医学
内科学
肺炎
肺炎严重指数
入射(几何)
胃肠病学
免疫学
队列
社区获得性肺炎
光学
物理
作者
Íñigo Rúa‐Figueroa,Javier Nóvoa,M. Isabel García-Laorden,Celia Erausquin,Miguel Ángel García Bello,Felipè Rodríguez de Castro,Estefanía Herrera‐Ramos,Soledad Ojeda,Juan Carlos Quevedo,Félix Francisco,Antonio Naranjo,Carlos Rodríguez‐Lozano,Carlos Rodríguez‐Gallego
标识
DOI:10.3899/jrheum.131470
摘要
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.
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