Autoanticuerpos y vasculitis sistémicas
DOI:
https://doi.org/10.31053/1853.0605.v67.n4.22576Palabras clave:
autoanticuerpos, vasculitis sistémicasResumen
El término vasculitis incluye un grupo heterogéneo de enfermedades que tienen en común la lesión inflamatoria de los vasos sanguíneos. La evolución de este proceso inflamatorio conduce a la isquemia o, en ocasiones, hemorragia de los órganos dependientes de esos vasos. La localización de los vasos y los tejidos afectados van a determinar la aparición de una amplia variedad de manifestaciones clínicas y, por tanto, de un pronóstico también muy variable. Las distintas entidades agrupadas bajo el término de vasculitis incluyen la granulomatosis de Wegener, el síndrome de Churg-Strauss, panarteritis nodosa clásica, poliangeítis microscópica, enfermedad de Kawasaki y vasculitis leucocito clásticas que afectan predominantemente a vasos de mediano y pequeño tamaño. La arteritis de células gigantes y la arteritis de Takayasu afectan sobre todo a vasos de gran tamaño. Podemos encontrar vasculitis primarias (sin asociación con otra enfermedad subyacente) o secundarias tanto a procesos infecciosos como a enfermedades autoinmunes (artritis reumatoide, lupus eritematoso sistémico, etc.). Los anticuerpos anticitoplasma de neutrófilo (ANCA) fueron descriptos inicialmente por Davies et al. (2) en pacientes con glomerulonefritis. Están dirigidos contra enzimas presentes en los gránulos azuròfilos de los neutrófilos (3,4). Trabajos posteriores han confirmado su asociación con la granulomatosis de Wegener (5,6), con la poliangeítis microscópica, glomerulonefritis idiopática necrotizante y otras enfermedades autoinmunes.
Descargas
Referencias
FAUCI, A. C.; LEAVITT, RY.: Systemic vasculitis. En: Lichtenstein L. M. Fauci AS ed. Current therapy in allergy, immunology and rheumatology-3. Toronto, Decker BC; 1988: 149-155.
DAVIES, D.; MORAN, J.; NIALL, J.; RYAN, G.: Segmental necrotising glomerulonefritis with antineutrophil antibody: possible arbovirus aetiology? BMJ 1982; 285: 606.
LUDEMANN, J.; UTECHT, B.; GROSS, W. L.: Anti-neutrophil cytoplasm antibodies in Wegener's granulomatosis reconize an elastinolytic enzyme: J. Exp. Med. 1990; 171: 357-362.
GOLDSCHMEDING, R; VAN DER SCHOOT, C. E.; BOKKEL-HUININK, D. et al.: Wegener's granulomatosis autoantibodies identify a novel diisopropyl fluorophosphatase binding protein in the lysosomes of normal human neutropltils. J. Clin. Invest. 1989; 84: 1577-1587.
GASKIN, G.; PUSEY, C. D.: Systemic vasculitis. In: CAMERON, J. S., DAVISON, A M., GRUNFELD, J. KERR DNS eds. Oxford textbook of clinical nephrology. Oxford: Oxford University Press, 1992; 612-636.
REINHOLD-KELLERE.; KEKOW, J.;SCHNABEL,A et al.: Influence of disease manifestation and antineutrhophil cytaplasmic antibody titre on the response to pulse cyclophosphamide therapy in patients with Wegener's granulomatosis. Arthirtis Rheum. 1994; 37: 919-924.
RAMIREZ, G.; KHAMASHTA, M. A.; HUGHES, G. R V.: The ANCA test: its clinical relevance. Ann. Rheum. Dis. 1990; 49: 741-742.
NASSBERGER,L.; SJOHOLM A. G; JONSSON, H.; STURFELT, G; AKESSON, A.: Autoantibodies against neutrophil cytoplasm components in systemic lupus erythematosus and in hydrallazine-induced lupus. Clin. Exp. Immunol. 1990; 81-380-383.
LEUNG, D. Y.M.; GEHA, R S.;NEWBURGER,J. W. et al.: Two monokines, intereukin 1 and tumor necrosis factor render cultured vascular endothelial cells susceptible to lysis by antibodies circulating during Kawasaki syndrome. J. Exp. Med. 1986; 164: 1958-1972.
HUNDER, H H; AREND,W. P.; BLOCH, D.A et al: The American College of Rheumatology 1990 criteria for the classification of vasculitis: introduction. Arthritis Rheum. 1990; 33: 1065-1067.
JENNETIE, J. c.; FALK, R J.; ANDRASSY, K. et al.: Nomenclature of systemic vasculitides. Proposal of an International Consesus Conference.Arthrits Rheum. 1994; 37: 187-192.
SAVAGE, C. O.; HARPER, L.; ADU, D.: Primary systemic vasculitis. Lancet 1997; 349: 553-558.
LIE, J. T.: Nomenclature and classification of vasculitis: Plus ça change, plus c'est la même chose. Arthritis Rheum. 1994; 37: 181-186.
WATTS, R A.: ABC of rlteumatology: Rasltes and vasculitis. B. M. J. 1995; 310: 1128-1132.
NILES, J. L.: Antineutrophil cytoplasmic antibodies in the classification of vasculitis. Annu Rev. Med. 1996; 47: 303-313.
BASU N;WATTS R, BAJEMA I et al. EULAR points to consider in the development of classification and diagnostic criteria in systemic vasculitis. Ann Rheum Dis 2010; 69: 1744-50.
WIES SLANDER, J.: How are antineutraphil cytaplasmic autoontibodies detected? Am J. Kidney 1991; 18: 154-158
CALAFAT, J.; GOLDSCHEMEDING, R; RINGENLING, P. L.; JANSSEN, H; VAN DER SCHOOT, C. E.: In situ localization of doublelabeling immunoelectron microscopy of antineutropltil cytoplasmic autoantibodies in neutropltils and monocytes. Blood 1990; 75: 242-250.
NILES, J. L.; McCLUSKEY, R T.; AHMAD, M. F.; ARNAOUT, M. A.: Wegener's granulomatosis autoantigen is a novel neutropltil serine proteinase. Blood 1989; 74: 1888-1894.
FALK, R J.; JENNETTE, J. C.: Anti-neutraphil cytoplasmic autoantibodies with specifity for myeloperoxidase in patients with systemic vasculitis and idiapathic necrotizing and crescentic glomerulonephritis. N. Engl. J. Med. 1988; 318:: 1651-1657.
VENNING, M. c.; QUINN, A.; BROOMHEAD, V.; BIRD, A G Antibodies directedagainst neutrophils (e-ANCA and p-ANCA) are of distinct diagnostic value in systemic vasculitis. Q. J. Med. 1990; 77: 1287-1296.
Van DerWOUDEN, F. J.; LOBATIO, S.; PERMIN, H et al.: Autoantibodies against neutrophils and monocytes: Tool for diagnosis and marker of disease activity in Wegener granulomatosis. Lancet 1985; 1: 425: 429.
NOLLE, B.; SPECKS, U; LUDEMANN, J. et al.: Anticytoplasmic autoantibodies: Their immuno-diagnostic value in Wegener' s granulomatosis. Ann Intern. Med. 1989; 111: 28-40.
MUSTILA, A; KORPELA, M.; MUSTONEN, J. et' al.: Perinuclear antuneutrophil cytaplasmic antibody in rheumatoid arthritis: A marker of severe disease with associated nephrapathy. Arthritis Rheum 1997; 40: 710-717.
GOMEZ -PUERTA JA, BOSCH X. Anti-neutrophil cytoplasmic antibody pathogenesis in small-vessel vasculitis: an update. Am J Pathol 2009; 175: 1790-98.
Van ROSSUM AP, RAROK AA, HUITEMA MG. et al. : Constitutive membrane expression of proteinase 3 (PR3) and neutrophil activation by anti-PR3 antibodies. J Leukoc Biol 2004; 76:1162-70.
RADFORD DJ, LORD JM, SAVAGE COS.: The activation of the neutrophil respiratory burst by anti-neutrophil autoantibody (ANCA) from patients with systemic vasculitis requires tyrosine kinases and protein kinase C activation. Clin Exp Immunol 1999;118: 171-79.
FALK RJ, TERREL RS, CHARLES LA, et al. : Antineutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro. Proc Natl Acad Sci USA 1990; 87: 4115-19.
VAN PAASSEN P, TERVAERT JWC, HEERINGA P.: Mechanisms of vasculitis: How pauci-immune is ANCA associated renal vasculitis? Nephron Exp Nephrol 2007; 105:10-16.
MULLER KOBOLD AC, VANWIJK RT, FRANSSEN CF et al.: In vitro up regulation of E-selectin and induction of interleukin- 6 in endothelial cells by autoantibodies in Wegener`s granulomatosis and microscopic polyangiitis. Clin Exp Rheumatol 1999; 17: 433-40.
TERVAERT JW.: Proteinase 3 : a cofactor for the binding of antineutrophil cytoplasm antibodies ( ANCA) to endothelial cells? Kidney Int 2000; 57: 2171-72.
CSERNOK E, ERNST M, SCHMITT W et al. : Activated neutrophils express proteinase 3 on their plasmamembrane in-vitro and in-vivo. Clin Exp Immunol 1994; 95: 244-51.
MULLER KOBOLD AC, VAN DER GELD YM, LIMBURG PC et al. : Pathophysiology of ANCA-associated glomerulonephritis. Nephrol Dial Transplant 1999; 14: 1366-75.
MULLER KOBOLD AC, KALLENBERG CG, TERVAERT JW.: Leucocyte membrane expression of proteinase 3 correlates with disease activity in patients with Wegener `s granulomatosis. Br J Rheumatol 1998; 37:901-7.
RADFORD DJ, SAVAGE COS, NASH GB.: Treatment of rolling neutrophils with antineutrophil cytoplasmic antibodies causes conversion to firm integrin-mediated adhesion. Arthritis Rheum 2000; 43: 1337-45.
SCHREIBER A, LUFT FC, KETTRITZ R. : Membrane proteinase 3 expression and ANCA-induced neutrophil activation. Kidney Int 2004;65: 2172-83.
LU X, GARFIELD A, RAINGER GE et al. : Mediation of endothelial cell damage by serine proteases, but not superoxide, released from antineutrophil cytoplasmic antibody-stimulated neutrophils. Arthritis Rheum 2006; 54: 1619-28.
WEISS S. : Tissue destruction by neutrophils. N E J Med 1989; 320: 365-76.
DOLMAN KM, STEGEMAN CA, VAN DEWIEL BA, et al. : Relevance of classic anti-neutrophil cytoplasmic autoantibody (C-ANCA) mediated inhibition of proteinase 3-alpha 1-antitrypsin complexation to disease activity in Wegener `s granulomatosis. Clin Exp Immunol 1993;93: 405-10.
SIBELIUS U, HATTAR K, SCHENKEL A et al. :Wegener `s granulomatosis : anti-proteinase 3 antibodies are potent inductors of human endothelial cells signaling and leakage response. J Exp Med 1998; 187: 497-503.
DE BANDT M, MEYER O, DACOSTA L, et al. Antiproteinase- 3(PR 3) antibodies (C-ANCA) recognize various targets on the human umbilical vein endothelial cell (HUVEC) membrane. Clin Exp Immunol 1999; 115: 362-68.
RADFORD DJ, LUU NT, HEWINS P et al. : Antineutrophil cytoplasmic antibodies stabilize adhesion and promote migration of flowing neutrophils on endothelial cells. Arthritis Rheum 2001; 44: 2851-
HEERINGA P, HUUGEN D, TERVAERT JW. : Antineutrophil cytoplasmic autoantibodies and leukocyte – endothelial interactions : a sticky connection? Trends Immunol 2005; 26: 561-64.
PRIMO VC, MARUSIC S, FRANKLIN CC, et al. : Anti-PR3 immune responses induce segmental and necrotizing glomerulonephritis. Clin Exp Immunol 2010; 159 ;327-337.
KAIN R, EXNER M, BRANDES R et al. Molecular mimicry in pauci-immune focal necrotizing glomerulonephritis. Nat Med 2008;14: 1088-96.
PENDERGRAFT WF, PRESTON GA, SHAH RR et al. Autoimmunity is triggered by cPR-3(105-201), a protein complementary to human autoantigen proteinase- 3. Nat Med 2004;10:72-9.
STEGEMAN CA, TERVAERT JWC, SLUITER WJ et al. Trimethoprim –sulfamethoxazole (co-trimoxazole) for the prevention of relapses of Wegener `s granulomatosis. N E J Med 1996;335: 16-20.
STEGEMAN C, COHEN TERVAERT J, KALLENBERG C. Co-trimoxazole and Wegener `s granulomatosis: more than a coincidence ? Nephrol Dial Trasplant 1997; 12: 652-55.
TERVAERT JW, MULDER L, STEGEMAN C, et al. Occurrence of autoantibodies to human leucocyte elastase in Wegener`s granulomatosis and other inflammatory disorders. Ann Rheum Dis 1993; 52: 115-20.
WIESNER O, RUSSELL KA, LEE AS, et al. Antineutrophil cytoplasmic antibodies reacting with human neutrophil elastase as a diagnostic marker for cocaineinduced midline destructive lesions but not autoimmune vasculitis. Arthritis Rheum 2004;50: 2954-65.
DOLMAN KM, GANS RO, VERVAAT TJ, et al. Vasculitis and antineutrophil cytoplasmic autoantibodies associated with propylthiouracil therapy. Lancet 1993; 342: 651-2.
HU CH, O `LOUGHLIN S, WINKELMANN RK. :Cutaneous manifestations of Wegener granulomatosis. Arch Dermatol 1977; 113:175-182.
Van Timmeren MM, Chen M, Heeringa P. Pathogenic role of complement activation in anti-neutrophil cytoplasmic auto-antibody associated vasculitis. Nephrology 2009; 14:16-25.
Haas M, Eustace JA. Immune complex deposits in ANCA-associated crescentic glomerulonephritis : a study of 126 cases. Kidney Int 2004; 65:2145-2152.
VogtW. Complement activation by mieloperoxidase products released from stimulated human polymorphonuclear leukocytes. Immunobiology 1996;195:334-346.
Johnson U, Ohlsson K, Olsson I. Effects of granulocyte neutral proteases on complement components. Scand J Immunol 1976;5:421-26.
Xiao H, Schreiber A, Heeringa P et al. Alternative complement pathway in the pathogenesis of disease mediated by anti-neutrophil cytoplasmic autoantibodies. Am J Pathol 2007; 170:52-64.
Tipping PG, Holdsworth SR. T cells in crescentic glomerulonephritis. J Am Soc Nephrol 2006; 17:1253-1263.
BoltonWK, Innes Jr DJ, Sturgill BC et al. T-cells and macrophages in rapidly progressive glomerulonephritis: clinicopathologic correlations. Kidney Int 1987;32:869-876.
Marinaki S, Neumann I, Kalsch AI et al. Abnormalities of CD4 T cell subpopulations in ANCA-associated vasculitis. Clin Exp Immunol 2005; 140:181-191.
Marinaki S, Kalsch AI, Grimminger P et al. Persistent T cell activation and clinical correlations in patients with ANCA –associated systemic vasculitis. Nephrol Dial Trasplant 2006; 21:1825-1831.
Wilde B, Dolff S, Cai X et al. CD4+CD25+ T-cell populations expressing CD134 and GITR are associated with disease activity in patients with Wegener’s granulomatosis. Nephrol Dial Trasplant 2009; 24:161-171.
DEL PAPA, N.; CONFORTI, G.; GAMBINI, D. et al.: Characterization of the endotelial surface proteins recognized by antiendothelial antibodies in primary and secondary autoimmune vasculitis. Clin. Immunol. Immunopathol. 1994; 70: 211-216.
FERRARO, G.; MERONI, P. L.; TINCANI, A. et al.: Antiendothelial cell antibodies in patients with Wegener's granulomatosis and mycropoliarteritis. Clin. Exp. Immunol. 1990; 79: 47-54.
SAVAGE, C. O.; POTTINGER,B.E.;GASKIN,G. et al.: Vascular damage inWegener's granulomatosis and microscopic polyarteritis: presence of antiendothelial cell antibodies and their relation to antineutrophil cytoplasm antibodies.Clin Exp. Inmunol. 1991;85: 14-21.
D'CRUZ, D. P.; HUSSIAU, F. A.; RAMIREZ,G. et al.: Antibodies to endothelial cells in systemic lupus erythematosus: A potential marker for nephritis and vasculitis. Clin. Exp. Immunol. 1991; 85: 254-261.
FRAMPTON, G.; JAYNE, Dr.; PERRY, G. J. et al.: Autoantibodies to endothelial cells and neutrophil cytoplasmic antigens in systemic vasculitis. Clin. Exp. Immunol. 1990; 82: 227-235.
BRASILE, L.; KREMER, J. M.; CLARKE, J. L. et al.: ldentification of an autoantibody to vascular endothelial cellspecificantigens in patients with systemic vasculitis. Am. J. Med. 1989; 87: 74-81.
ROLLINO, c.; ROCCA TELLO, D.; BORSA, S.; BELLONE, G.; PICOLLI, G.; EMANUELLI, G.: Antibodies directed to sonicated human endothelial cells in patients with vasculitis. Nephron 1996; 73: 346-347.
MATSUO, S.;KUKATSU, A.; TAUB, M. L., CALDWELL P.R.B.,BREN1JENS,J. R; ANDRES, G.:
Glomerulonefritis induced in the rabbit by endothelial cell antibodies. J. Clin. Invest. 1987; 79: 1798-1811.
MATSUDA, M: Experimental glomerular tissue injury induced by immunisation with cultured endothelial cell plasma membrane.Acta Pathol. Jpn 1988; 38: 823-839.
JAFFE, E. A.: Cell biology of endothelial cells. Human Pathol. 1987; 18: 234-239.
D'CRUZ, D. P.: Nuevos anticuerpos en las vasculitis. In: KHAMASHTA M A.; FONT, J.; HUGHES, G. R V. eds. Enfermedades autoinmunes del tejido conectivo. Barcelona: Ediciones Doyma S. A. 1992; p: 173-187.
ALARCON-SEGOVIA, D. et al.: Preliminary classification criteria for the antiphospholipid syndrome within systemic lupus erythematosus. Sem Arthritis Rheum. 1992; 21: 275-286.
ALARCON-SEGOVIA, D.; CARDIEL, M. H.; REYES; E.: Antiphospholipid arterial vasculopathy. J. Rheumatol. 1989; 16: 762-767.
GOLDBERGER, E.; ELDER, R. c.; SCHWARTZ, R A.; PHILIPIS, P. E.: Vasculitis in the antiphospholipid syndrome. A cause of ischemia responding to cortirosteroids. Arthritis Rheum. 1992; 35: 569-572.
TOUSSIROT,E. et al.: Association of cerebral vasculitis with a lupus anticoagulant. A case with brain pathology. Clin Rheumatol. 1994; 13: 624-627.
NORDEN, D. K; OSTROV, B. E.; SHAFRITZ, A. B.; Von FELDT, J. M.: Vasculitis associated with antiphospholipid syndrome. Semin. Arthritis Rheum. 1995; 24: 273-281.
ALARCON-SEGOVIA, D. et al.: Antiphospholipid antibodies and the antiphospholipid syndrome in systemic lupus erythematosus. Medicine 1989; 68: 353-365.
ALARCON-SEGOVIA, D.: Pathogenetic potential of antiphospholipid antibodies. J. Rheumatol. 1988; 15: 890-893.
DRENKARD, c.; VILLA,A. R; REYES,E.; ABELLO, M; ALARCON-SEGOVIA D.: Vasculitis in systemic lupus erythematosus. Lupus 1997; 6: 235-242.
DEL PAPA, N. et al.: Relationship between antiphospholipid and anti-endothelial cell antibodies III: b2 glycoprotein I mediates the antibody binding to endothelial membranes and induces the expression of adhesion molecules. Clin. Exp. Rheumatol. 1995; 13: 179-
185.
VISMARA, A. et al.: Relationship between anticardiolipin and anti-endothelial cell antibodies in systemü; lupus erythematosus. Clin. Exp. Immunol. 1988; 74: 247-253.
CERVERA, R KHAMASHTA, M A.; FONT, J. et al.: Antiendothelial cell antibodies in patients with antiphospholipid syndrome. Autoimmunity 1991; 11: 1-6.
DAVENPORT, A.; LOCK, R J; WALLINGION, T. B.; FEEST, T. G.: Clinical significance of antineutrophil cytoplasm antibodies detected by a standarised indirect immunofluorescence assay. Q. J Med. 1994; 87: 291-299.
EDGAR, J. D.; McMILLAN, S. A.; BRUCE, 1.; CONLAN, S. K: An audit of ANCA in routine clinical practice. Postgrad Med. J. 1995; 71: 605-612.
BRAUN, M. G.; CSERNOK, E.; SCHMITT, W. H.; GROSS, W. L.: lncidence, target antigens, and clinical implications of antineutrophil cytoplasmic antigens, and clinical implications of antineutrophil cytoplasmic antibodies inn rheumatoid arthritis. J. Rheumatol. 1996; 23:
826-830.
RAO, J. K; WEINBERG, M; ODDONE, E. 2.; ALLEN, N. B.; LANDSMAN, P.; FEUSSNER, J. R: The role of antineutrophil cytoplasmic antibody (c-ANCA) testing in the diagnosis ofWegener granulomatosis-A literature review and meta-analysis. Ann Intern. Med. 1995; 123: 925-932.
KERR, G. S.; FLEISHER, T. A.; HALLAHAM, C.W.; LEAVIIT, R Y.; FAUO, A. S.; HOFFMAN, G. S.: Limited prognostic value of change in antineutrophil cytoplasmic antibody titer in patients with granulomatosis de Wegener. Arthritis Rheum. 1993; 36: 365-371.
HOFFMAN, G. S.: Vasculitis syndromes. :Curr Opin-Rheumatol. 1995; 7: 1-3.
HOFFMAN, G. S.;KERR, G. S.: Rise in ANCA titer:to treat or not to treat. Am. J Med. 1995;98: 102-103.
EDGAR, J. D. M.: The clinical utility of ANCA positivity.: Ann Rheurn. Dis. 1996; 55: 494-496.
Descargas
Publicado
Número
Sección
Licencia
Derechos de autor 2010 Universidad Nacional de Córdoba
Esta obra está bajo una licencia internacional Creative Commons Atribución-NoComercial 4.0.
Se permite la generación de obras derivadas siempre que no se haga con fines comerciales. Tampoco se puede utilizar la obra original con fines comerciales.
Cómo citar
