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Aetiopathogenesis

 

The presence of both HLA-DRB1*04:01 and HLA-B*15:01 increases the susceptibility to cranial and extracranial giant cell arteritis


1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22

 

  1. Department of Rheumatology, Hospital Universitario Marqués de Valdecilla, Santander, and Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, IDIVAL, Santander, Spain.
  2. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, IDIVAL, Santander, Spain.
  3. Department of Immunology, Hospital Universitario Marqués de Valdecilla, Santander, Spain.
  4. Department of Rheumatology, Hospital Universitario Marqués de Valdecilla, Santander, and Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, IDIVAL, Santander, Spain.
  5. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, IDIVAL, Santander, Spain.
  6. Department of Rheumatology, Hospital Universitario Virgen del Rocío, Sevilla, Spain.
  7. Department of Rheumatology, Hospital Universitario y Politécnico La Fe, Valencia, Spain.
  8. Department of Rheumatology, Complejo Hospitalario Universitario Pontevedra, Spain
  9. Department of Rheumatology, Complejo Asistencial Universitario de León, Spain.
  10. Department of Rheumatology, Hospital Universitario de Basurto, Bilbao, Spain.
  11. Department of Rheumatology, Hospital Universitario de Basurto, Bilbao, Spain.
  12. Autoimmune Diseases Unit, Hospital Universitario San Cecilio, Instituto de Investigación Biosanitaria de Granada (IBS Granada), Department of Internal Medicine, University of Granada, Spain.
  13. Department of Rheumatology, Hospital Universitario San Agustín, Avilés, Spain.
  14. Division of Rheumatology, Hospital Universitario Lucus Augusti, Lugo, Spain.
  15. Department of Rheumatology, Hospital Universitario de la Princesa, IIS-Princesa, Cátedra EPID Future, Universidad Autónoma de Madrid (UAM), Madrid, Spain.
  16. School of Medicine, Universidad de Cantabria, Santander, Spain.
  17. Department of Rheumatology, Hospital Universitario Marqués de Valdecilla, Santander, and Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, IDIVAL, Santander, Spain.
  18. Health Research Institute of Santiago, and The NEIRID Group (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
  19. Instituto de Parasitología y Biomedicina ‘López-Neyra’, CSIC, PTS Granada, Spain.
  20. Department of Rheumatology, Hospital Universitario de la Princesa, IIS-Princesa, Cátedra EPID Future, Universidad Autónoma de Madrid (UAM), Madrid, Spain.
  21. Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, IDIVAL, Santander, Spain.
  22. Department of Rheumatology, Hospital Universitario Marqués de Valdecilla, Santander; Research Group on Genetic Epidemiology and Atherosclerosis in Systemic Diseases and in Metabolic Bone Diseases of the Musculoskeletal System, IDIVAL, Santander; School of Medicine, Universidad de Cantabria, Santander, Spain; and Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. miguelaggay@hotmail.com

CER14266
2021 Vol.39, N°2 ,Suppl.129
PI 0021, PF 0026
Aetiopathogenesis

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PMID: 33734973 [PubMed]

Received: 25/11/2020
Accepted : 01/02/2021
In Press: 18/03/2021
Published: 19/05/2021

Abstract

OBJECTIVES:
To determine if patients with the predominant extracranial large-vessel-vasculitis (LVV) pattern of giant cell arteritis (GCA) have a distinctive HLA-B association, different from that reported in biopsy-proven cranial GCA patients. In a further step we assessed if the combination of HLA-B and HLA-DRB1 alleles confers an increased risk for GCA susceptibility, either for the cranial and extracranial LVV phenotypes.
METHODS:
A total of 184 patients with biopsy-proven cranial GCA, 105 with LVV-GCA and 486 healthy controls were included in our study. We compared HLA-B phenotype frequencies between the three groups.
RESULTS:
HLA-B*15 phenotype was significantly increased in patients with classic cranial GCA compared to controls (14.7% versus 5.8%, respectively; p<0.01; OR [95% CI] =2.81 [1.54-5.11]). It was mainly due to the HLA-B*15:01 allele (12.5% versus 4.0%, respectively; p<0.01; OR [95% CI] =3.51 [1.77-6.99]) and remained statistically significant after Bonferroni correction. Similar HLA-B*15 association was observed in patients with the LVV-GCA (11.4% versus 5.8%, p=0.04, OR [95% CI] =2.11 [1.04-4.30]). This association was also mainly due to the HLA-B*15:01 allele (10.5% versus 4.0%, respectively; p=0.0054; OR [95% CI] =2.88 [1.19-6.59]). Noteworthy, the presence of HLA-B*15:01 together with HLA-DRB1*04:01 led to an increased risk of developing both cranial and extracranial LVV-GCA.
CONCLUSIONS:
Susceptibility to GCA is strongly related to the HLA region, regardless of the clinical phenotype of expression of the disease.

Rheumatology Article