Arthritis & Rheumatism, Volume 63,
November 2011 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Chicago, Illinois November 4-9, 2011.


CC Chemokine Receptor 5 Polymorphism in Behet's Disease.

Atzeni1,  Fabiola, Boiardi2,  Luigi, Casali3,  Bruno, Farnetti3,  Enrico, Sarzi-Puttini1,  Piercarlo, Pipitone2,  Nicolo, Olivieri4,  Ignazio

Rheumatology Unit, L. Sacco University Hospital of Milan, Milan, Italy
Ospedale Santa Chiara, Trento
Arcispedale S Maria Nuova, Reggio Emilia, Italy
Molecular Biology Laboratory, Arcispedale S. Maria Nuova,, Reggio Emilia, Italy
Rheumatology Department of Lucania, San Carlo Hospital of Potenza and Madonna delle Grazie Hospital of Matera, Potenza, Italy
Stabilimento Ospedaliero Misericordia, Prato, Italy
Dept. of Neurological Sciences, Ospedale Bellaria,, Bologna, Italy
Chair of Rheumatology, University of Ferrara,, Ferrara, Italy
Rheumatology Unit, University of Palermo, Palermo, Italy
Rheumatology Unit, Ospedale Niguarda,, Milan, Italy

Background/Purpose:

Behçet's disease (BD) is a primary systemic vasculitis characterised by oral and genital ulcerations associated with other clinical manifestations, such as skin lesions, uveitis and thrombosis. The aim of this study was to evaluate potential associations of CC chemokine receptor 5 (CCR5)D32 polymorphism with BD and disease expression.

Methods:

One hundred and ninety-six consecutive Italian patients satisfying the International Study Group criteria for BD followed up for seven years and 180 healthy controls were genotyped for CCR5D32 polymorphism by molecular methods. The patients were grouped on the basis of the presence or absence of clinical manifestations. The diagnoses of deep venous thrombosis (DVT) and superficial thrombophlebitis (ST) were initially made clinically, and then confirmed by means of ultrasonography or contrast venography.

Results:

The distribution of the CCR5D32 genotype was not significantly different in the BD patients and healthy controls (p corr = 0.072), but the CCR5D32 allele was more frequent in BD than in controls (p corr = 0.004, odds ratio [OR] 3.1, 95% CI 1.5–6.7). Carriers of the CCR5D32 allele (D 32/ D 32 + CCR5/DC32] were significantly more frequent in BD patients than in controls (p corr = 0.024, OR 2.37, 95% CI 1.1–5.1).

The CCR5D32 polymorphism was found more frequently in the BD patients with ST than in the controls (25.0% vs 5.6%, P=0.009), whereas there was no significant difference between BD patients with and without ST (25.0% vs 10.8%, P=0.07). There was no other significant association between clinical manifestations (including DVT) and the CCR5D32 polymorphism in the BD patients.

Conclusion:

The CCR5D32 polymorphism might be associated with an increased risk of developing BD. Chemokines may have a role in the pathophysiology of BD and in the development of ST.

To cite this abstract, please use the following information:
Atzeni, Fabiola, Boiardi, Luigi, Casali, Bruno, Farnetti, Enrico, Sarzi-Puttini, Piercarlo, Pipitone, Nicolo, et al; CC Chemokine Receptor 5 Polymorphism in Behet's Disease. [abstract]. Arthritis Rheum 2011;63 Suppl 10 :2390
DOI:

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