| Autor: |
Rodríguez-González D; Division of Central Laboratory, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain., García-González M; Division of Rheumatology, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain., Gómez-Bernal F; Division of Central Laboratory, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain., Quevedo-Abeledo JC; Division of Rheumatology, Hospital Doctor Negrín, 35010 Las Palmas de Gran Canaria, Spain., González-Rivero AF; Division of Central Laboratory, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain., Fernández-Cladera Y; Division of Central Laboratory, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain., González-López E; Division of Immunology, Hospital Universitario Marqués de Valdecilla, Instituto de Investigación Valdecilla (IDIVAL), 39011 Santander, Spain., Ocejo-Vinyals JG; Division of Immunology, Hospital Universitario Marqués de Valdecilla, Instituto de Investigación Valdecilla (IDIVAL), 39011 Santander, Spain., Jiménez-Sosa A; Research Unit, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain., González-Toledo B; Fundación Jimenez Díaz School of Nursing, Autonomous University of Madrid, 28040 Madrid, Spain.; Health Research Institute, Fundación Jiménez Díaz, 28040 Madrid, Spain., González-Gay MÁ; Division of Rheumatology, IIS-Fundación Jiménez Díaz, 28040 Madrid, Spain.; Deparment of Internal Medicine, University of Cantabria, 39005 Santander, Spain., Ferraz-Amaro I; Division of Rheumatology, Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain.; Department of Internal Medicine, University of La Laguna (ULL), 38200 Santa Cruz de Tenerife, Spain. |
| Abstrakt: |
The complement (C) system is implicated in the etiopathogenesis of rheumatoid arthritis (RA). However, there is a lack of studies characterizing all three C pathways in RA patients. This study aimed to evaluate the association between an in-depth examination of the C system and RA patient characteristics, focusing on disease activity and the presence of rheumatoid factor and anti-citrullinated protein autoantibodies (ACPA). In a cohort of 430 RA patients, functional assays of the three C pathways (classical, alternative, and lectin) and serum levels of their components were assessed. Components included C1q (classical); factor D and properdin (alternative); lectin (lectin); C1-inhibitor; C2, C4, and C4b (classical and lectin); C3, C3a, and C4b (common); and C5, C5a, and C9 (terminal). A multivariable linear regression analysis showed significant positive correlations between C-reactive protein and C system proteins and functional assays, especially in the terminal and common pathways. Disease activity, measured by scores with or without acute phase reactants, positively correlated with the classical pathway functional test and terminal pathway products. Conversely, rheumatoid factor or ACPA presence was associated with lower classical pathway values and decreased C3a and C4b levels, suggesting complement depletion. In conclusion, RA disease activity increases C molecules and functional complement assays, while rheumatoid factor or ACPA positivity is linked to C consumption. Our study offers a detailed analysis of the complement system's role in RA, potentially guiding the development of more targeted and effective treatment strategies. |
