title: Polymorphisms of the human platelet antigens HPA-1, HPA-2, HPA-3, and HPA-5 on the platelet receptors for fibrinogen (GPIIb/IIIa), von Willebrand factor (GPIb/IX), and collagen (GPIa/IIa) are not correlated with an increased risk for stroke.
abstract: OBJECTIVE
  A recent study has described a high incidence of the human platelet antigen (HPA)-1b alloantigen in patients with myocardial infarction. We investigated the distribution of gene polymorphisms of platelet glycoproteins (GPs) in patients with cerebrovascular disease (CVD) and stroke. The polymorphic systems we have studied are HPA-1 and HPA-3 on the fibrinogen receptor (GPIIb/IIIa), HPA-2 on the von Willebrand factor receptor (GPIb/IX), and HPA-5 on one of the platelet collagen receptors (GPIa/IIa).
  
  
  METHODS
  DNA was isolated from peripheral blood collected from 218 consecutive stroke patients, 165 neurological inpatients without signs of CVD, and 321 healthy blood donors. The genotypes of HPA-1, HPA-2, HPA-3, and HPA-5 were determined by sequence specific primer polymerase chain reactions.
  
  
  RESULTS
  The calculated allele frequencies were as follows: for CVD patients, HPA-1a/b 0.81/0.19, HPA-2a/b 0.91/0.09, HPA-3a/b 0.61/0.39, and HPA-5a/b 0.92/0.08; for inpatient HPA-1a/b 0.83/0.17, HPA-2a/b 0.91/0.09, HPA-3a/b 0.62/0.3 and HPA-5a/b 0.93/0.07; and for blood donors, HPA-1a 0.85/0.15, HPA-2a/b 0.94/0.06, HPA-3a/b 0.60/0.40, and HPA 5a/b 0.92/0.08. There were no statistically significant difference for the analyzed HPA polymorphism frequencies either between the CVD patients and the non-CVD inpatients or the CVD patients and blood donors. However, the HPA-1b genotype was slightly more frequent in patients (CVD and non-CVD) than in the healthy blood donors.
  
  
  CONCLUSIONS
  Our results indicate that the HPA-1, HPA-2, HPA-3, and HPA-5 polymorphisms are not associated with an increased risk for stroke.
authors.affiliation: Departments of Immunology and Transfusion Medicine, Ernst-Moritz-Arndt-University, Greifswald, Germany.
authors.forename: L E
authors.initials: LE
authors.lastname: Carlsson
authors.forename: A
authors.initials: A
authors.lastname: Greinacher
authors.forename: C
authors.initials: C
authors.lastname: Spitzer
authors.forename: R
authors.initials: R
authors.lastname: Walther
authors.forename: C
authors.initials: C
authors.lastname: Kessler
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D015703:Antigens, CD / Q000235:genetics* / Q000378:metabolism; D016824:Antigens, Human Platelet / Q000235:genetics* / Q000276:immunology; D001792:Blood Platelets / Q000737:chemistry; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000235:genetics; D002561:Cerebrovascular Disorders / Q000453:epidemiology / Q000235:genetics*; D003094:Collagen / Q000235:genetics / Q000378:metabolism; D000939:Epitopes / Q000235:genetics / Q000276:immunology; D005260:Female; D005838:Genotype; D006801:Humans; D039421:Integrin alpha2; D039661:Integrin beta3; D008297:Male; D008875:Middle Aged; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000235:genetics*; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000235:genetics* / Q000378:metabolism; D011110:Polymorphism, Genetic; D012307:Risk Factors; D014841:von Willebrand Factor / Q000235:genetics / Q000378:metabolism
chemical_list: C071221:2b alloantigen, human; C044561:3a alloantigen, human; C071092:5a alloantigen, human; D015703:Antigens, CD; D016824:Antigens, Human Platelet; D000939:Epitopes; C061248:ITGB3 protein, human; D039421:Integrin alpha2; D039661:Integrin beta3; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019038:Platelet Glycoprotein GPIb-IX Complex; D014841:von Willebrand Factor; D003094:Collagen