title: Association of haptoglobin genotype and common cardiovascular risk factors with the amount of iron in atherosclerotic carotid plaques.
abstract: BACKGROUND
  The aim of this study was to evaluate the iron burden of carotid atherosclerotic plaques removed from patients treated for carotid disease and find any relation with haptoglobin genotype and other common cardiovascular risk factors.
  
  
  METHODS
  Consecutive patients undergoing carotid endarterectomy were included in the study. All patients had high-grade carotid stenosis (>70%). The clinical characteristics and serum parameters of the study population were recorded and the haptoglobin genotype was determined. The presence of hemosiderin deposits in the plaques was identified using Perl's stain on adjacent serial sections.
  
  
  RESULTS
  70 specimens were processed for histologic examination: 27 plaques from diabetic patients (16 with the Hp 1-1 or 2-1 genotype and 11 with the Hp 2-2 genotype) and 43 plaques from non diabetic patients (20 with the Hp 1-1 or 2-1 genotype and 23 with the Hp 2-2 genotype). In plaques from diabetic patients the density of Perl's iron stain was significantly higher in the Hp 2-2 group compared with that in the Hp 1-1 or 2-1 group (p = 0.008). The correlation and regression analysis of all possible clinical and laboratory predictors of intraplaque iron deposition showed that four factors were independently associated with intraplaque iron deposition: male gender, serum homocysteine, Hp 2-2 genotype and diabetes mellitus treatment.
  
  
  CONCLUSIONS
  Male diabetic patients with increased plasma levels of homocysteine and the Hp 2-2 genotype had higher carotid plaque iron deposition. Current evidence and pathophysiological considerations suggest that the increased intraplaque iron deposition may be associated with increased oxidative stress, affecting the stability of the carotid plaque.
authors.affiliation: Department of Vascular Surgery, Red Cross Hospital of Athens, Greece. christoslioupis@yahoo.gr
authors.forename: Christos
authors.initials: C
authors.lastname: Lioupis
authors.forename: Calypso
authors.initials: C
authors.lastname: Barbatis
authors.forename: Aggeliki
authors.initials: A
authors.lastname: Drougou
authors.forename: Vasiliki
authors.initials: V
authors.lastname: Koliaraki
authors.forename: Avgi
authors.initials: A
authors.lastname: Mamalaki
authors.forename: Christos
authors.initials: C
authors.lastname: Klonaris
authors.forename: Sotirios
authors.initials: S
authors.lastname: Georgopoulos
authors.forename: Vasilios
authors.initials: V
authors.lastname: Andrikopoulos
authors.forename: Elias
authors.initials: E
authors.lastname: Bastounis
mesh_terms: D000368:Aged; D002318:Cardiovascular Diseases / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D016893:Carotid Stenosis / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D003920:Diabetes Mellitus / Q000188:drug therapy; D016894:Endarterectomy, Carotid; D005260:Female; D020022:Genetic Predisposition to Disease; D006115:Greece; D006242:Haptoglobins / Q000235:genetics*; D006485:Hemosiderin / Q000032:analysis; D006710:Homocysteine / Q000097:blood; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000150:complications; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007501:Iron / Q000032:analysis*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D010641:Phenotype; D058226:Plaque, Atherosclerotic / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D012737:Sex Factors; D013194:Staining and Labeling
chemical_list: C485359:HP protein, human; D006242:Haptoglobins; D007004:Hypoglycemic Agents; D006710:Homocysteine; D006485:Hemosiderin; D007501:Iron