S, Vega-Ostertag M, Liu X, Girardi G. Complement activation: a novel mechanism in the antiphospholipid syndrome. Ann N Y Acad Sci. 2005;1051:413–20.CrossRefPubMed
27.
Zurück zum Zitat Pierangeli S, Girardi G, Vega-Ostertag M, et al. Requirement of activation of complement C3 and C5 for antiphospholipid antibody-mediated thrombophilia. Arthritis Rheum. 2005;52:2120–4.CrossRefPubMed Pierangeli S, Girardi G, Vega-Ostertag M, et al. Requirement of activation of complement C3 and C5 for antiphospholipid antibody-mediated thrombophilia. Arthritis Rheum. 2005;52:2120–4.CrossRefPubMed
28.
Zurück zum Zitat Girardi G, Berman J, Redecha P, et al. Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. J Clin Invest. 2003;112:1644–54.CrossRefPubMedPubMedCentral Girardi G, Berman J, Redecha P, et al. Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. J Clin Invest. 2003;112:1644–54.CrossRefPubMedPubMedCentral
29.
Zurück zum Zitat Fischetti F, Durigutto P, Pellis V, et al. Thrombus formation induced by antibodies to b2-glycoprotein I is complement dependent and requires a priming factor. Blood. 2005;106:2340–6.CrossRefPubMed Fischetti F, Durigutto P, Pellis V, et al. Thrombus formation induced by antibodies to b2-glycoprotein I is complement dependent and requires a priming factor. Blood. 2005;106:2340–6.CrossRefPubMed
30.
Zurück zum Zitat Arfors L, Lefvert AK. Enrichment of antibodies against phospholipids in circulating immune complexes (CIC) in the anti-phospholipid syndrome (APLS). Clin Exp Immunol. 1997;108:47–51.CrossRefPubMedPubMedCentral Arfors L, Lefvert AK. Enrichment of antibodies against phospholipids in circulating immune complexes (CIC) in the anti-phospholipid syndrome (APLS). Clin Exp Immunol. 1997;108:47–51.CrossRefPubMedPubMedCentral
31.
Zurück zum Zitat Sammaritano LR, Ng S, Sobel R, et al. Anticardiolipin IgG subclasses. Association of IgG2 with arterial and/or venous thrombosis. Arthritis Rheum. 1997;40:1998–2006.CrossRefPubMed Sammaritano LR, Ng S, Sobel R, et al. Anticardiolipin IgG subclasses. Association of IgG2 with arterial and/or venous thrombosis. Arthritis Rheum. 1997;40:1998–2006.CrossRefPubMed
32.
Zurück zum Zitat Amengual O, Atsumi T, Khamashta MA, Bertolaccini ML, Hughes GVR. IgG2 restriction of anti-P-glycoprotein I as the basis for the association between IgG2 anticardiolipin antibodies and thrombosis in the antiphospholipid syndrome: comment on the article by Sammaritano et a1. Arthritis Rheum. 1998;41:1513–20.CrossRefPubMed Amengual O, Atsumi T, Khamashta MA, Bertolaccini ML, Hughes GVR. IgG2 restriction of anti-P-glycoprotein I as the basis for the association between IgG2 anticardiolipin antibodies and thrombosis in the antiphospholipid syndrome: comment on the article by Sammaritano et a1. Arthritis Rheum. 1998;41:1513–20.CrossRefPubMed
33.
Zurück zum Zitat Guerin J, Casey E, Feighery C, et al. Anti-Beta 2-glycoprotein I antibody isotype and IgG subclass in antiphospholipid syndrome patients. Autoimmunity. 1999;31:109–16.CrossRefPubMed Guerin J, Casey E, Feighery C, et al. Anti-Beta 2-glycoprotein I antibody isotype and IgG subclass in antiphospholipid syndrome patients. Autoimmunity. 1999;31:109–16.CrossRefPubMed
34.
Zurück zum Zitat Samarkos M, Davies KA, Gordon C, Walport MJ, Loizou S. IgG subclass distribution of antibodies against b2gpI and cardiolipin in patients with systemic lupus erythematosus and primary antiphospholipid syndrome, and their clinical associations. Rheumatology. 2001;40:1026–32.CrossRefPubMed Samarkos M, Davies KA, Gordon C, Walport MJ, Loizou S. IgG subclass distribution of antibodies against b2gpI and cardiolipin in patients with systemic lupus erythematosus and primary antiphospholipid syndrome, and their clinical associations. Rheumatology. 2001;40:1026–32.CrossRefPubMed
35.
Zurück zum Zitat Païdassi H, Tacnet-Delorme P, Garlatti V, et al. C1q binds phosphatidylserine and likely acts as a multiligand-bridging molecule in apoptotic cell recognition. J Immunol. 2008;180:2329–38.CrossRefPubMedPubMedCentral Païdassi H, Tacnet-Delorme P, Garlatti V, et al. C1q binds phosphatidylserine and likely acts as a multiligand-bridging molecule in apoptotic cell recognition. J Immunol. 2008;180:2329–38.CrossRefPubMedPubMedCentral
36.
Zurück zum Zitat Gropp K, Weber N, Reuter M, et al. Beta (2)-glycoprotein I, the major target in antiphospholipid syndrome, is a special human complement regulator. Blood. 2011;118:2774–83.CrossRefPubMed Gropp K, Weber N, Reuter M, et al. Beta (2)-glycoprotein I, the major target in antiphospholipid syndrome, is a special human complement regulator. Blood. 2011;118:2774–83.CrossRefPubMed
37.
Zurück zum Zitat Skerka C, Gropp K, Weber N, Reuter M, Micklisch S, Kopka I, Hallstroem T, Skerka C. Beta 2 glycoprotein 1 (beta 2GPI), the major target in anti-phospholipid syndrome (APS), regulates complement activation on the level of C3/C3b. Abstracts/Mol Immunol. 2011;48:1666–733. Skerka C, Gropp K, Weber N, Reuter M, Micklisch S, Kopka I, Hallstroem T, Skerka C. Beta 2 glycoprotein 1 (beta 2GPI), the major target in anti-phospholipid syndrome (APS), regulates complement activation on the level of C3/C3b. Abstracts/Mol Immunol. 2011;48:1666–733.
38.
Zurück zum Zitat Johnson E, Hetland G. Human umbilical vein endothelial cell synthesize functional C3, C5, C6, C8 and C9 in vivo. Scand J Immunol. 1991;33:667–71.CrossRefPubMed Johnson E, Hetland G. Human umbilical vein endothelial cell synthesize functional C3, C5, C6, C8 and C9 in vivo. Scand J Immunol. 1991;33:667–71.CrossRefPubMed
39.
Zurück zum Zitat van den Berg RH, Faber-Krol MC, Sim RB, Daha MR. The first subcomponent of complement, C1q, triggers the production of IL-8, IL-6, and monocyte chemoattractant peptide-1 by human umbilical vein endothelial cells. J Immunol. 1998;161:6924–30.PubMed van den Berg RH, Faber-Krol MC, Sim RB, Daha MR. The first subcomponent of complement, C1q, triggers the production of IL-8, IL-6, and monocyte chemoattractant peptide-1 by human umbilical vein endothelial cells. J Immunol. 1998;161:6924–30.PubMed
40.
Zurück zum Zitat Oku K, Atsumi T, Bohgaki M, et al. Complement activation in patients with primary antiphospholipid syndrome. Ann Rheum Dis. 2009;68:1030–5.CrossRefPubMed Oku K, Atsumi T, Bohgaki M, et al. Complement activation in patients with primary antiphospholipid syndrome. Ann Rheum Dis. 2009;68:1030–5.CrossRefPubMed
41.
Zurück zum Zitat Bećarević M, Majkić-Singh N. High-sensitivity C-reactive protein: discriminator between patients with primary and secondary antiphospholipid syndrome. Clin Biochem. 2008;41:1449–53.CrossRefPubMed Bećarević M, Majkić-Singh N. High-sensitivity C-reactive protein: discriminator between patients with primary and secondary antiphospholipid syndrome. Clin Biochem. 2008;41:1449–53.CrossRefPubMed
42.
Zurück zum Zitat Oku K, Amengual O, Hisada R, et al. Autoantibodies against complement component 1 q subcomponent (C1q) contribute to complement activation and recurrent thrombosis/pregnancy morbidity in antiphospholipid syndrome. Rheumatology (Oxford). 2016;55:1403–11.CrossRef Oku K, Amengual O, Hisada R, et al. Autoantibodies against complement component 1 q subcomponent (C1q) contribute to complement activation and recurrent thrombosis/pregnancy morbidity in antiphospholipid syndrome. Rheumatology (Oxford). 2016;55:1403–11.CrossRef
43.
Zurück zum Zitat Navratil JS, Manzi S, Kao AH, Krishnaswami S, Liu CC, Ruffing MJ, Shaw PS, et al. Platelet C4d is highly specific for systemic lupus erythematosus. Arthritis Rheum. 2006;54:670–4.CrossRefPubMed Navratil JS, Manzi S, Kao AH, Krishnaswami S, Liu CC, Ruffing MJ, Shaw PS, et al. Platelet C4d is highly specific for systemic lupus erythematosus. Arthritis Rheum. 2006;54:670–4.CrossRefPubMed
44.
Zurück zum Zitat Bećarević M, Ignjatović S. Proinflammatory proteins in female and male patients with primary antiphospholipid syndrome: preliminary data. Clin Rheumatol. 2016;35:2477–83.CrossRefPubMed Bećarević M, Ignjatović S. Proinflammatory proteins in female and male patients with primary antiphospholipid syndrome: preliminary data. Clin Rheumatol. 2016;35:2477–83.CrossRefPubMed
45.
Zurück zum Zitat • Barratt-Due A, Fløisand Y, Orrem HL, Kvam AK, Holme PA, Bergseth G, et al. Complement activation is a crucial pathogenic factor in catastrophic antiphospholipid syndrome. Rheumatology. 2016;55:1337–9. Showed that complement inhibition is a “life-saving” medical intervention for patients with CAPS CrossRefPubMedPubMedCentral • Barratt-Due A, Fløisand Y, Orrem HL, Kvam AK, Holme PA, Bergseth G, et al. Complement activation is a crucial pathogenic factor in catastrophic antiphospholipid syndrome. Rheumatology. 2016;55:1337–9. Showed that complement inhibition is a “life-saving” medical intervention for patients with CAPS CrossRefPubMedPubMedCentral
46.
Zurück zum Zitat •• Dragon-Durey MA, Blanc C, Marinozzi MC, van Schaarenburg RA, Trouw LA. Autoantibodies against complement components and functional consequences. Mol Immunol. 2013;56:213–21. Described auto Abs against various complement components and their associations with clinical manifestations of various diseases CrossRefPubMed •• Dragon-Durey MA, Blanc C, Marinozzi MC, van Schaarenburg RA, Trouw LA. Autoantibodies against complement components and functional consequences. Mol Immunol. 2013;56:213–21. Described auto Abs against various complement components and their associations with clinical manifestations of various diseases CrossRefPubMed
47.
Zurück zum Zitat Daha NA, Banda NK, Roos A, Beurskens FJ, Bakker JM, Daha MR, Trouw LA. Complement activation by (auto-) antibodies. Mol Immunol. 2011;48:1656–65.CrossRefPubMed Daha NA, Banda NK, Roos A, Beurskens FJ, Bakker JM, Daha MR, Trouw LA. Complement activation by (auto-) antibodies. Mol Immunol. 2011;48:1656–65.CrossRefPubMed
49.
Zurück zum Zitat Katsumata Y, Miyake K, Kawaguchi Y, et al. Anti-C1q antibodies are associated with systemic lupus erythematosus global activity but not specifically with nephritis: a controlled study of 126 consecutive patients. Arthritis Rheum. 2011;63:2436–44.CrossRefPubMed Katsumata Y, Miyake K, Kawaguchi Y, et al. Anti-C1q antibodies are associated with systemic lupus erythematosus global activity but not specifically with nephritis: a controlled study of 126 consecutive patients. Arthritis Rheum. 2011;63:2436–44.CrossRefPubMed
50.
Zurück zum Zitat Blanc C, Togarsimalemath SK, Chauvet S, et al. Anti-factor H autoantibodies in C3 glomerulopathies and in atypical hemolytic uremic syndrome: one target, two diseases. J Immunol. 2015;194:5129–38.CrossRefPubMed Blanc C, Togarsimalemath SK, Chauvet S, et al. Anti-factor H autoantibodies in C3 glomerulopathies and in atypical hemolytic uremic syndrome: one target, two diseases. J Immunol. 2015;194:5129–38.CrossRefPubMed
51.
Zurück zum Zitat Foltyn Zadura A, Memon AA, Stojanovich LJ, et al. Factor H autoantibodies in patients with antiphospholipid syndrome and thrombosis. J Rheumatol. 2015;42:1786–93.CrossRefPubMed Foltyn Zadura A, Memon AA, Stojanovich LJ, et al. Factor H autoantibodies in patients with antiphospholipid syndrome and thrombosis. J Rheumatol. 2015;42:1786–93.CrossRefPubMed
52.
Zurück zum Zitat Khamashta M, Taraborelli M, Sciascia S, Tincani A. Antiphospholipid syndrome. Best Pract Res Clin Rheumatol. 2016;30:133–48.CrossRefPubMed Khamashta M, Taraborelli M, Sciascia S, Tincani A. Antiphospholipid syndrome. Best Pract Res Clin Rheumatol. 2016;30:133–48.CrossRefPubMed
53.
Zurück zum Zitat Zhou XJ, Chen M, Wang SX, Zhou FD, Zhao MH. A 3-year follow-up of a patient with acute renal failure caused by thrombotic microangiopathy related to antiphospholipid syndrome: case report. Lupus. 2016;0:1–6. Zhou XJ, Chen M, Wang SX, Zhou FD, Zhao MH. A 3-year follow-up of a patient with acute renal failure caused by thrombotic microangiopathy related to antiphospholipid syndrome: case report. Lupus. 2016;0:1–6.
54.
Zurück zum Zitat Thachil J. Recurrent venous thromboembolism while on anticoagulant therapy. Blood Rev. 2012;26:175–81.CrossRefPubMed Thachil J. Recurrent venous thromboembolism while on anticoagulant therapy. Blood Rev. 2012;26:175–81.CrossRefPubMed
55.
Zurück zum Zitat Jordan SC, Choi J, Kahwaji J, Vo A. Complement inhibition for prevention and treatment of antibody-mediated rejection in renal allograft recipients. Transplant Proc. 2016;48:806–8.CrossRefPubMed Jordan SC, Choi J, Kahwaji J, Vo A. Complement inhibition for prevention and treatment of antibody-mediated rejection in renal allograft recipients. Transplant Proc. 2016;48:806–8.CrossRefPubMed
56.
Zurück zum Zitat Chandran S, Baxter-Lowe L, Olson JL, Tomlanovich SJ, Webber A. Eculizumab for the treatment of de novo thrombotic microangiopathy post simultaneous pancreas-kidney transplantation—a case report. Transplant Proc. 2011;43:2097–101.CrossRefPubMed Chandran S, Baxter-Lowe L, Olson JL, Tomlanovich SJ, Webber A. Eculizumab for the treatment of de novo thrombotic microangiopathy post simultaneous pancreas-kidney transplantation—a case report. Transplant Proc. 2011;43:2097–101.CrossRefPubMed
57.
Zurück zum Zitat Barilla-Labarca ML, Toder K, Furie R. Targeting the complement system in systemic lupus erythematosus and other diseases. Clin Immunol. 2013;148:313–21.CrossRefPubMed Barilla-Labarca ML, Toder K, Furie R. Targeting the complement system in systemic lupus erythematosus and other diseases. Clin Immunol. 2013;148:313–21.CrossRefPubMed
58.
Zurück zum Zitat Hallstensen RF, Bergseth G, Foss S, et al. Eculizumab treatment during pregnancy does not affect the complement system activity of the newborn. Immunobiology. 2015;220:452–9.CrossRefPubMed Hallstensen RF, Bergseth G, Foss S, et al. Eculizumab treatment during pregnancy does not affect the complement system activity of the newborn. Immunobiology. 2015;220:452–9.CrossRefPubMed
59.
Zurück zum Zitat Kocak B, Arpali E, Demiralp E, Yelken B, Karatas C, Gorcin S, et al. Eculizumab for salvage treatment of refractory antibody-mediated rejection in kidney transplant patients: case reports. Transplant Proc. 2013;45:1022–5.CrossRefPubMed Kocak B, Arpali E, Demiralp E, Yelken B, Karatas C, Gorcin S, et al. Eculizumab for salvage treatment of refractory antibody-mediated rejection in kidney transplant patients: case reports. Transplant Proc. 2013;45:1022–5.CrossRefPubMed
60.
Zurück zum Zitat Legendre C, Sberro-Soussan R, Zuber J, Rabant M, Loupy A, Timsit MA, Anglicheau D. Eculizumab in renal transplantation. Transplant Rev. 2013;27:90–2.CrossRef Legendre C, Sberro-Soussan R, Zuber J, Rabant M, Loupy A, Timsit MA, Anglicheau D. Eculizumab in renal transplantation. Transplant Rev. 2013;27:90–2.CrossRef
61.
Zurück zum Zitat Murdaca G, Colombo BM, Puppo F. Emerging biological drugs: a new therapeutic approach for systemic lupus erythematosus. An update upon efficacy and adverse events. Autoimmun Rev. 2011;11:56–60.CrossRefPubMed Murdaca G, Colombo BM, Puppo F. Emerging biological drugs: a new therapeutic approach for systemic lupus erythematosus. An update upon efficacy and adverse events. Autoimmun Rev. 2011;11:56–60.CrossRefPubMed
62.
Zurück zum Zitat Pickering MC, Ismajli M, Condon MB, McKenna N, Hall AE, Lightstone L, Cook HT, Cairns TD. Eculizumab as rescue therapy in severe resistant lupus nephritis. Rheumatology. 2015;54:2288–90. Pickering MC, Ismajli M, Condon MB, McKenna N, Hall AE, Lightstone L, Cook HT, Cairns TD. Eculizumab as rescue therapy in severe resistant lupus nephritis. Rheumatology. 2015;54:2288–90.
63.
Zurück zum Zitat Stewart ZA, Collins TE, Schlueter AJ, Raife TI, Holanda DG, Nair R, Reed AI, Thomas CP. Case report: eculizumab rescue of severe accelerated antibody-mediated rejection after ABO-incompatible kidney transplant. Transplant Proc. 2012;44:3033–6.CrossRefPubMed Stewart ZA, Collins TE, Schlueter AJ, Raife TI, Holanda DG, Nair R, Reed AI, Thomas CP. Case report: eculizumab rescue of severe accelerated antibody-mediated rejection after ABO-incompatible kidney transplant. Transplant Proc. 2012;44:3033–6.CrossRefPubMed
64.
Zurück zum Zitat Lonze BE, Singer AL, Montgomery RA. Eculizumab and renal transplantation in a patient with CAPS. N Engl J Med. 2010;362:1744–5.CrossRefPubMed Lonze BE, Singer AL, Montgomery RA. Eculizumab and renal transplantation in a patient with CAPS. N Engl J Med. 2010;362:1744–5.CrossRefPubMed
65.
Zurück zum Zitat Gustavsen A, Bergseth G, Volokhina E, van den Heuvel LP, Skattum L, Mollnes TE, Barratt-Due A. Eculizumab treatment in pregnancy complicated with APS—effects on mother and infant. Abstracts/Immunobiology. 2016;221:1131–225. Gustavsen A, Bergseth G, Volokhina E, van den Heuvel LP, Skattum L, Mollnes TE, Barratt-Due A. Eculizumab treatment in pregnancy complicated with APS—effects on mother and infant. Abstracts/Immunobiology. 2016;221:1131–225.
66.
Zurück zum Zitat Wig S, Chan M, Thachil J, Bruce J, Barnes T. A case of relapsing and refractory catastrophic anti-phospholipid syndrome successfully managed with eculizumab, a complement 5 inhibitor. Rheumatology. 2016;55:382–4.CrossRefPubMed Wig S, Chan M, Thachil J, Bruce J, Barnes T. A case of relapsing and refractory catastrophic anti-phospholipid syndrome successfully managed with eculizumab, a complement 5 inhibitor. Rheumatology. 2016;55:382–4.CrossRefPubMed
67.
Zurück zum Zitat Sheridan D, Yu ZX, Zhang Y, Patel R, Lasaro M, Bouchard K, Andrien B, Marozsan A, Wang Y, Tamburini P. Design and preclinical characterization of ALXN 1210: a next generation anti-C5 monoclonal antibody with improved pharmacokinetics and duration of action. Abstracts/Immunobiology. 2016;221:1131–225. Sheridan D, Yu ZX, Zhang Y, Patel R, Lasaro M, Bouchard K, Andrien B, Marozsan A, Wang Y, Tamburini P. Design and preclinical characterization of ALXN 1210: a next generation anti-C5 monoclonal antibody with improved pharmacokinetics and duration of action. Abstracts/Immunobiology. 2016;221:1131–225.
68.
Zurück zum Zitat Harder MJ, Kuhn N, Schrezenmeier H, et al. Mechanistic evidence for incomplete terminal pathway inhibition under eculizumab during strong complement activation. Abstracts/Immunobiology. 2016;221:1131–225. Harder MJ, Kuhn N, Schrezenmeier H, et al. Mechanistic evidence for incomplete terminal pathway inhibition under eculizumab during strong complement activation. Abstracts/Immunobiology. 2016;221:1131–225.
70.
Zurück zum Zitat Nishimura J, Yamamoto M, Hayashi S, Ohyashiki K, Ando K, Brodsky AL, et al. Genetic variants in C5 and poor response to eculizumab. New Engl J Med. 2014;370:632–9.CrossRefPubMed Nishimura J, Yamamoto M, Hayashi S, Ohyashiki K, Ando K, Brodsky AL, et al. Genetic variants in C5 and poor response to eculizumab. New Engl J Med. 2014;370:632–9.CrossRefPubMed
71.
Zurück zum Zitat Risitano AM, Marotta S. Therapeutic complement inhibition in complement-mediated hemolytic anemias: past, present and future. Semin Immunol. 2016;28:223–40.CrossRefPubMed Risitano AM, Marotta S. Therapeutic complement inhibition in complement-mediated hemolytic anemias: past, present and future. Semin Immunol. 2016;28:223–40.CrossRefPubMed
72.
Zurück zum Zitat Woodruff TM, Nandakumar KS, Tedesco F. Inhibiting the C5–C5a receptor axis. Mol Immunol. 2011;48:1631–42.CrossRefPubMed Woodruff TM, Nandakumar KS, Tedesco F. Inhibiting the C5–C5a receptor axis. Mol Immunol. 2011;48:1631–42.CrossRefPubMed
73.
Zurück zum Zitat Manthey HD, Woodruff TM, Taylor SM, Monk PM. Complement 801 component 5a (C5a). Intern J Biochem Cell Biol 2009;41:2114-7. Manthey HD, Woodruff TM, Taylor SM, Monk PM. Complement 801 component 5a (C5a). Intern J Biochem Cell Biol 2009;41:2114-7.
Metadaten
Titel
Antibodies Against Complement Components: Relevance for the Antiphospholipid Syndrome—Biomarkers of the Disease and Biopharmaceuticals
verfasst von
Mirjana Bećarević
Publikationsdatum
01.07.2017
Verlag
Springer US
Erschienen in
Current Rheumatology Reports / Ausgabe 7/2017
Print ISSN: 1523-3774
Elektronische ISSN: 1534-6307
DOI
https://doi.org/10.1007/s11926-017-0669-1

Weitere Artikel der Ausgabe 7/2017

Current Rheumatology Reports 7/2017 Zur Ausgabe

Pediatric Rheumatology (S Ozen, Section Editor)

Autoinflammatory Diseases with Periodic Fevers

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Notfall-TEP der Hüfte ist auch bei 90-Jährigen machbar

26.04.2024 Hüft-TEP Nachrichten

Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Bei schweren Reaktionen auf Insektenstiche empfiehlt sich eine spezifische Immuntherapie

Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.

Therapiestart mit Blutdrucksenkern erhöht Frakturrisiko

25.04.2024 Hypertonie Nachrichten

Beginnen ältere Männer im Pflegeheim eine Antihypertensiva-Therapie, dann ist die Frakturrate in den folgenden 30 Tagen mehr als verdoppelt. Besonders häufig stürzen Demenzkranke und Männer, die erstmals Blutdrucksenker nehmen. Dafür spricht eine Analyse unter US-Veteranen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.