Raúl Méndez1, Rosario Menéndez2, Isabel Amara-Elori3, Laura Feced3, Alba Piró3, Paula Ramírez4, Amparo Sempere5, Alicia Ortega6, Jesús F Bermejo-Martín7, Antoni Torres8. 1. Servicio de Neumología, Hospital Universitario y Politécnico La Fe / Instituto de Investigación Sanitaria (IIS) La Fe, Avenida Fernando Abril Martorell 106, 46026 Valencia, Spain; PhD program in Medicine and Translational Research, University of Barcelona, Barcelona, Spain. 2. Servicio de Neumología, Hospital Universitario y Politécnico La Fe / Instituto de Investigación Sanitaria (IIS) La Fe, Avenida Fernando Abril Martorell 106, 46026 Valencia, Spain; Center for Biomedical Research Network in Respiratory Diseases (CIBERES, CB06/06/0028), Madrid, Spain. Electronic address: rosmenend@gmail.com. 3. Servicio de Neumología, Hospital Universitario y Politécnico La Fe / Instituto de Investigación Sanitaria (IIS) La Fe, Avenida Fernando Abril Martorell 106, 46026 Valencia, Spain. 4. Center for Biomedical Research Network in Respiratory Diseases (CIBERES, CB06/06/0028), Madrid, Spain; Intensive Care Unit, Hospital Universitario y Politécnico La Fe / IIS La Fe, Valencia, Spain. 5. Hematology Department, Hematology Research Group, Hospital Universitario y Politécnico La Fe / IIS La Fe, Valencia, Spain; Center for Biomedical Research Network in Cancer (CIBERONC), Madrid, Spain. 6. Group for Biomedical Research in Sepsis (Bio∙Sepsis), Hospital Clínico Universitario de Valladolid / Instituto de Estudios de Ciencias de la Salud de Castilla Y León (IECSCYL), Valladolid, Spain. 7. Center for Biomedical Research Network in Respiratory Diseases (CIBERES, CB06/06/0028), Madrid, Spain; Group for Biomedical Research in Sepsis (Bio∙Sepsis), Hospital Clínico Universitario de Valladolid / Instituto de Estudios de Ciencias de la Salud de Castilla Y León (IECSCYL), Valladolid, Spain. 8. Center for Biomedical Research Network in Respiratory Diseases (CIBERES, CB06/06/0028), Madrid, Spain; Pneumology Department, Hospital Clínic / Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Abstract
OBJECTIVES: Lymphopenic (<724 lymphocytes/µL) community-acquired pneumonia (L-CAP) is an immunophenotype with an increased risk of mortality. We aimed to characterize the l-CAP immunophenotype though lymphocyte subsets and the inflammatory response and its relationship with severity at presentation and outcome. METHODS: Prospective study of 217 immunocompetent patients hospitalized for CAP. Lymphocyte subsets (CD4+, CD8+, CD19+, and natural killer [NK] cells) and inflammatory cytokines were analyzed on days 1 and 4, and immunoglobulin subclasses were analyzed on day 1 in a nested group. RESULTS: 39% of patients showed l-CAP, with decreased levels of all lymphocyte subsets with a partial recovery of CD4+ and CD8+ cells by day 4. l-CAP patients exhibited higher initial severity and systemic levels of interleukin (IL)-8, IL-10, granulocyte colony-stimulating factor, and monocyte chemoattractant protein-1. Initial IgG2 levels were lower in patients with <724 lymphocytes/µL and positively correlated with ALC, CD4+, and CD19+ cell counts. Low CD4+ counts (<129 cells/µL) also independently predicted 30-day mortality after adjusting for age, gender, and the CURB-65 score. CONCLUSIONS: l-CAP is characterized by CD4+ depletion, a higher inflammatory response, and low IgG2 levels that correlated with greater severity at presentation and worse prognosis. l-CAP is an immunophenotype useful for rapidly recognizing severity.
OBJECTIVES:Lymphopenic (<724 lymphocytes/µL) community-acquired pneumonia (L-CAP) is an immunophenotype with an increased risk of mortality. We aimed to characterize the l-CAP immunophenotype though lymphocyte subsets and the inflammatory response and its relationship with severity at presentation and outcome. METHODS: Prospective study of 217 immunocompetent patients hospitalized for CAP. Lymphocyte subsets (CD4+, CD8+, CD19+, and natural killer [NK] cells) and inflammatory cytokines were analyzed on days 1 and 4, and immunoglobulin subclasses were analyzed on day 1 in a nested group. RESULTS: 39% of patients showed l-CAP, with decreased levels of all lymphocyte subsets with a partial recovery of CD4+ and CD8+ cells by day 4. l-CAPpatients exhibited higher initial severity and systemic levels of interleukin (IL)-8, IL-10, granulocyte colony-stimulating factor, and monocyte chemoattractant protein-1. Initial IgG2 levels were lower in patients with <724 lymphocytes/µL and positively correlated with ALC, CD4+, and CD19+ cell counts. Low CD4+ counts (<129 cells/µL) also independently predicted 30-day mortality after adjusting for age, gender, and the CURB-65 score. CONCLUSIONS:l-CAP is characterized by CD4+ depletion, a higher inflammatory response, and low IgG2 levels that correlated with greater severity at presentation and worse prognosis. l-CAP is an immunophenotype useful for rapidly recognizing severity.
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