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Inicio Angiología Papel del HLA en la patogenia de los aneurismas de aorta abdominal
Información de la revista
Vol. 54. Núm. 2.
Páginas 102-110 (enero 2002)
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Vol. 54. Núm. 2.
Páginas 102-110 (enero 2002)
Acceso a texto completo
Papel del HLA en la patogenia de los aneurismas de aorta abdominal
Role of hla complex in the pathogenesis of abdomin alaortic aneurysms
papel do hla na patogenia dos aneurismas da aorta abdominal
Visitas
2376
G. Moñuxa, P. Vigilb, F.J. Serranoa,
Autor para correspondencia
fserrano@hcsc.insalud.es

correspondence: Servicio de Angiología y Cirugía Vascular. Hospital Clínico San Carlos. Profesor Martín Lagos, s/n. E-28040 Madrid. Fax: +34913 303 043.
, E. Gómez de la Conchab
a Servicio de Angiología y Cirugía Vascular.
b Servicio de Inmunología. Hospital Clínico San Carlos. Madrid, España.
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Bibliografía
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Summary
Introduction

Recently, changes in metaloproteinases matrix has been described in abdominal aortic aneurysms (AAA). This changes are due to inflamatory processes that could be implicated in their pathogenesis. There are few reports that study autoinmunity implication in the pathogenesis of this pathology.

Objective

To study the HLA class II and III complex to evaluate the implication of autoinmunity in the AAA.

Patients and methods

HLA class II and HLA class III corresponding to tumor necrosis factor and its promoter were typed in a group of 72 patients with an AAA. These results were compared with a group of 380 healthy volunteers as control group.

Results

HLA-II: HLA-DR4*401 was more frecuent in AAA than in control group (12.5% vs 5.2% p 0.02 OR 2.59). There were not any other difference between both groups. TNF: TNF α4β5 was more frecuent in AAA group than incontrol group but statistical differences were not encountered (p= 0.055). There were not any difference in the frecuencies of TNF promoters. Haplotypes: HLA-DR3-TNF α2β3 ancestral haplotipe was more frecuent in AAA than in control group (16.6% vs 8.4%, p= 0.03, OR = 2.17).

Conclusion

The relationship encountered between HLA-DR4*401 and ancestral haplotype HLA-DR3-TNF α2β3, that is associated with other autoinmune processes, suggest that autoinmunity could play an important role in the pathogenesis of abdominal aortic aneurysms.

Key words:
Abdominal aortic aneurysms
Ancestral haplotype
Autoinmunity
HLA
Major histocompatibility complex
Tumoral necrosis factor
Resumen
Introducción

En los últimos años, se han descrito alteraciones en el patrón de las metaloproteinasas en los aneurismas de aorta abdominal (AAA), secundarias aprocesos inflamatorios que podrían estar implicados en la patogenia de los mismos; existen muy escasos estudios que valoren el papel de la autoinmunidad en la etiopatogenia de esta enfermedad.

Objetivo

Estudiar el patrón HLA de clase II y III para valorar la participación de un proceso autoinmune en los AAA.

Pacientes y métodos

Se realizó el tipaje de los HLA-II y las zonas del HLA-III correspondientes al factor de necrosis tumoral (TNF) y su promotor en un grupo de 72 pacientes con AAA, y se comparó con una muestra control de 380 personas sanas.

Resultados

HLA-II: se encontró mayor incidencia de HLA-DR-4*401 en AAA respecto a controles (12,5% frente a 5,2%; p= 0,02; OR= 2,59). No hubo diferencias entre los demás alelos. TNF: la frecuencia de aparición del TNF α4β5 en el grupo de AAA mostró una tendencia a la significación (p= 0,055) sin encontrar otras diferencias respecto a los controles. Tampoco se encontraron diferencias en cuanto a los promotores del TNF. Haplotipos: el haplotipo HLA-DR3-TNF α2β3 fue significativamente más prevalente entre los AAA respecto a los controles (16,6% frente a 8,4%; p= 0,03; OR= 2,17).

Conclusiones

La relación encontrada entre el HLA-DR4*401 y el haplotipo ancestral HLA-DR3-TNFα2β3 que se encuentra asociado a otras enfermedades autoinmunes, sugiere que fenómenos de autoinmunidad pueden desempeñar un papel importante en lapatogenia de los aneurismas de aorta abdominal.

Palabras clave:
Aneurismas de aorta abdominal
Autoinmunidad
Complejo mayor de histocompatibilidad
Factor de necrosis tumoral
Haplotipo ancestral
HLA
Resumo
Introdução

Nos últimos anos, foram descritas alterações no padrão das metaloproteínas nos aneurismas da aorta abdominal(AAA), secundário a processos inflamatórios que poderiam estar implicados na patogenia dos mesmos, existindo raros estudos que avaliam o papel da auto-imunidade na etiopatogenia desta doença.

Objectivo

Estudar o padrão HLA de classe II e III para avaliar a participação de um processo auto-imune nos AAA. Doentes e métodos. Realizou-se a tipificação dos HLA-IIe as zonas do HLA-III correspondentes ao factor de necrose tumoral (TNF) e seupromotor no grupo de 72 doentes com AAA, comparando-o com uma amostra de controlo de 380 indivíduos sãos.

Resultados

HLA-II: encontrou-se maior incidência de HLA-DR-4*401 no AAA em relação aos controlos (12,5% contra 5,2%; p= 0,02; OR= 2,59), não houveram diferenças entre os restantes alelos. TNF: a frequência de aparecimento de TNF α4β5 no grupo de AAA mostrou uma tendência para ser significativo (p= 0,055) sem encontrar outras diferenças no que dizrespeito aos controlos; da mesma forma, não se encontraram diferenças quanto aos promotores do TNF.Aplotipos: o haplotipo HLA-DR3-TNFα2β3 foi significativamente mais prevalente entre os AAA do que diz respeito aos controlos (16,6% contra 8,4%; p= 0,03; OR= 2,17).

Conclusões

A relação encontrada entre oHLA-DR4*401 e haplotipo ancestralHLA-DR 3-TNF α2β3, que está associada a outras doenças auto-imunes, sugere que fenómenos de auto-imunidade po-dem representar umpapel importante na patogenia dos aneurismas da aorta abdominal.

Palavras clave:
Aneurismas da aorta abdominal
Auto-imunidade
Complexo major de histocompatibilidade
Factor de necrose tumoral
Haplotipo ancestral
HLA
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Bibliografía
[1.]
D. Tilson, J.M. Reilly, M. Brophy, E. Webster, T.R. Barnett.
Expression and secuence of the gene for tissue inhibitor of metalloproteinases in patients with abdominal aortic aneurysms.
J Vasc Surg., 18 (1993), pp. 266-270
[2.]
K.M. Newman, J. Jean-Claude, L. Hong, J.V. Scholes, Y. Ogata, H. Nagase, M.D. Tilson.
Cellular localization of matrix metalloproteinases in the abdominal aortic aneurysm wall.
J Vasc Surg., 20 (1994), pp. 814-820
[3.]
K.M. Newman, Y. Ogata, A.M. Malon, E. Irizarry, R. Ghandi, H. Nagase, M.D. Tilson.
Identification of matrix metalloproteinases 3 (streptomelisin) and 9 (gelatinase B) in abdominal aortic aneurysm.
Arterioescler Thromb Vasc Biol, 14 (1994), pp. 1315-1320
[4.]
K.M. Newman, A.M. Malon, R.D. Shin, J.V. Scholes, W.G. Ramey, M.D. Tilson.
Matrix metalloproteinases in abdominal aortic aneurysms: caracterization, purification and its possible sources.
Connest Tissue Res, 30 (1994), pp. 265-276
[5.]
W.H. Pearce, I. Sweis, J.S. Yao, W.J. Mc Carthy, A.E. Koch.
Interleukin 1 beta and tumor necrosis factor-alpha release in normal and diseased human infrarenal aortas.
J Vasc Surg., 16 (1992), pp. 784-789
[6.]
M.D. Tilson, K. Ozsvath, H. Hirose, X. Shichao.
A genetic basis for autoimmune manifestations in the abdominal aortic aneurysm resides in the MHC class II locus DR beta 1.
N Y Acad Sci., 800 (1996), pp. 208-217
[7.]
H. Hirose, M. Tagaki, N. Miyagawa, H. Hashiyada, M. Noguchi, S. Tada, et al.
Genetic risk factor for abdominal aortic aneurysm: HLA-DR2(15): a japanese study.
J Vasc Surg., 27 (1998), pp. 500-503
[8.]
R.H. Armour.
Survivors of ruptured abdominal aortic aneurysm: The iceberg's tip.
Br Med J, 2 (1977), pp. 1055-1057
[9.]
A.K. Samy, G. MacBain.
Abdominal aortic aneurysm: Ten year's hospital population study in the city of Glasgow.
Eur J Vasc Surg., 7 (1993), pp. 561-566
[10.]
A.E. Koch, K. Haines, R. Rizzo, J. Radosevich, R. Pope, P. Robinson, et al.
Human abdominal aortic aneurysms.
Immunophenotypic analysis suggesting an immune mediated response. Am J Pathol, 137 (1990), pp. 1199-1213
[11.]
G.S. Herron, E. Unemori, M. Wong, J.H. Rapp, M.H. Hibbs, R.J. Stoney.
Conective tissue proteinases and inhibitors in abdominal aortic aneurysms: involvement of the vasa vasorum in the pathogenesis of aortic aneurysms.
Arterioscler Thromb, 11 (1991), pp. 1667-1677
[12.]
C.H. Evans, H.I. Georgescu, C.W. Lin, D. Mendelow, D.L. Steed, M.W. Webster.
Inducible synthesis of collagenase by cells of aortic origin.
J Surg Res, 51 (1991), pp. 399-404
[13.]
N. Vine, J.T. Powell.
Metalloproteinases in degenerative aortic disease.
Clin Sci., 81 (1991), pp. 233-239
[14.]
E. Irizarry, K.M. Newman, R.H. Ghandi, G.B. Nackman, V. Halpern, S. Wishner, et al.
Demonstration of interstitial collagenase in abdominal aortic aneurysm disease.
J Surg Res, 54 (1993), pp. 571-574
[15.]
A.K. Gregory, N. Yin, J. Capella, S. Xia, K.M. Newman, M.D. Tilson.
Features of autoimmunity in the abdominal aortic aneurysm.
Arch Surg., 131 (1996), pp. 85-88
[16.]
C.M. Weyand, J.J. Grononzy.
Functional domains on HLA-DR mollecules: implications for the linkage of HLA DR genes for different autoimmune disease.
Clin Immunol Immunopathol, 70 (1994), pp. 91-98
[17.]
T.E. Rasmussen, J.V. Hallett, R.L. Mathewu-Metzger, D.M. Richardson, J.J. Gronzy, C.M. Weyand.
Genetic risk factor in inflammatory abdominal aortic aneurysms: polymorphic residue 70 in the HLA DRB1 gene is a key element.
J Vasc Surg., 25 (1997), pp. 356-364
[18.]
P. Price, C. Witt, R. Allcock, D. Sayer, M. Garleep, C. Choy Kok, et al.
The genetic basis for the association of the 8.1 ancestral haplotype (A1, B8, DR3) with musltiple immunopatholological disease.
Immunol Rev, 167 (1999), pp. 257-274
[19.]
M.A. Hall, J.S. Lanchbury, P.J. Ciclitira.
Hla class II region genes and susceptibility to dermatitis herpetiformis: DPB1 and TAP2 associations are secundary to those of the DQ subregion.
Eur J Immunogenet, 23 (1996), pp. 285-296
[20.]
F.T. Christiansen, W.J. Zhang, M. Griffiths, S.A. Mallal, R.L. Dawkins.
Major histocompatibility complex (MHC) complement deficiency, ancestral haplotypes and systemic lupus erythematosus (SLE): C4 deficiency explains some but not all of the influence of the MHC.
J Reumatol, 18 (1991), pp. 1350-1358
[21.]
A.G. Wilson, F.E. Clay, A.M. Crane, M.J. Cork, G.W. Duff.
Comparative genetic association of human leucocyte antigen class II and tumor necrosis factor alpha with dermatitis herpetiformis.
J Invest Dermatol, 104 (1995), pp. 856-858
[22.]
M.A. Degli-Esposti, A. Andreas, F.T. Chistiensen, B. Schalke, E. Albert, R.L. Dawkins.
An approach to the localization of the susceptibility genes for generalised myasthenia gravis by mapping recombinant ancestral haplotypes.
Immunogenetics, 35 (1992), pp. 355-364
[23.]
J.E. Volanakis, Z.B. Zhu, F.M. Schaffer, K.J. Macon, J. Palermos, B.O. Barger, et al.
Major histo-compatibility complex class III genes and susceptibility to immunoglobulin A deficiency and common variable immunodeficiency.
J Clin Invest, 89 (1992), pp. 1914-1922
[24.]
C.G.M. Kallenberg, J.M. van der Voort-Beelem, J. D'Amaro, T.H. The.
Increased frecuency of B8/DR3 in scleroderma and association of the haplotype with impaired cellular immune response.
Clin Exp Immunol, 43 (1981), pp. 478-485
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