SPP1 rs9138 variant contributes to the severity of radiological damage in anti-citrullinated protein autoantibody-negative rheumatoid arthritis
| Autor: | Gabriel J. Tobón, Thierry Schaeverbeke, Philippe Dieudé, Steven Gazal, Valérie Devauchelle-Pensec, Pierre-Antoine Juge, Hanna W. van Steenbergen, Bernard Combe, Arnaud Constantin, Annette H M van der Helm-van Mil, Delphine Nigon |
|---|---|
| Přispěvatelé: | Biologie de l'Os et du Cartilage : Régulations et Ciblages Thérapeutiques (BIOSCAR (UMR_S_1132 / U1132)), Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of rheumatology, Leiden University Medical Center (LUMC), Epidémiologie et analyses en santé publique : risques, maladies chroniques et handicaps (LEASP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Immunologie et Pathologie (EA2216), Université de Brest (UBO)-IFR148, Université Paris Diderot - Paris 7 (UPD7), Infection, Anti-microbiens, Modélisation, Evolution (IAME (UMR_S_1137 / U1137)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC), Département de Rhumatologie[Montpellier], Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie, Centre d'Investigation Clinique (CIC - Brest), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM), Lymphocyte B et Auto-immunité (LBAI), Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO), CHRU Brest - Service de Rhumatologie (CHU - BREST - Rhumato), Centre Hospitalier Régional Universitaire de Brest (CHRU Brest), Service de rhumatologie, Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse], Department of Rheumatology, Service de rhumatologie [Bichat], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Investigation Clinique INSERM 1412 (CIC 1412 - BREST), Mécanismes, Conséquences et Modulation de l'Inflammation Ostéo-articulaire, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-AP-HP - Hôpital Bichat - Claude Bernard [Paris]-Université Paris Diderot - Paris 7 (UPD7), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM) |
| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Oncology
Male Pathology MESH: Osteopontin [SDV]Life Sciences [q-bio] Arthritis Rheumatoid MESH: Genotype 0302 clinical medicine Early Rheumatoid Arthritis Immunology and Allergy MESH: Autoantibodies MESH: Genetic Variation MESH: Radiography MESH: Aged 0303 health sciences education.field_of_study MESH: Arthritis Rheumatoid MESH: Middle Aged MESH: Genetic Predisposition to Disease Middle Aged Connective tissue disease MESH: Case-Control Studies [SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system Rheumatoid arthritis Cohort Disease Progression Female MESH: Disease Progression Adult musculoskeletal diseases medicine.medical_specialty MESH: Hand Joints Genotype Hand Joints Immunology Population Rheumatoid Arthritis Peptides Cyclic General Biochemistry Genetics and Molecular Biology MESH: Foot Joints 03 medical and health sciences Rheumatology Gene Polymorphism Internal medicine Foot Joints medicine Humans Genetic Predisposition to Disease education Genotyping MESH: Peptides Cyclic 030304 developmental biology Aged Autoantibodies 030203 arthritis & rheumatology MESH: Humans business.industry Autoantibody Genetic Variation MESH: Adult medicine.disease MESH: Male Minor allele frequency Radiography Case-Control Studies Ant-CCP Osteopontin Gene polymorphism business MESH: Female [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology |
| Zdroj: | Annals of the Rheumatic Diseases Annals of the Rheumatic Diseases, BMJ Publishing Group, 2014, 73 (10), pp.1840-3 Annals of the Rheumatic Diseases, 73(10), 1840-1843 Europe PubMed Central |
| ISSN: | 0003-4967 1468-2060 |
| Popis: | Objective We recently reported an association of the SPP1 rs9138 and rs11439060 functional variants with the risk of rheumatoid arthritis (RA), the association being greater in anti-citrullinated protein autoantibody (ACPA)-negative patients. We hypothesised that SPP1 may contribute to the severity of joint destruction in RA, specifically in the ACPA-negative population. Methods Patients with RA in the ESPOIR cohort underwent genotyping for SPP1 rs9138 and rs11439060. Radiographs of the hands and feet were obtained at the first visit and at 1- and 2-year follow-up. Association analyses were performed by ACPA status. A replication study of the relevant subset of the Leiden Early Arthritis Clinic (EAC) cohort was performed. Results In the ESPOIR cohort (652 patients), rs9138 was significantly associated with radiological progression of joint destruction at 2 years, the association being restricted to 358 ACPA-negative patients (p=0.034). In the replication study with the Leiden EAC cohort (273 ACPA-negative patients), rs4754, which is in complete linkage disequilibrium with rs9138, was significantly associated with joint damage progression in ACPA-negative patients at 2- and 7-year follow-up (p=0.019 and p=0.005, respectively). Combined analysis of the two cohorts revealed a 0.95-fold rate of joint destruction per year per minor allele (p=0.022). Conclusions The SPP1 rs9138 variant contributes to joint damage progression in ACPA-negative RA. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|