PT - JOURNAL ARTICLE AU - Iñigo Rúa-Figueroa AU - Javier Nóvoa AU - María Isabel García-Laorden AU - Celia Erausquin AU - Miguel García-Bello AU - Felipe Rodríguez de Castro AU - Estefanía Herrera-Ramos AU - Soledad Ojeda AU - Juan Carlos Quevedo AU - Félix Francisco AU - Antonio Naranjo AU - Carlos Rodríguez-Lozano AU - Carlos Rodríguez-Gallego TI - Clinical and Immunogenetic Factors Associated with Pneumonia in Patients with Systemic Lupus Erythematosus: A Case-Control Study AID - 10.3899/jrheum.131470 DP - 2014 Sep 01 TA - The Journal of Rheumatology PG - 1801--1807 VI - 41 IP - 9 4099 - http://www.jrheum.org/content/41/9/1801.short 4100 - http://www.jrheum.org/content/41/9/1801.full SO - J Rheumatol2014 Sep 01; 41 AB - Objective. To determine the incidence of pneumonia and associated factors in a single-center systemic lupus erythematosus (SLE) cohort. Methods. We included all our SLE patients [1997 American College of Rheumatology (ACR) criteria] with ≥ 1 pneumonia event, and 196 age and sex-matched SLE controls with no pneumonia events. Cumulative clinical data, weighted Systemic Lupus International Collaborating Clinics/ACR damage index (wSLICC/ACR-DI), comorbidities, and risk factors for pneumonia were retrospectively collected. The standardized incidence ratio (SIR) of pneumonia was estimated. Polymorphisms at genes coding for mannose binding lectin (MBL), MBL-associated serine protease 2, Fc-gamma receptors, and surfactant proteins A1, A2, and D were determined, and their potential association with pneumonia was analyzed. Patients with and without pneumonia were compared using a multivariate logistic regression model for adjustment of pneumonia-associated factors. Results. Thirty-six of 232 patients with SLE had experienced ≥ 1 pneumonia event. SIR for pneumonia was 5.1 (95% CI 3.5–7.4; p < 0.0001). Excluding patients receiving immunosuppressive therapy at the time of pneumonia (13%), associations were found for Katz Severity Index (KSI) (p = 0.016), wSLICC/ACR-DI (p = 0.044), number of SLE criteria (p = 0.005), hospital admissions (p < 0.001), FCGR2A HH genotype (p = 0.03), previous use of immunosuppressive therapy (p = 0.049), cutaneous ulcers (p < 0.001), and vasculitis (p = 0.008) in bivariate analyses. In the multivariate analysis adjusted to previous immunosuppressive treatment, only KSI and FCGR2A HH genotype remained statistically significant (p = 0.05 and p = 0.03, respectively). Conclusion. The incidence of pneumonia in patients with SLE is higher than that in the general population, and particularly high in severe SLE, regardless of immunosuppressive therapy. The HH genetic variant of FCGR2A appears to predispose patients with SLE to pneumonia.