Unique Changes in the Incidence of Acute Chest Syndrome in Children With Sickle Cell Disease Unravel the Role of Respiratory Pathogens: A Time Series Analysis.

COVID-19 pandemic acute chest syndrome attributable fraction child influenza nonpharmaceutical interventions pneumococcus respiratory pathogens sickle cell disease time series analysis

Journal

Chest
ISSN: 1931-3543
Titre abrégé: Chest
Pays: United States
ID NLM: 0231335

Informations de publication

Date de publication:
05 Aug 2023
Historique:
received: 23 05 2023
revised: 27 07 2023
accepted: 30 07 2023
pubmed: 7 8 2023
medline: 7 8 2023
entrez: 6 8 2023
Statut: aheadofprint

Résumé

Acute chest syndrome (ACS) is a life-threatening complication of sickle cell disease (SCD). Although respiratory pathogens are frequently detected in children with ACS, their respective role in triggering the disease is still unclear. We hypothesized that the incidence of ACS followed the unprecedented population-level changes in respiratory pathogen dynamics after COVID-19-related nonpharmaceutical interventions (NPIs). What is the respective role of respiratory pathogens in ACS epidemiology? This study was an interrupted time series analysis of patient records from a national hospital-based surveillance system. All children aged < 18 years with SCD hospitalized for ACS in France between January 2015 and May 2022 were included. The monthly incidence of ACS per 1,000 children with SCD over time was analyzed by using a quasi-Poisson regression model. The circulation of 12 respiratory pathogens in the general pediatric population over the same period was included in the model to assess the fraction of ACS potentially attributable to each respiratory pathogen. Among the 55,941 hospitalizations of children with SCD, 2,306 episodes of ACS were included (median [interquartile range] age, 9 [5-13] years). A significant decrease was observed in ACS incidence after NPI implementation in March 2020 (-29.5%; 95% CI, -46.8 to -12.2; P = .001) and a significant increase after lifting of the NPIs in April 2021 (24.4%; 95% CI, 7.2 to 41.6; P = .007). Using population-level incidence of several respiratory pathogens, Streptococcus pneumoniae accounted for 30.9% (95% CI, 4.9 to 56.9; P = .02) of ACS incidence over the study period and influenza 6.8% (95% CI, 2.3 to 11.3; P = .004); other respiratory pathogens had only a minor role. NPIs were associated with significant changes in ACS incidence concomitantly with major changes in the circulation of several respiratory pathogens in the general population. This unique epidemiologic situation allowed determination of the contribution of these respiratory pathogens, in particular S pneumoniae and influenza, to the burden of childhood ACS, highlighting the potential benefit of vaccine prevention in this vulnerable population.

Sections du résumé

BACKGROUND BACKGROUND
Acute chest syndrome (ACS) is a life-threatening complication of sickle cell disease (SCD). Although respiratory pathogens are frequently detected in children with ACS, their respective role in triggering the disease is still unclear. We hypothesized that the incidence of ACS followed the unprecedented population-level changes in respiratory pathogen dynamics after COVID-19-related nonpharmaceutical interventions (NPIs).
RESEARCH QUESTION OBJECTIVE
What is the respective role of respiratory pathogens in ACS epidemiology?
STUDY DESIGN AND METHODS METHODS
This study was an interrupted time series analysis of patient records from a national hospital-based surveillance system. All children aged < 18 years with SCD hospitalized for ACS in France between January 2015 and May 2022 were included. The monthly incidence of ACS per 1,000 children with SCD over time was analyzed by using a quasi-Poisson regression model. The circulation of 12 respiratory pathogens in the general pediatric population over the same period was included in the model to assess the fraction of ACS potentially attributable to each respiratory pathogen.
RESULTS RESULTS
Among the 55,941 hospitalizations of children with SCD, 2,306 episodes of ACS were included (median [interquartile range] age, 9 [5-13] years). A significant decrease was observed in ACS incidence after NPI implementation in March 2020 (-29.5%; 95% CI, -46.8 to -12.2; P = .001) and a significant increase after lifting of the NPIs in April 2021 (24.4%; 95% CI, 7.2 to 41.6; P = .007). Using population-level incidence of several respiratory pathogens, Streptococcus pneumoniae accounted for 30.9% (95% CI, 4.9 to 56.9; P = .02) of ACS incidence over the study period and influenza 6.8% (95% CI, 2.3 to 11.3; P = .004); other respiratory pathogens had only a minor role.
INTERPRETATION CONCLUSIONS
NPIs were associated with significant changes in ACS incidence concomitantly with major changes in the circulation of several respiratory pathogens in the general population. This unique epidemiologic situation allowed determination of the contribution of these respiratory pathogens, in particular S pneumoniae and influenza, to the burden of childhood ACS, highlighting the potential benefit of vaccine prevention in this vulnerable population.

Identifiants

pubmed: 37544426
pii: S0012-3692(23)05256-X
doi: 10.1016/j.chest.2023.07.4219
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Financial/Nonfinancial Disclosures The authors have reported to CHEST the following: N. O. reports travel grants from GlaxoSmithKline, Pfizer, and Sanofi. A. R. reports travel grants from Pfizer and AstraZeneca and personal fees from MSD outside the submitted work. A. V. reports personal fees from Sanofi, Moderna, GlaxoSmithKline, and MSD. R. C. reports speaking and lecture fees from Pfizer, Sanofi, GlaxoSmithKline, and MSD; and funding and travel grants from Pfizer. E. V. reports grants from Santé Publique France, Pfizer, and MSD. F. A. reports honoraria from Pfizer, GlaxoSmithKline, MSD, and Sanofi outside the submitted work. None declared (Z. A., Z. V., F. K., A. L., L.-L. P., L. L., A. F., M. C., C. L., F. G., B. K.).

Auteurs

Zein Assad (Z)

Department of General Pediatrics, Pediatric Infectious Disease and Internal Medicine, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; INSERM UMR 1137, Infection, Antimicrobials, Modelling, Evolution (IAME), Paris Cité University, Paris, France. Electronic address: zein.assad@aphp.fr.

Zaba Valtuille (Z)

Centre d'Investigation Clinique, INSERM CIC1426, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; EA7323 Perinatal and Pediatric Pharmacology and Therapeutic Assessment, Paris Cité University, Paris, France.

Alexis Rybak (A)

INSERM UMR 1123, ECEVE, Paris Cité University, Paris, France; Urgences Pédiatriques, Hôpital Trousseau, Assistance Publique-Hôpitaux de Paris, Sorbonne Université, Paris, France; Association Clinique et Thérapeutique Infantile du Val-de-Marne (ACTIV), St Maur-des-Fossés, France.

Florentia Kaguelidou (F)

Centre d'Investigation Clinique, INSERM CIC1426, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; EA7323 Perinatal and Pediatric Pharmacology and Therapeutic Assessment, Paris Cité University, Paris, France.

Andrea Lazzati (A)

Department of General Surgery, Centre Hospitalier Intercommunal de Créteil, Créteil, France.

Emmanuelle Varon (E)

National Reference Center for Pneumococci, Centre de Recherche Clinique et Biologique, Centre Hospitalier Intercommunal de Créteil, Créteil, France.

Luu-Ly Pham (LL)

INSERM UMR 1137, Infection, Antimicrobials, Modelling, Evolution (IAME), Paris Cité University, Paris, France; Department of General Pediatrics, Jean Verdier University Hospital, Assistance Publique-Hôpitaux de Paris, Bondy, France.

Léa Lenglart (L)

INSERM UMR 1137, Infection, Antimicrobials, Modelling, Evolution (IAME), Paris Cité University, Paris, France; Service d'Accueil des Urgences Pédiatriques, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.

Albert Faye (A)

Department of General Pediatrics, Pediatric Infectious Disease and Internal Medicine, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; INSERM UMR 1123, ECEVE, Paris Cité University, Paris, France.

Marion Caseris (M)

Department of General Pediatrics, Pediatric Infectious Disease and Internal Medicine, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.

Robert Cohen (R)

Association Clinique et Thérapeutique Infantile du Val-de-Marne (ACTIV), St Maur-des-Fossés, France; Centre Hospitalier Intercommunal, Research Centre, Université Paris Est, IMRB-GRC GEMINI, Créteil, France.

Corinne Levy (C)

Association Clinique et Thérapeutique Infantile du Val-de-Marne (ACTIV), St Maur-des-Fossés, France; Centre Hospitalier Intercommunal, Research Centre, Université Paris Est, IMRB-GRC GEMINI, Créteil, France.

Astrid Vabret (A)

Department of Virology, Caen University Hospital, Caen, France; Univ Caen Normandie, Univ Rouen Normandie, INSERM UMR 1311, DYNAMICURE, Caen, France.

François Gravey (F)

Univ Caen Normandie, Univ Rouen Normandie, INSERM UMR 1311, DYNAMICURE, Caen, France.

François Angoulvant (F)

Paris Sorbonne University, Centre de Recherche des Cordeliers, INSERM UMRS 1138, Paris, France.

Bérengère Koehl (B)

Department of Child Hematology, Reference Center for Sickle-Cell Disease, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; INSERM UMR S1134, Integrated Biology of Red Blood Cells, Paris Cité University, Paris, France.

Naïm Ouldali (N)

Department of General Pediatrics, Pediatric Infectious Disease and Internal Medicine, Robert Debré University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France; INSERM UMR 1137, Infection, Antimicrobials, Modelling, Evolution (IAME), Paris Cité University, Paris, France; INSERM UMR 1123, ECEVE, Paris Cité University, Paris, France.

Classifications MeSH