title: Investigation of platelet glycoprotein IIIa polymorphism using flow cytometry in patients with rheumatoid arthritis.
abstract: OBJECTIVE
  Previous work has shown that the human platelet antigen (HPA) 1b polymorphism of platelet glycoprotein IIIa (GPIIIa) is implicated in the development of ischaemic vascular disease. HPA1b positive platelets have a lower threshold for activation and may exert a greater thrombotic tendency than those without the 1b allele. However, platelets heterozygous for the polymorphism are also more sensitive to aspirin than those homozygous for the 1b allele, which have a similar sensitivity to those without the 1b allele. A flow cytometric method has become available to identify this polymorphism. The aim of our study was to evaluate the use of this assay in patients with rheumatoid arthritis (RA) and to determine the incidence of the 1b allele in these patients. We also compared platelet aggregation and platelet/white blood cell interaction in patients with or without this polymorphism.
  
  
  METHODS
  We enrolled 99 patients and measured platelet aggregation in whole blood and platelet-rich plasma (prp), platelet/white blood cell interaction and C-reactive protein (CRP).
  
  
  RESULTS
  Thirty-four of the 99 patients were unsuitable for analysis because their baseline expression of GPIIIa was outwith the normal range, making the results outwith the limits of the flow cytometric method. The incidence of the 1b allele in the patients was 29%, with incidence being higher in females, although this failed to reach statistical significance. The number of circulating platelet aggregates and adenosine diphosphate (ADP)-induced aggregation in prp was significantly higher in those patients with the 1b allele.
  
  
  CONCLUSIONS
  This method may be of use as an initial screening test.
authors.affiliation: Vascular Diseases Research Unit, The Institute of Cardiovascular Research, Department of Medicine, Ninewells Hospital and Medical School, Dundee, Scotland, UK. m.mclaren@dundee.ac.uk
authors.forename: M
authors.initials: M
authors.lastname: McLaren
authors.forename: A
authors.initials: A
authors.lastname: Waring
authors.forename: B
authors.initials: B
authors.lastname: Galarraga
authors.forename: A
authors.initials: A
authors.lastname: Rudd
authors.forename: K
authors.initials: K
authors.lastname: Morley
authors.forename: J J F
authors.initials: JJ
authors.lastname: Belch
mesh_terms: D000328:Adult; D000368:Aged; D016824:Antigens, Human Platelet / Q000097:blood / Q000235:genetics*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000453:epidemiology / Q000235:genetics*; D001792:Blood Platelets / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D039661:Integrin beta3 / Q000097:blood / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000235:genetics; D011110:Polymorphism, Genetic; D015995:Prevalence
chemical_list: D016824:Antigens, Human Platelet; D039661:Integrin beta3; C083451:human platelet antigen 1b; D002097:C-Reactive Protein