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THU0005 Increased frequency of hla dr 11 and decreased frequency of hla dr 1 in caucasian europeans with abdominal aortic aneurysms
  1. A Schmarda1,
  2. H Schennach1,
  3. P Klein-Weigel2,
  4. C Goldberger3,
  5. D Schönitzer1,
  6. KP Pfeiffer4,
  7. G Fraedrich2,
  8. M Schirmer3
  1. 1Central Institute for Blood Transfusion
  2. 2Vascular Surgery
  3. 3Internal Medicine
  4. 4Biostatistics, Innsbruck University Hospital, Innsbruck, Austria


Background A genetic predisposition has been reported to play a key role in the pathogenesis of abdominal aortic aneurysms (AAA) in Japanese and a subgroup of North American patients with inflammatory AAA.

Objectives The aim of this study was to evaluate a possible association of HLA DR phenotypes with AAA in a European population sample.

Methods Consecutive patients with AAA larger than 3 cm presenting at our outpatient clinic were analysed for HLA class II genotypes using the PCR-SSP technique at low resolution level. DR phenotypes were deduced from these results. Patients with any history of an autoimmune disease were excluded from the study. The frequencies of HLA DR phenotypes were compared to those of a cohort of consecutive and ethnically matched organ donors using the appropriate statistical methods. Classification trees have been applied to increase the predictive value and to consider more than one variable.

Results HLA DR genotyping was performed in 54 European AAA patients (44 males) and 296 controls (203 males). At the HLA DRB1* locus, 19/54 AAA patients (35,2%) and 63/296 controls (21,3%) were found to be 1*11 positive (p = 0,035; OR = 2,01, 95% c.i.: 1,08–3,75). Subanalysis of male patients revealed 17/44 (38,6%) AAA patients and 39/203 (19,2%) in controls to be 1*11 positive (p = 0,009; OR = 2,65, 95% c.i.: 1,31–5,33). Regarding HLA DRB1*01, 4/54 AAA patients (7,4%) and 64/296 controls (21,6%) turned out to be 1*01 carrier (p = 0,014; OR = 0,29, 95% c.i.: 0,10–0,83). Subanalysis of male patients revealed 2/44 (4,5%) and 48/203 (23,6%) DRB1*01 carrier in AAA patients and controls, respectively (p = 0,003; OR = 0,15, 95% c.i.: 0,04–0,66). No associations for DRB1*11 and 1*01 were observed in female patients.

Conclusion These data suggest a positive association between AAA and DR 11 and a possible protective effect of DR 1 in male Caucasian Europeans suffering from AAA. This finding supports the hypothesis that MHC class II genes play a role in the pathogenesis of AAA.

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