metricas
covid
Buscar en
Revista Colombiana de Reumatología
Toda la web
Inicio Revista Colombiana de Reumatología Espondiloartritis y su asociación con el Complejo Mayor de Histocompatibilidad ...
Journal Information
Vol. 18. Issue 1.
Pages 34-41 (March 2011)
Share
Share
Download PDF
More article options
Vol. 18. Issue 1.
Pages 34-41 (March 2011)
Full text access
Espondiloartritis y su asociación con el Complejo Mayor de Histocompatibilidad “Spondylarthritis and the association with Major Histocompatibility Complex”
Visits
3549
Wilson A. Bautista-Molano1,
Corresponding author
wbatu@hotmail.com

Correspondencia.
, John D. Londoño2, Consuelo Romero Sánchez3, Mabel Ávila3, Rafael R. Valle4
1 Médico Internista. Residente Reumatología. Universidad Militar Nueva Granada. Hospital Militar Central
2 Médico Internista. Reumatólogo. Hospital Militar Central. Profesor Universidad de la Sabana
3 Docente Inmunología. Universidad Militar Nueva Granada. Laboratorio de Inmunología. Servicio de Reumatología. Hospital Militar Central
4 Médico Internista. Reumatólogo, Jefe del Servicio de Reumatología. Hospital Militar Central. Profesor Universidad Militar Nueva Granada y Universidad de la Sabana
This item has received
Article information
Resumen

Las espondiloartritis corresponden a un grupo heterogéneo de enfermedades crónicas caracterizadas por entesitis tanto axial como periférica, artritis y menos comúnmente manifestaciones extra articulares. Se encuentran fuertemente ligadas a factores genéticos y en algunos pacientes a infecciones por bacterias artritogénicas. Su presentación y curso clínico se encuentran influenciados por la etnia, el género y la edad de inicio de la enfermedad.

La Espondilitis Anquilosante (EA) como prototipo de espondiloartritis es una enfermedad hereditaria con un 90% de susceptibilidad atribuible a factores genéticos. Desde el descubrimiento de la asociación del alelo HLA-B*27 en los años setenta, las bases moleculares de esta asociación, una de las más fuertes entre una molécula del Complejo Mayor de Histocompatibilidad y una enfermedad, permanecen sin esclarecer. La fuerte asociación del HLA-B*27 confiere a este alelo un papel significativo de susceptibilidad para el desarrollo de la enfermedad. Varios estudios han informado la asociación de otros genes dentro del Complejo Mayor de Histocompatibilidad con la susceptibilidad para el desarrollo de la enfermedad en varios grupos poblacionales.

Palabras clave:
espondiloartritis
poblaciones
asociación
Summary

Spondylarthritis refers to a heterogeneous group of chronic diseases characterized by both axial and peripheral enthesitis, arthritis and extra articular manifestations. There is strongly linked to genetic factors and in some patients is related to clinical infections by arthritogenic bacteria. The clinical presentation and evolution are influenced by ethnicity, gender and age of onset.

Ankylosing Spondylitis as a prototype of Spondylarthritis is an inherited disease with 90% of susceptibility related to genetic factors. Since the publication of the association of HLA-B*27 in the 70's, the molecular component of this association, one of the strongest between a molecule of Major Histocompatibility Complex and disease, remains unclear. The strong association of HLA-B*27 gives to this allele a significant role in susceptibility related to disease development. Several studies have reported the association of other genes within the Major Histocompatibility Complex to susceptibility for development of the disease in others population groups.

Key words:
spondylitis
population
association
Full text is only aviable in PDF
Referencias
[1.]
A. Iglesias, R. Valle, J. Restrepo.
Historia de las Espondiloartropatías seronegativas.
Rev Col Reum, 11 (2004), pp. 181-198
[2.]
B.M. Rothschild, D.R. Prothero, C. Rothschild.
Origins of spondyloarthropathy in perissodactyla.
Clin Exp Rheumat, 19 (2001), pp. 628-632
[3.]
B.M. Rothschild, R.J. Woods.
Spondyloarthropathy as an World phenomenon.
Semin Arthritis Rheum, 21 (1992), pp. 306-316
[4.]
Samano-Tirado José, Gustavo.
Ausencia de Espondiloartropatías en los indígenas pimas en la época colonial.
Rev Mex Reumat, 14 (1999), pp. 89-92
[5.]
A. Hrdlièka.
American Anthropologist, (1904), pp. 54-59
[6.]
A. Ruffer.
Studies in palaeopathology: Arthritis deformans and spondylitis in ancient Egypt.
J Pathol Bacteriol, 22 (1919), pp. 152-196
[7.]
M.A. Khan.
An overview of clinical spectrum and heterogeneity of spondyloarthropathies.
Rheum Dis Clin North Am, 18 (1992), pp. 1-10
[8.]
C.S. Lau, R. Burgos-Vargas, W. Louthrenoo, M.Y. Mok, P. Wordsworth, Q.Y. Zheng.
Features of spondyloarthropathies around the world.
Rheum Dis Clin North Am, 24 (1998), pp. 753-770
[9.]
V. Wright.
Psoriasis and arthritis.
Ann Rheum Dis., 15 (1956), pp. 348-356
[10.]
T. Burns, A. Narder, E. Becks.
Undifferentiated spondyloarthropathies: a nosological missing link?.
Arthritis Rheum, 25 (1982), pp. 142-149
[11.]
J.M. Moll, I. Haslock, I.F. Macrae, V. Wright.
Associations between ankylosing spondylitis, psoriatic arthritis, Reiter's disease, the intestinal arthropathies, and Behçet's syndrome.
Medicine (Baltimore), 53 (1974), pp. 343-364
[12.]
V. Wright, J.M.H. Moll.
Seronegative Polyarthritis.
North Holland Publish Co, (1976), pp. 26-79
[13.]
V. Wright.
Seronegative polyarthritis: an unified concept.
Arthritis Rheum, 21 (1978), pp. 619-633
[14.]
B. Rogoff, R.H. Freyberg.
The familial incidence of rheumatic spondylitis.
Ann Rheum Dis, 8 (1949), pp. 139-142
[15.]
J. Klein, A. Sato.
The HLA System.
New Engl J Med, 343 (2000), pp. 782-786
[16.]
J.L. Tiwari, P.I. Terasaki.
HLA and disease associations.
Springer-Verlag, (1985),
[17.]
E. Thorsby.
Invited anniversary review: HLA associated diseases.
Hum Immunol, 53 (1997), pp. 1-11
[18.]
R.A. Flavell, D.A. Hafler.
eds. Autoimmunity.
Curr Opin Immunol, 11 (1999),
[19.]
D.R. Madden, J.C. Gorga, J.L. Strominger, D.C. Wiley.
The three-dimensional structure of HLA-B27 at 2.1 A resolution suggests a general mechanism for tight peptide binding to MHC.
Cell, 70 (1992), pp. 1035-1048
[20.]
M.J. Turner, M.L. Delay, S. Bai, E. Klenk, R.A. Colbert.
HLA-B27 up-regulation causes accumulation of misfolded heavy chains and correlates with the magnitude of the unfolded protein response in transgenic rats: implications for the pathogenesis of spondylarthritis-like disease.
Arthritis Rheum, 56 (2007), pp. 215-223
[21.]
J.A. López de Castro.
HLA-B27 and the pathogenesis of spondyloarthropathies.
Immuno Lett, 108 (2007), pp. 27-33
[22.]
L.A. Bird, C.A. Peh, S. KoUnberger, T. Elliott, A.J. McMichael, P. Bowness.
Lymphoblastoid cells express HLA-B27 homodimers both intracellularly and at the cell surface following endosomal recycling.
Eur J Immunol, 33 (2003), pp. 748-759
[23.]
S. Kollnberger, P. Bowness.
The role of B27 heavy chain dimer immune receptor interactions in spondyloarthritis.
Adv Exp Med Biol, (2009), pp. 277-285
[24.]
R.E. Hammer, S.D. Maika, J.A. Richardson, J.P. Tang, J.D. Taurog.
Spontaneous inflammatory disease in transgenic rats expressing HLA-B27 and human beta 2m: an animal model of HLA-B27-associated human disorders.
Cell, 63 (1990), pp. 1099-1112
[25.]
R.L. Allen, C.A. O’Callaghan, A.J. McMichael, P. Bowness.
Cutting edge: HLA-B27 can form a novel p2- microglobulin-free heavy chain homodimer structure.
J Immunol, 162 (1999), pp. 5045-5048
[26.]
L.S. Tam, J. Gu, D. Yu.
Pathogenesis of Ankylosing Spondylitis.
Nat Rev Rheumatol, 6 (2010), pp. 399-405
[27.]
M.A. Brown, et al.
Susceptibility to ankylosing spondylitis in twins: the role of genes, HLA, and the environment.
[28.]
M.A. Khan.
Epidemiology of HLA-B27 and arthritis.
Clin Rheumatol, 15 (2006), pp. 10-12
[29.]
J.D. Reveille, A.M. Sims, P. Danoy, D.M. Evans, P. Leo, J.J. Pointon, et al.
Genome-wide association study of ankylosing spondylitis identifies non-MHC susceptibility loci.
Nat Genet, 42 (2010), pp. 123-127
[30.]
D.A. Brewerton, F.D. Hart, A. Nicholls, M. Caffrey, D.C. James, R.D. Sturrock.
Ankylosing spondylitis and HL-A 27.
Lancet, 1 (1973), pp. 904-907
[31.]
L. Schlosstein, P.I. Terasaki, R. Bluestone, C.M. Pearson.
High association of an HL-A antigen, W27, with ankylosing spondylitis.
N Engl J Med, 288 (1973), pp. 704-706
[32.]
J.A. López de Castro.
HLA-B27 and the pathogenesis of spondyloarthropathies.
Immunol Lett, 108 (2007), pp. 27-33
[33.]
P. Wordsworth, M. Brown.
HLA-B27, ankylosing spondylitis and the spondyloarthropathies.
Oxford University Press, (1998), pp. 179-193
[34.]
D. John, Reveille.
Major histocompatibility genes and ankylosing spondylitis.
Best Practice & Research Clinical Rheumatology, 20 (2006), pp. 601-609
[35.]
M.A. Brown.
Genetics and the pathogenesis of ankylosing spondylitis.
Curr Opin Rheumatol., 21 (2009), pp. 318-323
[36.]
M.A. Brown.
Genetics of ankylosing spondylitis.
Curr Opin Rheumatol, 22 (2010), pp. 126-132
[37.]
S. Gonzales-Roces, M.V. Alvarez, S. Gonzalez, A. Dieye, H. Makni, D.G. WoodWeld, et al.
HLA-B27 polymorphism and world-wide susceptibility to ankylosing spondylitis.
Tissue Antigens, 49 (1997), pp. 116-123
[38.]
M.A. Blanco-Gelaz, A. Lopez-Vasquez, S. Garcia-Fernandez, et al.
Genetic variability, molecular evolution, and geographic diversity of HLA B27.
Hum Immunol, 62 (2001), pp. 1042-1050
[39.]
M.A. Khan.
HLA-B27 polymorphism and association with disease.
J Rheumatol, 27 (2000), pp. 1110-1114
[40.]
Y. Almanos, N.G. Papadopoulos, P.V. Voulgari, A. Karakatsanis, C. Siozos, A.A. Drossos.
Epidemiology of ankylosing spondylitis in Northwest Greece, 1983-2002.
Rheumatology, 43 (2004), pp. 615-618
[41.]
E.K. Gunal, F.O. Sarvan, S. Kamali, A. Gul, M. Inanc, M. Carin.
Low frequency of HLA-B27 in ankylosing spondylitis patients from Turkey.
Joint Bone Spine, 75 (2008), pp. 299-302
[42.]
J.L. Fernandez-Sueiro, C. Alonso, F.J. Blanco, M. Rodriguez-Gomez, F. Galdo, M.A. Gonzalez-Gay.
Prevalence of HLA-B27 and subtypes of HLA-B27 associated with ankylosing spondylitis in Galicia, Spain.
Clin Exp Rheumatol, 22 (2004), pp. 465-468
[43.]
M.A. Khan.
HLA System in Biology and Medicine: A Resource Book.
Jaypee Brothers Medical Publishers, (2010), pp. 422-446
[44.]
M.A. Brown, G.L. Kennedy, C. Darke, K. Gibson, K.D. Pile, J.L. Shatford, et al.
The effect of HLA-DR genes on susceptibility to and severity of ankylosing spondylitis.
[45.]
W. Miehle, M. Schattenkirchner, D. Albert, M. Bunge.
HLA-DR4 in ankylosing spondylitis with different patterns of joint involvement.
Ann Rheum Dis, 44 (1985), pp. 39-44
[46.]
W.P. Robinson, S.M. Van Der Linden, M.A. Khan, H.U. Rentsch, A. Cats, A. Russell, et al.
HLA-Bw60 increases susceptibility to ankylosing spondylitis in HLA-B27 patients.
Arthritis Rheum, 32 (1989), pp. 1135-1141
[47.]
M.D. De Juan, A. Reta, J. Cancio, J. Belzunegui, E. Cuadrado.
HLA-A*9 a probable secondary susceptibility marker to ankylosing spondylitis in Basque patients.
Tissue Antigens, 53 (1999), pp. 161-166
[48.]
G. Vargas Alarcon, J.D. Londoño, G. Hernandez Pacheco, C. Pacheco Tena, E. Castillo, M.H. Cardiel.
Effect of HLA-DR genes on susceptibility to and severity of spondyloarthropathies in Mexican patients.
Ann Rheum Dis, 61 (2002), pp. 714-717
[49.]
G. Vargas-Alarcón, A. García, S. Bahena, H. Melín-Aldana, F. Andrade, G Ibañez-de-Kasep, et al.
HLAB and complotypes in Mexican patients with seronegative spondyloarthropathies.
Ann Rheum Dis, 53 (1994), pp. 755-758
[50.]
H. Mielants, E.M. Veys, R. Joos, L. Noens, C. Cuvelier, M. De Vos.
HLA antigens in seronegative spondyloarthropathies: reactive arthritis and arthritis in ankylosing spondylitis: relation to gut inflammation.
J Rheumatol, 14 (1987), pp. 466-471
[51.]
M. Siala, N. Mahfoudh, H. Fourati, R. Gdoura, M. Younes, A. Kammoun.
MHC class I and class II genes in Tunisian patients with reactive and undifferentiated arthritis.
Clin Exp Rheum, 27 (2009), pp. 208-213
[52.]
M. Kchir, W. Hamdi, L. Laadhar, S. Kochbati, D. Kaffel, K. Saadellaoui.
HLA-B D.R. DQ antigens polymorphism in Tunisian patients with ankylosing spondylitis (a case-control study).
Rheumatol Int, 30 (2010), pp. 933-939
[53.]
B. Silva-Ramirez, G. Vargas-Alarcon, J. Granados, Burgos-Vargas R.
HLA antigens and juvenile onset spondyloarthritides: negative association with non-B27 alleles.
Clin Exp Rheumatol, 23 (2005), pp. 721-723
[54.]
A. Yamaguchi, N. Tsuchiva, H. Mitsui, et al.
Association of HLA-B39 with HLA-B27 negative ankylosing spondylitis and pauciarticular juvenile rheumatoid polyarthritis in Japanese patients.
Arthritis Rheum, 38 (1995), pp. 1672-1677
[55.]
W.P. Robinson, S.M. van der Linden, M.A. Khan, et al.
HLA-BW60 increases susceptibility to ankylosing spondylitis in HLA-B27+ patients.
Arthritis Rheum, 32 (1989), pp. 1135-1141
[56.]
M.A. Brown, K.D. Pile, L.G. Kennedy, A. Calin, C. Darke, J. Bell, et al.
HLA class I associations of ankylosing spondylitis in the white population in the United Kingdom.
Ann Rheum Dis, 55 (1996), pp. 268-270
[57.]
J.C. Wei, W.C. Tsai, H.S. Lin, C.Y. Tsai, C.T. Chou.
HLAB60 B61 are strongly associated with ankylosing spondylitis in HLA-B27-negative Taiwan Chinese patients.
Rheumatology, 43 (2004), pp. 839-842
[58.]
J.D. Londoño, L. González, L. Ramírez, P. Santos, M. Ávila, A.M. Santos.
Caracterización de las espondiloartropatías y determinación de factores de mal pronóstico en una población de pacientes colombianos.
Rev Col Reum, 12 (2005), pp. 195-197
[59.]
J. Márquez, L. Pinto, D. Candia, M. Restrepo, E. Uribe, O. Rincón, et al.
Espondiloartritis en el Hospital Pablo Tobón Uribe. Descripción de una cohorte.
Rev Col Reum, 17 (2010), pp. 80-85

Grupo de Espondiloartritis. Servicio Reumatología e Inmunología. Hospital Militar Central. Universidad de la Sabana. Bogotá. Transversal 3 # 49-00 Tercer Piso. Teléfono 0571-3486868 Ext. 5050.

Los autores declaran no presentar ningún conflicto de interés al momento de la redacción del manuscrito.

Copyright © 2011. Asociación Colombiana de Reumatología
Download PDF
Article options