P1A1/A2 polymorphism of the platelet glycoprotein receptor IIIa and risk of cranial ischemic complications in giant cell arteritis

Carlo Salvarani, Bruno Casali, Enrico Farnetti, Nicolò Pipitone, Debora Formisano, Davide Nicoli, Pierluigi Macchioni, Luca Cimino, GianLuigi Bajocchi, Maria Grazia Catanoso, Giovanna Restuccia, Alessandra Ghinoi, Luigi Boiardi

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Abstract

Objective. To investigate potential associations of the P1A1/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 P1A1/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 P1A1/A2 genotype was investigated, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Results. The distribution of the P1A1/A2 genotype differed significantly between GCA patients with and those without visual loss caused by anterior ischemic optic neuritis (P = 0.016, corrected P [Pcorr] = 0.048). The P1A2 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, Pcorr = 0.046, OR 2.4 [95% CI 1.2-4.8]). Homozygosity for the P1A2 allele was significantly more frequent among GCA patients with anterior ischemic optic neuritis than among those without (P = 0.019, Pcorr = 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]). Conclusion. 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.

Original languageEnglish
Pages (from-to)3502-3508
Number of pages7
JournalArthritis and Rheumatism
Volume56
Issue number10
DOIs
Publication statusPublished - Oct 2007

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Integrin beta3
Giant Cell Arteritis
varespladib methyl
Optic Neuritis
Odds Ratio
Confidence Intervals
Alleles
Genotype
Polymyalgia Rheumatica
Italy
Population
Genes
Therapeutics
Biopsy

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

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P1A1/A2 polymorphism of the platelet glycoprotein receptor IIIa and risk of cranial ischemic complications in giant cell arteritis. / Salvarani, Carlo; Casali, Bruno; Farnetti, Enrico; Pipitone, Nicolò; Formisano, Debora; Nicoli, Davide; Macchioni, Pierluigi; Cimino, Luca; Bajocchi, GianLuigi; Catanoso, Maria Grazia; Restuccia, Giovanna; Ghinoi, Alessandra; Boiardi, Luigi.

In: Arthritis and Rheumatism, Vol. 56, No. 10, 10.2007, p. 3502-3508.

Research output: Contribution to journalArticle

Salvarani, C, Casali, B, Farnetti, E, Pipitone, N, Formisano, D, Nicoli, D, Macchioni, P, Cimino, L, Bajocchi, G, Catanoso, MG, Restuccia, G, Ghinoi, A & Boiardi, L 2007, 'P1A1/A2 polymorphism of the platelet glycoprotein receptor IIIa and risk of cranial ischemic complications in giant cell arteritis', Arthritis and Rheumatism, vol. 56, no. 10, pp. 3502-3508. https://doi.org/10.1002/art.22922
Salvarani, Carlo ; Casali, Bruno ; Farnetti, Enrico ; Pipitone, Nicolò ; Formisano, Debora ; Nicoli, Davide ; Macchioni, Pierluigi ; Cimino, Luca ; Bajocchi, GianLuigi ; Catanoso, Maria Grazia ; Restuccia, Giovanna ; Ghinoi, Alessandra ; Boiardi, Luigi. / P1A1/A2 polymorphism of the platelet glycoprotein receptor IIIa and risk of cranial ischemic complications in giant cell arteritis. In: Arthritis and Rheumatism. 2007 ; Vol. 56, No. 10. pp. 3502-3508.
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abstract = "Objective. To investigate potential associations of the P1A1/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 P1A1/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 P1A1/A2 genotype was investigated, and odds ratios (ORs) and 95{\%} confidence intervals (95{\%} CIs) were calculated. Results. The distribution of the P1A1/A2 genotype differed significantly between GCA patients with and those without visual loss caused by anterior ischemic optic neuritis (P = 0.016, corrected P [Pcorr] = 0.048). The P1A2 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, Pcorr = 0.046, OR 2.4 [95{\%} CI 1.2-4.8]). Homozygosity for the P1A2 allele was significantly more frequent among GCA patients with anterior ischemic optic neuritis than among those without (P = 0.019, Pcorr = 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]). Conclusion. 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.",
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T1 - P1A1/A2 polymorphism of the platelet glycoprotein receptor IIIa and risk of cranial ischemic complications in giant cell arteritis

AU - Salvarani, Carlo

AU - Casali, Bruno

AU - Farnetti, Enrico

AU - Pipitone, Nicolò

AU - Formisano, Debora

AU - Nicoli, Davide

AU - Macchioni, Pierluigi

AU - Cimino, Luca

AU - Bajocchi, GianLuigi

AU - Catanoso, Maria Grazia

AU - Restuccia, Giovanna

AU - Ghinoi, Alessandra

AU - Boiardi, Luigi

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N2 - Objective. To investigate potential associations of the P1A1/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 P1A1/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 P1A1/A2 genotype was investigated, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. Results. The distribution of the P1A1/A2 genotype differed significantly between GCA patients with and those without visual loss caused by anterior ischemic optic neuritis (P = 0.016, corrected P [Pcorr] = 0.048). The P1A2 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, Pcorr = 0.046, OR 2.4 [95% CI 1.2-4.8]). Homozygosity for the P1A2 allele was significantly more frequent among GCA patients with anterior ischemic optic neuritis than among those without (P = 0.019, Pcorr = 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]). Conclusion. 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.

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