title: PlA1/A2 polymorphism of the platelet glycoprotein receptor IIIA and risk of cranial ischemic complications in giant cell arteritis.
abstract: OBJECTIVE
  To investigate potential associations of the PlA1/A2 polymorphism of the platelet glycoprotein IIIa (GPIIIa) gene with susceptibility to, and clinical expression of, giant cell arteritis (GCA).
  
  
  METHODS
  One hundred forty patients with biopsy-proven GCA who were residents of Reggio Emilia, Italy, and 241 population-based healthy controls from the same geographic area were genotyped for the PlA1/A2 polymorphism of the platelet GPIIIa gene by molecular methods. The patients were divided into subgroups according to the presence or absence of polymyalgia rheumatica and cranial ischemic complications. The distribution of the PlA1/A2 genotype was investigated, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.
  
  
  RESULTS
  The distribution of the PlA1/A2 genotype differed significantly between GCA patients with and those without visual loss caused by anterior ischemic optic neuritis (P = 0.016, corrected P [P(corr)] = 0.048). The PlA2 allele was found significantly more frequently in GCA patients with anterior ischemic optic neuritis than in those without anterior ischemic optic neuritis (P = 0.023, P(corr) = 0.046, OR 2.4 [95% CI 1.2-4.8]). Homozygosity for the PlA2 allele was significantly more frequent among GCA patients with anterior ischemic optic neuritis than among those without (P = 0.019, P(corr) = 0.038, OR 7.1 [95% CI 1.64-30.6]). Cranial ischemic complications occurred in 8 of 19 patients (42.1%) receiving antiplatelet therapy, compared with 22 of 118 patients (18.6%) not receiving such therapy (P = 0.03, OR 3.2 [95% CI 1.1-8.8]).
  
  
  CONCLUSIONS
  Our findings show that A2/A2 homozygosity is associated with an increased risk of visual loss due to anterior ischemic optic neuritis in GCA patients. Antiplatelet therapy, however, was not effective in reducing the risk of ischemic events in this population of GCA patients.
authors: Arcispedale S. Maria Nuova, Reggio Emilia, Italy. salvarani.carlo@asmn.re.it
authors: Carlo
authors: C
authors: Salvarani
authors: Bruno
authors: B
authors: Casali
authors: Enrico
authors: E
authors: Farnetti
authors: Nicolò
authors: N
authors: Pipitone
authors: Debora
authors: D
authors: Formisano
authors: Davide
authors: D
authors: Nicoli
authors: PierLuigi
authors: P
authors: Macchioni
authors: Luca
authors: L
authors: Cimino
authors: GianLuigi
authors: G
authors: Bajocchi
authors: Maria
authors: M
authors: Grazia Catanoso
authors: Giovanna
authors: G
authors: Restuccia
authors: Alessandra
authors: A
authors: Ghinoi
authors: Luigi
authors: L
authors: Boiardi
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D002545:Brain Ischemia / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D013700:Giant Cell Arteritis / Q000150:complications / Q000235:genetics* / Q000473:pathology; D006720:Homozygote; D006801:Humans; D039661:Integrin beta3 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009902:Optic Neuritis / Q000235:genetics; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: C061248:ITGB3 protein, human; D039661:Integrin beta3