PMID- 11436079
OWN - NLM
STAT- MEDLINE
DCOM- 20010809
LR  - 20121003
IS  - 0741-5214 (Print)
IS  - 0741-5214 (Linking)
VI  - 34
IP  - 1
DP  - 2001 Jul
TI  - Genetic similarity in inflammatory and degenerative abdominal aortic aneurysms: a 
      study of human leukocyte antigen class II disease risk genes.
PG  - 84-9
AB  - PURPOSE: Clinically, abdominal aortic aneurysms (AAAs) display a spectrum of 
      inflammation that extends from apparently noninflamed (degenerative) AAAs to the 
      classic inflammatory variant. Genes encoded in the human leukocyte antigen (HLA) 
      region are important in the development of both variants of AAA; however, their 
      role in progression to the inflammatory variant is unknown. The purpose of this 
      study was to compare HLA class II genes in patients with degenerative versus 
      classic inflammatory AAAs and to quantify their impact as disease risk factors. 
      METHODS: Genotypes of the 12 major alleles of the HLA-DR B1 locus were determined 
      in patients with degenerative (102) and inflammatory (40) AAAs who were compared 
      with controls (118). Univariate and multivariate logistic regression analyses 
      were used to determine allele distributions and to quantify disease risk. 
      RESULTS: Distribution of the HLA-DR B1 alleles was nonrandom and similar in both 
      degenerative and inflammatory AAA groups compared with controls. The B1*02 and 
      B1*04 alleles were enhanced in both degenerative (39.2% vs. 25.4%, P =.03; and 
      35.3% vs. 24.6%, P =.08 respectively) and inflammatory (47.5% vs. 25.4%, P =.01; 
      and 32.5% vs. 24.6%, P =.09, respectively) AAAs compared with controls. The B1*02 
      and B1*04 alleles were associated with risk for both degenerative (odds ratio 
      [OR] 2.2; 95% CI, 1.2-4.0; and OR 2.0; 95% CI, 1.1-3.7, respectively) and 
      inflammatory AAAs (OR 3.7; 95% CI, 1.8-8.6; and OR 2.5; 95% CI, 1.1-6.1). 
      CONCLUSION: This study demonstrates that identical HLA alleles function as 
      genetic risk factors for both inflammatory and degenerative AAAs. These results 
      support the concept of a common, immune-mediated pathogenesis for AAAs that may 
      be modulated by HLA-independent factors.
FAU - Rasmussen, T E
AU  - Rasmussen TE
AD  - Division of Vascular Surgery, Mayo Clinic and Mayo Medical School, Rochester, MN 
      55905, USA.
FAU - Hallett, J W Jr
AU  - Hallett JW Jr
FAU - Schulte, S
AU  - Schulte S
FAU - Harmsen, W S
AU  - Harmsen WS
FAU - O'Fallon, W M
AU  - O'Fallon WM
FAU - Weyand, C M
AU  - Weyand CM
LA  - eng
GR  - R01-AI-44142/AI/NIAID NIH HHS/United States
GR  - R01-AR-42527/AR/NIAMS NIH HHS/United States
GR  - R01-EY11916/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Vasc Surg
JT  - Journal of vascular surgery
JID - 8407742
RN  - 0 (HLA-DR Antigens)
SB  - IM
MH  - Aged
MH  - Aortic Aneurysm, Abdominal/*genetics/pathology
MH  - Female
MH  - HLA-DR Antigens/*genetics
MH  - Humans
MH  - Inflammation/genetics
MH  - Male
MH  - Risk Factors
EDAT- 2001/07/04 10:00
MHDA- 2001/08/10 10:01
CRDT- 2001/07/04 10:00
PHST- 2001/07/04 10:00 [pubmed]
PHST- 2001/08/10 10:01 [medline]
PHST- 2001/07/04 10:00 [entrez]
AID - S0741-5214(01)74934-8 [pii]
AID - 10.1067/mva.2001.115603 [doi]
PST - ppublish
SO  - J Vasc Surg. 2001 Jul;34(1):84-9. doi: 10.1067/mva.2001.115603.