PMID- 12920695
OWN - NLM
STAT- MEDLINE
DCOM- 20031216
LR  - 20111117
IS  - 0049-0172 (Print)
IS  - 0049-0172 (Linking)
VI  - 33
IP  - 1
DP  - 2003 Aug
TI  - Genetic markers of disease susceptibility and severity in giant cell arteritis 
      and polymyalgia rheumatica.
PG  - 38-48
AB  - BACKGROUND AND OBJECTIVES: Giant cell arteritis (GCA) and polymyalgia rheumatica 
      (PMR) are common and often overlapping diseases that generally occur in elderly 
      patients. In this article, we examine the role of different genes as markers of 
      disease susceptibility and severity in GCA and PMR. METHODS: The influence of 
      human leukocyte antigen (HLA)-DRB1 and tumor necrosis factor alleles, as well as 
      the different allelic polymorphisms, on the susceptibility and severity to GCA 
      and PMR was examined. A review of the literature was conducted. RESULTS: Most 
      studies have described an association of GCA with HLA-DRB1(*)04 alleles. However, 
      HLA-DRB1 association in patients with PMR varies from one population to another. 
      In Northwest Spain, patients with GCA and PMR exhibited different tumor necrosis 
      factor microsatellite polymorphism associations. Studies of intercellular 
      adhesion molecule-1 biallelic polymorphisms have yielded contradictory results. 
      Interleukin 1 cluster and tumor necrosis factor alpha polymorphisms increased 
      susceptibility to GCA and PMR slightly. In Northwest Spain, interleukin 6 
      promoter polymorphism at position -174 modulated the phenotypic expression of PMR 
      in biopsy-proven GCA. In the same population, regulated upon activation, normal T 
      cell expressed and presumably secreted gene promoter biallelic polymorphism at 
      position -403 was a marker for PMR susceptibility but not for GCA, and 
      corticotropin-releasing hormone polymorphism appeared to be implicated in the 
      risk of severe ischemic complications in patients with GCA. CONCLUSIONS: The 
      present analysis confirms that GCA and PMR are polygenic diseases. The search for 
      additional genes is necessary to better understand the pathogenesis of these 
      conditions.
CI  - Copyright 2003 Elsevier Inc. All rights reserved.
FAU - Gonzalez-Gay, Miguel A
AU  - Gonzalez-Gay MA
AD  - Division of Rheumatology, Hospital Xeral Calde, Lugo, Spain. 
      miguelaggay@hotmail.com
FAU - Amoli, Mahsa M
AU  - Amoli MM
FAU - Garcia-Porrua, Carlos
AU  - Garcia-Porrua C
FAU - Ollier, William E r
AU  - Ollier WE
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Genetic Markers)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DRB1 Chains)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Genetic Markers
MH  - *Genetic Predisposition to Disease
MH  - Giant Cell Arteritis/*genetics
MH  - HLA-DR Antigens/genetics
MH  - HLA-DRB1 Chains
MH  - Polymorphism, Genetic
MH  - Polymyalgia Rheumatica/*genetics
MH  - Tumor Necrosis Factor-alpha/genetics
RF  - 96
EDAT- 2003/08/16 05:00
MHDA- 2003/12/17 05:00
CRDT- 2003/08/16 05:00
PHST- 2003/08/16 05:00 [pubmed]
PHST- 2003/12/17 05:00 [medline]
PHST- 2003/08/16 05:00 [entrez]
AID - S0049017203500348 [pii]
AID - 10.1053/sarh.2002.50025 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2003 Aug;33(1):38-48. doi: 10.1053/sarh.2002.50025.